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Storey

The Chicken Health Handbook

I his must-have reference for the small flock owner covers theproblems and diseases common to chickens of a l l breeds and allages. Generously illustrated, The Chicken Health Handbookteaches you how to:

V hatch healthy chicksV provide proper nutritionV fight parasitesV spot diseases and infections in their early stagesV protect flocks from predatorsV build safe houses and yards

Practical charts in The Chicken Health Handbook help pin-point common symptoms and causes of disease. An extensive

alphabetic listing of diseases provides quick access to treatmentsand remedies for everything from poor egg production to crookedtoe syndrome.A first-rute guide . . . Flawless.

- AMERICAN LIBRARY ASSOCIATION

If you don't have any bonks on chickens, thisis the only one you need. If you have u book-shelf full of books, you still need litis one.

- POULTRY PRKSS

A small-scale farmer in Tennessee, GailDamerow lias written numerous articles 011 rais-ing chickens. She is the editor o(Rural Heritagemagazine and the author of seven books, includ-

ISBN 978-0-88266-611-2

ing Chickens in Your Backyard, Ducks and Geesein Your Backyard, and Your Chickens: A KidsGuide to Raising and She/wing.

9 ,PETS & PET CARE

Storey Publishingwww.storey.com

S19.95 US

978088266611251995Z<

Gail Damerow

P

WStorey Publishing

The m ission of Storey Publishing is to serve our customers bypublishing practical information that encourages

personal independence in harmony with the environment.

Edited by Amanda R. HaarCover design by Meredith MakerText design and production by Cynthia McFar landCover photograph ©John Colivell from Grant Heilmann PhotographyL ine drawings by Elayne Sears except chapter opener line art

and diagramart on pages 6 and 216 by Cynthia

McFarlandIndexed by Gail Damerow

© 1994 by Gail Damerow

All rights reserved. No part of this book may be reproduced without written per-mission from the publisher, except by a reviewer who may quote brief passages orreproduce illustrations in a review with appropriate credits; nor may any part ofthis book be reproduced, stored in a retrieval system, or transmitted in any formor by any means — electronic, mechanical, photocopying, recording, or other— without written permission from the publisher.

The information in this book is true and complete to the best of our knowledge.All recommendations are made without guarantee on the part of the author orStorey Publishing. The author and publisher disclaim any liability in

connectionwith the use of this information. For additional information, please contact StoreyPublishing, 210 MASS MoCA Way, North Adams, MA 01247.

Storey books are available for special premium and promotional uses and forcustomized editions. For further information, please call 1-800-793-9396.

Printed in the United States by Versa PressJO 29 28

Library of Congress Cataloging-in-Publication DataDamerow, Gail.

Chicken health handbook / Gail Damerowp. cm.

Includes bibliographical references (p. ) and index.ISBN 978-0-88266-611-2 (pbk.)

1. Chickens — Diseases. 2. Chickens — Health. 3. ChickensSF99S.D33 1994636.5'089—dc20

— Parasites. I. Title.

93-33385CIP

Charts...............................................................................vForeword by Jeanne Smith, D.V.M...................................viiIntroduction......................................................................1Chicken Health.................................................................3Health and Nutrition.......................................................26Anatomy of a Chicken....................................................43External Parasites...........................................................58Internal Parasites: Worms...............................................77Internal Parasites: Protozoa............................................97Infectious Diseases.......................................................107Environment-Related Problems....................................132Diagnostic Guides.........................................................147Postmortem Examination.............................................165Therapy........................................................................181Enhancing Immunity.....................................................197Incubation and Brooding..............................................208Chickens and Human Health........................................230Diseases and Disorders................................................244Glossary.......................................................................315Suppliers......................................................................324State Poultry Pathology Laboratories...........................325

Recommended Reading...............................................331Index............................................................................333

CHAPTER 1 CHICKEN HEALTH1- 1..............................................................Diseases Spread by Carriers

81 -2 Minimum Space Requirements........................................................151 -3 Survival Ability of Disease-Causing Organisms...............................181 -4 Chemical Disinfectants....................................................................20

Chapter 2 HEALTH AND NUTRITION2- 1............................................................Vitamin Benefits and Sources

302-2 Nutritional Diseases and Disorders...................................................332-3 Nutritional Symptoms.......................................................................342-4 Feeding Schedule.............................................................................362-5 Feeder Space....................................................................................372-6 Restricted Feeding Schedule for Pullets...........................................382-7 Diseases Affecting Water Consumption ...........................................392-8 Diseases Related to Drinking Water.................................................392-9 Environmental Temperature and Water Consumption.....................402-10 Signs of Water Deprivation.............................................................412- 11.....................................Waterer Space and Minimum Water Needs

41

Chapter 3 ANATOMY OF A CHICKEN3- 1................................................Diseases Involving the Cloacal Bursa

453-2 Air Sacs.............................................................................................483- 3.......................................Disorders by the Body System They Affect

56

Chapter 4 EXTERNAL PARASITES4- 1.............................................Diseases Spread by External Parasites

594-2 Lice...................................................................................................654-3 Mites.................................................................................................684- 4............................................................................................Chiggers

72

Chapter 5 INTERNAL PARASITES: WORMS5- 1.....................................................................................Roundworms

865-2 Tapeworms.......................................................................................905- 3................................................................................................Flukes

92

Chapter 6 INTERNAL PARASITES: PROTOZOA6- 1...........................................................................Protozoan Diseases

976-2 Coccidia Affecting Chickens............................................................1006-3 Drugs Used to Treat Coccidiosis.....................................................103

v

Chapter 7 INFECTIOUS DISEASES7-1 Bacterial Diseases..........................................................................1107-2 Viruses Infecting Chickens.............................................................1207-3 Forms of Newcastle Disease...........................................................1257-4 Forms of Marek's Disease...............................................................1277-5 Differences Between Lymphoid Leukosis and Marek's Disease.....1287- 6................................................................................FungaJ Diseases

1 30

Chapter8 ENVIRONMENT-RELATED PROBLEMS8- 1...............................................................................Fungal Poisoning

1418-2 Toxic Plants....................................................................................1428-3 Rodent Droppings.... ....................................................-................1438- 4......................................................................................Rodenticides

146

Chapters DIAGNOSTIC GUIDES9- 1......................................................................................Flock History

1489-2 Signs of Health ..............................................................................1489-3 Diseases Causing a Change in Droppings......................................1529-4 Diseases Interfering with Movement..............................................1549-5 Diseases and Conditions Affecting Egg Production........................1569-6 Diseases Causing Breathing Difficulties.........................................1589-7 Diseases Causing Discoloration......................................................1599-8 Diseases Causing Off Odors...........................................................1609-9 Diseases Affecting the Eyes...........................................................1619-10 Diseases Causing Sores in the Mouth...........................................1629-11 Diseases Causing Temperature Changes.....................................1629-12 Diseases Causing a High Rate of Death.......................................1639- 13.........................................Diseases Causing Sudden Death ..........

164

Chapter 10 POSTMORTEM EXAMINATION10- 1.........................................................................Postmortem Findings

17410-2 Inflamed Conditions......................................................................17910- 3............................................................Nutritionally Related Findings

180

CHAPTER 11 THERAPY11- 1..........................................................................Reportable Diseases

196Chapter 12 ENHANCING IMMUNITY

12- 1..........................................................................Vaccination Methods205

Chapter 13 INCUBATION AND BROODING

vi

13- 1................................................Nutrition-Related Hatching Problems217

13-2 Incubation Trouble-Shooti ng.......................................................21813- 3...........................................................Nutritional Problems in Chicks

228

Chapter 14 CHICKENS AND HUMAN HEALTH14- 1......................................................Poultry-Related Human Diseases

23114-2 Food-Borne Bacteria.......................................................................238

14-3 Bacterial Food Poisoning Quick-Check..........................................240

vii

ForewordIN MY VETERINARY PRACTICE I work with many poultry fanciers and backyardpoultry farmers. I am often asked what books I could recommend to help themlearn better management and gain a better understanding of the diseases thatmay affect their birds. I have been unable to help them much with their requests,as most of the texts on avian diseases are written for veterinarians, of limited use-fulness to the layperson. Very few books are available for the fancier, and thosethat I have seen are generally incomplete and not particularly accurate.

Therefore, I am delighted to see this publication being made available to thepoultry fancier. Gail Damerow has covered the topic of small-flock poultry healthmanagement very completely and competently. The information is presentedaccurately and in enough detail to give the fancier a full understanding of the dis-eases, their prevention and treatments. Yet this is done in an easily understoodmanner through careful attention to definitions and explanations. It is not an easytask to convert scientific information that veterinarians study for years to under-stand into useful, management-bottom-line information for the average back-yard poultry giower. I believe Ms. Damerow has accomplished this in her book.

Ms. Damerow has also presented her information in a quite accessible formatfor the fancier. She not only describes each disorder as a distinct entity, which canbe looked up by the fancier who has just received a diagnosis and wants to learnmore about the disease, but she also has provided a section arranged by clinicalsigns. The fancier, seeing certain clinical signs in the flock, can go to the

viii

book andlook up what the possible causes are. Both of these approaches will have theirusefulness for the fancier.

Prevention of disease through good management is essential when raisingpoultry, especially small flocks of poultry, which are often not vaccinated for manyof the diseases that commercial poultry are, which often travel to and from shows,and which are maintained in multi-age facilities. Also, the generally low monetaryvalue of individual birds makes costs of diagnosis and treatments impractical inmany cases. Having a book such as this which outlines good disease preventionstrategies, as well as disease management strategies should problems occur, is avaluable asset to the poultry fancier.

I believe the best use of this book is to read it through for the disease preven-tion management information whether you are having disease problems in yourbirds or not. Implement whatever management practices you are not already us-ing. Then keep the book handy as a reference if you see a problem pop up in yourflock.

Jeanne Smith, D.V.M.Avian Health Services

3220 Quail Drive, Placerville, CA 95667

ix

Introduction

THIS BOOK WAS BORN out of years of frustration in trying to deal withchicken diseases and not being able to find a clearly understandable, in-depthsource of information. Books diat are easy to understand are usually not com-plete — often failing to contain the very information needed most. On theother hand, comprehensive books rarely make sense to the non-specialist.Making matters worse, most printed information is geared toward operators oflarge commercial flocks, who deal with quite a different set of problems fromthose experienced by small flock owners.

Since I couldn't find the book I needed, after years of experience raisingchickens I decided to write it. I've tried to include all the i nformation necessaryto keep a small (lock healthy, while avoiding technical details that have nopractical application (do you really need to know which bacteria are gram-negative, polar-staining, and non-motile?).

1 can't promise to have described every conceivable problem your chick-ens might experience, but I've covered all the common problems and manyless common ones you'll likely never see but will surely be interested in, if oneof diem turns up in your flock.

Years ago, when I was secretary of the Pacific Poultry Breeders Associationand was responsible for putting out the organization's newsletter, I was ac-cused of placing too much emphasis on diseases. Complainers grumbled

1

2 THF. CHICKEN HEALTH HANDBOOK

thatchicken-keepers (especially novices) might get the idea that raising chickensinvolves a constant battle with diseases.

Those complaints haunted me as I wrote this book, so I wish to make clearthat my aim is not to discourage you from keeping chickens. It is, rather, tohelp you line tune your management practices so you can avoid diseases, andto increase your disease awareness so you can recognize any problem thatmight occur and take action before the problem gets out of hand.

How you approach injury or disease in your flock depends a great deal onyour purpose in keeping chickens, whether it is to enjoy healthful meat andeggs, to have fun showing your birds, or to make money selling homegrownmeat or eggs. This book provides information pertaining to all three situations.It is not for the commercial grower who takes an impersonal view of individual

birds, who crowds them and thereby induces stress and disease, who medi-cates them to the max, and who breeds for ever-greater growth or productionat the expense of disease resistance. (Diseases found primarily in commercialflocks are described here, however, so you can watch out for them if you live ina major poultry-producing area.)

I wish to diank Randy Holliman of Hoechst-Roussel Agri-Vet Company inMurfreesboro, Tennessee, for helping me learn how to do a home fecal test; L.Dwight Schwartz, D.V.M., avian health consultant with Avicon, Inc. inOkemos, Michigan, for reviewing my chapter on "Diseases and Disorders" andhelping fill in the gaps; Arthur A. Bickford, D.V.M., of the California VeterinaryLaboratory in Turlock for his thorough review and numerous helpful sugges-tions; and Jeanne Smith, D.V.M., of Avian Health Services in Placerville,California, for her technical review and wonderful insights into die problemsof small-flock ownership.

3


Chicken Health

DURING THE PAST CENTURY, most of the serious diseases that once plaguedpoultry' keepers have been brought under control. It wasn't that long ago, forexample, that we discovered viruses and invented vaccines against them, orthat we first began to understand the life cycles of internal parasites and werefinally able to control them.

While we have been busy learning to control old diseases, new ones haveappeared. Some were always there, to be discovered as technology improved.Others have popped up out of the blue. Still others have been caused by theway modern poultry flocks are managed. So, while technology gives us newways to fight diseases, it also gives us new diseases to fight.

What Is Disease?Disease is defined as a departure from health and includes any condition thatimpairs normal body functions. Disease results from a combination of indirectcauses (called "stress") that reduce resistance and direct causes that

producethe disease.

Direct causes of disease can be divided into two categories: infectious andnon-infectious. Infectious diseases result from invasion of the body by anotherliving organism — bacteria, viruses, fungi, protozoa, and a variety of internaland external parasites. Non-infectious diseases are caused by nutritionalproblems (deficiency or excess), chemical poisons, traumatic injury, or evenexcessive stress.

5


Technically speaking, all infectious diseases are parasitic, and all parasiticinvasions are infectious. By convention, the word "parasite" is often used toidentify infectious diseases caused byanimal forms, most of which can beseen with the naked eye (worms, lice,mites, and the like).The word "infection" is generally re-

served for invasion by other forms,which all happen to be microscopic(bacteria, virus, fungi, etc.). The dis-tinction breaks down, however, in thecase of protozoa, which are both ani-mal forms and microscopic. (In thisbook, protozoa are grouped with the

other animal forms.)Regardless of a disease's cause, be-

fore you can effectively control it, youmust know how diseases in general areintroduced and how they spread.

BACTERIA

Microorganisms causing infectiousdisease

CHICKEN HEALTH 7

Reservoirs of InfectionDiseases are introduced from reservoirs of infection, defined as any

sourceor site where a disease-causing organism survives or multiplies and fromwhich it can be transferred to a host — in this case, a chicken. A reservoir ofinfection may be animate or inanimate.


Animate or living reservoirs include:• chickens and other domestic poultry• exotic and cage birds• wild birds• wild animals (including rodents)• livestock• household pets• humans• earthworms, snails, and slugs• arthropods (fleas, mites, ticks, lice, and mosquitoes that bite; sow bugs,crickets, and grasshoppers that chickens eat)Some disease-causing organisms, such as the infectious bronchitis

virus,are species specific for chickens, meaning they affect only chickens. Others areshared among different kinds of poultry, such as the avian reovirus, which in-fects both chickens and turkeys. Some microbes are harmless to one type offowl but devastating to others, such as the Marek's disease virus that's com-mon and harmless in turkeys but potentially deadly to chickens. Somemicrobes, including Salmonella bacteria, infect a wide variety of vertebratesincluding humans. A few infectious organisms spend part of their life cyclesliving in arthropods that parasitize chickens or that spread disease to chickensthrough their bites.

A chicken may serve as its own reservoir of infection, as occurs when adisease is caused by an organism the chicken normally carries on or in its body.Examples are streptococci and Pasteurello bacteria, both of which infect a birdafter its resistance has been reduced by some other cause. Dead chickens, im-properly disposed of, can also serve as reservoirs of infection, if their bodies arepecked by susceptible chickens.

CHICKEN HEALTH 9

Inanimate reservoirs of infection include:• feed containing fungi or bacteria• water, usually stagnant and rich in organic matter, in which bacteria,fungi, or protozoa thrive• litter, soil, and dust harboring spore-bearing organisms that producedisease when they get into a chicken's tissue, often through a wound• so-called "fomites" — articles that can be contaminated by disease-causing organisms. Examples of fomites include a crate used forcarrying chickens, an incubator used for hatching chicks, or a brooderin which chicks are raised. A fomite can be either a reservoir of infec-tion or merely a vehicle that serves as a means of spreading infectiousorganisms from one place to another.


How Diseases SpreadOnce a disease has been introduced, it may spread from one chicken

toanother in two ways:

• vertically — from an infected hen to her chicks by means of hatchingeggs (or, in the case of some viruses, from an infected cock throughsemen fertilizing the eggs);• horizontally — from one bird to another through direct or indirectcontact.Direct contact occurs when an infected bird and a susceptible bird

peck,preen, or mate one another. Diseases that spread through contact with theskin of an infected bird include pox and influenza (caused by viruses) and sta-phylococcal and streptococcal infections (caused by opportunisdc bacteria).Staph and strep infections also spread through direct mucus-to-mucus con-tact during mating.

Indirect contact occurs by means of a vehicle (sometimes called a"mechanical vector"). A vehicle is anything, living or otherwise, capable oftransporting disease-causing organisms from one place to another. Like reser-voirs of infection, vehicles can be either animate or inanimate.

HORIZONTAL TRANSMISSION

1

VERTICALTRANSMISSION

Infectedcock or hen

Susceptiblecock or hen

Infected cock or hen

Infected INDIRECT Susceptiblecock or hen CONTACT cock or hen

CHICKEN HEALTH 11

Animate vehicles include:• wild birds, rodents, household pets, and other animals that carryinfectious organisms on their feet, feathers, or fur (as distinct fromdiseased animals that spread infection through their saliva, droppings,or urine);• flies and other arthropods tiiat carry disease on their feet or bodies (asdistinct from infected arthropods that spread disease by injectingcontaminated saliva);• humans who carry disease-causing organisms on their clothing, shoes,skin, or hair, including fanciers who visit one another, vaccinationcrews that travel from place to place, meter readers, electricians,plumbers, and feed delivery personnel.

Inanimate vehicles include:• shed skin, feathers, droppings, broken eggs, and other debris frominfected birds;• feed and drinking water contaminated by body discharges frominfected birds, including undrained puddles and streams that run pastone flock and then another;• air, which wafts dust, fluff, fine bits of dried droppings, and droplets ofrespiratory' moisture expelled by breathing, sneezing, or coughing(most airborne infections do not spread far);• needles that contaminate the blood of susceptible chickens duringflockwide vaccination of infected and susceptible birds alike;• used equipment, egg cartons, waterers, feeders, feed sacks, tires (ofcars, trucks, or wheelbarrows), and other fomites to which bodydischarges containing disease-causing microbes may cling, to betransported for hundreds of miles.

CarriersMany diseases are spread by earners. A carrier is a bird that does not

showsymptoms of a disease, yet harbors the organism that causes the disease. Car-riers may be active or passive. An active carrier once had symptoms of thedisease but has since recovered. A passive carrier never developed


symptoms.Whether active or passive, a carrier sheds and spreads disease-causing or-ganisms.

Diseases that produce carriers usually are not worth curing. You can cure abird of infectious coryza, for instance, but you have no way of knowing if thebird will become a carrier and spread the disease to susceptible birds in diefuture.

The older a bird is, the more exposure it has had to disease-causing organ-

CHICKEN HEALTH 13

isms, and die more likely it is to be a carrier. Since growing and adult birdscarry levels of microbes that chicks and young birds can't resist, birds of vari-ous ages should never be mixed together.

CHART 1 -1Diseases Spread by Carriers

Disease Cause Incidence

Air-sac disease bacteria commonArizonosis bacteria rareBlackhead protozoa rareBluecomb unknown rareCampylobacieriosis bacteria commonCanker protozoa rareChlamydiosis bacteria rareCholera bacteria not

commonChronic respiratory disease

bacteria common

Erysipelas bacteria rareInfectious bronchitis virus commonInfectious coryza bacteria commonInfectious laryngotracheitis

virus common

Infectious synovitis bacteria not common

Influenza virus rareLeucocytozoonosis protozoa rareListeriosis bacteria rareLymphoid leukosis virus commonMarek's disease virus commonNewcastle virus commonNewcastle (exotic) virus rareParasites worms very

commonParatyphoid bacteria commonPox virus common


Pullorum bacteria rareThrush fungus commonTyphoid bacteria rareUlcerative enteritis bacteria common

CHICKEN HEALTH 15

Biosecurity"Biosecurity" is the latest buzzword in the world of poultry health. It meansprotecting your flock from infectious diseases and it encompasses any precau-tion you take to prevent diseases from entering or surviving in your yard.

Different sectors of the poultry industry place emphasis on differentbiosecurity measures. The USDA favors all-in, all-out management, whichworks fine for commercial broiler and layer operations, but not for an ongoingbackyard flock. Manufacturers of pharmaceuticals promote (lie use of antibi-otics and other drugs as a means of controlling disease, but the use of drugs fornon-medical purposes has serious drawbacks in commercial and backyardflocks alike.

No single biosecurity measure provides the perfect answer to preventingdisease. Instead, protect your flock with a well-thought-out program of inter-related precautions, thoroughly grounded in old-fashioned common sense.As part of your common sense biosecurity program:

• keep a flock history• start with good foundation stock• maintain a closed flock• breed for resistance• medicate only as necessary• provide a sound environment• practice good sanitation• minimize stress• feed a balanced ration

Flock HistoryA flock history is basically a diary that includes anything and

everydiingpertaining to your flock. Start it the moment you acquire your first birds, not-ing the date (or date of hatch — if you purchase by mail, it will be on theshipping carton), source, strain (if applicable), anything the seller tells youabout the birds' past history, and any health certificates that come with die birds.


Document your feeding and management practices and any changes youmake, including vaccinations you give and medications you use. Write thingsdown as you go along. It may seem like a time-consuming chore, but it's a loteasier than trying to reconstruct events later if you need the information tohelp trace a health problem.

The "Flock History" chart 011 page 148 lists additional information to in-clude in your flock history.

CHICKEN HEALTH 17

Foundation StockIt's difficult to maintain a healthy flock unless you start out witii

healthystock. The best way to make sure the birds are healthy is to purchase locally, soyou can see whether or not they come from a healthful environment. You canthen ask the seller, eye to eye, about the birds' ages and healdi history, and youcan see for yourself if any of the seller's birds have symptoms of diseases thatmight be carried by the birds you plan to buy.

You'll have the least chance of getting diseased birds if you start with newlyhatched chicks. The older the bird, the more disease problems it has been ex-posed to. If you do purchase older birds, take time to check their appearance.Make sure they have glossy plumage, look perky and active, and don't showany signs of stress behavior.

Flocks enrolled in the National Poultry Improvement Plan (NPIP) are cer-tified to be free of pullorum and typhoid. Some are also free of mycoplasmosis.(Information on how to obtain the latest NPIP directory is offered in the ap-pendix.) Unfortunately, you may not find an NPIP member who has the kindof birds you want.

Don't buy birds if you are not totally satisfied with their background interms of genetics, management, sanitation, or health history. Above all, avoidbirds from live-bird auctions, flea markets, wheeler-dealers, traders,uncertified hatcheries, and any other source where birds are brought togetherfrom far-flung flocks.

Closed FlockEach llock is exposed to a unique set of disease-causing organisms, so

thateach develops its own distinct set of immunities. Birds from two healthy


flocks can therefore give each other diseases for which the others have nodefenses.

Once your flock is established, the best way to avoid diseases is to keep aclosed flock. Keeping a closed flock means avoiding direct or indirect contactwith other birds. Complete avoidance isn't always possible, but knowing thedangers helps keep them to a minimum.Maintaining a closed flock means you don't:

• mix birds from various sources• bring in new birds• return a bird to your property' once it's been elsewhere• visit other llocks• let owners of other llocks visit yours• borrow or lend equipment

CHICKEN HEALTH 19

♦hatch eggs from other flocks• allow wild birds free access toyour yardUnfortunately for biosecurity, visit-ing other flocks is part of the fun ofhaving chickens. If you do visit otherflocks, slip plastic grocery bags over yourshoes and tie the handles around yourankles. When the visit is over, seal dietwo bags in a third bag for disposal. Ifother flock owners visit you, ask them todo the same. You may feel foolish wear-ing plastic bags on your feet, but you'llfeel even more foolish if you spread a dis-ease to someone else's birds or bring adisease home to your flock.

Trading and showing birds are otherfun activities that breach biosecurity. Al-though diseases are more likely to be spread by trading than by showing,occasionally a highly contagious disease (most often infectious laryngo-tracheitis) does make the show rounds. To be on the safe side, isolate anyreturning show bird or incoming new bird with two or three sacrificial cullsfrom your flock. If your old chickens remain healthy after about a month,chances are good the incoming chicken is not a carrier.

Breeding for ResistanceOld poultry books make frequent references to "constitutional vigor."

Theconcept is quite simple: in every flock some individuals are less affected bydiseases than otiiers. Susceptible birds get sick or die when exposed to a dis-ease. Resistant birds (those with "constitutional vigor") get mildly sick andrecover quickly or don't get ill at all.

Developing your Hock's genetic resistance means breeding only thosebirds that are less affected by disease, so you'll raise more like them. The re-mainder should be culled. In this context, cull means kill — it does not meanpassing on your problem birds to someone else.


Some poultry specialists take the position that small-flock owners shouldpurchase new stock each year and that raising chicks from your own breederflock only promotes disease. Quite the contrary will be true, //"you take care tocull sick birds so that your flock gradually develops genetic resistance. Fred P.Jeffrey (backyard fancier, retired professor of poultry science, and author of

Excluding Wild Birds

Wild birds are seriously endan-gered due to the cutting downof forests, draining ofwetlands,and other disturbances to theirnatural environment. Insteadof trapping or poisoning wildbirds to keep them away fromyour flock, cover your run withwire or plastic mesh. If yourchickens are range fed, so thatan overhead cover is impracti-cal, place their feeders indoorsso spilled grain won't attractwild birds.

CHICKEN HEALTH 21

Chicken Diseases) advocates die rigid culling of all snifflers, droopers, featherrufflers, poor eaters, and pale-headed birds to be sure they don't reproducetheir kind.

Guidelines on Breeding for Besistance• Keep a minimum breeding flockof about fifty birds, so you'll have

the leewayto cull vigorously and still maintain a viable flock.

• Use breeders that are at least two years old, which opposes the conventionalwisdom that the older the bird, the more diseases it has been exposed to andthe less healthy it is likely to be. Chicks hatched from survivors of diseaseexposure are particularly hearty and may carry maternal antibodies thatgive them further immunity. (Be sure that the disease cannot be egg-transinitted from survivor-carriers to their chicks.)

• "Progeny test" or evaluate your breeders based on (he performance of theiroffspring. Progeny testing requires pedigreeing your birds; in other words,you must know exactly which cock and hen produced each chick (for ideason how to keep track of chicks, see "Chick Identification," page 221). Forprogeny testing, Jeffrey suggests this criterion: if the majority of progenyfrom a particular mating live for 1 x/z years, keep the parents in your breederflock; if the majority of progeny do not survive that long, cull the parents andthe remaining progeny.

• Find indicators or factors known to be related to susceptibility or resistanceto diseases prevalen l in your area. Some indicators can be identified throughblood typing, a potentially impractical, expensive, and time-


consumingpractice. Other indicators are more accessible to the owner of a small flock.Forexample, resistance to pullorum is associated with a higher than normalbody temperature in chicks during their first six days of life.

• Give your flock a leg up on resistance by starting with a breed or strain thatalready has some natural resistance to the diseases and parasites they willencounter in your area. Leghorns and other light breeds, for example, aremore resistant to pullorum than Rocks, Reds, and other heavy breeds; RhodeIsland Reds are more resistant to worms than White Leghorns.

Breeding for genetic resistance does have its down side: your birds candevelop resistance only to diseases present in your yard. If a new disease isintroduced, your chickens may have no defenses against it. Since no flock canbe exposed to all possible diseases, no flock can be immune to all possible dis-eases. Even if you breed for genetic resistance, you must still take care not tointroduce new diseases.

Another aspect to breeding for resistance is that disease-causing organ-isms are likely to evolve right along with your resistant strain of birds. These

CHICKEN HEALTH 23

evolving new forms of bacteria and viruses make breeding for resistance anever-ending process.Medication Schedule

Using drugs casually, rather than controlling disease through proper man-agement, will only increase your problems and your costs. Instead, work out adisease prevention program based on the problems prevalent in your area.Vaccinate against serious diseases your flock is likely to be exposed to, espe-cially epidemic tremor, infectious bronchitis, infectious bursal disease, andMarek's disease. Pay attention to your flock and know what to look for, so if aproblem does occur you'll be ready to treat it properly and promptly.

Sound EnvironmentThe way you house your chickens influences their state of health.

Poultryhousing falls into four basic categories:

• cage confinement — common for show birds, pedigreed breeders, andlarge, mechanized laying flocks

• confinement housing — common for broilers, breeder flocks, andfloor-managed layers

• free range — favored for backyard laying flocks and range-fed or so-called "organic" meat birds

• yard and coop — preferred for backyard flocks in the suburbs andother areas where space is limited

Commercial flocks are confined indoors, in cages or on the floor, for sev-eral reasons: lighting can be strictly controlled, air can be filtered, and diseasesthat are spread by flying insects and wild birds can be excluded. While con-fined flocks are protected from some diseases, as a trade-off diey incur


otherhealth problems due to lack of sunshine, fresh air, and activity. In addition, if acontagious disease does manage to get in, it spreads like wildfire.

No matter how you choose to house your chickens, they need protectionfrom cold, heat, rain, and wind. A sound fence protects them from four-footedpredators; a covered yard protects them from flying predators. The yard or penshould be free of junk and weeds to discourage mice and rats.

The single most important feature of any chicken house is ease of clean-ing. If cleanup is a hassle, you won't do it as often as you ought. The tighter theconstruction, the easier cleaning is and the fewer cracks and crevices there willbe where pathogens and parasites can hide.

Smooth surfaces are easier to clean than rough or porous surfaces. Old-time poultry keepers used to spray crankcase oil along the bottoms of walls

CHICKEN HEALTH 25

and on wood and cement floors, to make these surfaces less penetrable andtherefore easier to clean. The practice has the additional advantage of control-ling roundworms, as well as common insects, but it has the disadvantage ofcreating a fire hazard in wood structures.Floors. Flooring can be one of four basic types:

• A dirt floor is simple and cheap, and it keeps birds cool in warmweather. Its disadvantages are that it draws heat in cold weather, doesnot exclude burrowing rodents, and cannot be effectively cleaned.

• A wood floor invariably has cracks that get packed with tilth, and mostare built too close to the ground, providing a shallow air space thatinvites invasion by rodents.

• Droppings boards made of wood battens or welded wire have theadvantage of allowing droppings to fall through where chickens can'tpick in them. Like a wood floor, droppings boards must be placed highenough to discourage rodents.

• Concrete, if well finished, is the most expensive type of flooring, butrequires minimal repair and upkeep, is easy to clean, and discouragesrodents.

Floor Space. Crowded conditions get filthy fast, reduce the flow of fresh air,and cause stress — all inducements to disease. The minimum floor space re-quirements, including those listed inthe accompanying chart, may needadjustment to suit your specificmanagement practices.

To keep chickens evenly spreadover the available space, use severalfeeders and waterers and spread themaround in different locations. In ex-tremely cold weather conditions,provide heat to prevent huddling.


Litter management. When chickensare kept on a flooring other than drop-pings boards, use litter to absorbdroppings and moisture expelled bythe flock. For chicks, use 3 inches (7.5cm) or more of clean litter that's absor-bent, non-toxic, free of mold, and hasparticles too large to be eaten. For adultbirds, litter should be at least 8 inches(20 cm) deep. Dry pine shavings make

RoostsSince droppings tend to accu-mulate where chickens perch atnight, roosts should be placedover wooden battens or weldedwire droppings boards. Allow atleast 8 inches (20 cm) of roost-ingspaceperbird. Roosts shouldbeapproximately 2 inches (5 cm)in diameter (1 inch [2.5 cm] forbantams) and free of splintersand sharp edges that can causefoot injuries. To prevent breastblistersandbumblefoot in broil-ers and in cocks of the heavybreeds, do not allow theseheavier birds to roost.

CHICKEN HEALTH 27

CHART 1-2Minimum Space Requirements

excellent litter. Hardwood shavings, on the other hand, should be avoided dueto the danger of aspergillosis.

Remove and replace litter around feeders if it becomes thick with drop-pings. Remove and replace moist litter around waterers. Moist litter favors thegrowth of molds (such as those causing aspergillosis) and bacteria (that pro-duce ammonia and odier unpleasant gases), and aids the survival of viruses,protozoa (such as those causing coccidiosis), and nematodes (worms).

Birds Age Open Housing,sq ft/Bird Birds/sq m

ConfinedHonsingsq It/Bird Birds/sq m

Cagedsq in/Bird sq cm/Bird

Heavy

1-7 days _ _ 0.5

20 (Do not house

1-8 weeks

1.0

10 2.5

4 heavy breeds

9-15' weeks

2.0

5 5.0

2 on wire)

15-20 weeks

3.0

4 7.5

1.5

21 weeks +

4.0

3 10.0

1

Light 1 day-1week

- - 0.5

20 25 160

1-11 weeks

1.0

10 2.5

4 45 290

12-20 weeks

2.0

5 5.0

2 60 390

21 weeks +

3.0

3 7.5

1.5 75 480

Bantams

1 day-1 week

- - 0.3

30 20 130

1-11 weeks

0.6

15 1.5

7 40 260

12-20 weeks

1.5

7 3.5

3 55 360

21 weeks +

2.0

5 5.0

2 70 450

*or age of slaughter


At least once a year, empty your coop, clean out and replace all the litter,and scrape manure from the walls and perches. Fall is the best time for thischore, since it puts your flock on clean litter at the start of winter, when badweather keeps chickens indoors much of the time. Compost the used litter orspread it on a field where chickens will not range for at least one year.

If you use the built-up litter system of management (whereby litter is onlyinfrequently removed and replaced), compost the litter if you plan to intro-duce a replacement flock. The heat produced during composting will destroymost pathogens and parasites.

Ventilation. Fresh air dilutes the population of microbes and reduces thebuildup of airborne diseases. Good ventilation also keeps air in motion (with-out causing drafty conditions) and removes suspended dust and moisture.Moisture tends to be particularly high in a chicken house because chickens

CHICKEN HEALTH 29

Pine shavingsmake excellentlitter to absorbdroppings andmoisture.

breathe rapidly, thereby using more air in proportion to their size than anyother animal. Another important benefit of good ventilation is preventing thebuildup of ammonia fumes from accumulated droppings.

Providing an adequate flow of fresh air may require a fan to move out staleair and bring in fresh air. Fans are sold according to how many cubic feet of airthey move per minute (cfm). A good rule of thumb is to get a fan that provides5 cfm (.03 cubic meters per minute) per bird.

Ammonia CheckIligh levels of ammonia in the air can reduce feed consumption, affecting thegrowth rate of young birds and the production of laying hens. Ammonia gasdissolves in fluid around the eyes, causing irritation, inflammation, and blind-ness. Symptoms of ammonia-induced conjunctivitis are rubbing the eye with awing and reluctance to move or go into sunlight. High levels of ammonia canalso damage the mucous membranes of a bird's respiratory tract, allowingbacteria, dust, and viruses to travel down the tract to cause disease.


Ammonia that is concentrated enough to cause conjunctivitis or respira-tory tract damage is concentrated enough to be detected by the human sense ofsmell. To check the ammonia level in your coop, squat or bend down until yourhead is 1 foot (30 cm) above the litter, or about the height of a chicken's head.Breathe normally for a moment or two. If your eyes, nose, or throat burn, theammonialevel is too high for your birds—decrease litter moisture and improveventilation. Once the condition is corrected, a chicken's cells that were dam-aged by ammonia fumes should repair themselves within 2 weeks.

CHICKEN HEALTH 31

SanitationAfter a period of continuous use, chicken housing becomes

contaminatedwith disease-causing organisms that may eventually reach infectious levels.Regular cleanup does not eliminate microorganisms, but it does keep them atbay. You can remove an estimated 95 percent of contamination with a thor-ough cleaning.

Dry cleaning is not nearly as effective as cleaning with water, and hot watercleans better than cold water. Detergent (or a 4 percent washing soda solution)added to the hot water reduces surface tension and helps the water penetrateorganic matter. In addition, detergents are mildly germicidal.

During cleanup, wear a dust mask and avoid inhaling poultry dust, whichcan cause human respiratory problems. Methodically follow these steps:

• Choose a warm day so facilities will dry quickly.• Suppress dust by lightly misting equipment and walls with water and abit of detergent.• Remove portable equipment, such as feeders, waterers, nests, andcages.• Remove litter and droppings; compost them or spread diem on landwhere your chickens will not range for at least a year.• Use a broom, brush, or shop vac to remove dust and cobwebs from theceiling and walls.• Brush, blow, or vacuum dust from fans, vents, and any electricalequipment.• Use a hoe or other scraper to remove manure and dirt clinging to thefloor, walls, and perches; as long as you can see manure or dirt,


keepscraping.• Turn off electricity and protect electrical equipment and outlets withwatertight covers or duct tape.• Apply detergent or washing soda and hot water systematically to theceiling, walls, floor, and washable equipment with a brush or fruit-treesprayer that delivers 400 psi (pounds per square inch) or 28 kg per sqcm for good penetration.• Open doors and windows, and turn on the ventilation fan, to air outand dry housing before letting the chickens back in.• Finish the job by removing any debris that has accumulated aroundthe yard since your last cleanup.

DisinfectionThoroughly cleaning a chicken house is more important than

disinfectingit, since many disease-causing organisms cannot survive long in an environ-

CHICKEN HEALTH 33

CHART 1-3Survival Ability of Disease-Causing Organisms

Disease Cause Survival of BirdsChlamydiosis bacteria hours to daysCholera bacteria month or moreCoccidiosis protozoa monthsErysipelas bacteria yearsInfectious bronchitis virus week or lessInfectious bursal disease

virus months

Infectious coryza bacteria hours to daysInfectious laryngotracheitis

virus days

Influenza virus days to weeksMarek's disease virus yearsMycoplasmosis bacteria hours to daysNewcastle disease virus month or lessPox virus monthsSalmonellosis bacteria weeks to monthsTuberculosis bacteria months to years

ment away from birds or their debris. In addition, the microbes that causesome diseases—including infectious bursal disease, coccidiosis, and tubercu-losis — resist disinfectants. Disinfection, in most cases, should be used only asa way to zap stragglers following cleanup.

Disinfection becomes a necessity if you acquire used equipment or yourflock experiences an infection. Not all disinfectants work equally well againstall disease-causing organisms. A veterinarian or poultry pathologist can helpyou select the appropriate disinfectant for your situation.

Check the date on any disinfectant to be sure it is not outdated. Store thedisinfectant in a cool place. Some chemicals are quite toxic and should bestored away from children, pets, livestock, food, and feeds. To avoid a tragicerror, keep disinfectants in their original containers with the labels intact.

Dilute a disinfectant according to either directions on the label or instruc-


tions provided by a vet or pathologist. Some disinfectants work best in hotwater, but some evaporate too quickly in warm or hot water. Never mix differ-ent kinds of disinfectant, or you may render them all ineffective. Before mixinga disinfectant with detergent, lye, washing soda, or other cleaning product,check the label for information on compatibility.

Organic matter inhibits penetration by a disinfectant, and in some casesactually deactivates the disinfectant, so follow the above steps for thoroughcleanup before applying a disinfectant. If surfaces cannot be scrubbed clean,

CHICKEN HEALTH 35

use a disinfectant that is not readily deactivated by organic matter. Take care,though — such disinfectants are quite toxic and should never be applied with aspray.

Wear goggles to protect your eyes, and avoid inhaling disinfectant chemi-cals. Alter scraping and scrubbing housing clean, close doors and windowsbefore applying the disinfectant. Work systematically, starting with the ceiling,then the walls, and finally the floor. Afterward, don't forget to disinfect yourshovel, broom, rake, hoe, and other clean-up tools. Wait at least 20 minutesbefore rinsing equipment and tools to give the disinfectant time to do its job.

To protect your chickens from skin injury and from respiratory irritationdue to inhaled chemicals, allow housing to dry thoroughly, and leave the facili-ties empty for as long as possible. The safe time between application andletting your chickens in varies from 4 hours to 2 days. Consult the label.

Chemical DisinfectantsChemical disinfectants include:Hypochlorites — chlorine-based disinfectants such as chlorine bleach

(which contains 5 percent available chlorine) and swimming pool chlorine(which contains 15 percent). Common brand names are Clorox and Halazone.Chlorines work best in warm water but evaporate rapidly, so prepare a freshsolution right before use. Chlorine is destructive to fabric, leather, metal andsome kinds of plastic.

Iodine, organic—mixture of iodine with some other chemical. Commonbrand names include Betadine and Isodyne. When the amber color fades, or-ganic iodine is no longer effective.

Quat— quaternary ammonium compound (sometimes also referred to asQAC). Quats vary in composition and are widely available at drugstores, petshops, feed stores, and poultry supply outlets. Common brand names


includeGermex and Zephiran. Quats have no strong odor, leave no stains, and arenon-corrosive, non-irritating, and relatively non-toxic. They cannot be com-bined with soap or detergent and will not work on surfaces that are notcompletely free of soap or detergent.

Phenol — another name for carbolic acid, a coal tar derivative and thestandard by which all other disinfectants are measured. Common brandnames include Lysol and Orthophenylphenol. Most chicken keepers considerphenols too expensive for use in poultry houses.

Cresols — coal tar product related to phenol and similar in bactericidalproperties, once found on every farm. Cresl-400 is one common brand name.Cresylic acid is cresol with soap added.

Quicklime— also called "slaked lime" is used primarily for damp yardswhere the sun does not shine (and where birds shouldn't be kept, anyway).Quicklime is highly caustic, so keep birds away until the area dries thoroughly.

CHICKEN HEALTH 37

CHART 1-4Chemical Disinfectants

Iodine

Qucit

Chlorine

Cresol

Pheno

Used for:

Eggs yes yes yes no yes

Incubator yes yes yes no yes

Housing yes yes no yes yes

Equipment yes yes yes yes yes

Troughs yes yes yes no yes

Drinking Water yes no yes no no

Bootbath yes yes no yes yes

Effective against:Bacteria yes mo

styes yes y

es

Bacterial spores

some

no some

no no

Fungi yes some

yes most

most

Viruses some

some

some

some

some

Usage level (ppm):

Disinfect 100 600 200 varies

varies

Sanitize 25 200 50 varies

500

Application:


Water temperature

<110"F

hot <110°F

hot hot

(43.5°C)

(43.5°C)

Effective pH acid alkaline

acid acid acid

Deactivated byalkaline water yes no yes no n

oDeactivated byhard water no some

whatno no n

oDeactivated byorganic matter yes some

whatyes no n

oApply with brush

yes yes yes yes yes

Apply with spray

yes yes yes no no

Other Properties:Toxicity low low low high hi

gh

Residual effect no yes no yes yes

Odor little

none

strong strong

strong

Nonchemical DisinfectantsNot all disinfectants are chemicals. Here's the rundown on readily

avail-able nonchemical disinfectants:

Hot water increases the effectiveness of some chemical disinfectants, andboiling water and live steam are both effective disinfectants in their own right.

CHICKEN HEALTH 39

Sanitation TerminologyProducts with names ending in "cide" kill the disease-causing agent named inthe first part: abactericide kills bacterial cells, a fungicide kills molds and fungi,a viricide kills or inactivates viruses, a germicide kills bacteria, but not necessar-ily their spores (most germicides are also viricides).

Products ending in "stat" retard the growth of the organism named in theFirst part: a bacteriostat slows the growth of bacteria, a fungistat slows thegrowth of molds or fungi, and so forth.Antiseptic — destroys or retards the growth of microorganismsDetergent— improves the cleaning action of water, acts as a wetting agent orsurfactant to help water penetrate the surface of organic matter, and ismildly germicidal

Disinfectant — inactivates or kills microorganisms, but not necessarily theirspores

Sanitizer — reduces microbial contamination to a level considered safeSterilizer—destroys all microbes, including bacteria, spores, fungi, and viruses

Resting housing by keeping chickens out for 2 to 4 weeks after cleanuphelps reduce the microorganism population, since many cannot live long inthe absence of chickens.

Drying also reduces the population of microorganisms, but killing a sig-nificant number of microbes by drying takes a long time.

Sunlight speeds up drying of portable equipment (such as feeders, water-ers, cages, and nests) and housing that can be readily opened up to direct rays.Sunlight does not penetrate deeply, but will destroy microbes on the surface.Sunlight and normal soil activity will effectively disinfect a yard or run fromwhich surface organic wastes have been removed.

Heat produced by composting will destroy most of die bacteria, viruses,coccidial oocysts, and worm eggs present in litter. Heap the litter into a pile(but not on a wood floor, oryou could start a fire). If the litter is dry, dampen ita little to start fermentation. Let the pile heat up to at least 125°F (52°C),


leave itfor 24 hours, then turn it so the outside is on the inside. Let it heat for another24 hours before spreading the litter back out. Composting litter to destroy itsmicrobes is a good idea, whether die litter will be reused for chickens or used tofertilize a garden or field.

Flame is an effective disinfectant, but a hazardous one, especially aroundwood structures. It is best reserved to disinfect concrete pads and to sear awayfeathers stuck to wire cages, but take care: if you hold a torch to galvanizedwire long enough for the wire to get hot, the galvanizing will be damaged.

CHICKEN HEALTH 41

Stress ManagementStress encompasses anything that reduces resistance to disease.

Some mi-crobes are so strong (or "virulent") that they readily overcome a bird's normalresistance. Many microbes, on the other hand, cause no illness or only mildillness, unless stress lowers the bird's resistance.

Some diseases are themselves stress factors — they are not serious, butthey lower a bird's resistance to a more serious infection. Internal parasites(worms) are a prime example of a mild infection that can open the door tosomething more serious or that can become serious in combination witii otherstress factors.

No matter how much natural resistance a chicken has, its resistance willbe reduced to some extent by stress. Stress cannot be avoided. It is normal inevery chicken's life. Most chickens are able to adapt, even to limes of peakstress: hatching, reaching maturity, and molting. Additional stresses arecaused by the environment (such as chilling, heating, and excessive humidity)and by routine management procedures (debeaking, vaccinating, and anyprocedure in which birds are handled or herded).

Stress management involves providing clean, dry litter and range, ad-equate protection from the elements, good ventilation without draftiness,contamination-free feed and water, adequate feed and water space, propernutrition, and freedom from crowding. Avoidance of crowding is especiallyimportant for chicks, since they grow fast and can quickly outgrow their livingquarters. As birds grow, they develop immunities through gradual exposure todisease-causing microbes. Stress due to crowding can cause disease instead ofimmunity.

Stress reduction also involves avoiding die indiscriminate or improper useof medications, as well as avoiding handling birds at critical times, includingwhen pullets are just starting to lay, when a (lock has recentiy been moved


orvaccinated, and when the weather is extremely hot or cold.

Gentle handling as a stress-reduction measure is more important tochicken health than fancy housing, according to a study by W. B. Gross at Vir-ginia Tech. Gently treated birds are easier to handle and experience less stressduring procedures that require handling. Compared to birds that are ignoredor are treated roughly, birds that are handled gently grow to a more uniformsize and are more resistant to infections.

Preconditioning is another stress-reduction technique. Whenever youmake a management change, precondition your birds by making the changegradually so that each step is relatively minor. If, for example, you plan to cageyour pullets for laying, move them at least a week before you expect them tostart production. If you plan to move or separate breeders, give them plenty oftime to adjust to their new surroundings before the start of breeding season.

CHICKEN HEALTH 43

Showing and StressShowing causes stress by exposing a bird to unfamiliar and confusing

sur-roundings, strange people, different-tasting water, and any number of newand potentially frightening experiences. Excessive showing can be so stressfulthat it affects the fertility and hatchability of eggs. Hens are more easilystressed by showing than cocks.

If you show your chickens, precondition diem by coop training them priorto the show so they'll get used to being caged alone and handled frequently. Atshow time, bring along your own feed and water — if your chickens don't likethe feed or water at the show, they won't eat or drink well, their stress level willgo up, and they'll be more susceptible to diseases. Some exhibitors add antibi-otics or electrolytes to water during a show, but if a bird doesn't like the taste itwon't drink, increasing its stress level.

Stress BehaviorIf you're familiar with the way your chickens normally act, you can

readilynotice changes caused by stress and can take appropriate action. You may beable to alleviate the stress behavior through a simple management change.Continuing stress that causes long-term behavioral changes seriously reducesa chicken's resistance to disease. Sometimes the stress behavior itself is a firstsign of disease.Stress behavior falls into three basic categories:

• diarrhea• labored breathing• changes in normal behavior or activity patternsDiarrhea becomes evident as a stress sign when you grab a bird

suddenlyand it reacts by pooping on you. Diarrhea can also be a sign that there's some-


thing wrong with the feed or water or that your birds are suffering from adigestive disorder. Labored breathing can be caused by crowding, panic, hightemperatures, and respiratory distress. Changes in normal behavior or activitycan be triggered by any number of factors including boredom, fear, crowding,constant introduction of new birds, frequent showing, insufficient or unpalat-able water, uncomfortable temperatures, and disease.

The study of animal behavior and its relationship to healdi is called "vet-erinary ediology." For observation purposes, ethologists divide the behaviorof chickens into eleven distinct areas:

Reflex behavior involves any automatic reaction, such as flinching or shy-ing away from sudden movement. A frightened chicken, for example, mightshake its head from side to side. A sick chicken reacts more slowly than usual toperceived danger.

Feeding behavior includes both the frequency of visiting feed or water

CHICKEN HEALTH 45

troughs and the amount ingested. Under normal circumstances, a chicken vis-its feed and water stations often and eats or drinks a little at a time. Stressusually makes a bird eat and drink less, although some diseases increase thirst.Anomalous feeding behaviors that call for management action include featherpicking, cannibalism, drinking excessive amounts of water, eating litter or soil,and eating eggs.Rest patterns, including sleep, are easily disturbed during times of

stress. Aclassic example is restlessness at roosting time, caused by anticipation of beingbitten by external parasites that feed 011 birds at night.

Exploratory behavior satisfies the need to investigate new things in the en-vironment, including new birds. Excess stress can be induced by the suddenintroduction of something a bird can't see or doesn't understand (such as theloud noise of machinery operating nearby). Excessive stress leads to over-reaction, often in the form of fiighiiness (the "Chicken Little syndrome").Flightiness is relative, however, since some breeds naturally tend to be moreHighly than others. Anomalous behavior that may be an early sign of disease isloss of interest by a bird in its surroundings.

Body activity relates to motion, including moving from place to place orwing flapping for the sheer joy of it. A stressed-out chicken may pace up anddown, indicating either frustration (as in the case of one cock trying to get awayfrom another) or boredom (in the case of a caged chicken).

Grooming activities include head scratching, preening, mutual grooming,and dust bathing. If you're not familiar with dust-bath behavior, the first timeyou see your chickens laid out in the din, you'll surely think they died a suddendeath. Loss of interest in grooming behavior, so that birds take on a scruffylook, is a common early sign of disease.


Sexual behavior on the part of a cock involves courtship (pecking theground, waltzing, and wing fluttering) and crowing (to establish location andwarn off competitors — a behavior that's territorial as well as sexual). Sexualbehavior 011 the part of a hen largely involves crouching when a cock puts hisfoot on her back in preparation for mating. Hens that are low in the peckingorder will crouch as the rooster nears and will be mated more often than otherhens. You can readily identify these subordinate hens by the broken or missingfeathers 011 their backs or sometimes by wounds inflicted by the mountingcock. Such wounds may be serious enough to require isolation and treatment.

Parental behavior refers to the relationship between a hen and her chicks,since a cock develops no special relationship with his offspring. A hen protectsher chicks, leads them to feed and water, and communicates with them (andthey with her) through a series of vocalizations t hat each have a specific mean-ing. Anomalous parental behavior includes leaving the nest before the eggshatch (perhaps because the hen was bothered by mites), attacking chickswhen they hatch, or abandoning chicks. Some breeds, particularly those best

CHICKEN HEALTH 47

known for their laying abilities, have been selectively bred not to have thebrooding instinct.

Territorialism involves aggressive behavior used in an effort to maintainpersonal and territorial space. Crowding increases aggression, which in-creases stress. Stress behavior in the form of so-called "displacement" activitycommonly occurs when one cock of a sparring pair suddenly starts preeningor pecking the ground. Anomalous territorial behavior includes attacking in-truders, other chickens, or humans and refusing (or being unable) to move dueto fear.

Social relations in a flock of chickens boil down to the peck crder. Birdsthat are low in peck order get chased away from feeders, don't get enough toeat, and don't grow as well or lay as many eggs as others. The more birds youhave, the more important it is to have several feeders and waterers, and tospread them around. Stress goes up when die peck order is disrupted for anyreason, such as sickness or the removal or addition of birds. As a result, birdseat less, grow slowly or lose weight, and lay fewer eggs.

Relationship to man starts with imprinting, a phenomenon occurring inchicks during their first day of life. By the time a chick is 3 days old, it startsexperiencing fear, which is why you'll never develop the same friendly rela-tionship with mail-order chicks that you can have with chicks hatched in yourincubator. Whether or not your chickens are imprinted on you, minimizestress by talking or singing softly when you work among them, and by movingcalmly and avoiding abrupt movements.


Balanced RationsThe best way to ensure that your chickens are getting a balanced

ration isto purchase commercially prepared feed designed to suit your flock's stage ofmaturity: chick starter for young and growing birds, layer ration for table-eggproduction, and breeder (or gamebird) ration for hatching-egg production.The relationship between health and nutrition is covered in the next chapter.

Health and Nutrition

HEALTH AND NUTRITION INTERACT in many ways. Disease isn't alwayscaused by bacteria, viruses, or odier parasites. Disease can also be caused by anutritional deficiency. The nutritional deficiency may, in turn, inhibit thebody's immune response, opening the door to infection.

Conversely, an infectious disease may reduce a bird's appetite or inhibitabsorption of nutrients from its digestive system. The resulting nutritional de-ficiencies may eidier delay recovery or further reduce the bird's resistance,increasing its susceptibility to secondary infection.

NutrientsFree-ranged flocks are able to forage for natural sources of the nutrients theirbodies need. Other nutrients are manufactured within their bodies, aided bysunlight. Some nutritional deficiencies occur only in chickens confined in-doors, away from sunlight. Others occur due to incorrect formulation orimproper storage of prepared feeds.

49


More than thirty-six nutrients have been identified as being essential tochickens. Since 110 single ingredient contains all the necessary nutrients, thebest ration includes a combination of ingredients that together satisfy achicken's requirements.

Nutritional problems don't always result from deficiencies, but can becaused by excess. Too much of any nutrient, or a lack of balance between nu-

HEALTH AND NUTRITION 51

trients, can be just as devastating as a deficiency, so don't be too quick to pumpyour birds full of nutritional supplements.

ProteinA chicken's body uses protein to produce antibodies that fight

disease.During infection, a bird rapidly loses its protein stores, causing its protein re-quirement to go up. If the bird cannot obtain additional protein, its resistancelevel drops.

Feathers are 85 percent protein. Protein requirements therefore increaseduring the annual molt, when all of a bird's feathers are replaced with newones. When your flock is about to molt — as indicated by plumage taking on adull look — begin tossing a handful of dry cat food into the yard every otherday, and continue until the molt is over. Use cat food, rather than dog food,

Free-ranged chickens

forage for natural

sources of nutrients.


because cat food contains animal protein (which is rich in amino acids), whilemost brands of dog food are top-heavy with grains.

A hard molt — where feathers fall rapidly but grow back slowly — mayindicate animal protein deficiency. Another indicator is feathers that becomebritde and break easily. If the deficiency is unlikely to be caused by a dietaryproblem, look for a disease (recent or current) that may be inhibiting proteinabsorption.

Genera] symptoms of protein deficiency are similar to general symptomsof infection: decreased appetite, slow growth in chicks or weight loss in ma-ture birds, decreased laying, and smaller egg size.

Excess protein in a chicken's diet is converted to uric acid and deposited ascrystals in joints, causing gout. The excess use of meat scraps as a source of


protein can also result in an imbalance of phosphorus (described later in thischapter).

VitaminsVitamins are divided into two groups: fat soluble and water soluble.

Thefat soluble vitamins (A, D, E, and K) are retained in body fat and used as theyare needed. The water soluble vitamins (C and the B complex) are not storedby the body, which uses only what it immediately needs and expels any excessin droppings. Water-soluble vitamins must therefore be replenished more of-ten than fat-soluble vitamins.

Every known vitamin is needed by chickens in some amount. A flock's vi-tamin requirements are interrelated with and must be balanced against othernutritional components — protein, minerals, and energy. Of all the nutrients,chickens are most likely to be deficient in vitamins A, D, and B2 (riboflavin).

Caged birds are more prone to vitamin deficiencies than floor-raisedbirds, since the latter pick up some of the vitamins they need from litter. Simi-larly, housed chickens are more prone to deficiencies than free-ranged flocks,since the latter enjoy a more diverse diet.

Stress, including disease-induced stress, increases the effects of a vitamindeficiency. Heat stress causes birds to eat less and worsens a deficiency. A vita-min supplement will give your chickens' immune systems a boost duringtimes of stress, such as when their bodies are battling a disease, when theweather is unpleasant, during a move, before and after a show, and duringbreeding season. Chicks will get off to a good start if you give them a vitaminsupplement during their first 3 weeks of life.


Fat-Soluble VitaminsVitamin Ays needed for vision, growth, and bone development. It is

calledthe ' anti-infection" vitamin because it helps maintain the immune system. Italso aids disease resistance by playing a role in maintaining the linings of thedigestive, reproductive, and respiratory tracts.

Vitamin A deficiency is unlikely to result from improper diet, but may becaused by a health condition that interferes with nutrient absorption, such ascoccidiosis or worm infestation.

If a chicken misses the mark when pecking, suspect poor eyesight due tovitamin A deficiency. An increase in blood spots in eggs may be another sign,since the amount of vitamin A needed to minimize blood spots is higher thanthe amount needed to keep a laying hen healthy.

Vitamin A deficiency can cause nutritional roup which produces respira-tory symptoms similar to those of infectious bronchitis or infectious coryza; itcan also cause the upper digestive tract to develop blisters resembling those of


fowl pox. The damage caused to linings of the upper digestive and respiratorytracts can open the door to bacterial or viral invasion. Deficiency increases theseverity of respiratory infections such as bronchitis and chronic respiratorydisease, and increases a chicken's susceptibility to parasites such as coccidia.

Cod liver oil mixed into mash at the rate of 2 percent is a good source ofvitamin A. Take care not to go overboard — too much vitamin A is toxic tochickens.

Vitamin D is necessary for the absorption of calcium to make strongbones, beaks, claws, and eggshells. A bird's body synthesizes vitamin D fromsunshine, making deficiency more likely in caged or housed chickens than inpenned or range-fed flocks. Deficiency can also occur in chickens fed rationsintended for other livestock, since chickens need vitamin D3 while most otherstock require vitamin D2.

A typical sign of vitamin D deficiency is a continuing cycle of normal eggproduction followed by the appearance of thin- and soft-shelled eggs followedby a drop in production followed by a return to normal production. A deficienthen may have weak legs right before she lays an egg, causing her to squat in apenguin-like stance. If the deficiency is not corrected, her beak, claws, and keelwill become soft and her eggs will be small with reduced hatchability. Defi-ciency can be easily corrected by adding cod liver oil to mash at die rate of 2percent or by adding vitamin AD&E powder to drinking water three times aweek.

A chicken's need for vitamin D is intimately tied with its needs for the min-erals calcium and phosphonis. A deficiency in any of these three nutrients


canresult in rickets (in young birds) or cage fatigue (in older birds). A deficiencymay also cause egg eating.

Excess vitamin D causes kidney damage. One sign of too much vitamin Din a hen's diet is calcium "pimples" on eggshells that, when scraped off, leavelittle holes in die shell.

Vitamin E is necessary for normal reproduction and for resistance toEscherichia coli infection (colibacillosis). Wheat germ oil is a good source ifused fresh — vitamin E in fortified rations degenerates rapidly, especiallywhen temperature and humidity are high. Deficiency is most likely to occur inconfined young birds fed a diet that's high in soy bean oil or cod liver oil and inbirds fed rations containing rancid fats. Deficiency in chicks can result inencephalomalacia, exudative diathesis, or white muscle disease. Deficiency incocks can cause loss of fertility.

Vitamin K is necessaiy for normal blood clotting. Signs of deficiency areprofuse bleeding from slight wounds and internal bleeding (under the skin orinto the body cavity). Vitamin K may trigger infectious anemia, especially inchicks treated for extended periods with the coccidiostai sulfaquinoxaline. Al-falfa leaves are a good source of vitamin K.


Water-Soluble VitaminsVitamin B is actually a whole group of unrelated substances whose

nameschange so often it's hard to keep up. Vitamin B deficiency was not an issue inthe days when chickens roamed pastures, freely picking in cow patties andhorse apples. Health problems occurred when breeders started to specializeand began penning their chickens. In those early days, poultry keepers kepttheir flocks healthy by tossing them fresh horse or cow manure, but no oneknew why it worked until 1948, when researchers discovered that manure con-tains vitamin B12. This B vitamin is unique among nutrients in being foundalmost exclusively in animal products.

Today, deficiency is not a problem where poultry keepers have returned tothe practice of letting chickens run with other livestock. Chickens raised onCHART 2-1

Vitamin Benefits and Sources

Benefitvision, growth, bone develop-ment, resistance to diseases &parasites

B complexthiamin (Bl)riboflavin (B2)

pyridoxine (B6)nicotinic acid(niacin)pantothenic acidbiotin (H)

inositolpara-amino-benzoic acidcholinefolic acid (folacin)B12

Dwhole cereal grainsleafy greens, grass, milk,yeastmany sourcesmeat protein, whole grain

many sourcesbrewer's yeast, leafy greens,molassesmany sourcesyeast, many sources

many sourcesgreen leavesmeat protein

ascorbic acidcod liver oilAD&E powderwheat germ oilAD&E powder

growth &hatchability

VitaminSourcecod liver oilAD&E powder


stress reductionstrong bones, beaks,

claws, &eggshells;

hatchabilityfertility, resistance tocolibacillosis


normal blood clottingalfalfa leavesK


built-up floor litter get enough vitamin B12 by picking in the litter. Deficiencycan occur in housed flocks, especially those fed soymeal as the sole or mainsource of protein.

Curled-toe paralysis in chicks is a sign of riboflavin (vitamin B2) defi-ciency, occurring when penned breeder hens are fed unsupplemented layration. Greens, including young grass, are good sources of riboflavin. Milk,whey, and other dairy products are also good sources, but too much can causediarrhea.

All the B vitamins, along with other vitamins, are added to commercial ra-tions and are otherwise so readily available in a wide variety of feedstuff's that,in a properly managed flock, deficiency is unlikely.

Vitamin Chelps prevent diseases by reducing the harmful effects of stress.Chickens make dieir own vitamin C and do not need a supplement exceptwhen die absorption of vitamin C and other nutrients is inhibited by stress,such as might be induced by high environmental temperatures.

MineralsWhile vitamins have their origins in organic plant or animal matter,

min-erals are inorganic elements. They give bones rigidity and strength, and dieyinteract with other nutrients to keep the body healthy. Just as caged birds aremore prone to vitamin deficiencies than floor-raised birds, they're also moreprone to mineral deficiencies. But, unlike vitamins, minerals do not go stale.Most commercial feeds contain adequate amounts, with the possible excep-tion of calcium.

Calcium and phosphorus are needed by chicks for bone formation and byhens for eggshell formation. Calcium and phosphorus are interrelated, andboth require the presence of vitamin D to be metabolized. A deficiency in


vita-min D can cause a deficiency of calcium and/or phosphorus.

Regardless of the cause, a deficiency of calcium and phosphorus increasesa chicken's susceptibility to parasitic infection. Beetles and other hard-shelledbugs contain lots of calcium and phosphorus; ironically, they may also be asource of parasitic infection. A good supplemental source of calcium is groundoyster shells or limestone (but not "dolomitic" limestone, which can inhibitegg production).

Older hens need more calcium than younger hens, and all hens need morecalcium in warm weadier. Rough eggshells are a sign that a hen is getting toomuch calcium.

Magnesium is needed for bone formation, eggshell formation, and themetabolism of carbohydrates. A chicken's diet is more likely to have too muchmagnesium than too litUe, leading to diarrhea and smaller eggs widi thin shells.

Salt in the form of sodium and chlorine can be deficient in a flock's diet,


causing chicks to grow slowly and hens to abruptly lay fewer, smaller-sizedeggs, lose weight, and become cannibalistic. But chickens are more likely to gettoo much salt than too little. The result is increased thirst, inability to stand,weak muscles, convulsions, and death. A lethal dose of salt is 0.06 ounce perpound (4g/kg) of body weight.

Chicks are more susceptible to salt poisoning than adults. Salt poisoningcan occur when a flock's sole source of drinking water is saline water, al thoughchickens can tolerate salt in water up to 0.25 percent. Poisoning can also occurwhen chickens pick in rock salt used for de-icing sidewalks and driveways.

Salt poisoning can be caused by a normal amount of salt in rations duringsummer, if chickens run out of water, and during winter, if drinking waterfreezes. Obviously, the way to avoid salt poisoning is to be sure your chickenshave fresh, clean water at all times.

Potassium deficiency can occur during times of heat or other stress, result-ing in decreased egg production, thin shells, and general weakness.

Manganese is needed for normal bones, for good eggshell quality, and toprevent slipped tendon. Coccidiosis interferes with its metabolism.

Copperdehciency can cause aloss of feather color in New Hampshires andRhode Island Reds. As with manganese, the metabolism of copper is affectedby coccidiosis.

Selenium deficiency is associated with white muscle disease; an excess ofselenium increases susceptibility to salmonellosis. Corn and other grains maybe low in selenium if they are grown east of the Mississippi River and in thePacific Northwest, where the soil is selenium deficient. Grains may be espe-


cially high in selenium if they are grown in the Great Plains or parts of Canadawhere soils contain an excess of selenium.

EnergyA chicken's protein requirement goes up during the annual molt, its

vita-min and mineral needs remain fairly constant year around, and its energyrequirements fluctuate with outside temperature. Where the temperaturerange is extreme, energy must be adjusted seasonally — upward during coldmonths, downward during warm months. Energy can be lowered by addingwheat bran (but too much affects laying). Energy can be increased by increas-ing protein or carbohydrates.

Although protein contains a certain amount of energy, the cheapest formof energy is carbohydrates found in cereal grains. Grains are also the most ca-loric form of energy, so diey must be used judiciously. Since a chicken eats tosatisfy its energy needs, if its ration is too high in carbohydrates, the bird getsfat; if too low, the bird becomes underweight. In both cases, the bird is moresusceptible to disease.


CHART 2-2Nutritional Diseases and Disorders

Disease caused by:

Deficiency of: Excess of:

Cage fatigue calcium/phosphorus

Curled-toe paralysis riboflavin(vitamin

B2)Egg binding calcium/

phosphorusEncephalomalacia vitamin EExudative diathesis vitamin EFatty liver syndrome

carbohydrate

Gout water proteinInfectious anemia vitamin KProlapsed oviduct calcium/

phosphorusRickets vitamin DRoup (nutritional) vitamin ASlipped tendon calcium/

phosphorusmanganesevitamins

White muscle disease

vitamin Dvitamin E/selenium

Nutritional DiseasesNutritional research has traditionally focused on broiler chicks and layinghens. More is therefore known about the requirements for rapid early growthin heavy breeds and about the maintenance needs of light laying breeds thanabout the requirements of breeder flocks, especially in the heavy breeds. Com-mercial feeds designed for mature birds are formulated for maintenance,ensuring that hens lay well but not necessarily providing sufficient nutritionfor die eggs to develop into strong viable chicks. (See chapter 13 for more aboutthe influence of nutrition on the hatchability of eggs and viability of chicks.)


Chickens, like humans, depend for good health on the existence of benefi-cial bacteria and other microorganisms living in their digestive tracts. A bird'snutritional requirements go up when the delicate balance of these microflorais upset by illness, drugs, stress, or an abrupt change in feed.

A bird's nutritional requirements can also be increased by any conditionthat causes nutrients to be destroyed before they can be absorbed or diat in-hibits the chicken's ability to absorb them. Interference with the absorption ofnutrients, called "malabsorption," can be caused by parasite loads includingworms or coccidia, infection, drug use, and environmental stress due to lowhumidity or temperature extremes. Any of these conditions can make even themost perfectly formulated rations insufficient to prevent a deficiency.


Deficiency SymptomsA nutritional deficiency may be:

• borderline — resulting in slow growth, poor or rough feathering, lackof energy, lack of appetite, a slight drop in egg production, and slightlyreduced hatchability;• serious — birds become crippled, hens stop laying;• extreme — ending in deadi.Nutritional diseases tend to be quite similar to one another, making

it hardto tell specifically which nutrient is lacking. In addition, deficiencies are rarelysimple (having a single cause) but are more likely to be multiple (caused by thelack of more than one nutrient). Symptoms of a simple deficiency are deter-mined by deliberately putting chickens on a deficient diet and observing theresults. In a real-life multiple deficiency, symptoms combine tocomplicate thediagnosis.

CHAKT 2-3Nutritional Symptoms

Body Part Disease/Condition Deficiency Excess

BeakBloodBones

BrainClawsDroppingssoltexcessive bleedingbrittle

soft

greenish yellowsoftloose & ninnyvitamin Dvitamin Kcalciumvitamin D

calciumphosphorusvitamin Dvitamin Evitamin Dsaltmagnesium

blood spotssmall

vitamin AEggsmagnesiumproteinvitamin Avitamin Dvitamin

Ecalcium


pale yolkcalcium pimpleslow fertilitylow hatchability* magnesiumvitamin Apotassiumprotein vitamin A

low production


Body Part

Disease/Condition Deficiency

Eggs (cont.)

no production calcium

soft shell calcium/vitamin D

thin shellpotassiumvitamin D

no shell vitamin Deating of calcium

vitamin DEyes pale vitamin A

poor vision vitamin Awatery vitamin A

Feathers black, in ermine pattern

vitamin D

brittle proteincurled proteinhard molt proteinmissing proteinpale, in black & red breeds

copper

ruffled vitamin AKeel deformed vitamin DLegs stiff walk biotin

penguin squat vitamin Dweak or bowed vitamin D

Mouth whitish sores vitamin AMuscle swollen joints vitamin D

weak muscles vitamin ERespiratory

general symptoms vitamin A

Ribs collapsed (adult) vitamin Dbeaded (chick) vitamin D

Skin inflamed biotinSusceptibility

general vitamin A

colibacillosis vitamin Eparasites calcium &

phosphorussalmonellosisslipped tendon manganese

Weight emaciation vitamin Afatslow growth protein

vitamin Avitamin D


weight loss carbohydrateprotein

Excess

magnesium

salt

pantothenicacid

selenium

carbohydrate

*See "Nutrition-Related Hatching Problems," p. 217.


FeedsCertain feedstuff's themselves affect digestion and nutrient absorption. Thegrowth rate of chicks, for example, is retarded by uncooked soybeans andsoymeal. Deficiencies sometimes occur when commercial feecs are manufac-tured under new technologies. When processors switched from the expellermethod to the solvent method of extracting soybean meal, feeds were deficientin folic acid and had to be reformulated to include an increased amount of thatB vitamin. liven feedstuffs that are high in nutrients may contain them in"bound" form, meaning the nutrients are unavailable to or poorly utilized bychickens.

If you stockpile feed or continuously buy from the same stockpiled source,diagnosis of a nutritional deficiency may involve analyzingyour feed. For mostsmall flocks, though, feed is bought in small batches, and one batch is not likelyto be around long enough to cause a serious deficiency, let alone be analyzedfor its nutritional content.

A good rule of thumb is to buy only as much feed as you can use within 6weeks of manufacture. Store the feed in such a way that it won't go rancid,moldy, or stale. Mold and other spoilage organisms destroy nutrients, andeven the best commercial rations lose nutritional value during prolonged stor-age at a warehouse or on your back porch. Despite the inclusion ofantioxidants to retard deterioration, nutrients are destroyed over time by heat,sunlight, and oxygen.

CHART 2-4Feeding Schedule


Flock Type

Roasters and CaponsLayers and Breeders

1 day-6 weeks6-13 weeks13-20 weeks

or I day-20 weeks20 weeks

finisher + cornstartergrowerpullet developerstarter/growerlay ration + oyster shellor limestone grit

Feed

AgeBroilers 1 day-5

weeksstarterfinisherstarter/grower

5-7 weeksor 1 day-7 weeks

7 weeks-slaughter


Nutritional content holds up best in feed stored in a cool, dry, place, awayfrom direct sunlight. Once you open a bag, transfer its contents to a sealedcontainer such as a clean plastic garbage can with a tight-fitting lid; don't storefeeds in metal cans, which sweat in warm weather, causing the feed to gomoldy. Never feed chickens moldy rations, whether the mold developed in astorage container or in a sack that got wet.

Avoid cheap feeds that don't contain animal protein or high-fiber ingredi-ents such as alfalfa or wheat products. Such feeds start out missing nutrientsand go downhill from there. Also avoid the temptation to save money by feed-ing your flock copious amounts of scratch grains or stale bakery products, bothof which will upset the nutritional balance of even the best feeding program.Corn and other treats should never make up more than 5 percent of a flock'stotal diet.

FeedersFeeder design can affect health byallowing droppings to accumulate inthe feed. Droppings can be excludedby hanging feeders from the rafters orby fitting them with perch guards thatrotate and dump any bird trying toroost on diem.Feeder design can also affecthealth by allowing feed to be scatteredon the ground, where it not only at-tracts rodents but combines with

CHART 2-5Feeder Space

Space per Bird

Age

Layers:0-6 weeks7- 18

weeks19 weeks and upBroilers:1 day-1 week1 -4 weeks4-8 weeks8- 20

weeks21 weeks and up

1.0"2.0"3.0"

2.5 cm5.0 cm7.5 cm

2.5 cm5.0 cm5.0 cm10.0 cm12.5 cm

1.0"2.0"2.5"4.0"5.0"


manure and moisture to provide agood environment for disease-caus-ing organisms. Billing out (the bad habit chickens have of using their beaks totoss feed out of a trough) can be prevented by using a feeder with an inwardlyrolled lip and by positioning the feeder so the hopper is approximately theheight of die birds' backs. Here, again, a hanging feeder is ideal because itsheight can easily be adjusted as birds grow.

Feed AmountHow much chickens eat varies with the ration's palatability, texture,

en-ergy, and protein content, as well as with the chickens' breed and strain,degree of activity, and condit ion of health. How much a chicken eats also var-ies with environmental temperature. Chickens subjected to cold wintertemperatures need more feed than chickens raised in a warm climate or in a


controlled environment. Hot weather causes a chicken to eat less; the ration'snutritional value must therefore be increased to meet the bird's needs.

Depending on dieir breed and purpose, chickens may be either fed freechoice (given a constantly ready suppy) or placed on a restricted feedingschedule. Broilers and roasters should be fed free choice, since the idea is to getthem to butchering age as quickly as possible. Pullets of the lightweight layingbreeds may also be fed free choice, since diey have been bred for efficient feedutilization.

Older lightweight hens, as well as breeders in the dual-purpose or meatcategories, should be kept on a restricted diet. Restricting the feed intake ofpullets past the age of 4 weeks slows their growth and delays the onset of lay-ing, causing them to do better when they become layers and/or breeders.Restricting the intake of mature breeders keeps them from getting unhealthilyfat and developing fatty liver syndrome.

CHART 2-6Restricted Feeding Schedule forPullets

Age* Body Weight** Feed per Birdweeks pounds grams pounds grams

Laying Breeds:4 0.59 270 0.06 286 0.88 400 0.07 368 1.32 600 0.08 3910 1.60 730 0.09 4212 1.87 850 0.09 4514 2.09 950 0.10 4916 2.55 1160 0.11 5318 2.72 1240 0.14 6420 3.03 1380 0.14 79

Meat Breeds:4 1.16 530 0.19 906 1.68 765 0.22 1008 2.01 915 0.23 105


10 2.34 1065 0.25 11512 2.67 1215 0.27 12514 3.17 1445 0.29 13516 3.72 1695 0.33 15018 4.30 1955 0.37 17020 4.89 2225 0.41 190

*To age 4 weeks, each layer pullet averages 1.47 pounds (672 grams) of feed, each broilerpullet averages 1.09 pounds (954 grams! .**Average expected body weight under restricted feeding program.


Rations-Related ProblemsStarvation occurs when newly hatched chicks do not learn to eat

quicklyenough, causing them to lose energy rapidly until they can no longer activelyseek food. In older birds, starvation occurs when rations are too high in fiber(common in cheap feeds). Starvation may also be related to climate: duringcold weather, chickens may not get enough to eat to keep warm; during ex-tremely diy weather, vegetation may be scarce for free-ranged chickens.

Obesity is most likely to occur in chickens kept as pets and in caged birdsthat are inactive and therefore eat more energy-rich feed tiian they need. Somebreeds, especially New Hampshires and other dual-purpose breeds, have anatural tendency to put on fat. Fat hens do not lay well and are prone to heatstroke, reproductive problems, and fatty liver syndrome.

Xanthomatosis, a condition in which thick yellow or orange patches ap-pear on the skin, is apparently caused by toxic fats in rations.

WaterA chicken's body is 50 percent water and an egg is 65 percent water, makingwater the most important nutrient in a chicken's diet. Water serves many func-

CHART 2-7

Diseases AffectingWater

ConsumptionIncrease DecreaseConsumption ConsumptionBlackhead Infectious coryza

Cholera OmphalitisEnteritisTyphoidInfectious bursaldiseaseLeucocytozoonosis


Newcastle diseaseSalmonellosisSpirochetosisCHART 2-8

Diseases Related to

Drinking Water

Disease* CauseAlgae poisoning

algae toxins in

surface waterBluecomb stress

triggered bylack of water

Botulism rotting organicmatter in water

Gout insufficient drinkingwater

Salt poisoning

insufficient or salinedrinking water

Thrush water contaminatedwith fungus

*Numerous bacteria, protozoa, and virusesare spread by means of drinking water

contaminated with droppings or mucus frominfected birds.


tions; among them is to transport othernutrients throughout the body and tokeep the body cool through evapora-tion.

An old saying points out the perver-sity of chickens: "A flock's water supplyis no better than the poorest drinkingwater available." You can bring yourflock the purest, freshest water, yetyour birds will persist in drinking fromfilthy puddles. Good yard drainage pre-vents stagnant puddles in whichdisease-causing microbes and para-site-carrying insects thrive. If your soil is neither sandy nor gravelly, enhancedrainage by locatingyour coop on a slight slope. Many microbes and parasitescan't survive long in the absence of moisture.

Provide your flock with water from a clean, reliable source. Avoid surfacetanks, ponds, or streams, all of which are easily contaminated. Chickens preferdrinking water with a temperature of about 55°F (13°C), and will drink less ifwater is much above or below that.

The average chicken drinks between 1 and 2 cups (237 to 474 ml) of waterper day, depending on numerous factors including its size, the environmentaltemperature, water palatability, feed intake, feed composition, condition ofhealth, and whether or not the bird is laying.

The average layer drinks twice as much as the average non-layer. Somedisease conditions cause chickens to drink more, as do rations that are high inprotein or salt. Chickens drink less if the water contains medication or an ex-cessive amount of dissolved minerals that die birds find unpalatable. Chickensthat don't drink enough because water is unpalatable, dirty, or warm (or theresimply isn't enough) can die from kidney failure.

Under normal conditions, a chicken will drink approximately twice asmuch as it eats, by weight. A layer, for example, may eat '/a pound (224 g) of feedand drink 2 cups (474 ml) of water per day. As the temperature goes up,


theratio of water to feed also goes up, as high temperatures cause a chicken to

eatless and drink more.

DehydrationA chicken can survive longer witiiout feed dian without water. Chickens

drink only a little at a time, so they must drink often. Insufficient water slowsgrowth in chicks and reduces egg production in hens.

Ratioof Water to

Temperature One Pan Feed60° F

16°C

1.8 parts

70 21 2.080 27 2.890 32 4.9100

38 8.4

Water deprivation can occur at any age and for a variety of reasons. Water

CHART 2-9Environmental

Temperatureand Water Consumption


may be available to chicks, but perhapsthey are too small to reach it. Chickensof any age will be deprived of water ifthe water quality is poor or they simplydon't like the taste of it. Diarrheacauses dehydration by passing waterthrough the body too quickly to be ab-sorbed. Hens may have plenty of waterin winter, but if the water freezes, eggproduction will drop. In warmweather, water deprivation occurswhen a flock's water needs go up but the supply remains the same.

If a laying hen goes without water for as little as 24 hours, she may take aslong as 24 days to recover. If she goes without water for 36 hours, she may gointo a molt, followed by a lengthy period of poor laying from which she maynever recover.

CHART 2 - 1 1

Layers:

CHART 2-10Signs of Water DeprivationBody Part Change

Comb and wattles

Tendons on backsof legsDroppings

shrunkenand bluishstand outprominentlyoff color

WateringWaterer Space

Trough/Bird Birds/Fount

Age1 quart1 liter

2quarts 2 liters1 gallon 4 liters1.5 gallons

6 liters

1 day-1 week1-4 weeks4-12 weeks12 weeks and upDouble in hot weather


0-6 weeks 1.0"

2.5 cm

100 25 15

7-18 weeks 1.0"

2.5 cm

50 12 8

19 weeks and up

2.0"

5.0 cm

30 12 8

Founts or Cups/100 Birds

Broilers:1 day-1 week

1.0"

2.5 cm

1

1-6 weeks 1.0"

2.5 cm

2

8 weeks and up

1.0"

2.5 cm

2

Breeders: 1.0"

2.5 cm

2*


Minimum Water Needs

Water Per Dozen Birds

Age

Caged Birds/Cup Nipple

42 TIIF. CHICKEN HEALTH HANDBOOK

WATERERSA good waterer is designed so chickens can't step in the water or roost

overit, and it holds enough to last until it can conveniently be refilled. Automaticwatering is, of course, ideal, provided you check it daily to make sure die sys-tem is functioning properly. Once a week, add 1 tablespoon of sodiumbicarbonate (baking soda) per gallon to the automatic watering tank to keepslime from forming in the pipes, valves, and drinkers. Diseases can be spreadthrough drinking water, so clean and disinfect all waterers regularly.

In winter, coils or a heating pan will keep water from freezing. In summer,place waterers in a shady place where the water won't be warmed by the sun. Agravel or sand bed beneath the waterer, topped with droppings boards, willkeep chickens from drinking spills and picking in moist, filthy soil that invari-ably surrounds a waterer.

Anatomy of a Chicken

DIFFERENT DISEASES AFFECT DIFFERENT PARTS of a chicken's body in dif-ferent ways. When a bird gets sick, knowing what pan of its body is affectedmay help you determine what disease the bird has.

If your flock keeps getting diseases that always affect the same body sys-tem, some management change may be in order. Frequent bouts withdigestive disorders, for example, may indicate a need for improved sanitation,while repeated respiratory problems may signal a need for improved ventilation.

Vital Statistics

Maximum Life Span: 30-35 yearsMaximum Productive Life: 12-15 yearsBody Temperature

adult 103°F (39.5°C)chick 106.7°F (41.5°C)

Respiratory Ratecock 12-20 breaths per minutehen 20-36 breaths per minute

Heart Rate*adult 250-350 beats per minutechick 350-450 beats per minute

*Heart rate varies with breed and sex; a mature New Hampshire cock has a heartrate of 250 beats per minute, a mature Leghorn hen 350 beats per minute.

84

Immune SystemA chicken's first defense against disease is its skin, the largest organ and themain one by which a bird comes into contact with its environment. The major-ity of disease-causing organisms can enter a chicken's body only through theskin protecting the outside of its body or the mucous membranes lining theopenings on the inside of its body.

On the skin live certain microbes that, through competition, keep othermicroorganisms away. If the skin is broken, even these "good" microbes mayget into the body and cause disease. Microbes have an easier time gettingthrough mucous membranes than through the skin. They are kept out by mov-ing fluids (mucus and tears) and by enzymes that destroy invaders.

If a microorganism manages to break through the defenses of the skin ormucous membranes, the bird's lymphatic system takes up the battle. All bodytissues are lubricated by watery fluid, called "lymph," that's derived from thebloodstream and that accumulates in the spaces between tissue cells. Thelymphatic system drains lymph from all over the body and returns it to thebloodstream, after passing it through lymph glands (or lymph nodes) that filt erout microbes and odier foreign bodies.

Lymph contains specialized white blood cells of several kinds, technicallycalled "lymphocytes" but popularly known by such names as "engulfing"

Where antibodies are produced

TEARS

SALIVA

LYMPHOCYTES

SPLEEN

MUCOUS MEMBRANES

BLOOD PLASMA

85 TI IN CHICKEN HEALTI I HANOH< HJK


cells and "killer" cells. Lymphocytesneutralize or destroy invading mi-crobes, which they recognize asantigens. An antigen is, quite sim-ply, a protein that differs from anynatural protein in the body.When lymphocytes detect anantigen, they respond by producingsubstances to fight the invader.These substances are called "anti-bodies" or "immunoglobulins." Noone knows exactly how antibodiesare produced. What is known is that antibodies attach themselves to antigens,making it easier for engulfing cells, killer cells, and other lymphocytes to de-stroy the antigens.

Antibodies are also produced by the spleen (the additional function ofwhich is to remove and destroy worn-out blood cells). Many diseases affect thespleen, causing it to swell (paratyphoid), turn mushy (histoplasmosis), or atro-phy (infectious anemia). The spleen is not a vital organ, however, and if itceases to function, other parts of the body take over its job.

Immunity is controlled and antibody production is activated in chicks by arose-shaped organ behind the cloaca, called the "cloacal bursa" (or "bursa ofFabricius"). Some viral diseases damage the cloacal bursa, permanently com-promising the bird's immune system. Infectious bursal disease, the mostcommon cause of immunosuppression, is a fairly common infection of chicks3 to 6 weeks old that attacks lymph tissue and destroys the cloacal bursa.Marek's disease, a common tumor disease of birds 3 to 6 months old, may alsodamage the cloaca! bursa.

CHART 3-1Diseases Involving the

Cloacal BursaDisease EffectInfectious anemia atrophyInfectious bursal disease

atrophyLymphoid leucosis tumorMarek's disease tumorRunting syndrome atrophy

Location of cloacal bursa, organ responsible for antibody production

ANATOMY or A CHICKEN 87


Digestive SystemA chicken has no teeth. Saliva starts breaking down feed as soon as it enters thebird's mouth. Its tongue pushes the feed toward the back of its mouth. Thefeed then slides down the esophagus, a tube leading to the crop where the feedis temporarily stored. You can sometimes see a full crop bulging at the base ofa bird's neck.

Occasionally the crop becomes impacted (see "Crop Impaction," page264). Crop impaction may occur when feed is withheld preparatory to worm-ing, causing chickens to eat too much at once afterward. Crops may also getpacked when birds are free ranged where little is available to eat but tough,fibrous vegetation. Even if the bird continues to eat, nutrition cannot getthrough. The swollen crop may cut off the windpipe, suffocating the bird. Cropimpaction is not likely to occur in properly fed birds.

Digestive System



From the crop, feed is moved to the proventriculus or true stomach, whereenzymes break it down further. It is then passed along to the gizzard, or me-chanical stomach, an organ with strong muscles, a tough lining, and acollection of small stones or grit for grinding up grains.

A chicken fed only commercially prepared mash or pellets does not needgrit. Its digestive efficiency will be impaired, however, if it eats grains withouthaving access to grit for its gizzard. If a bird eats a small, sharp object such as atack or staple, the object is likely to lodge in its gizzard and, due to the stronggrinding motion of the gizzard muscles, may eventually pierce the gizzardwall. As a result, die bird will grow thin and eventually die — a good reason tokeep the yard free of nails, glass shards, bits of wire, and the like.

From the gizzard, feed passes into the small intestine for absorption. Theupper portion of the small intestine, called the "duodenum," forms a loop.Enclosed by the duodenal loop is the pancreas, which secretes enzymes to aiddigestion, bicarbonate to neutralize acids, and hormones to regulate bloodsugar.

Between the duodenal loop and the lower small intestine is connected theliver, an organ that secretes green bile (or gall) to aid in the absorption of fats inthe intestine. Attached to the liver is a transparent pouch, the gall bladder,where bile is stored until it is needed.

Branching off between the small and large intestine are two blindpouches, called the "ceca" (one is a "cecum"), that have no known function.The ceca empty their contents two or three times a day, producing pasty drop-pings that often smell worse dian regular droppings.

The last portion of the intestine, the large intestine or "rectum," is rela-tively short. It absorbs water from feedstuffs as they pass through.

Both the small and large intestine are normally populated by beneficialbacteria, referred to as "microflora" (micro meaning very small and flora

meaning plants). Microflora aid digestion and enhance immunity by guardingtheir territory against invading microbes. An intestinal disease occurs whenthe balance of microflora is upset or the normal microflora are overrun by toomany foreign organisms (usually eaten in contaminated feed or water). Theresult is enteritis or inflammation of the intestines; symptoms include diar-rhea, increased thirst, dehydration, loss of appetite, weakness, and weight lossor slow growth.

Enteric diseases tend to be complex. Combinations of and interactionsbetween various organisms — worms, bacteria, protozoa, viruses, and naturalmicroflora — determine the severity of the disease. Successfully treatingenteritis requires knowing what organism, or combination of organisms, iscausing the illness.

The large intestine ends at the cloaca, where the digestive, reproductive,and excretoiy tracts meet. The cloaca has three chambers:


92 THE CI IICKEN HEAI.TI I HANDBOOK

• the fecal chamber, at the end of the rectum• the urogenital chamber, where the excretory and reproductive systemscome together• the vestibule, into which the cloacal bursa emptiesIn the fecal chamber, a final bit of moisture is absorbed from

feedstuffsleaving the body, which are then expelled through the vent in the form of drop-pings. In a healthy chicken, feed passes through the entire digestive system in 3to 4 hours.

Excretory SystemThe excretory system consists basically of the kidneys (lying along thechicken's back) connected to the cloaca's urogenital chamber by means oftubes called "ureters." The kidneys are responsible for filtering and removingwastes from the blood. In humans, these waste products are expelled in urine.A healthy chicken does not excrete urine, but expels blood-wastes in the formof semi-solid uric acid, called "urine salts" or "urates," that appear as white,pasty caps on droppings.

Urates may be improperly metabolized due to water deprivation, excessdietary protein or calcium, or certain diseases. Droppings may then containmore than the usual amount of urates (as occurs in spirochetosis), or uratesmay accumulate as pasty deposits in the joints (articular gout) or collect ascrystals that block the ureters (as in the case of infectious bronchitis).

Respiratory SystemThe function of the respiratory system is to circulate oxygen throughout thebody and to aid in temperature regulation. Parts of the respiratory system in-clude the nose, throat, trachea or windpipe, lungs, air sacs, and certain bones.

Chickens, like other birds, are peculiar in having an extensive system of air

sacs, or thin-walled pockets, t hat circulate air from the lungs into other parts ofthe body. The system of air sacs extends around the internal organs and intoCHART 3-2

Air SacsNumber Name

abdominalcervicalinterclavicularthoracic, anteriorthoracic, posteriorsurrounding intestineneck, above esophagusshoulderbeneath lungbehind lung


Location

22

2

2


some bones, called "pneumatic" bones, that are hollow. While the lungs arerigid, air sacs are flexible. All but one come in pairs. The largest pair is in theabdomen, surrounding the intestine.

Respiratory DiseaseRespiratory disease has always been a problem in poultry. At one

time, allrespiratory diseases were lumped together as "colds" or "roup." During diemiddle part of the 20th century, they were recognized as a group of separate,sometimes unrelated, infections with common characteristics similar to a hu-man cold: labored breathing, coughing, sneezing, sniffling, gasping, runnyeyes and nose.

Fn these modern times, respiratory diseases are classified according totheir cause, whether nutritional, parasitic, bacterial, fungal, viral, or

SINUS

Respiratory System

environ-mental. Most serious respiratory diseases are caused by viruses, for whichthere is no cure and which are easily spread in moisture expelled by a sick birdthat coughs, sneezes, or simply breathes. Respiratory distress can also occur asa reaction to vaccination, especially against Newcastle disease or infectiousbronchitis.

Respiratory diseases often occur in combination, so that a flock cured



of one disease may continue to have symptoms produced by a second disease.The best defense against respiratory illness is to develop your flock's geneticresistance. The best management practices are to provide good ventilationand avoid introducing carriers into your flock.

Skeletal SystemThe skeletal system of a chicken has three functions:

• to support the bird• to transport calcium• to aid respirationRespiration is aided by a system of hollow pneumatic bones. Calcium

transport is aided by a system of so-called "medullary" bones, from which ahen gets 47 percent of the calcium used in eggshell formation.

Skeletal problems can be caused by insufficient calcium, eitiier becausethe diet is deficient or because a disease or other condition keeps calcium frombeing properly metabolized. Common problems include crooked or humpedback, crooked keel, and wry tail (that flops to one side).

By far the most common problem is weak legs, which may be related togenetics, nutrition, infection, or some combination thereof. In hens, die prob-lem is usually the result of mineralimbalance. Leg weakness is morelikely to occur in heavy breeds than inlight breeds. Guard against it by keep-ing young birds off slippery surfaces,by feeding a balanced diet, and by notbreeding lame or deformed birds. Beaware that lameness is not always askeletal disorder, but may result fromnerve or muscle damage.

Another common skeletal problemis inflammation of the joints and syn-ovial membranes — thin membraneslining joint cavities and tendonsheaths. The synovial membranes se-crete synovia, a fluid resembling thinegg white that lubricates joints.

Inflammation of the synovial mem-branes, called "synovitis," causesexcess synovia to be secreted, makingSkeletal System die joint swell and become warm and



painful. The most likely joint affected is the hock. Non-infectious synovitismay be caused by injury or nutritional problems. Infectious synovitis may becaused by bacteria, staphylococci, or viruses.

Near the joints, at places where a tendon or muscle crosses a bone ormuscle, are small, fluid-filled sacs, called "bursa," that cushion pressurepoints. Inflammation of the bursa (bursitis) can be caused by pressure, fric-tion, or injury to the membrane surrounding the joint. If the bird is notreinjured or does not become infected, after a time the excess fluid is re-absorbed by the bloodstream. The most common form of bursitis is keelbursitis, popularly known as "breast blister." Breast blister is caused by pres-sure against the keel, usually in a bird with weak legs (so it cannot keep itsweight off the keel while resting) and/or poor feathering (that offers little pro-tection to die keel).

Reproductive SystemA cock's reproductive system consists of two sperm-producing testes and theaccompanying equipment necessary to get the sperm into a hen. A hen's re-productive system consists of one ovary and a passageway or oviduct that'sslightly more than 2-feet long.

A female chick embryo actually starts out with two ovaries, but the rightone atrophies. Only the left one continues to develop and become functional.For some unknown reason, occasionally the right oviduct develops partiallyand becomes cystic, eventually growing so large it presses against other inter-nal organs and causes death.

The functioning left ovary consists of a clump of undeveloped yolks or ova(one is an "ovum") located just beneath the hen's backbone, approximatelyhalfway between the neck and tail. As each ovum develops and matures,

it isreleased into the oviduct, usually about an hour after the previous egg was laid.Double-yolked eggs, laid most often by pullets and by heavy-breed hens, occurwhen two yolks are released within 3 hours of each other.

During a yolk's journey through the oviduct, it is fertilized (if sperm arepresent), encased in albumen or egg white, wrapped in a membrane, andsealed in a shell. The whole process takes about 25 hours, causing a hen to layher egg a little later each day. Since a hen rarely lays in the evening, as the cycleprogresses she'll eventually skip a day and start a new cycle the followingmorning. A group of eggs laid within one cycle is called a "clutch." A hen witha longer cycle (say, 28 hours) lays fewer eggs per clutch than a hen with ashorter cycle.

Any interruption in normal cycling can result in abnormal shell patterns.Abnormal patterns also occur when yolks are released less than 25 hours apart,causing two eggs to move through the oviduct close to each other. The second



egg will have a thin, wrinkled shellriiat's flattened toward the pointyend. If it bumps against the first egg,the shell may crack.

Egg shape is inherited, so you canexpect to see family similarities. Oc-casional variations are normal, andso are seasonal variations. Shells willbe thicker and stronger in winter,but will get thinner in warm weatherdue to a reduction in calcium mobi-lization. Soft-shelled eggs arecommon when production peaks inspring.

A hen lays best during her firstand second year. Thereafter, as longas she is healthy she will continue tolay, but not efficiently enough forcommercial production. Regardlessof a hen's age, the number of eggsshe lays, their size, shape, and inter-nal quality, and shell color, texture,and strength can be affected by avariety of things including environ-

Reproductive System of a Hen

OVA ARE

OVIDUCT

CLOACA

mental stress, improper nutrition,medications, vaccinations, para-sites, and disease.

Reproductive DisordersSoft-shelled, thin-shelled, or misshapen eggs, ruptured yolks witiiin eggs, re-duced production, and prolapse may be the result of either poor nutrition orinfection. Watery whites and weak or misshapen shells with altered textureand strength can be caused by a viral respiratory disease, such as infectiousbronchitis or Newcastle, or sometimes by vaccination. A coccidiostat in ahen's rations may alter egg size, color, and shell texture.

Tumors occur in the reproductive organs of hens more often than in anyother animal and are a common cause of poor laying. Some tumors haveknown causes — notably lymphoid leukosis and Marek's disease — others donot. Slow-growing tumors occuring in older hens are understood least of all,since only young hens are kept in commercial Hocks that sponsor most of theresearch.



Prolapsed oviduct, also called "blowout" or "pickout," is a condition inwhich the lower part of a hen's oviduct turns inside out and protrudes throughthe vent. Prolapse occurs most often when a hen starts laying at too young anage, is too fat, or lays unusually large eggs. Caught in time, the prolapse cansometimes he reversed by applying a hemorrhoidal cream (such as Prepara-tion H) and isolating the hen until she improves. Otherwise, the odier chickenswill pick at her vent, eventually pulling out her oviduct and intestines andcausing the hen to die from hemorrhage and shock. Not all vent picking is dueto prolapse, but instead may result from faulty management — feeders, water-ers, and roosts may be positioned in such a way that birds below can pick at thevents of birds above.

A false layer is a hen whose egg-laying mechanism malfunctions due todamage in chickhood, usually by infectious bronchitis. The hen acts normal,visits the nest regularly, but leaves no egg. Instead, yolks drop into the hen's

Wrinkled andmisshapen eggs

ANATOMY OF A CHICKF.N 103

abdominal cavity and are partially reabsorbed by the hen's body. A postmor-tem examination (see Chapter 10) of a false layer will reveal large quant ities oforange fat in the body and coagulated, cooked-looking yolk in the abdominalcavity. The latter is called "yolk peritonitis" and can be caused, as well, by avariety of bacterial infections.

An internal layer is a hen with partially or fully formed eggs in her abdomi-nal cavity, caused by reverse peristaltic action (die rhythmic, wavelike motionthat moves an egg through the oviduct). No one knows what causes peristalticaction to reverse, and no treatment is known. An internal layer is easily recog-nized by her lowered rear end, causing her to stand like a penguin.

Salpingitis, or inflammation of the oviduct, derives its name from theGreek word "Salpinx," meaning trumpet — the shape of the oviduct.Salpingitis is the most common cause of death in layers. It usually results froma respiratory infection, in which bacteria invade the oviduct via one of the ab-


Egg BindingAn egg travels down the oviduct pointed end first. When it gets to the urogenitalchamber of the cloaca, it turns end for end so it will come out large end first.Sometimes an egg gets stuck. The egg may be too large (for example, if a pulletlays unusually large eggs), or a disease may cause the oviduct to swell or itsmuscles to become partially paralyzed. The stuck egg then causes future eggs toaccumulate behind it, distending the hen's abdomen. Unless you can get thingsmoving again, the hen will die.

Lubricate a forefinger with mineral oil or KY Jelly and insert it into thevent. With your other hand, push gently against the hen's abdomen to force theegg toward the vent. If you can see the egg, but it is too big to pass through thevent, puncture the shell and remove it in pieces (with great care not to let a sharpshard injure the hen). Rinse the cloaca with hydrogen peroxide.

If the egg was stuck in the cloaca too long, cloacal tissue may protrudethrough the vent. In that case, protect the hen from cannibalism by isolatingher until her muscle tone is back to normal.

dominal air sacs. Most hens die within 6 months of becoming infected; survi-vors do not lay. If you conduct a postmortem on such a hen, you will find acheesy mass in the oviduct. The longer the infection has gone on, the biggerthe mass will be.

Atrophy of the ovary can occur due to disease or to severe stress caused bylack of feed or water. Symptoms, in addition to cessation of laying, are emacia-tion and dehydration accompanied by a neck or body molt.

Spontaneous sex change is a phenomenon whereby an old hen developsthe characteristics of a cock, perhaps because an infected ovary has causedhormonal changes. The hen's comb grows larger, she molts into male


plum-age, and she may crow or mount other hens. If the infection is successfullytreated, die "cock" will revert back to a hen at the next molt. If the infection iscured before the next molt, the "cock" will lay eggs. This phenomenon wasonce considered witchcraft, the most famous case being a "cock" named Baselwho was burned at die stake in 1474 for laying eggs.

Nervous SystemThe nervous system is the network coordinating all the other systems. It con-sists of two parts:

• die central nervous system, responsible for voluntary movements(like eating)


• the peripheral nervous system, responsible for involuntary bodyfunctions (like breathing)

The nervous system can be disrupted by poisoning (as in die case of botu-lism), by a virus (such as the herpes vims causing Marek's disease), or by ahereditary defect (such as the recessive genetic trait that causes congenitaltremor). Typical symptoms of a nervous disorder are incoordination, trem-bling, Uvitching, staggering, circling, neck twisting, convulsions, and paralysisof a wing, leg, or the entire body.

Circulatory SystemBlood type influences a chicken's resistance to disease, a hen's egg productionand vigor, and the hatchability of her eggs. A chicken may have one of twelveblood types: A, B, C, D, E, H, I, J, K, L, P, and R, which explains why certainbreeds and strains are more vigorous and less susceptible to disease dian oth-ers. The resistance factor B21, for example, is found in birds that are immuneto Marek's disease.

Blood is part of the circulatory system, which includes the heart and a net-work of blood vessels. The heart is a pump that keeps blood circulatingthrough the vessels. The function of the circulatory system is to transport oxy-gen, hormones, and nutrients throughout the body, but it can also transportdisease-causing microbes.

The blood may be invaded by bacteria, viruses, fungi, protozoa, and otherparasites diat get into die blood through mucous membranes or through theskin, introduced by wounds or insect bites. Some species of parasitic wormstemporarily travel through the blood stream on their way to the organ or


tissuein which they will grow to maturity.

Septicemia occurs when any infectious organism enters the bloodstreamand becomes "generalized" or "systemic" by invading the whole body. Typicalsymptoms that a disease has gone septicemic are weakness, listlessness, lackof appetite, chills, fever, and prostration. In acute septicemia, chickens that arein good flesh and appear healthy die suddenly. Sudden death with a full crop isa good indication of acute septicemia, since any other fatal condition is likelyto cause loss of appetite.

Anemia, or "going light," is a condition in which the blood is deficient inquantity (blood loss) or quality (low hemoglobin, red blood cell count, orboth). Anemia may be caused by dietary iron deficiency, worms, bloodsuckingparasites (mites and lice), coccidiosis, and some infectious diseases — notablyinfectious anemia, caused by a virus known as "chicken anemia agent." Signsof anemia include pale skin arid mucous membranes, loss of energy, loss ofweight, and death.

108 THE CHICKEN HEALTH HANDBOOK

Chart 3-3Disorders by the Body System They Affect

ANATOMY OF A CHICKFN 109

Skin Joint and Bone NervousBreast blister Arthritis Algae poisoningBumblefoot Cage fatigue BotulismFavus Gout (articular) Congenital tremorFlukes Infectious synovitis Epidemic tremorLice Kinky back ErgotismMites Osteopetrosis Marek's diseaseNecrotic dermatitis Rickets Newcastle diseasePox (dry) Slipped tendon Toxoplasmosis

Twisted legDigestive GeneralizedArizonosis Respiratory (Entire Body)Blackhead Air-sac disease AflatoxicosisBluecomb Aspergillosis ArizonosisCampylobacteriosis Chlamvdiosis BlackheadCanker Cholera CampylobacteriosisCholera Chronic respiratory ChlamydiosisCoccidiosis disease CholeraColibacillosis Cryptosporidiosis Chronic respiratoryCrop impaction Emphysema diseaseNecrotic enteritis Flukes ColibacillosisNewcastle (exotic) Gapeworms ErysipelasParatyphoid Infectious bronchitis HistoplasmosisPasted Vent Infectious Infectious bursal

diseasePullorum laryngotracheitis Infectious stuntingRotaviral enteritis Infectious synovitis syndromeRoundworms Influenza ListeriosisInfectious stunting Newcastle disease Lymphoid leukosis

syndrome Pox (wet) Marek's diseaseTapeworms Roup (nutritional) Newcastle disease.Thrush Swollen head

syndromeParatyphoid

Typhoid PseudomonasUlcerative enteritis Blood and Pullorum

Cardiovascular Runting syndromeReproductive Ergotism SpirochetosisEgg drop syndrome Infectious anemia StaphylococcosisFlukes Leucocytozoonosis StreptococcosisFusariotoxicosis Malaria Toxoplasmosis

TuberculosisTyphoid

ANATOMY OF A CHICKFN 110

Temperature ControlA second function of the circulatory system is to aid in regulating body tem-perature. The normal body functions of a chicken depend on a relativelysteady temperature of just under 107T (42°C).

A chicken's temperature normally decreases slightly at night and duringcool weather. Heat is lost through droppings, evaporation (primarily from thelungs), conduction (sitting on a cool surface), and radiation (heat lost to sur-rounding air that is appreciably cooler than the bird). In an infection thatcauses fever, a drop in body temperature to below normal means death is near.

Body heat normally increases slightly during the day and in warmweather. A rise in body heat also occurs naturally during physical activity anddigestion. Fever is a symptom of certain infections, including influenza, infec-tious bursal disease, and spirochetosis, and any infection that becomessepticemic.

General Symptoms of Systems DiseasesEnteritis: diarrhea, increased thirst, dehydration, loss of appetite, weakness,

weight loss or slow growthNervous Disorder: incoordination, trembling, twitching, staggering, circling,

neck twisting, convulsions, paralysisRespiratory Disease: labored breathing, coughing, sneezing, sniffling,

gasping,runny eyes and nose

Septicemia: weakness, listlessness, lack of appetite, chills, fever, prostration

Acute Septicemia: sudden death in an apparently healthy bird in good flesh witha full crop

External Parasites

A PARASITE IS A LIVING ORGANISM that invades the body of another livingorganism and survives without providing benefit. Any living thing that invadesa chicken's body and produces an infectious disease is, by definition, a para-site. Those organisms commonly called parasites, however, have certaincharacteristics that set diem apart from other infectious agents.

• They are animals, while other infectious agents are primitive plantforms.• They primarily cause mechanical damage to the body, rather thenpoisoning the body with toxins, as do odier infectious agents.• They normally cause a long-term decline in health, rather than theusual brief life-or-deadi struggle triggered by other infectious agents.

111

112 Tin; CHICKEN HEALTH HANDBOOK

Parasites are divided into two groups: internal parasites that invade dieinternal organs (discussed in the next two chapters), and external parasitesthat generally stay on the outside of a chicken's body.

Externa] parasites, in turn, are divided into two groups: insects (bugs,fleas, flies, lice) and mites (chiggers, mites, ticks). Most external parasites pro-duce similar results: weight loss or slow growth, reduced egg production, andaesthetic damage to meat birds. Serious infestations may cause deadi, particu-larly to young birds. Some parasites carry diseases from one bird to another.

EXTERNAL PARASITES 113

Chart 4-1Diseases

Spread by External Parasites

Transmitted

by Disease

ChlamydiosisCholeraEpidemic tremorLeucocytoz

ooMa

sh

smosquitoesMarek's disease

PoxSpiroche

Transmitted by

Disease


to

si

Insects

Bugs, fleas, flies, and lice all belong to class Insecta. They all have three-partbodies and three pairs of legs attached to the middle part. They develop tomaturity in stages, and young insects do not look like mature ones.

Most insects spend at least part of their lives off the bird's body, making itpossible to control them by eliminating their


favorite hiding places and breed-ing grounds — cracks and crevices inside buildings, junk piles outside.

BugsBugs

are flat-bodied insects belonging to the family Cimicidae, orderHemiptera. They all bite to get a blood meal. In doing so, they inject saliva thatcauses itching and swelling.

The poultry bug (Haematosiphon modoru) — also called "adobe bug,""curuco," or


"Mexican chicken bug" — occurs in southern and western states.It attacks humans as well as chickens.

The swallow bug (Oeciacus vicarius) is spread to poultry flocks by barnswallows. It has a fierce bite and, like the poultry bug, attacks humans.

The cone-nose assassin bug (Triatoma sanguisuga in California, Florida,Maryland, and Texas, T. protrata in California and Utah) bothers chickens


butis a relatively minor pest.

BedbugThe most common bug that affects chickens isthe bedbug (Cime.x lectularius in temperate areas,C. boueti and C. hemipterus in the tropics and sub-tropics). This bloodsucking parasite is sowell-known for attacking humans that it is men-tioned in an old nursery rhyme ending with the line,"Don't let die bedbugs bite."


The bedbug infests cracks, crevices, and litter,

Bedbugwhere it can survive for as long as a year without a (Cimex lectularius)


blood meal. It feeds at night, forabout 10 minutes at a lime, and israrely seen on birds during the day.Evidence of bedbug infestation isblack fecal spots deposited on eggsand in cracks, and the characteristicunpleasant odor created by thebugs' stink glands.

Adult bedbugs are up to lA inch(0.5 cm) long. The female lays sev-


eral eggs per day until she hasproduced between 70 and 200 eggs.Depending on the temperature, theeggs hatch in 6 to 17 days. In 1 to 3months, again depending on tem-perature, young bedbugs gothrough several stages to reach ma-turity and begin reproducing.Control includes removing infestedlitter, cleaning out housing, anddusting cracks and crevices with aninsecticide


approved for poultry.

FleasFleas

are insects (order Siplion-aptera) with an enlarged third pairof legs that allow them to jump.They spend most of their lives offtheir host, usually in bedding orgrass. They live for weeks off thehost, but survive for up to a year ifthey temporarily return for a blood feeding. Females lay several eggs per day,which hatch in bedding, litter, or grass.


Most fleas are brown and are large enough to see with the naked eye. Theyare particularly abundant in temperate and warm climates. Of the six speciesdial attack poultry, three are important in North America.

The European chick flea (Ceratophyllusgallinae) is most likely to be foundin northeastern areas. It lives in nests and liner, and stays on birds only longenough for a blood meal.


Life cycle of the Darkling Beetle(Alphatobius diapernus)

eggs

jgjpre®* Imeal worm!

Darkling BeetleThe darkling beetle (Alphatobiusdiaperinus) and its larvae, the lessermealworm, are not, strictly speak-ing, parasites ofchickens, but they'reoften found in and around poultryhouses. This beetle is about V* inch(0.5 cm) long and likes to hide incorners and under feeders. It is diffi-cult to control unless you can takeadvantage of its extreme sensitivityto low temperatures: if the tempera-ture falls below 40°F (8"C), thor-oughly clean out the coop and openit up to the chill.


The western hen flea (C. niger) is common along the Pacific Coast andnorthward into Alberta. It is similar to the European chick flea, but occurs in a


different geographical area. It breeds in poultry droppings and only occasion-ally returns to birds for feeding.Sticktight FleasThe sticktight flea (Echidnophaga galliiiacea) —also called "soutiiern chicken Ilea" or "tropical henflea" — is quite common all across the southernUnited States and as far north as New


York. It is par-ticularly prevalent in sandy areas.The tiny, reddish brown fleas measuring fi/u>o ofan inch (1.5 mm) attack humans and odier mammalsas well as chickens. They attach themselves in clus-

Sticktight Fleaters of 100 or more to the skin of a chicken's head, (Echidnophagawhere they remain for weeks. Sometimes


they imbed macea'their mouths permanently into the skin to suck the chicken's blood. The re-sulting blood loss may cause death, especially to young birds.

Sticktight fleas are easy to control on birds using a flea salve or poultry-approved insecticide. Unfortunately, they are difficult to remove fromhousing, due to the female's habit of forcefully ejecting eggs so they will lodgeand hatch in


sand or litter. Control involves removing infested litter andheavily dusting the floor with an approved insecticide. Repeal die applicationtwo or three times at 10- to 14-day intervals to kill fleas that hatch in the mean-time.

Sunlight, heat, excessive moisture, and freezing all inhibit sticktight andother fleas. Moisture may be used to control Ileas when housing is empty be-tween flocks. Sunlight,


heat, or cold may be used effectively in a clean coopthat can be opened up for complete exposure.

FliesFlies are

insects of the order Diptera, meaning "nvo-winged." One pair ofwings is for flying, the other is for balance. Flies that bother chickens fall intotwo categories: biting flies and filth flies. Both kinds spread diseases and para-sitic infections.

Biting Flies


Biting flies are found primarily around bodies of water. The two mainkinds that bother chickens are black flies and biting gnats.

Blackflies (Siinulium spp) — also called "buffalo gnats" or "turkey gnats"— are found at the edge of flowing water. They are approximately the same sizeas mosquitoes, but are chunkier and have rounded or humped backs. Theytransmit leucocytozoonosis and


sometimes attack in swarms large enough to


cause anemia and deadi.

Blackflies are difficult to control. Your best bet is tocontrol larvae in spring (using an insecticide locallyapproved for the purpose), before adults emerge.Chickens kept in strict confinement may be pro-tected from blackflies by windows fitted withfine-mesh screens.

Biting gnats (Culicoides spp) — also called"midges," "no-see-ums," "punkies," or "sandflies"

pupa

Life cycle of House Fly(Musca domesticalthird larval stage o eggsxj first larval stage

SECOND LARVAl STAGEW


— are found in swampy ar-eas. Attacks irritate chickens, causing them to become resdess and to eat less.Like blackflies, biting gnats are difficult to control. A good start is to eliminatesources of stagnant water.

Filth FliesThe

common house fly (Musca domestical and odier filth-breeding fliesdon't bite, but they irritate birds, transmit tapeworm (by ingesting tapeworm


eggs that infect a chicken when it eats die fly), and spread bacterial diseases.Flies also leave annoying specks on eggs, and they bother neighbors, some-times leading to nuisance-abatement lawsuits.

Fly problems are a direct result of housing a flock in an artificial environ-ment without providing proper management. Flies breed in damp litter andmanure. An important fly-control measure is


keeping litter dry by guardingagainst leaky waterers, leaky roofs, and run-off seepage due to improper grad-ing outside.

Good ventilation also helps dry out manure and litter. Since flies don't likemoving air, a ceiling fan not only improves ventilation on hot days, but keeps

Blackfly'Simulium spp)


flies from bothering chickens.

A common mistake that can lead to awarm-weather population explosion offlies is to remove litter without thor-oughly cleaning the coop. When manureaccumulates and dries out, it attracts flyparasites and predators that naturallycontrol flies. If you remove litter and ma-nure, you also remove the natural flypredators.

Letting manure accumulate


duringwarm weather, and making sure it staysdry, is a good fly-control method. An-other is cleaning out litter and manure atleast once a week. The cleaning must beabsolutely thorough — one small clumpof manure contains enough fly eggs toproduce hundreds of flies. Dispose of thelitter by composting it, burying it, orspreading it on a field where chickenswon't roam within the next year.

If flies get out of


hand, avoid usinginsecticides or you'll run the risk ofbreeding a resistant fly population. Onealternative is to introduce fly predators, purchased from one of several mail-order sources. Another alternative is to buy or make fly traps.

Mosquitoes

The occasional mosquito does not seriously bother a chicken, but a massattack lowers egg production and can cause death. Several


mosquito species(Aecies and Culex spp) transmit poultry diseases, including malaria and pox.Such diseases are most likely to occur in late summer and early fall, when coolnights attract mosquitoes to the warmth and lights of a poultry house.

Control mosquitoes by eliminating their principal breeding grounds —stagnant water in persistent puddles, old tires, and swampy areas. Wheremosquitoes


are dense, vaccinate against pox.

LiceLice

come in two varieties: blood-sucking and chewing. Bloodsucking liceattack only mammals. Chewing or biting lice (order Mallophaga) attack both

Homemade Fly TiapHow many traps you need de-pends on how bigyour chickenhouse is and on how bad the flyproblem is. Foreach trap,you'llneed a milk jug or similar con-tainer. Cut four 3-inch (6 cm)diameter holes into the upperone-third of the jug, one holein each face. In the bottom ofthe jug, place 2 tablespoons ofcommercial fly bait granulescontaining the fly sex phero-mone (common brand namesinclude Muscalure and Tri-colure). Hang the jug close tothe ceiling. Flies will enter thejug to feed on die bait and diebefore they can leave. As deadflies accumulate, replace thejug with a new one.


mammals and birds. Several species infest chickens, and a bird may be in-fected by more than one species at a time.

Lice are species specific, meaning a louse that prefers chickens doesn't likeany other kind of bird or animal. How seriously chickens become louse-infested, or lousy, depends in part on their strain — some strains are moreresistant than others. Debeaked


birds, because they can't groom properly, aremore likely to become seriously infested than other chickens.

An infested bird becomes so irritated from being chewed on that it doesn'teat or sleep well. Egg production may drop as much as 15 percent, and fertilitymay also drop. Chickens get restless and injure themselves by scratching andpecking their own bodies. In the process, feathers get damaged — an impor-


tant consideration if the birds are raised for show. In a serious infestation,especially in chicks, birds die.

Louse infestation (technically called "pediculosis") often accompaniespoor management and associated problems such as malnourishment, inter-nal parasites, and other infections. Whether louse infestation causes theseproblems, or these other problems make chickens more susceptible


to lice, isarguable but entirely academic.

Lice SpeciesLice

species vary in shape and size, ranging in length from V25 to [A inch (1to 5 mm) — big enough to see with the naked eye. Most liceare yellow or straw-colored, making them difficult to see011 white chickens, but easy to spot on dark-feathered vari-eties.

Among the different species that attack


chickens, eachhas a preference for feeding on certain parts of the body,resulting in descriptive common names such as winglouse, head louse, and fluff louse. Most lice eat feathers,skin scales, and other organic matter on the skin. An ex-ception is the body louse, which chews through skin andpunctures growing quills to get blood. Body and head liceare the two most serious louse pests of poultry.

In a heavy


infestation of body lice (Menacanthusstramineus), you'll find numerous scabs on the bird's skinand pearl-colored egg masses at die base of feathers. Bodylice move fast — when you part a

bird's T

he head louse

it*-. r ?

Head Louse(Cuclotogasterheterographa)

d ^ —ki

Jjgfc1fc:;:v

Body Louse(Menacanthusstramineus)


(Cuclotogaster heterographus) is themost serious louse pest of young birds, particularly inheavily feadiered breeds like Polish and Cochin. It spreadsfrom a hen to her chicks, causing the little guys to become


Chart 4-2Lice

Common NameScientific Name

Body PartAffected

WherePound

Appearanceof Louse

AppearanceofEgR

Commonin NorthAmerica

head louseCuclotogasterheterographus

head andneck

base offeathers

oblong, grayish,0.1" (2.5 mm)long

white,attachedto down orfeather base

very

small body louseMenacanthuscornutus

vent,breast,head,under wings

close toskin

like bodylouse, butsmaller

like bodylouse eggs,but smaller

110

body louseM. stramineus

vent, breast,head,under wings

close toskin insparselyfeatheredareas

straw-colored,moves

in clustersnear featherbase

very

small body louseM. pallidulus

vent, breast,head,under wings

close toskin

like bodylouse, butsmaller

tike bodylouse eggs,but smaller

no

shaft louseMenopongallitiae

leathershafts

bodyfeathers

like bodylouse, butsmallerand paler

in stringson feathers

yes

wing louseLipeurus caponis

featherbarbules

wing, tail,back, andneckfeathers

slender, gray,moves slowly

in clustersnear

feather base

yes

fluff louseGoniocotesgallinae

body featherfluff

backand vent

small, broad,yellow, slow

in clustersnear featherbase

no

large chickenlouseGoniodes gigas

body andfeathers

bodyfeathers

dark. in clusterssmokey gray near feather0.25" (5 mm) long base

no

brown chicken feathers body large, in clusters no


louseG. dissimilis

feathers

reddishbrown

near featherbase


droopy and weak. Seriously infested chicks may die before they reach 1 monthof age.

The shaft louse (Menopon gallinae), which does not infest young birdsuntil they become well feathered, is a possible transmitter of chlamydiosis. Itpunctures soft feather quills near the base and leaves strings of light-coloredeggs on feathers. It likes to rest on feather shafts, but scurries toward the bird'sskin when you part the feathers.


The fluff louse (Goniocotes gallinae) is fairly common. It stays mainly onfluff and is relatively inactive, so it causes little irritation or injury. Similarly, thebrown chicken louse (Goniodes dissimilis) which occurs primarily in theSouth, lives on body feathers. Two species of small body lice (Menacanthuscornutus and M. pallididus) are similar to each other, and both are often mis-


taken for immature body lice. These and other lice species are not particularlycommon in North America.

Life Cycle and Treatment

A louse lives for several months, going through its entire life cycle on abird's body. It can survive less dian a week off the body. The female louse laysher eggs, called "nits," on a chicken's feathers and makes sure they stay thereby sticking them down with glue.


Nits hatch in 4 to 7 days. Young lice, called "nymphs," are unlike otherinsects in that they look like adults, only diey're smaller and nearly transpar-ent. They go through several molts and develop color as they grow.

When a louse matures, it mates on the bird and starts laying nits. One fe-male may lay as many as 300 nits in her lifetime. Since lice go through onegeneration in about 3 weeks, in just a few months one


pair explodes into120,000.

Lice usually travel to chickens by way of wild birds or used equipment.They spread by crawling from bird to bird or through contact with infestedfeathers, especially during a molt.

Lousiness is usually worse in fall and winter. Suspect lice if your chickensare restless and constantly scratch and pick themselves. Look for moving liceon feathers and skin, and for white or


grayish egg clusters at the base of feath-ers. If you see lice on one bird, chances are good the whole flock has them, orsoon will.

Inspect your birds at least once a month. As soon as you spot lice, treat the(lock by spraying or dusting with an insecticide approved for poultry. Spraycaged birds from the bottom as well as from the sides and top. Treat litter-reared birds by sprinkling powder on the litter and in preferred dusting


areas.Treat individual birds by placing a pinch of powder beneath each wing and inthe vent area. For head lice, mix insecticide powder with Vaseline and rub it on


each bird's head and neck. Since no insecticide kills nits, repeat the treatmenttwice at 7-day intervals.

MitesMites belong to the tribe Arthropoda, characterized by exterior skeletons andjointed limbs. They are members of the class Arachnida, a group of spider-likecreatures with single-segmented bodies and four pairs of legs.Mites are quite small, usually


under '/2s inch (1 mm) inlength; some are microscopic. All have mouths designed forpiercing or chewing. Depending on the species, they live onblood, tissue cells, or feathers.Most mites spend a lot of time off the bird and are spreadby contaminated equipment, shoes, or clothing. They are alsospread by infested birds, including wild ones.Some mites remain on a chicken's skin. Others hide infeather


parts, burrow under the skin, or make their way deepwithin the body to live in the lungs, liver, or other organs. Miteinfestation (technically called "acariasis") causes irritation,low vitality, plumage damage, increased appetite accompanied by low eggproduction, reduced fertility, retarded growth in young birds, and sometimesanemia and death.

Red MitesThe red

mite (Dermanyssusgallinae)


— also called "chicken mite," "poul-try mite," or "roost mite" — is the most common mite found in warm climatesand is a bigger problem in summer than in winter, since it becomes inactivewhen the temperature drops. The red mile is more likely to be found on litter-raised birds than on those kept in cages.

Red mites are grey until they suck a chicken's blood and turn red. They liveand lay their eggs in cracks near


roosts or nests. They survive for up to 6months off chickens, so housing may remain infested long after chickens havebeen removed.

The red mite population increases rapidly in hot weather; one female laysas many as 120,000 eggs. The mites feed at night. In a heavy infestation, somemites may stay on birds during the day and can kill chicks and setting hens. Ina particularly severe infestation, red mites


invade die roof of a bird's mouth,causing serious anemia. Red mites, when abundant, will also attack humans.

Check birds at night, when mites are on the prowl. You'll see little speckscrawling on the roost or on the birds themselves. Red mites can be controlledsolely by cleaning up the birds' environment — 110 need to treat individual

- H1 |,

rtM V' 1 }'Red Mite(Dermanyssusgallinae)


Chart 4-3

Mites

Sarcoptidae

KnemicestnutansK. gallinae

EpidermoptidaeEpiderm

bilRivoltasiabifurcata

Cytoditidae Cytodites rntdus

Laminosioptidae LamcysticolaAnaldesidae

MgalliMDermogylph

usminorD. elongaPteobtusesNeosca.ameTrombiculaalfT. batatasT. spleMyobi

idae

Syringophilus

bipectinatusDermanyssidae Dermanyssus

gallinae

OmithonyssussylviarumO. bursa

Argas spp.Amblyomm

Ioc/5

Commonin NorthAmerica

Wherefound

Commonname

Family Species

Prerolichidae

ArgasidaeIxodidae

Ixodidae


aamericanumA. rnaculatumscaly-legmitedeplumingmitescaly-skinmite

fea

ther-eating mite

air-

sac

m

i

t

e

c

y

s

t

m

i

t

e

f

e

a

t

h

e

r

mi

tefeather mitequill mite

quill m

itefeather mitechicken

chi

Trombiculidae Acomatacarus galli chigger


ggerchigger

chiggerred bug

quill

mit

e

red

mit

e

northernfowl mitetropical fowlmitefowl ticklone startickGulf Coasttickun

feathered

part of legs

in skin at base

of feathersbody

and upperlegs on birds

respiratorysystemunder skin

legs and headon


birdsinside quills

inside quills

on flight and

tail feathershe

dgerows and

dense brush

inside quills

at night in n

estsand cracks; duringday on birdson birds

on birds

wood litter

southernstates

very

northernstateswarmregionsyessouthernstatessouthernstates


, crackswood litter, cracks

wood litter, cracks

yes

no

no

unknow

n

unknow

n

no


birds. Clean facilities thoroughly and dust with a pesticide powder approvedfor poultry, with particular attention to cracks and crevices. Repeat the dustingin 5 to 7 days.

Fowl MitesThe Northern fowl mite (Ornithonyssus sylvia-rum) is the most serious external parasite ofchickens and the most common one found in coolerclimates. It completes its entire life cycle in less thana week, so an infestation worsens rapidly. In con-trast to red mites, Northern fowl mites increasemore rapidly in cold weather.This mite differs from the red mite in anotherway — it survives only about a month off the bird. Itlives its entire life on the bird and therefore doesmore damage than the red mite.Evidence that northern fowl mites are presentincludes mites crawling on eggs in nests, large num-bers of mites on the skin of birds during the day,darkened vent feathers, and blackened, scabby skinaround the vent. This mite moves quickly and willcrawl up your arms when you handle your chickens.Control involves dusting individual birds with a pes-ticide approved for poultry. Repeat the dustingagain in 5 to 7 days.The tropical fowl mite (Ornithonyssus bursa) re-sembles the northern fowl mite and seems toreplace it in warm areas. Like the northern fowl mite, Lhe tropical mite lives itsentire life on the bird, but by contrast is more likely to lay eggs in poultry nests.Control involves dusting nests as well as individual birds.

Skin MitesThe scalv-leg mite (Knemidocoptes mutatis) is a pale gray, round,

tinycreature, only about Vioo of an inch (0.5 mm) in diameter. It is more likely toattack older birds, but also affects young birds kept with old birds. It burrowsinto the unfeathered portion of the skin on a chicken's shanks, raising the


scales by generating debris that accumulates beneath them. As a result, thelegs thicken and crust over. In severe infestations, this mite attacks combs andwattles as well as legs.

The scaly-leg mite spends its entire life on the chicken. Once it invades,

Northern Fowl Mite(Ornithonyssus

sylviarum) found in coolclimates

Nearly identical TropicalFowl Mite (Ornithonyssusbursa) found in warmerareas


you'll have a hard time getting rid of it. The best approach is to cull affectedbirds. Treatment involves smothering the mites by applying a kerosene-linseed oil mixture (see box) to the

chicken's legs every 10 days until theproblem clears up. Coat the legs with mineral oil or warmed petroleum jelly(Vaseline) to loosen old, crusty scales, but don't expect raised scales to returnto normal.

Scaly-skin mite (Epidermoptes bilobatus) is a relatively rare parasite thatcauses avian scabies. The mite burrows into the skin of a chicken's body andthighs, causing inflammation and itchiness. The skin thickens with brownish-yellow scabs that may become infectcd with fungus. A serious infestationcauses emaciation and death. The scaly-skin mite is difficult to control. Keep itfrom spreading by isolating or culling infested birds.

Feather MitesFeather mites live on and eat plumage, ruining feathers by chewing

stripesacross them or by damaging the featiier base. Luckily, these mites are not com-mon in North America.


Perhaps the most common among them is the depluming mite

Scaly-leg mites spread slowly by traveling from bird to bird. They can becontrolled by brushing perches and chickens' legs once a month with a mixtureof one part kerosene to two parts linseed oil (not motor oil).

Scaly-leg and other burrowing mites can be controlled in exhibition birdswith ivermectin (trade name Ivomec), an over-the-counter cattle wormer soldat most feed stores. Give a bantam 5 to 7 drops by mouth; give a larger bird lA ccby mouth. Since the withdrawal time is not known, ivermectin should not beused on birds kept for meat or eggs.

Controlling Scaly-Leg Mites


(Knemidocoptesgallinae), a tiny creature that is barely visible to the naked eye.It burrows into the skin at the base of feathers, causing the chicken to scratchand pull out its feathers in an effort to reduce the irritation. The problem in-creases in warm weather. This mite is difficult to control; cull birds to avoid itsspread. Treatment involves dipping individual birds in a solution made up of 1ounce (30 grams) soap, 2 ounces (60 grams) sulfur, and 1 gallon (4 liters) warmwater.

The quill mite (Syringophilus bipectinatus) inhabits a feather quill, result-ing in partial or total loss of the feather. Evidence of its presence is the powderyresidue it leaves in the quill stump. Since diese mites hide inside feathers, theonly known way to control them is to dispose of affected birds and thorougltlyclean their housing. Quill mites occur in the eastern states, but are quite rare.

Also rare are:• the feather-eating mite (Rivoltasia bifurcata), which does litde

damage• the Canadian feather mite (Meginnia gallimdae), which causes

crustyheads and the loss of leg scales

• the soudiern feather mite (M. cubitalis), which is similar to the Cana-dian feather mite but occurs primarily in the southern United States.

Internal MitesAlthough mites are basically external parasites, they sometimes

invade theinside of a chicken's body, either by burrowing under the skin or by invadinginternal organs. No one knows how common they are. Since they do not causeserious health problems, few people look for them. As a result, little is knownabout them.


The cyst mite (Laminosioptes tysticola) — also called "flesh mite" or "sub-cutaneous mite" — is a tiny creature visible only under a microscope. Itburrows into a chicken's skin, where it does little damage until it dies. Then itbecomes encased in a yellowish nodule (somewhat resembling a nodulecaused by tuberculosis). The main problem cyst mites cause is destroying dieaesthetic appeal of meat birds. The only known way to get rid of them is todestroy infected birds.

The air-sac mite (Cytodites nudus) invades a chicken's respiratory system,where it seems to do little damage unless it becomes abundant. A serious infes-tation produces symptoms that resemble avian tuberculosis: emaciation,anemia, and death. During postmortem examination (see chapter 10), you cansee the mites as slow-moving white dots on the air-sac surfaces. The onlyknown method of control is to cull affected birds. Unlike other mites, whichhatch from eggs and molt several times to reach maturity, air-sac mites areborn live and spend their entire life cycles in a chicken's windpipe, lungs, ait-sacs, and bone cavities.

72 TIN; Chicken Health Handbook

CHIGGER MITESChigger mites — also called "jiggers," "harvest mites," and "red

bugs" —infest the skin of birds, humans, and other animals. Of the 700 known species,only 4 are common in the United States and Canada. Chiggers are most preva-lent east of the Rockies, although some species occur in Arizona andCalifornia. The adult, identified by its red, figure-eightshaped body, feeds on plants. Only the larval stage isparasitic. In southern states chiggers go through severalgenerations per year; in the north, they go through onlytwo or three generations.

Chigger larvae have diree pairs of legs, instead of theusual four of other mite forms. They are about V150 inch(0.17 mm) long — so small they can barely be seen withthe naked eye. They are straw-colored, making themeven more difficult to see until after they feed, when theylook like red dots.

Chiggers are fond of attacking a chicken's neck, breast, and wings. Theypierce the skin with their mouths, inject poisonous saliva that liquifies the skin,and feed on liquified skin for up to 6 days before dropping off. The bite causesitching, swelling, and irritating scabs that may last for weeks. Young birds be-come droopy, stop eating and drinking, and sometimes die.

Since chiggers prefer tall weeds, they can be a problem for free-rangedchickens. The best method of control is to keep weeds mowed around yourcoop. Where chiggers are especially numerous, repel them by dusting orspraying widi sulfur.Chart 4-4

Chiggers

Species Distribution Habitat

Acomatacants galli southern grassy meadows, dense


U.S. brushNeoschongastia a. americana

southern U.S.

dry soil and rocks

Trombicula alfreddugesi

widespread dry, brushy areas

T. batatas tropical areas sunlit, grassy meadowsT. splendens eastern U.S. swamps, bogs, rotten

logs

Scavenger MitesScavenger mites (family Uropodidae) live in poultry litter and feed on

fungi. They are especially numerous where new pine shavings are thrown on

Chigger Mite Larvae(Trombiculaalfreddugesi)


top of old litter. Discovering an infestation of scavenger mites can be alarming,but don't worry — these mites do not attack chickens.Ticks

Ticks are really nothing more than big mites. They are divided into threefamilies, two of which are parasitic — Argasidae or soft ticks and Ixodidae orhard ticks.

Soft TicksOf several species of soft ticks, Argas persicus is the most prevalent

in theUnited States. It is commonly known as the "fowl tick," "adobe tick," "bluebug," "chicken tick," or "tampan." It mainly occurs in the southwestern statesand along the Gulf Coast.

Fowl ticks are leathery, egg-shaped, flattish and up to '/a-inch (12 mm) long.They feed only on blood and can survive as long as 4 yearsbetween feedings. They are tan or reddish-brown until theyfeed, then they turn bluish.A female tick lays as many as seven batches of eggs con-taining up to 150 eggs each. She deposits her eggs under treebark and in coop walls. In warm weather, the eggs hatch inabout 10 days; in cool weather, they take up to 3 months.Tick larvae crawl around until they find a host, attach them- Fow| ^selves, and feed for about a week. They leave the bird to (Argas persicus)molt, then return for another blood meal.

Ticks are particularly active during dry, warm weather. They hide in cracksand crevices during the day and come out at night to feed, feeding takes 15 to30 minutes and leaves red spots on the bird's skin. Chickens that expect to bebitten become restless at roosting time.

Other signs of infestation are raffled feathers, weakness, depressed appe-tite, weight loss, a drop in laying, and sometimes diarrhea. The bite woundmay become infected with bacteria. In a growing or mature hen, toxins


re-leased from the ticks' saliva can cause transient paralysis that is sometimesmistaken for botulism or Marek's disease. Soft ticks also spread a number ofdiseases, including cholera epidemic tremor, and spirochetosis. A large infes-tation causes anemia, emaciation, and death.

Control includes housing chickens in a metal building (to eliminate hidingplaces), and installing suspended roosts or keeping birds in cages (so tickscan't easily climb onto diem). Eradicating ticks is difficult. It involves thor-oughly cleaning housing and spraying with a pesticide labeled for ticks that isapproved for use with poultry. Use a high-pressure sprayer and pay specialattention to cracks and crevices. If birds must be individually treated for larval


ticks, dipping is more effective than spraying.Since ticks molt several times before reaching adulthood, and the

entireprocess takes about 8 weeks (longer, in winter), spray every week for at least 8weeks to destroy all stages in the life cycle, then spray once a month thereafter.Alternate the type of insecticide you use so the ticks don't become resistant toone type.

A serious tick infestation involving the transmission of a disease may re-quire such drastic measures as cutting down and burning nearby trees inwhich chickens roost and/or burning down infested housing. Moving tick-infested chickens to new housing will, however, only move the problem to anew location.

Hard TicksHard licks are most likely to be found on free-ranged chickens in

temper-ate and tropical climates. Two kinds affect chickens in North America.

The lone star tick (Amblyominaamericanum) occurs from southern Iowa

eastward to the Atlantic Coast and southward into Mexico. It is found in wood-

land and brushy areas, and attacksdogs and humans as well as chickens. Since

it transmits human diseases, you don't want one of these tobite you.

The adult female lone star tick is pear-shaped and chest-nut-brown with a pale spot on her back. She'll lay between5,000 and 7,000 eggs, which take 32 clays to hatch. The lar-vae, called "seed licks," are straw-colored and crawlaround in bunches. Nymphs are light to dark tan and aresmaller than adults. The lone star tick has a 1 -year life cycle,during which it feeds three times on three different hosts.The Gulf Coast tick (Amblyomina macula turn) is chest-nut-brown with colorful patterns on its back. It occurs along the Atlantic Coastfrom Virginia southward into Florida and westward along the Gulf Coast intoTexas, decreasing in numbers as it moves inland. Although it attacks chickens,it prefers humans, dogs, and other large animals. Each female lays


15,000 to19,000 eggs, which take 19 to 28 days to hatch. Larvae usually attach them-selves to die neck area and feed in groups.

Parasite ControlNot all external parasites are equally common in all areas of the country. Yourstate Extension poultry specialist can tell you which parasites are most likely tobe found in your area and can advise you on currently approved methods fortheir control.

Many parasites can be controlled through good management, including

r 'iJ > '

Lone Star Tick(Amblyommaamericanum)


giving housing a periodic thorough cleaning. Once parasites invade a coop,sometimes die only way to get rid of diem is to use a pesticide.

Methods for applying pesticides to birds can be divided into two catego-ries: individual treatment and flock treatment. Individual treatment is moreeffective, but Hock treatment is more practical for a large flock.

No pesticide destroys parasite eggs. To avoid reinfestation when eggshatch, a repeat application is necessary, timed to coincide with the hatchingcycle of the parasite involved.

Pesticide UseThe list of pesticides recommended for poultry is fairly short and changes oftendue to two things: continuing development of resistant strains of parasites andnew knowledge about the dangers of various products. Even approved pesti-cides are toxic and should be handled with care. Always read the label and followall precautions.

Before applying any pesticide, remove or cover feeders and waterers andgather eggs. Wear gloves and a face mask, and avoid inhaling sprays or dusts. Ifyou spill any on yourself, wash your skin and launder your clothing. Afterapplying a pesticide, wash your clothing separately.

Store pesticides away from children, pets, livestock, foods, and feeds. Keepthem in their original containers with their labels intact. Puncture emptycontainers so they can't be reused. Due to laws regarding toxic wastes, gettingrid of empty containers can be difficult. Check with your local waste-disposalagency.

Some pesticides approved for poultry are restricted, meaning you mustobtain a permit to use them. Contact your county Extension office or statepoultry specialist for details. Obviously, your best bet is to avoid using toxicchemicals by managing your flock so you don't need them.

Pyrethrum. One fairly safe natural pesticide is pyrethrum, a plant extractthat's relatively non-toxic to humans and birds but is highly toxic to insects.Put into a squeeze bottle and puffed into cracks and crevices, or


powderedonto vent fluff and beneath wings, it wards off body parasites and flies.

Dust baths. Old-time poultry keepers controlled external parasites by pro-viding their flocks with bins of fine road dust or ashes, sometimes adding sulfuror lime-and-sulfur garden dust to enhance the beneficial effects of the dustbath. Chickens instinctively dust themselves to keep clean and rid themselvesof external parasites, which they dislodge by pulling leathers through theirbeaks while grooming. But dusting in ashes, sulfur, or other chemicals involvesa trade-off — chickens are highly susceptible to respiratory problems, and in-


haling exotic materials makes matters worse.Nicotine sulfate. Another old-time treatment that works wonderfully

wellis the gardening pesticide nicotine sulfate (sold as a 40 percent solution underdie trade name Black Leaf-40). It works by evaporating when it is warmed by abird's body heat. It's painted on roosts just before nightfall or dabbed on ventfluff. As a 2 percent dust it's puffed into vent feathers. The use of nicotine sul-fate on poultry has been banned in some states because it is highly toxic ifspilled on the skin of chickens (or humans). Old-timers could sometimes re-vive a poisoned bird by tossing it into the air, causing the bird to llap its wingsand inhale oxygen by reflex, but the trick didn't always work and the bird oftendied.

Petroleum oil. A safer old-time method that's messy but effective againstparasites living off a bird's body is to paint petroleum oil onto roosts and nestsand into cracks and crevices. It works by coating and smothering lice andmites, but can create a fire hazard in a wooden building.

Dog clip/shampoo. Two other products that work quite well for chickensare flea dips and flea-tick-louse shampoo for dogs. Shampooing is ideal if youwash your birds for exhibition anyway. On a warm, sunny day, wash each birdin warm water, soaking the bird thoroughly and working a good lather amongthe feathers. Rinse the bird at least twice in warm water. Pat the feathers drywith towels. Let the bird dry in a warm area, away from drafts, or hasten dryingwith a blow dryer.

Systemic inhibitors. A fairly new idea being developed for chickens is theuse of systemic inhibitors that minimize infestation by making a chicken'sbody unpleasant to parasites. Commonly used systemic inhibitors includebrewer's yeast fed to cats to ward off fleas, and vitamin B taken by humans to


keep mosquitoes away. Some drugs, including the coccidiostat sulfaquin-oxaline and the catde wormer ivermectin, work similarly.

PrecautionDespite the success of extra-label ttses such as those suggested

above, itisn't a good idea to experiment wit h products that are not specifically intendedfor poultry unless: a) you do not plan to eat meat or eggs from your flock in thenear future, and b) you're prepared to lose birds treated with inappropriateproducts.

Internal Parasites: Worms

INTERNAL PARASITES ARE DIVIDED into two major categories — protozoa(discussed in the next chapter) and the group commonly known as worms.Worms can become a problem in ground-reared flocks, particularly wherechickens are kept in the same place year after year. Most infestations developrather slowly.

Under good management, worms and chickens become balanced inpeaceful co-existence. Through gradual exposure, birds can develop resis-tance to most parasites. An overload is usually caused by disease or stress.

If the scale tips in favor of the worms, the chickens may gradually loseweight as the worms interfere with food absorption and other digestive pro-cesses. Some worms, instead of invading the digestive tract, invade therespiratoiy system, causing breathing difficulties and gradual blockage of air-ways. Less common worms invade other parts of die body.

Worms are divided into two main groups, according to the shapes of theirbodies. Roundworms or Nemathelminthes have cylindrical bodies; flatwormsor Platyhelminthes have flattish bodies. In turn, roundworms, are divided

184

INTERNAL PARASITES: WORMS 185

intonvo groups, nematodes (also called "roundworms") and acanthocephalans(thorny-headed worms). Flatworms are also divided into two groups, cestodes(tapeworms) and nematodes (flukes).


Intermediate HostSome worms have direct life cycles whereby female worms living in a chicken'sbody shed eggs that pass out of the chicken in droppings and are eaten by thesame or another chicken to begin a new life cycle. Other worms have an indi-rect cycle that requires an intermediate host. A host is any living thing in which

Roundworm eggsor tapewormoo1 segments

ccxp p o" 3 c containing eggs4}. are possed in

are poss*chicken'sdroppings

Direct Life Cycle of Roundworm

Indirect Life Cycle of Roundworm or Tapeworm

1Roundworm- or tapeworm-infested chicken

Chicken acquiresparasite by eating JEggs eaten byintermediate host (beetlefly. slug, earthworm,grasshopper, etc.)


Roundworm eggTopeworm egg


a parasite resides. In an indirectcycle, worm eggs expelled by achicken are eaten by a grasshopper,earthworm, or other intermediatehost. A chicken becomes infected orreinfected by eating the intermediatehost (or being bitten by the interme-diate host, which releases parasitelarvae in its saliva).More than half the nematodesand all the tapeworms that invadechickens require an intermediatehost. These indirect-cycle parasitescreate greater problems in late summer, when beetles, grasshoppers, andother intermediate hosts proliferate. Knowing which parasites have indirectlife cycles, and which intermediate hosts are involved, is an important part ofany parasite control program.

Controlling WormsControlling parasitic worms requires good management rather than constantmedication. Not only can parasites become resistant to medication, butworming becomes an expensive and never-ending cycle unless you eliminatethe source of infection.

Reducing the need for worming medications includes providing aproper diet; a diet that's high in vitamins A and B and animal protein en-hances immunity to roundworms. Good management involves thesesensible parasite-control measures:

• practice good sanitation• eliminate intermediate hosts• rotate the range of free-ranged

birds• avoid mixing chickens of

different ages• don't raise turkeys with chick-

ens


Most worms spend part of theirlife cycles away from the bird's body,offering a good handle on parasite pre-vention and control. To avoiddirect-cycle parasites, design housing

Parasitic Wormsof Chickens

Nemathelmimhes (roundworms)Nematodes (roundworms)Acanthocephalans (thorny-headed worms)Platyhelminthes (flatworms)Cestodes (tapeworms)Trematodes (flukes)

General Symptomsof Worm InfestationUsual SymptomsPale head (anemia)Droopiness/depressionReduced layingGradual weight loss

Ocassional SymptomsFoamy diarrheaDeath


so chickens can't pick in their own droppings. To avoid indirect-cycle para-sites, keep intermediate hosts away from the coop. Take care when usinginsecticides, though, since chickens can be poisoned from eating poisoned in-sects. When possible, use an insecticide only in an unoccupied house, thenthoroughly clean up before introducing a Hock.Wormers

A healthy chicken can tolerate a certain amount of parasitic invasion.Avoid using a wormer unless parasites cause your chickens to look scrawnyand scruffy, lose weight, and lay fewer eggs. If worms get out of control andreach the point where they begin to affect the chicken's health, you may haveno choice but to use a wormer. Wormers are more properly called

WormersDifferent brands of the following anthelmintics come in varying strengths. Dos-

ages vary accordingly. Always follow label directions.Coumaphos (Meldane) is a feed additive approved for large

roundworms,capillary worms, and cecal worms. It is not readily available for small-scale use.For replacement pullets, 10 to 14 days before laying starts coumaphos is added tomash at the rate of 0.004 percent. For hens that are already laying, the rate is 0.003percent for 14 days. Since coumaphos has cumulative toxic effects, it should not beused within 3 weeks of a previous worming. The withdrawal period is 7 days.

Hygromycin B is a feed additive approved for large roundworms, capillaryworms, and cecal worms. It is not readily available for small-scale use. Minuteamounts are added to mash at a continuous rate of0.00088-0.00132 percent. Thewithdrawal period is 7 days.


Piperazine is a readily available wormer approved for large roundworms.Despite its wide safety margin, it is currently under FDA scrutiny and may one daybe withdrawn for use in chickens. Piperazine is rapidly absorbed and rapidlyexcreted. It acts as a narcotic, weakening and paralyzing adult worms and causingthem to be expelled from the chicken, live, with a bird's digestive wastes, butrequires a high concentration to be effective. Piperazine works best as a one-timeoral dose of 50 to 100 mg per bird. The next most effective method, and one that'smore practical for large flocks, is to add piperazine water-wormer to the birds' solesource of drinking water at the rate of 0.1 to 0.2 percen t (3 ml per gallon) for 4 hours.Repeat the dosage in 7 to 10 days. The withdrawal period is 7 days.Phenothiazine is approved for cecal worms. Itworksonly against cecal worms

and has a narrow margin of safety, so take care not to exceed the recommended


"anthelmintics" (from the Greek words antimeaning "against" and helminsmeaning "worms").

How often your chickens need worming, if they need it at all, depends inpart on the way your flock is managed. Chickens on open range may needworming more often than confined chickens. Caged chickens need wormingleast often of all. Flocks in warm, humid climates, where intermediate hostsare prevalent year-around, are more likely to need worming than flocks in coldclimates, where intermediate hosts are dormant part of the year.

To ensure a wormer's effectiveness (especially if you're battling tape-worm), withhold feed from the flock for 18 hours before worming. About anhour after worming, feed a moist mash, which causes hungry chickens to eatslowly.

Afteryou've used one wormer for a time, parasites will become resistant to

dosage of 0.05 grams per bird for 1 day only. The withdrawal period is 7 days.Drugs not approved for poultry use (withdrawal periods are therefore not

made public):levamisole, the active ingredient in telramisole, is effective against a

widevariety of nematodes. It actson a worm's nervoussystem, paralyzing the worm andcausing it to be expelled, live, with digestive wastes. Levamisole drench (for oraluse) is added to water at the rate of 0.03 to 0.06 percent (10 ml per gallon) for oneday only. Levamisole injectable is injected subcutaneously (beneath the skin) onetimeonly at the rateof 25 mgper 2 pounds of body weight (25 mg/kg). Levamisole'stherapeutic effect in treating a variety of infectious diseases is under investigation.


Th ia bendazoleis a rap i d ly absorbed, rapidly metabolized, rapidly excretedwormer used to kill gapeworm and common roundworm. It is less potent thanmore slowly absorbed and excreted products, making a divided dose (adminis-tered over a period of time) more effective than a single dose. The dosage rate infeed is 0.5 percent for 14 days; individual treatment calls for 75 mg for each 2pounds of a bird's weight (75 mg/kg). Due to its extended treatment period,thiabendazole is effective against emerging worm larvae as well as adult parasites.Since thiabendazole moves through a chicken quickly, the withdrawal time isrelatively short.

Mebendazole is based on thiabendazole and is used for spiral stomachworm, common roundworm, and thorny-headed worm. The dosage rate is 10 mgfor each 2 pounds of body weight (10 mg/kg) for 3 days.

Ivermectin is effective against a wide variety of internal and external para-sites (excluding flukes and tapeworm). It can be toxic to chickens in relatively smallamounts. Given orally, Vi cc is enough to worm a large chicken; up to 7 drops willworm a bantam.


it. Resistance takes between eight and ten generations. To minimize the devel-opment of resistant strains, avoid always using the same anthelmintic. Don'talternate too quickly, diough, or the parasites may become resistant to «// thewormers you use. For maximum benefit, rotate wormers annually.

In the old days, anthelmintics worked against a narrow range of parasites.Today's more potent wormers work against a wider variety of parasites. Theywork in two ways: by interfering with the parasite's feeding pattern (in otiierwords, by starving it), or by paralyzing the parasite so it is expelled live in thechicken's body wastes.

A wormer may be administered to chickens in one of two ways:• orally (added to feed, water, or given directly by mouth), to

be ab-sorbed through the digestive tract;

• injected, to be absorbed from tissue under a chicken's skin.Either way, die wormer is transported throughout the chicken's body,

me-tabolized, and eventually excreted.

Withdrawal PeriodDifferent wormers require different amounts of time before they

disap-pear entirely from a bird's body. Each drug approved for use in poultry has anestablished "withdrawal period" — the amount of time it takes before the drugno longer shows up in the bird's meal or eggs. The withdrawal period for mostwormers is 1 week.

Because an approved drug against a particular parasite isn't always avail-able, many flock owners use drugs that are not approved. Such use isconsidered "experimental" (a designation diat allows the drug to be used byqualified researchers) or "extra label" (a designation that allows veterinarians


to prescribe die drug as needed). Since no witiidrawal period has been estab-lished for them, drugs that are not approved should not be used on chickenskept for meat or eggs. (Chickens raised for meat reach butchering age soquickly that worming them shouldn't actually be necessary.)

Ding approval keeps changing, so what was "in" today is "out" tomorrow,and vice versa. Check with your state poultry specialist, veterinarian, or veteri-nary products supplier regarding the latest regulations. Carefully follow thelabel directions of any dnig you use.

RoundwormsIn the number of species involved and the damage they do to chickens, round-worms are die most significant parasitic worm. They belong to the phylumNemathelminthes (nema means "thread" and lielrnins means "worm" inGreek). Most nematodes are long and thin, appearing somewhat threadlike.


Nematodes are less common in caged layers than in floor-reared birds.Direct-cycle nematodes and those requiring an indoor-living intermediatehost (such as cockroaches or beetles) are more of a problem in penned birds;indirect-cycle nematodes requiring an outdoor-living intermediate host (suchas grasshoppers and earthworms) are more of a problem in free-ranged flocks.

EmbryonationNot all nematode eggs are infective when they are expelled from a

chicken.Some require development or "embryonation" to become infective. Someeggs embryonate in as little as 3 days, others require 30 days or more.

In order to embryonate, nematode eggs must encounter just the right con-ditions of temperature and humidity. In less than favorable conditions,embryonation may take longer or may not occur at all. In general, eggsembryonate more quickly under fairly warm, humid conditions. Minimizingmoisture inhibits embryonation and slows the buildup of parasite loads.

Large RoundwormThe large roundworm (Ascaridia galli) is one of the most common

poultryparasites. Roundworm or ascarid infestation is called "ascaridiasis." The largeroundworm is approximately the same thickness as pencil lead and grows aslong as 4'/2 inches (9 cm) — big enough to be seen without a magnifying glass.

Adult large roundworms roam a chicken's small intestine. Occasionallyone will migrate from the intestine up the cloaca and get trapped inside anewly forming egg — a decidedly unappetizing occurrence. Such a round-worm can easily be detected during candling.

One female roundworm lays up to 5,000 eggs, which take 10 days or moreto embryonate. Embryonated eggs survive in the soil for a year or longer.Roundworms are spread by direct cycle — embryonated eggs arc picked


up bya chicken from droppings, soil, feed, and water.

Birds that are over 3 months old are more resistant to ascaridiasis thanyounger birds. Heavier breeds such as Rhode Island Red and Plymouth Rockare more resistant than lighter breeds such as Leghorn and Minorca. Chickensdiat eat primarily animal protein are more resistant than chickens diat eat pri-marily plant protein.

Signs of ascaridiasis are pale head, droopiness, weight loss or slow growth,emaciation, and diarrhea. In a severe infestation, the intestines becomeplugged with worms, causing deadi. Even a somewhat mild infestation may bedevastating when combined widi some other disease, particularly coccidiosisor infectious bronchitis. In addition, ascarids have been implicated in thespread of avian reoviruses (see "Viral Diseases," page 119).


Of the drugs approved for ascarids in chickens, only piperazine is readilyavailable to owners of small-scale llocks, although levamisole is often used forbackyard flocks, particularly exhibition birds. Piperazine affects only adullroundworms. When an embryonated egg hatches in a chicken's intestine,within 7 days the new young worm attaches itself to the bird's intestinal lining.Although ibis immature form does more damage than an adult roundworm,during the 10 days it remains imbedded in the lining, piperazine can't touch it.Whenever you worm your flock, repeat the worming in 7 to 10 days, givingyoung worms time to release their hold on the intestinal lining.

Capillary WormSix species of Capillaria or capillarids invade chickens, causing

"capil-lariasis." Capillarids are white, hairlike or threadlike worms. Most are too smallto be seen with die naked eye, but may be seen with the aid of a magnifyingglass. They usually lodge in a chicken's crop, ceca, and/or intestines. In a seri-ous infestation, worms may move into the bird's throat or mouth.

Most capillarids have an indirect cycle, with earthworms as the intermedi-ate host. Some have a direct cycle. One species (C. Contorta) is both direct andindirect. Capillarid eggs are small and difficult to identify during fecal exami-nation (described later in this chapter).

Symptoms ofcapillariasis are pale head, poor appetite, droopiness, weak-ness, emaciation, and sometimes diarrhea. Chickens may sit around with theirheads drawn in. Postmortem examination (described in chapter 10) may re-veal adult worms in a thickened and inflamed crop.


Capillariasis is most likely to occur in llocks kept on built-up litter. No ap-proved treatment is readily available to small-Dock owners; levamisole is often used.

Crop WormEasily confused with capillary worm, the threadlike crop worm

(Gonglyonema ighwicola) invades the crop and sometimes the esophagus andproventriculus (stomach). Its indirect cycle involves beetles and cockroaches.

Unless they get out of hand, crop worms do little damage. Signs of a seri-ous infection are droopiness, weakness, lack of activity, reduced appetite, andthickening of the crop wall. Crop worms can be controlled by controllingbeetles and cockroaches.

Cecal WormThe cecal wonn (Heterakisgallinamm) is die most common

parasitic wonn inNorth American chickens. As its name implies, it invades a bird's ceca. Other


than carrying blackhead, to which most chickens are immune, the cecal wormdoes not seriously affect a bird's health. Leghorns are more susceptible to thisparasite than heavier breeds such as Rhode Island Red and Wyandotte.

Cecal worms are slender, white, and about Va-inch long, making them easyto see. Their cycle is direct. Eggs embryonate in 2 weeks (longer in coolweather) and survive for long periods tinder a wide range of environmentalconditions. Phenothiazine is the approved method of treatment, althoughmany backyard flocks are treated with levamisole.

Strongyloses avium is another parasite that invades the ceca, primarily inchickens raised in Puerto Rico. This worm is unusual for two reasons. First,rather than hatching in mi animal host, it's eggs hatch in soil, where matureworms live and grow. Second, only the female worm parasitizes chickens. In-festation can be deadly to young birds, but may cause no symptoms in adultbirds. No approved treatment is available for small flocks; levamisole is often used.

Stomach WormThe stomach worm (Tetrameres americana) invades a chicken's

proven-triculus, causing anemia, emaciation, diarrhea, and in a severe infestation,death. This worm is such a bright red color that you can sometimes see itthrough the wall of an unopened stomach during postmortem examination(see chapter 10). On close inspection, you will find worms of two shapes: theelongated ones are male, the roundish ones are female.

T. americana lias an indirect lifecycle involving cockroaches and grass-hoppers. Its near relative T. fissispina, which is identical but considerably


smaller, is carried by the same intermediate hosts and also by earthworms andsand hoppers. Control of the stomach worm involves controlling its inter-mediate hosts.

Eye WormEye worm (Oxyspirura niansoni) is prevalent in the southern United

Stales, Hawaii, the Philippines, and other tropical and subtropical areas. It is asmall white worm that lodges in die corner of a chicken's eye. The eye becomesswollen, inflamed, and watery, impairing the chicken's vision. The eyelids maystick together and the eye may turn cloudy and eventually be destroyed.Meantime, die chicken scratches the eye, trying to relieve irritation.

Eye worms have an indirect cycle. Worm eggs deposited in the eye passinto the tear duct, are swallowed by the chicken and expelled in droppings,and are eaten by the Surinam cockroach (Pycnoscelus surinarnerisis). When achicken eats an infective cockroach, worm larvae migrate up the esophagus tothe mouth, through the tear duct, and into the eye. Wild birds are also infected


Chart 5-1

Roundworms (Nematodes)

Common Name

Intermediate

Scientific Name

Appearance Host

capillary worm (capillarid)

C. annulatacapillary worm (capillarid)

C. contorta

capillary worm (capillarid)C. obsignata

capillary worm, threadworm (capillarid)C. bursata

capillary worm, threadworm (capillarid)C. caudinflata

cecal wormHeterakis gallinarum

cecal wormStrong)'loides avium

cecal wormSubulura brumpti

cccal wormS. sirongylina

crop wormGongylonema ingluvicolaeye worm, Manson's eye worm

Oxyspirura mansoni

gapeworm, forked worm, red wormSyngamus trachea

gizzard wormCheilospirura hamulosa

roundworm, commonTrichostrongulus tenuis

roundworm, large (ascarid)Ascaridia galli

white, threadlike, 0.04-2.4"(1-60 mm) longwhite, threadlike, 0.3-2.4"(8-60 mm) long

white, threadlike, 0.3-0.7"(7-18 mm) longwhite, threadlike, 0.4-1.4"

(11-35 mm) longwhite, threadlike, 0.3-1"

(9-25 mm) longyellowish-white, thin,

0.3-0.6"(7-15 mm) long

white, free- living, tiny, 0.08"(2.2 mm) long

white, 0.3-0.6" (7-14 mm) long

white, 0.2-0.7" (4.5-18 mm)long

white, threadlike, 0.7-2.2"(17-55 mm) long

white, slender, 0.3-0.8"(8-20 mm) long

red, Y-shaped, 0.2-0.8"(5-20 mm) long

reddish, 0.4-1" (9-24 mm) long

while, slender, 0.2-0.4"(5.5-11 mm) long

yellowish white, thick, 2-4.5"(50-115mm) long

capillary worm (capillarid)Capillaria anatis

white, threadlike, 0.3-1"(8-28mm) long

earthworm

none orearthworm

none

earthwor

m

earthwor

m

none

beetle, earwig,grasshopperbeetle,cockroach,grasshoppercockroach,beetle

cockroach

none orearthworm,slug, snailbeetle,grasshoppernone


stomach worm

Tetrameres americanastomach wormT.fissiprina

stomach worm, spiralDispharynx nasuta

bright red, male: long, 0.2" (5mm) female: round, 0.16" (4mm)similar to T. americana butsmaller 0.06-0.16"(1.5-4.1 mm) long

white, coiled, 0.3-0.4"(7-10 mm) long

cockroach,grasshoppercockroach,earthworm,grasshopper,sandhoppernone


"Use not approved — consult a veterinarian.


OrganAffected

Symptoms Severity Treatment

cecum,sometimes smallintestine, cloaca

weakness, emaciation,possible diarrhea, death

moderate-severe

levamisole*

crop, esophagus

emaciation, death moderate-severe

levamisole*

crop, esophagus,sometimesmouth

weakness, emaciation, reluctance tomove, possible diarrhea, death

severe levamisole*

small intestine,cecumsmall intestine

huddling away from flock, weakness,emaciation, possible diarrhea, deathpale head, inactivity, reduced appetite,slow growth, possible diarrhea, death

severe

moderate-severe

levamisole*

levamisole*

small intestine

cecum

pale head, inactivity, reduced appetite,slow growth, possible diarrhea, deathweakness, weight loss (carriesblackhead)

moderate-severemild

levamisole*

phenothiazine(Wormal)levamisole*

cecum,sometimes smallintestine

none or pasty cecal discharge, turningthin and bloody (found in Puerto Rico)

mild-severe,severe inyoung birds

levamisole*thiabendazole*

cecum none mild levamisole*

cecum none, (found in Puerto Rico and S.America, not N. America)

mild levamisole*

crop, sometimesesophagus,proventriculuseye

droopiness, weakness, inactivity,reduced appetite, slow growth,thickened crop wallscratching of eyes; watery, inflamed,swollen eyes; eyelids stuck together

mild

moderate

controlintermediatehostivermectin (3drops in eyetwice daily)

windpipe,bronchi, lungs

gasping, coughing, eyes closed, headdrawn in, yawning, head shaking,death

mild-moderate inadult birds

levamisole*

gizzard usually none mild-moderate

controlintermed. host

cecum,sometimes

primarily in young birds: weight loss,

severe thiabendazole*


smallintestine

anemia, deaths peak in spring and fall

mebendazole*

small intestine,sometimesesophagus, crop,gizzardproventriculus

pale head, inactivity, reduced appetite,slow growth, diarrhea, death

diarrhea, anemia, emaciation, death

moderate

moderate-severe

piperazine(Wormal)levamisole*controlintermed. host

proventriculus

diarrhea, anemia, emaciation, death

moderate-severe

controlintermediatehost

proventriculus,sometimesesophagus

heavily infested birds may die moderate-severe

mebendazole*


by eye worm, and may help spread it to chicken Hocks. Eye worm is controlledby controlling cockroaches around the hen house.

Veterinary treatment, usually reserved for valuable birds, involves apply-ing a local anesthetic to the eye, carefully lifting the third eyelid, applying 1 or 2drops of 5 percent cresol solution, and immediately flushing out the eye withclean water. If the eye is treated in the early stage of infection, it should clear upin 2 or 3 days.

An alternative (unapproved) treatment involves putting 3 drops ofivermectin into the chicken's eye, twice a day, until the eye worms are gone.Gapeworm

The gapeworm (Synganuts trachea) buries its head in the lining of a bird'swindpipe or other part of the respiratory system, causing "the gapes" or"gapes." Gapeworms get their name from the habit an infected bird has ofcontinually yawning or gasping for air. These worms, which are big enough tobe seen without magnification, are also called "red worms" or "forked worms"— each blood-red female has a somewhat paler male pennanently attached,forming the letter Y.

Gapeworms can cause considerable losses in free-ranged flocks, particu-larly those associated with adult turkeys. This parasite is especially serious inyoung birds; older chickens become resistant.

An infected chicken coughs up worm eggs, swallows them, and expelsthem in droppings. The cycle is either direct or indirect, involving earthworms,slugs, and snails. Eggs take up to 2 weeks to embryonate and may survive in soilfor as long as 416 years.


Symptoms of gapes are yawning, grunting, gasping, sneezing, coughing(sometimes coughing up a detached worm), choking, loss of energy, loss ofappetite, weakness, emaciation, closed eyes, head shaking, frequent throwingof head forward witii mouth open to gasp for air, and convulsive shaking of thehead (to dislodge worms from the windpipe). Gapeworms multiply rapidly,eventually suffocating the bird.

Infected small flocks are treated with either thiabendazole or levamisole.Thorny-Headed Worm

The thorny-headed worm (Acanthocephalans) is more common in Asiathan in North America. It invades a chicken's intestine, causing anemia andweakness. Like the nematode, it is cylindrical in shape. It can be identified byits tubular sucking appendage, or proboscis, sporting curved hooks or spines.

These worms have an indirect life cycle. Intermediate hosts includesnakes, lizards, and a variety of arthropods (spiders, mites, ticks, centipedes,and insects). Mebendezole, although not approved, is used as a treatment.


FlatwormsFlatworms belong to the phylum Platyhelminthes (platys meaning "flat" andhelminsmeaning "worm" in Greek). Flatworms come in two versions, ribbon-shaped tapeworms (cestodes) and leaf-shaped flukes (nematodes).

TapewormAn estimated 50 percent of all chickens in small flocks are infested

withtapeworms. Like roundworms, tapeworms come in many species. The eightspecies that invade chickens range in size from microscopic to 13 V2 inches (34cm) long. Infestation is called "cestodiasis."

Most tapeworms are host specific — those infecting chickens invade onlychickens and tiieir close relatives. All tapeworms lodge in the intestinal tract,attaching their heads to the intestine wall with four pairs of suckers. Each spe-cies prefers a different portion of the intestine.

During postmortem examination (see chapter 10), most tapeworms caneasily be seen without benefit of magnification. The exception is the micro-scopic tapeworm Davciinea proglottinci. To see it, open a portion of theduodenal loop and place it in water. The loose ends of the tapewonns will floataway from the intestinal tissue.

Ironically, this smallest species is also the most deadly. As many as 3,000have been found in one bird. Symptoms include dull feathers, slow move-ment, emaciation, breathing difficulty, paralysis, and death. Generalsymptoms of cestodiasis are weight loss and decreased laying. Leghorns tendto be more resistant than Plymouth Rocks.

All tapeworms require an intermediate host; an ant, beetle, earthworm,


housefly, slug, snail, or termite. Caged birds are likely to be infected by wormswhose cycle involves Hies. Litter-raised flocks are likely to be infected byworms whose cycle involves beetles. Free-ranged chickens are likely to be in-fected by worms whose cycle involves ants, earthworms, slugs, or snails.

A tapeworm's body is made up of individual segments, one or more ofwhich break away each day. A chicken starts shedding segments widiin 2 to 3weeks after eating an infective intermediate host. I11 a severe infestation, youmay see segments in droppings or clinging to the area around the vent, lookinglike bits of white rice. Each segment contains hundreds of eggs — in its life-time, each tapeworm releases millions of eggs, ensuring that some survive.

Tapeworm ControlTo control tapeworm, you must control the intermediate host. Since

symptoms are similar for most tapeworm species, it's important to knowwhich species you're dealing with so you'll know which intermediate liost(s)


you are looking for.Exterminating beetles is particularly troublesome, since not all

beetlesfound in and around chicken coops are harmful. In fact some are beneficial.To complicate the matter, tapeworms are carried by numerous species includ-ing darkling, dung, and ground beeties. Ask your county Extension agent orstate poultry specialist for information on problem beetles and their control inyour area.

Although no drug is currendy approved to combat tapeworm, a veterinar-ian can provide a suitable medication. Luckily, tapeworm is not a majorpoult ry disaster.

FlukesTrematodes or flukes belong to the same phylum (Platyhelminthes)

andclass (Cestoda) as tapeworms, but are in the order Galliformes. Their only simi-larity to tapeworms is that both are flat. The fluke is leaf-shaped rather than

Chart 5-2Tapeworms (Cestodes)

Common NameScientific Name Appearance Intermediate

Host

large chicken tapeworm

Choanotaeniainfundibulum

large chicken tapewormRaillietina cesticillus

large chicken tapewormR. enchinobothrida

large chicken tapewormR. tetragona

microscopic tapewormDauainea proglottina

short tapewormArnoeboiaenia

cuneatashort tapewormHymenolepiscantaniana

threadlike tapewormI I. caricca

very white, flat, segmented,up to 9" (23 cm) long

white, flat, segmented, up to6" (15 cm) long


white, Flat, wide, segmented,up to 13.5" (34 cm)white, flat, wide, segmented,up to 10" (25 cm) longwhite, flat, segmented, lessthan .16" (4 mm) longwhitish, flat, segmented, lessthan 0.16" (4 mm) longwhite, flat, segmented, up to0.8" (2 cm) long

white, flat, segmented,slender, threadlike, up to 0.5"(12 mm) longbeetle (severalspecies), housefly

histerid and darklingbeetle

ant

ant

slug, snail

earthwormdung beetle(S. carabeidae)

dung and groundbeetle, termite


ribbon-shaped. It is not as host specific as the tapeworm, so it may be intro-duced to an area by wild birds.

Flukes are rarely serious except where poor living conditions allow a mas-sive infestation. The four species that infect chickens each prefer a differentpart of the body — eye, skin, oviduct, or lower excretory system — where theyattach themselves with two suckers.

The oviduct fluke causes a hen's oviduct to swell and sometimes rupture,resulting in the hen's death. Early symptoms of infection include droopiness,weight loss, chalky white droppings, reduced egg production, soft-shelledeggs, and finding a fluke encased in an egg.

The skin fluke forms Vfe- to Vi-inch (4-6 mm) cysts under the skin, usuallynear the vent. The cysts, each containing two flukes, ooze and attract flies,leading to a possibly fatal bacterial infection. Meantime, the chicken suffersfrom depressed appetite and has difficulty walking. Treatment requires surgi-cally removing the flukes.

Flukes have complicated life cycles dial involve two intermediate hosts.

Part of IntestineAffected

Symptomssmall intestine

duodenal loop,small intestinelarge intestine

Severity Treatmentmoderate

none-mild

severe


noneapproved for

— poultry; seeyour

veterinarian

duodenal loop

duodenal loop

duodenal loop

moderate-large intestineweight loss, severe

— decreasedlaying severeduodenal loop severe

mild

none-mild

none-mild


Breaking the cycle is therefore easier than breaking the cycles of roundwormsor tapeworms. The scenario goes something like this: Fluke eggs pass out of aninfected chicken, are picked up by and develop within a snail, are released bythe snail in water, swim around until they're eaten by a dragonfly or mayfly,and infect a chicken that eats the dragonfly or mayfly. The

easiest way to con-trol flukes is to keep chickens away from ponds, lakes, or

swamps wheredragonflies and mayflies abound.

Chart 5-3FlukesBody Part Affected

Collyrichnn fabaPliilophthalinus gralliProsthogonimus macrorchis (P. ovatus)Tanaisia bragai

skineyeoviductlower excretory system

Fecal Test

Some internal parasites can be identified by signs that appear in die infectedbird's droppings. Checking droppings may therefore help you identify theparasite so you can determine appropriate management changes and/ortreatment, and so you can avoid the unnecessary use of wormers due to guess-work. You may discover that your chickens are not seriously infected withparasites, giving you reason to look for some other cause if your flock is experi-encing problems.

Checking droppings, or more properly called "conducting a fecal exami-nation," can be done by any veterinarian, usually for only a few dollars.

Fluke


Thereare, however, good reasons to learn how to do your own testing. Aveterinarian's office might not be handily nearby, discouraging you from test-ing as often as you would like. Mailing samples doesn't solve the problem,since samples diy out and parasite eggs may hatch or disintegrate. Even whenyou do your own testing, if you find something that looks serious, you mightthen wish to have your findings confirmed by a veterinarian before makingdrastic management changes or initiating drug treatment.

Home TestConducting your own fecal examinations is not difficult. To get an

ideawhat's involved, take a fecal sample to your veterinarian and ask to have a look


when the sample is placed under a microscope. The vet will help you identifyanything that is found. Once you know what you're looking for, you will havean easier time identifying signs of parasites on your own.

The parasites in a bird's digestive tract release eggs, larvae, cysts, seg-ments, and sometimes mature adults in a bird's droppings. Parasites in therespiratory system may be coughed up and swallowed to appear in the bird'sfeces. Even external parasites, especially mites, are sometimes pecked by abird and turn up in its droppings.

You can collect droppings from the ground or floor, if you're certainthey're fresh. Otherwise, obtain a sample directly from a bird: place your handinside a plastic bag, persuade the bird to do its duty, and wrap the sample byturning the bag inside out over the sample. If you're checking the whole llockrather than individual birds (for example, new birds you're just bringing in),collect about a dozen samples and mix them together.

Examine die sample for clearly visible signs of dead worms or tapewormsegments. Whether or not you find anything, the next step is to examine thesample under a microscope. The most likely thing you'll see is parasite eggs.Some eggs are unique and easy to recognize. Others are quite similar within agroup, making it difficult to tell one species from another. Either way, you'llneed a pictorial guide such as Veterinary Clinical Parasitology (listed in the ap-pendix).

Be aware that some things a bird eats that turn up in its droppings mayresemble parasites. Such "pseudo-parasites" include mold spores, pollen


grains, grain mites, and corn smut spores. The latter can easily be mistaken fortapeworm eggs.

Examination KitTo conduct a fecal examination, you'll need a microscope, preferably

onethat magnifies from 100 times to 400 times. A good microscope can cost hun-dreds of dollars, unless you find one at a flea market or garage sale. Aninexpensive microscope, designed to introduce children to science, is suffi-cient for most home purposes. As an alternative to purchasing a microscope,you might persuade a local high school or college biology instructor to let youbring in your samples for examination.

Most of the other things you'll need are ordinary items found around theaverage house. If your microscope is an inexpensive one, you'll need a light forit — which can be as simple as a well-directed strong flashlight beam or ahand-held egg candler.

The most difficult to find items, though not expensive, are microscopeslides and test tubes. Look for them at medical supply oudets or ask your drug-gist to get them for you. If you purchase a student microscope, it may come


with a variety of things you need, including microslides and covers, but even-tually you'll need replacement covers.

Unless you plan to test more than one sample at a time, you'll need onlyone test tube (it doesn't hurt to have at least one spare). To hold die test tube inan upright position, make a stand by drilling a hole in a block of wood orstyrofoam so the tube fits snugly.

To speed up the separation of eggs from other fecal matter, professionalsuse a centrifuge (a machine that spins to separate particles of varying densi-ties). At home, your options are to examine a simple smear or use the flotationmethod.

Fecal Examination Kit

Description MicroscopeSpecimen cupsWooden sticksStrainer15 cc test tubeTest tube holderFlotation solutionMedicine dropperMicroslides with cover slipsPincersIdentification guide100X to 400X magnification

3 ounce (90 ml) paper cupstongue depressors or Popsicle stickssmall tea strainerVTx4" (12 mm x 10 cm) longwooden or styrofoam blocksugar and tap watereye dropperstandard 3" x 1" (75 x 25 mm)tweezersVeterinary Clinical Parasitology

Simple Smear MethodThe simple smear method is not very accurate, but it's better than

nothing,and it gives you something to do while you're waiting for eggs to

Equipment


separate forthe flotation method.

Begin by placing your microscope on a piece of a magazine or newspaperin such a way that you can look through the microscope to read the print. Put aslide into the microscope and use an eye dropper to place a drop of water in thecenter of the slide.

With a toothpick, pick up a '/a-inch (3 mm) blob of droppings and stir itinto the water droplet until the water turns cloudy. You should still be able tosee the printed page through die moistened sample. If necessary, use tweezersto pick out large pieces of debris. Place a cover slide over the sample and sys-tematically examine the sample through die microscope.


Flotation MethodThe aim of the flotation method is to separate out eggs or larvae so

you canmore readily see them. When you combine the feces sample with a flotationsolution, eggs will float and heavier fecal matter will sink.

To make the flotation solution, combine 2>/4 cups of sugar (454 g) with IV2cups (355 ml) of tap water in a small saucepan. Stirring, heat the mixture untilit turns clear. Pour the soludon into a clean, labeled jar and keep it in the refrig-erator until you need it.

When you're ready for the test, use a wooden stick to transfer a L/2-inch (2-3 g) blob of fresh fecal matter into a paper cup (more is not better here — toomuch fecal matter will make your sample too thick to strain). Measure out oneand a half test tubes of flotation solution into the cup. With the wooden stick,mix the sample and solution thoroughly, taking care not to stir up air bubbles.Pour die liquid through a strainer into a second paper cup. Stir and press out asmuch liquid as you can.

Important sanitation measure: Before proceeding, seal the first cup con-taining solid fecal matter in a plastic bag for disposal and clean the strainer bypouring boiling water through it.

Place the test tube in a holder and pour the liquid from the second cup intothe test tube. If necessary, use an eye dropper to top off the test tube with freshflotation solution until the liquid rises above the rim, but does not run over theedge. Using tweezers, place the slide cover slip on top, taking care not to leavean air bubble beneath the slip or jostle the tube so it overflows.


Leave the cover slip on the test tube for 3 to 6 hours, during which parasite

Fecal samples can be examined for

nematodes and oocysts using a low-

powered microscope.

Flotation solution rising above testtube rim.


eggs will float to the top. A good thickness of material should slick to the bot-tom of the slip.

With tweezers, carefully lift the slip straight upward and put it in the centerof a microscope slide, taking care not to create air bubbles. Avoid squeezingthe slide and cover together, or you might mash the evidence.

Place the slide in the microscope and systematically examine it under 400Xmagnification. (For protozoan oocysts, described in chapter 6, set the micro-scope at 100X). Compare anything you find with photos in your identificationguide.

Finding a few parasite eggs is normal and no cause for alarm. A count ofmore than 500 eggs per gram of feces (F.PG) is considered a moderate infesta-tion, which translates into about 1,000 eggs per '/2-inch blob of droppings. Acount of more than 1,000 EPG (or about 1,200 eggs per V2-inch blob) meansprompt treatment is necessary. Of course, you would need a centrifuge to spinthis many eggs from any sample, but you can see that there's a vast differencebetween finding a few eggs on your slide and even a "moderate" infestation.

When you're done with your fecal test, clean out the test tube with an oldtoothbrush labeled for the purpose. Rinse all your materials with boiling waterand set them on a paper towel to dry before putting them away. Store yourmicroscope away from moisture and dust.

Internal Parasites: Protozoa

PROTOZOA ARE SINGLE-CELLED CREATURES that look round when viewedthrough a microscope. They are the simplest members of the animal kingdomand also the smallest, ranging in size from 1 to 50 microns (0.00004 inch orVi ,ooo mm) — too small to see with the naked eye. Many protozoa are harmless.Others are parasites, causing serious diseases.

Two phyla of protozoa affect chickens: Apicomplexa and Sarcomasti-gophora. Included in them are several genera that cause a variety of diseases in

Chart 6-1Protozoan Diseases

Genera Disease Affects Prevalence

Cryptosporidium

cryptosporidiosis

cloaca, cloacal bursa,

common

lungs, air sacs, eye lids

Eimeria coccidiosis ceca or intestines commonHistomonas blackhead ceca and liver very rareLeucocytozoon

leucocytozoonosis

blood, liver, lung, spleen,

rare

brain

224

INTERNAL PARASITES: PROTAZOA 225

Plasmodium malaria blood, liver, lung, spleen,

rare

brainToxoplasma toxoplasmosis central nervous

systemvery rare

Trichomonas canker mouth and throat rare


chickens, some of them quite serious. Luckily, the worst protozoan parasitesare rare or are not found in North America.

CoccidiosisCoccidiosis is die most common and most widely known protozoal disease ofpoultry. It is caused by severed different species of protozoa known as coccidia,most of which are in die Eimeria genera. Cocci is the most likely cause of deathin growing birds, usually striking chicks 3 to 6 weeks of age. The worst cases arelikely to occur at 4 to 5 weeks.

Coccidia are found wherever diere are chickens. Even in the healthiestflock, coccidia are present in the intestines of most birds over 3 weeks old.Many species cause no disease or only mild disease, in which case die chickensare said to have "coccidiasis."

Gradual exposure (or surviving an infection) allows a chicken to becomeimmune to the disease-causing coccidia in its environment, so by maturitymost chickens are immune. Chickens with Marek's disease are an exception,since they don't always develop the same immunity to coccidiosis as healthychickens do. Immune chickens won't gel coccidiosis, unless dieir resistance isreduced by some other disease or diey're exposed to a new species of coccidia.

A devastating outbreak may occur when a large number of growing ormature birds are brought together from different sources, since they may notall have been exposed to (and dierefore developed immunity to) die same coc-cidia species. Outbreaks also occur where sanitation is poor and/or birds arestressed due to overcrowding, an abrupt change in rations, being


transported,or some drastic change in the weadier.

Life CycleCoccidia have short, complex, direct life cycles. A chicken eats an

infectiveegg, or oocyst, containing eight coccidia in a form known as a "sporozoite."The oocyst is crushed in the bird's gizzard, releasing the eight sporozoites,which lodge in the bird's intestine wall and begin to reproduce. Within 4 to 6days, die reproductive cycle goes through two or more generations (the lengdiof time and number of generations vaiy witii coccidia species), at the end of

which millions of oocysts are released inthe chicken's droppings.

The life cycle of protozoa resultingfrom the first oocyst is now over, making

coccidiosis a self-limiting disease withpotentially inconsequential results.

How seriously a bird is infected depends

Oocysts: E. tenella (left), E. acervulina(right).


on the number of oocysts it eats—in a highly contaminated environment, onechicken may eat between one thousand and one million infective oocysts.

To become infective, the oocysts must develop or "sporulate" (the proto-zoal equivalent of embryonation in nematodes). For most species of coccidia,sporulation takes 18 hours or less. When a chicken eats a sporulated oocyst,the cycle begins again.

Infected and recovering birds shed oocysts diat contaminate dust, soil,damp litter, feed, and drinking water. As birds either die or recover and theinfection plays out, the number of shed oocysts decreases. Oocysts are sensi-tive to ammonia, molds, and bacteria, so they do not survive long in litter.Continuing litter contamination requires constant shedding by infected birds.

In soil, given the right moisture and temperature, oocysts can survive forseveral weeks (up to 18 months under ideal conditions). They can't survivelong in dry soil, and they don't survive at temperatures below freezing or above130°F (55°C). The danger of an outbreak is therefore greatest during warm,humid weather. Chicks hatched in late winter or early spring therefore tend tobe healthier than chicks hatched during the warmer, more humid summermonths.

The first outbreak of coccidiosis in a new chicken coop is usually the worst,a phenomenon known as "new-house coccidiosis syndrome." The reason isthat the first birds raised on new ground have little exposure to infective oo-cysts. When they eventually become exposed, they have little or no immunityand die outbreak is particularly serious.


Oocysts are spread on the feet of wild birds (even though the wild birdsthemselves don't become infected), on the bodies of insects and other ani-mals, on people's shoes, on the tires of feed delivery trucks, and on usedequipment that hasn't been tiioroughly cleaned.

SymptomsCoccidia irritate die intestinal lining, interfering with the absorption of

nu-trients. Outbreaks range from so mild you don't notice your chickens are sickto so severe they die. In mature birds, the chief sign is slow or no egg produc-tion. Breeds with yellow shanks and skin may turn pale due to their reducedability to absorb pigments from feeds. Older birds that appear healthy becomea source of infection for younger birds.

In young birds, symptoms include slow growth, a change in the droppings(runny, off-color, sometimes tinged with blood), and dehydration due to diar-rhea. The disease may come on slowly, or bloody diarrhea and deaths maycome on fast. The weakened chickens become more susceptible to otiier para-sites and diseases. Intestinal (issue damage causes the birds to be especiallysusceptible to bacterial infections such as salmonellosis or necrotic enteritis.


Coccidia Affecting ChickensSpecies

, <S Eimeria acervulina** duodenal loop

lower small intestine and ceca

duodenal loop

middle portion of small intestine

lower small intestine

entire intestine (starts in upperportion and works its way down)

middle portion of small intestine

Invades

Chart 6-2

E. brunettf *E.

hagani

C"—'3 '

/£ E. maxima**

E. mitis.'*) E.mivati**

/)•'" E. necatrix**

C J


duodenal loop

ceca

**Main causes of clinical outbreaks.

E. praecox

E. tenella**

*See Chapter 10.


Symptoms Postmortem Findings* Oocysts

(usually in chicks 3 to 6 weeks old)slow growth, pale skin

roughened wall of duodenal loopwith gray or white round orstriped patches (under magni-fication), sometimes overlapping

oval

slow growth, bloody droppings,up to 30% mortality; survivorsdo not grow well

peeling away of intestinelining

large,oval

watery diarrhea tiny bloody spots alongduodenal loop wall

oval toround

(usually chicks 3-6 weeks old)slow growth, pale skin, roughfeathers, yellow, gray, or browndiarrhea, loss of appetite, weightloss, high mortality

reddened, distended,thickened small intestinefilled with grayish, pinkish,or orange brown mucus

large,yellow-ish, oval

slow growth, weight loss, pale skin none significant small,round

slow growth thickened intestine wallwith patches similar toE. acervulina but rounder

roundish

(usually in birds 8 to 18 weeks old)comes on fast; weight loss, watery,bloody diarrhea, up to 25% mortality

portions of intestine may betwice the normal size, filledwith blackish blood clots, liningthickened, mottled with whitespots or bloody (red or black) dots

roundish

slow growth, pale skin, water,'diarrhea, dehydration

intestine filled with wateryfluid, small red dots alonglining

roundishto oval

(usually in chicks 3 to 6 weeks old)comes on fast; slow growth, weightloss, bloody diarrhea, severe anemia

ceca filled with clotted bloodand dead tissue that turnsblackish, hardens and is

large,round


high mortality (bacterial infection);survivors do not grow well

eventually expelled in droppings


Coccidiosis is worse in a flock that's combating another disease; cocci oftenfollows an outbreak of infectious bursal disease.

In severe cases, destruction of the intestinal lining causes hemorrhagingand death. In any case, internal damage is often done before you notice thefirst symptoms. Seriously damaged birds never become as productive as unaf-fected birds. It's therefore best to manage your flock with cocci in mind, ratherthan to wait and treat the disease after it occurs.

If you do suspect coccidiosis, a fecal test (described in chapter 5) will tellyou whether or not your birds are shedding oocysts and will help you pinpointthe species. Several tests may be required to identify the species, since an in-fected chicken does not shed oocysts at a steady rate. In diagnosing the causeof an outbreak, you can pretty safely eliminate any species that previously in-fected your flock. If you conduct a postmortem examination (see chapter 10),do so immediately after death — within an hour, changes occur that makediagnosis more difficult.

Coccidia SpeciesEimeria protozoa come in many species that infect nearly every kind

oflivestock, but each is highly species specific — the coccidia that invade chick-ens do not affect other kinds of livestock, and vice versa. Even different kindsof birds are infected by different species of coccidia.

In chickens, coccidiosis is caused by nine species of Eimeria protozoa,some more serious than others. One bird may be infected with more than onespecies at a time. Each species is identifiable by a number of traits includingthe portion of a chicken's intestinal tract it prefers, the appearance of its oo-cysts (size, shape, and color), and the symptoms it produces.


E acervulina is the most common cause of coccidiosis in North America.E. tenella and E. necatrixare the most serious, coming on rapidly and resultingin high death rates. E. tenella, a form of cecal coccidiosis, generally infectschicks 3 to 6 weeks of age. E. necatrix, a form of intestinal cocci, takes longer tobuild up and so is more likely to occur in maturing birds 8 to 18 weeks old.

Cocci ControlMeasures for controlling coccidiosis involve, in order of preference:

• good management• the use of drugs• vaccinationGood management includes providing adequate diy litter, clean

drinkingwater, and proper nutrition. /\ll ground-fed chickens are exposed to infective


oocysts throughout their lives. Awell-managed flock quickly de-velops resistance. The soonerthat happens, the healthier thechickens will be.Coccidiosis is generally lessof a problem in free-rangedflocks, being more serious whenchickens are concentrated in asmall area. Chicks raised on wireand moved to litter when they'repartially grown become seriouslyinfected, since they have not had a chance to develop resistance throughgradual exposure. Resistance is not necessaty for caged layers and cage-managed show stock, since they are unlikely to be exposed to coccidia (unlesstheir drinking water becomes contaminated).

Vaccination against coccidiosis has limited success, although it is some-times used for breeder pullets. Vaccination is seldom used for broilers — themild infection produced by the vaccine slows growth, making the option un-economical. Genetically engineered antigens, now on the horizon, may oneday be used to immunize young chicks.

AnticoccidialsA number of drags are available to prevent or control coccidiosis.

Whichone you use, if any, and how you use it depends on whether your intent is toprevent infection, permit a mild infection that allows resistance to develop, ortreat an existing infection. The type of drag used and the dosage needed alsovary with the species of coccidia involved — not all coccidiostats are effectiveagainst all species.

Drugs designed for treatment require high dosage levels, yet an excessivedose can poison chickens. Since the toxic level of sulfamethazine is close to thelevel required for treatment, poisoning can occur at normal doses if high


tem-perature causes an increase in treated water intake. Symptoms of poisoningare depression, paleness, and slow growth. At temperatures over 80°F (27°C),avoid poisoning by using only one-third the recommended dose.

The use of some anticoccidials, particularly amprolium, causes vitamindeficiency. It's a good idea, therefore, to offer a vitamin supplement alter youtreat your flock. Do not use a vitamin supplement during treatment, becausevitamin deprivation is one of the ways amprolium controls coccidia. Sincecoccidiosis increases a flock's susceptibility to bacterial infections, using anantibiotic along with the anticoccidial improves the rate of recovery.

CHART 6-3Drugs Used to Treat Coccidiosis*

WithdrawalApplication Time

DrugAmproliumSulfadimethoxineSulfamethazineSulfaquinoxaline

waterwaterwaterfeed

none5 days10 dayslOdays

For dosage and length of treatment, followdirections on label.


Some of the same drugs used to treat cocci, plus a few additional ones, areused in low dosages to prevent a serious outbreak in young birds while (at leasttheoretically) allowing them to develop immunity through gradual exposure.The use of drugs for this purpose, usually from the day of hatch to 16 weeks ofage, does have drawbacks:

• Although drugs used for treatment are equally effective in prevention— since they reduce die protozoa population by killing any coccidia achicken eats — the chickens may not be exposed to adequate numbersof coccidia to become immune, so an outbreak may occur when thedrug is withdrawn.

• Drugs designed specifically for control (ratiier than treatment) suppos-edly reduce the degree of infection while allowing immunity todevelop, but some only arrest the development of immunity, pavingthe way for an outbreak when they are withdrawn. Some are toxic athigh levels and/or produce side effects. Any continuous low dose ofmedication in water or feed can lead to the development of drug-resistant strains of coccidia, requiring rotation of drugs used.

• The medication has a withdrawal time of 30 days, so if you raise meatbirds, you'll have to find a non-medicated brand of feed during thatlast month. That being the case, why not seek out the alternative brandand use it right from the start? Feeds containing preventive medica-tion are designed for commercial producers who bring in as many as30,000 broilers at a time, and raise one batch right after another. In asmall flock, the use of medication is a poor substitute for goodmanagement.


CryptosporidiosisCiyptosporidiosis is the one form of coccidiosis that is not caused by Eimeria,but rather by the protozoa Cryptosporidium baileyi. Unlike the other forms ofcoccidiosis, ciyptosporidiosis is not specific to chickens; it infects other birdsand is possibly spread by wild species. Although C. baileyi does not invademammals, it may be spread from flock to flock on the feet of animals andhumans.

Like odier coccidioses, ciyptosporidiosis is spread by oocysts, but eachcontain four (rather than eight) sporozoites. The oocysts are considerablysmaller than those of other coccidia, and detecting them requires special labo-ratory techniques.

Like other coccidia oocysts, Cryptosporidia oocysts are sensitive to ammo-nia in litter. They are also somewhat sensitive to chlorine bleach as adisinfectant, and they cannot survive temperatures above 140° F (60°C).


Unlike Eimeria oocysts, those of Cryptosporidium are infective when theyleave the host's body. Some may not leave at all, but remain and developwithin the same host (called "autoinfection"). As few as 100 oocysts in one birdcan quickly produce a serious infection.

Although it has not been studied as thoroughly as other forms ofcoccidiosis, intestinal cryptosporidiosis is apparently quite common in chick-ens. It is usually mild, often producing no symptoms other than pale skin inyellow-skinned breeds. Once infected, birds become immune.

Oocysts may be inhaled as well as ingested, causing respiratory infectionthat is less common though more severe than the intestinal form. Respiratorycryptosporidiosis is likeliest to affect birds in the 4- to 17-week age group. Sur-vivors begin recovering in 2 to 3 weeks. E. coli often produces a secondaryinfection, and an existing infection with E. coli or infectious bronchitis virusmakes respiratory cryptosporidiosis worse.

Cryptosporidia invade other parts of the body, including the eyelid and thecloacal bursa, from which they may travel up the urinary tract. No means ofprevention or treatment is known. Chickens develop natural immunity whenexposed to oocysts at low levels, leading to the possibility of a vaccine inthe future.

HistomoniasisInfection with Histomonas meleagridis protozoan parasites is commonlyknown as "blackhead" because an infected bird's face tends to darken, al-though this is neither a sure sign of the disease nor necessarily characteristic ofit. The disease — caused by round, microscopic histomonads — is serious inturkeys, but chickens are normally immune.

Blackhead is more common in range-fed than housed or caged chickens,


since die disease occurs when a chicken eats an earthworm carrying eggs ofthe cecal worm (Heterakis gallinarum), which in turn are harboring histo-monads. The parasites lodge in the chicken's cecum, enter the bloodstream,and eventually migrate to the liver.

Histomonads shed by infected chickens may reinfect the same chicken orinfect another chicken that picks in droppings or eats a fly, sowbug, grasshop-per, or cricket carrying the parasite on its body. Once shed, histomonadscannot survive long in the environment unless they are protected by a cecalworm egg or an earthworm.

Chicks 4 to 6 weeks old are the most susceptible to histomonad infection.Mild strains produce no symptoms; virulent strains may cause deaths in the 20to 30 percent range. Drugs approved in the United States are not particularlyeffective. Since survivors continue to shed histomonads, control requires con-trolling cecal worms (see "Cecal Worm," page 84),


ToxoplasmosisThe protozoan Toxoplasma gondii causes toxoplasmosis in warm-bloodedanimals including chickens and humans. It is mainly a disease of the centralnervous system, but may also affect the reproductive system, muscles, and in-ternal organs.

This protozoa has a complex life cycle. A chicken may become infected inmany different ways: picking in infected droppings of chickens, cats, or otheranimals; picking at an infected chicken, live or dead; eating earthworms har-boring toxoplasma oocysts. Toxoplasma may be spread from one area toanother on the feet of rodents.

Control involves keeping litter diy, controlling filth flies, cockroaches, androdents, and keeping the yard free of cats. No effective cure is known.

TrichomoniasisThe protozoan parasite Trichomonas occasionally infects chickens, causing amouth and throat disease known as "canker." It is primarily a disease of pi-geons that may be spread to chickens through feed or water contaminatedwith discharge from an infected bird's mouth. Control involves keeping pi-geons away from chickens and isolating infected chickens so the parasite doesnot spread.

Blood ParasitesA chicken's blood may be invaded by a variety of protozoan parasites, most ofwhich are not common in North America.

Leucocytozoon are found near swampy areas and are spread by blackfliesand biting midges, causing anemia and sometimes death due to hemorrhage.

Plasmodium protozoa, transmitted by mosquitoes, cause malaria found


in chickens in Africa, Asia, and South America, but so far (knock on wood) notin North America.

Avoid these blood infections by controlling biting and bloodsucking in-sects such as blackflies, biting midges, mosquitoes, and flies. Do not allowweeds and trash to accumulate, as they provide breeding grounds for insects.

Infectious Diseases

THE INFECTIOUS DISEASES described in this chapter are caused by plant-like microscopic parasites — bacteria, viruses, and fungi. Some of thesemicroflora are always present but cause disease only under certain circum-stances, such as when a chicken's resistance is low due to stress. Suchmicrobes are called "opportunists."

A few microbes produce disease wherever they occur. They are commonlyknown as "germs," but technically they are "pathogens," and are described asbeing "virulent" or "pathogenic." Variations in padiogenicity among strainscause the same disease to appear in different degrees of severity or even indifferent forms altogether.

The vast majority of microbes are either harmless or beneficial. Beneficialmicroflora may live on a chicken's skin or within its body, aiding digestionand/or enhancing the bird's immunity by fending off pathogenic microbes, aprocess known as "competitive exclusion."

87% OF AIL MICROBES ARE BENEFICIAL OR HARMLESS

244

INFECTIOUS DISEASES 245

10% ARE OPPORTUNISTIC 3% ARE PATHOGENIC


Bacterial DiseasesBacteria are single-celled microbes that are abundant in die soil, water, andair. They were first discovered in the 17th century, when the microscope wasinvented. Some can move only on air or water currents; others (like salmo-nella) have tails that let them swim through liquids.

Some bacteria multiply by producing spores (individual cells encasedwithin a tough membrane). Others multiply by dividing themselves in half;under ideal conditions, they multiply so rapidly that within hours, one bacte-rium becomes millions.

Pathogenic bacteria enter the body through the digestive system, respira-tory system, or cuts and wounds. If they settle in an organ or tissue, theinfection becomes chronic or long term. If they travel throughout the body bymeans of the bloodstream (a condition called "septicemia"), die infection


isacute or short term, often ending in death.

Bacteria produce diseases in two ways: by causing mechanical damage tothe body and by generating toxins that poison the body. Some bacterial dis-eases are caused by damage, some by poisoning, and some by both.

Most bacterial diseases share one or more of these four properties: dieyproduce carriers; they are transmitted from breeders to chicks through hatch-


ing eggs; they are spread by rodents and wild birds; they survive for a long timein poultry housing. Owners of commercial flocks control bacteria by periodi-cally depoptilating their housing and thoroughly disinfecting before bringingin new, clean stock (all-in, all-out management).

Bacteria are divided into four related groups according to dieir shapes, vis-ible by magnifying diem 1,000 times under a microscope. The major ones thatare harmful to chickens fall into three categories:

• rod-shaped, called "bacilli," such as the organisms that causecolibacillosis, clostridial diseases, erysipelas, infectious coryza,listeriosis, cholera, pseudomonas, salmonellosis, and tuberculosis;

• round, called "cocci," such as the organisms that cause chlamydiosis,

Bacterial .Shapes

SPIRILLA

STAPHYLOCOCCUS

STREPTOCOCCUS

COCCI


staphylococcosis, streptococcosis, and mycoplasmosis (aldioughmycoplasmas are unique in their ability to change shape);• spiral, called "spirilla," such as the organisms dial causecampylobacteriosis and spirochetosis.

CampylobacteriosisCampylobacteriosis is an intestinal disease that infects a wide range

ofanimals including dogs, humans, and especially chickens. Poultry experts esti-mate diat 90 percent of all commercial broilers are infected.

Several species of Campylobacter cause the disease. The species mostlikely to affect chickens, as well as humans, is C. jejuni. Campylobacters are


Chart 7-1

Bacterial DiseasesDisease Cause Prevalenc

eCampylobacteriosis Campylobacter jejuni commonChlamydiosis Chlamydia psittaci very rareClostridial diseases

Botulism Clostridum botulinum rareNecrotic dermatitis C. septicum rareNecrotic enteritis C. perfringens rareUlcerative enteritis C. colinum common

Colibacillosis Escherichia coli commonAir-sac disease E. coli and other bacteria commonChronic respirator)' disease

E. coli common

Omphalitis E. coli commonSwollen head syndrome E. coli rare

Coryza, infectious Haemophilus paragallinarum

common

Erysipelas Erysipelothrix rhusiopathiae

rare

Listeriosis Listeria monocytogenes

very rare

MycoplasmosisAir-sac disease Mycoplasi na

gallisepticumcommon

and other bacteriaChronic respiratory disease

M. gallisepticum and other

common

bacteriaPasteurellosis

Cholera, (acute) Pasleurella multocicla commonCholera, (chronic) P. multocida not common

Pseudomonas very rareSalmonellosis

Arizonosis Salmonella arizonae rareParatyphoid S. heidelberg

S. enteriditisS. typhimurium and other spp

very common

Pullorum S. pullorum rareTyphoid S. gallinarum rare

Spirochetosis Borrelia anserina rareStaphylococcosis


Arthritis, staphylococcic Staphylococcus aureus commonBumblefoot S. aureus commonOmphalitis S. aureus and other

bacteriacommon

Streptococcosis Streptococcus zooepidemicus

not common

Omphalitis Streptococcus faecalis andother bacteria common

Synovitis, infectious M. synoviae not commonTuberculosis Mycobacterium avium fairly

common


spread among chickens dirough infectious droppings in feed and water. Themain symptoms are depression and watery, mucousy, or bloody diarrhea.

No effective way has been found to treat an infected flock.Campylobacters are, however, particularly sensitive to drying and can beeliminated from housing by thoroughly cleaning and disinfecting, followed byleaving the coop empty for at least a week before introducing new birds.

Clostridial DiseasesClostridial diseases result from toxins produced by bacteria in die

Clostri-dium group. Some clostridial bacteria do not cause disease unless a chicken'sresistance has first been reduced by coccidiosis or by an illness (such as infec-tious bursal disease) that damages the immune system.

Clostridium colinum causes ulcerative enteritis, a short-term intestinaldisease spread by infectious droppings in litter, feed, and water. The disease isknown as "quail disease" because it was first identified in quail, the most sus-ceptible of all avian species. The bacteria are able to survive under a variety ofconditions, so once an outbreak occurs, housing is permanently contami-nated. Control then involves replacing litter between flocks or keeping yourbirds on wire. Ulcerative enteritis may be avoided by taking care not to bring acarrier into your flock.

Clostridium septicum is commonly found in soil and in the intestines ofchickens. It usually causes infection in combination with otiier bacteria, oftenafter the chicken's immunity has been reduced by some other illness, espe-cially infectious bursal disease. Alone or in combination, the bacteria causenecrotic dermatitis, characterized by patches of dead skin and/or suddendeath. Necrotic dermatitis can easily be avoided through good managementand proper sanitation.


Clostridium perfringens is commonly found in air, soil, water, and feces.The bacteria generate a potent toxin that causes necrotic enteritis in youngand growing birds raised intensively on litter. The disease appears suddenly(often after a change in feed) and progresses rapidly, causing deaths within afew hours, sometimes without symptoms. It is easy to treat with antibioticsand easy to avoid through good management.

Clostridium botulinum, bacteria that commonly live in the intestines ofchickens, are not themselves pathogenic. When they multiply in the carcassesof dead animals or in rotting solid vegetables such as cabbages, they generatesome of the world's most potent toxins. Birds become poisoned after peckingat rotting organic matter or after drinking water into which it has fallen.

A poisoned bird gradually becomes paralyzed from the feet up. Initiallythe bird sits around or limps if you make it move. As paralysis progressesthrough its body, its wings droop and its neck goes limp (giving the disease its


common name, "limberneck"). By the time the eyelids are paralyzed, the birdlooks dead, but it continues to live until either its heart or its respiratory systembecomes paralyzed.

If the bird isn't too far gone, you might bring it around with antitoxin (froma veterinarian) or by squirting cool water and an epsom salt solution into itscrop (see "Flushes," page 192). Botulism is another disease that can easily beavoided through good sanitation.

ColibacillosisColibacillosis is a group of infectious diseases caused by one or more

strains of Escherichia coli, the so-called "coliform" bacteria commonly foundin the environment worldwide. Many strains, including some that normallylive within chickens, do not cause disease. Other strains are opportunistic.

The illnesses caused by E. coli are varied and often complex. The bacteriamay infect alone or may combine with or follow other diseases, especiallychronic respiratory disease, infectious bronchitis, infectious synovitis, andNewcastle. A bird's susceptibility to coliform invasion is increased by stressand by damage to its respiratory system caused by ammonia fumes or dust.

Coliform infections range from severe and acute to mild and chronic. Thesusceptibility of chickens varies with the bird's strain and age — infection ismore common in young birds than in older ones. The bacteria are transmittedthrough die shells of hatching eggs, causing dead embryos or chicks with in-fected navels (omphalitis). In die brooder, E. coli bacteria spread rapidly bymeans of infected droppings picked from litter, feed, or water.

The bacteria enter a chicken by way of either the digestive or the respira-tory system but may eventually settle in the bird's eye, heart, liver, navel,oviduct, leg joints, or wing joints. They may get into the bloodstream,


causingacute septicemia and the sudden death of an apparently healthy bird.

Coliform bacteria survive for long periods in dry litter and dust and arespread through the droppings of infected rodents and chickens. Respiratorycolibacillosis can be prevented by minimizing stress, providing good ventila-tion, and keeping chickens free of mycoplasmal and viral infections. Intestinalcolibacillosis is more difficult to avoid but can be minimized by controllingrodents and keeping feed and drinking water free of chicken droppings.

CoryzaInfectious coryza is a respiratoiy disease caused by Haemophilus

paragal-linarum bacteria that are prevalent in the southeastern United States and inCalifornia. The disease can be difficult to recognize because it resembles odierrespiratory diseases and often occurs in combination with them. Its chief


symptoms are swelling oi the face and, in chronic cases, the unmistakableodor of nasal discharge.

Infectious coryza is spread mainly through contact with carrier birds,which include all survivors of the disease and other birds in the same flock,even though they may never have had symptoms. The disease is easily intro-duced by unknowingly bringing growing or mature carriers into an establishedflock. A vaccine is available, but should be used only to prevent future out-breaks once Infectious coryza has been diagnosed in your flock.

The only way you can get rid of infectious coryza is by disposing of theinfected flock, disinfecting the premises, and leaving housing vacant for atleast 3 weeks before introducing new birds. Infectious coryza is not transmit-ted through hatching eggs, making it possible to start a new flock by incubatingeggs from infected breeders, provided you take great care to raise the chicks inan uncontaminated environment.

ErysipelasErysipelas, caused by Erysipelothrix rhusiopathiae bacteria, is rare

inchickens. It is significant as a disease chickens share with many other birds andanimals, notably turkeys, pigs, sheep, and humans.

Bacteria shed in die droppings of infected birds or other animals survivefor years in alkaline soil. Chickens 011 range that previously held infected tur-keys, sheep, or pigs may become infected through open wounds that resultfrom fighting, cannibalism, or clubbing. The disease is most likely to occuramong cockerels on free range — cockerels, because they commonly woundeach other in peck-order fights; free range, because it provides contact withpotentially contaminated soil.


The most startling symptom is the sudden death of apparently healthycockerels, while birds in nearby flocks (on uncontaminated soil) dirive. Sincesurvivors continue to shed bacteria, and since this disease poses a health riskto humans, the only sensible approach is to dispose of an infected flock andstart a new flock on fresh ground. Erysipelas is not transmitted through hatch-ing eggs, making it possible to start a new flock by hatching eggs from infectedbreeders, provided you keep the new birds away from contaminated ground.

MycoplasmosisMycoplasmosis encompasses any disease caused by mycoplasma

bacte-ria, the smallest living organisms capable of free existence. A mycoplasma isabout die same size as a virus, but (unlike a virus) can multiply outside a livingcell. The two important mycoplasmas affecting chickens are Mycoplasmasynoviae, which causes air-sac disease in young birds and infectious synovitis


in all ages, and M. gallisepticum, which causes air-sac disease in young birdsand chronic respiratory disease in growing and mature birds.

Diseases caused by mycoplasmas can be difficult to recognize withoutlaboratory work, since they often occur in combination with other bacteriaand with viruses. They are spread from infected breeders through hatchingeggs and by direct contact with infected or carrier birds. Survivors become im-mune to f uture infection but remain carriers. The bacteria cannot survive longaway from a bird's body.

At one time, all chickens carried mycoplasma and became infectious inresponse to stress. Today, mycoplasma-free strains are available among diecommercial breeds. The bacteria threaten primarily commercial operationswith high concentrations of large flocks in relatively confined geographic areas.The farther your flock is from an infected tlock, the lower its risk of exposure.

ChlamydiosisChlamydia psittaci, a bacteria-like organism, affects all species of

birds. Itis like a virus in that it multiplies only within the cell of another life form, butotherwise it behaves like a bacteria and can be treated with antibacterial drugs.It produces an infection commonly known as "psittacosis" or "parrot fever"because it was first identified in psittacine birds (parrots). Outbreaks are cycli-cal and, among poultry, are more common in turkeys than in chickens, whichare naturally resistant. Chlamydiosis is significant because it infects humansas well as birds.


SalmonellosisThe genus Salmonella contains over 2,000 different species.

Although theyall have the potential of causing disease in chickens, only about a dozen cause70 percent of die salmonella outbreaks. Evidence suggests that 75 percent of allchickens are infected with one or more kinds of salmonellae at some time intheir lives.

These bacteria create a serious problem for poultry keepers becausechickens that appear perfectly healthy are often earners. Symptoms may betriggered at any time by stress due to crowding, molting, feed deprivation, drugtreatment, or simply being transported.

The bacteria are transmitted by earners to their offspring through hatch-ing eggs (a process called "transovarian" transmission) in one of two ways:

• die yolk is infected as the egg is being formed in the body of an infectedhen;

• die shell is contaminated as the egg is being laid or when it lands in a

dirty nest; the bacteria then penetrate the shell (most likely because dieshell gets cracked or wet) and multiply within the egg.

An infected embryo may die in the shell toward the end of incubation ormay hatch into an infected chick. The disease spreads to healthy chicks orchickens that come into contact with infected chickens or other infected ani-mals (including humans). It spreads by means of contaminated droppings inlitter, drinking water, and damp soil around waterers. It is spread mechanicallyby flies, rodents, wild birds, used equipment, shoes, truck tires, and the like.Salmonellae may also be present in rations containing contaminated livestockby-products.

Salmonellae generally enter a bird's body by way of mouth. They causeinflammation of the intestines, or Ulcerative enteritis, and so are often referredto as "enteric" bacteria. Acute Ulcerative enteritis is indicated by watery diar-rhea, sometimes smelling bad or containing blood. Symptoms of chronicUlcerative enteritis are emaciation and persistent diarrhea, which may appearmucousy or bloody. If die disease becomes septicemic, the bird's head, comb,and wattles turn dark and purplish.

Salmonella bacteria are divided into four groups with symptoms so similarthat laboratory identification is required to tell them apart.

1. S. pullorum causes pullorum, a disease that affects only poultry, prima-rily chickens. Because it is always associated with diarrhea topped with whiteurates, it was once called "white diarrhea." Pullorum is spread by infectedbreeders dirough hatching eggs, causing deadi to embryos in the shell or tochicks soon after they hatch. Since some states require exhibition birds to beblood tested, a home-testing kit is now available. Local laws may require

INFECTIOUS DISEASES 2 6 0

you topass an examination in order to test your own flock.

2. S. gallinarum causes typhoid that is also specific to poultry, primarilychickens. Like pullorum, typhoid is rare in North America.

3. Paratyphoid infection (para meaning resembles) is caused by over 150different species of salmonellae that invade a large number of animal species.Paratyphoid is the most important bacterial disease in the hatching industry,since it causes deaths among chicks and stunts survivors. This group is alsoimportant in the meat and egg industiy, since it is responsible for causing foodpoisoning in humans. The most common paratyphoid strains in chickens areS. Heidelberg and S. typhimurium; at present, the most serious to humans is S.enteriditis.

4. S. arizonae, like the paratyphoid group, infects a large number of ani-mal species. These salmonellae cause avian arizonosis, mainly among turkeys.Rarely do chickens get the disease, which is similar in appearance and treat-ment to paratyphoid.


Controlling SalmonellaeSalmonellae readily survive and multiply in the environment, making

their control difficult. They survive for years in infected droppings, feathers,dust and hatchery fluff, and for almost a year in garden soil fertilized with in-fected droppings. The bacteria cannot survive long at 140°F (fiO°C), atemperature well below that of healing compost. The bacteria thrive in freshlitter, but cannot live long in built-up litter, due to the high pH of ammonia.

Antibiorics can be used to control a salmonella outbreak, but culling ispreferable to treatment for at least three reasons:

• antibiotics alter intestinal microflora, interfering with recovery;• the use of antibiotics causes antibiotic-resistant strains of

bacteria todevelop;

■ survivors are carriers and continue to spread die disease.In 1935, the National Poultry Improvement Plan (NPIP) was organized

tostandardize pullorum blood-testing and eliminate reactors from breedingflocks. Later, tests for other salmonelloses were added to the program. Ap-proximately two-diirds of the states are now classified as "Pullorum-TyphoidClean." Information on NPIP, which publishes a directory of pulJorum-freebreeding flocks, appears in the appendix.

Avoid salmonellosis by purchasing birds from disease-free flocks and pur-chasing rations that do not con lain slaughterhouse wastes. Keep feed andwater free of droppings. Minimize stress. Clean and disinfect facilities betweenflocks; clean and disinfect incubators and brooders between hatches. If an out-break occurs, cull heavily. Remember, survivors are carriers — you'll never getrid of salmonellae unless you get rid of the carriers.

SpirochetosisSpirochetosis is rare in North America, although the tick diat carries it

isquite common in the Southwest. Symptoms include yellowish-green

2 6 2 Tin; CHICKEN HEALTH HANDBOOK

diarrheacontaining large amounts of white urates, and a high rate of deaths. Controldie disease by controlling fowl ticks and by keeping susceptible birds awayfrom birds diat are immune earners due to exposure to fowl ticks.

StaphylococcosisStaphylococcus aureus bacteria commonly live on a chicken's skin

or mu-cous membranes. Normally they increase the bird's resistance to otherinfections, but will themselves cause infection if they get into the body througha break in the skin. Procedures such as dubbing, cropping, debeaking, and toeclipping open the way lo a staph infection.


Staph bacteria are the most likely cause of infection in feet (bumblefoot),joints (arthritis), and breast blisters. Newly hatched chicks become infectedthrough open navels (omphalitis). If a chicken's immune system has been per-manently damaged by infectious bursal disease or Marek's disease, staph mayget into the bloodstream, causing sudden death, laying hens in hot weatherare particularly susceptible. Ironically, mild stress increases a chicken's resis-tance to staph infections.

StreptococcosisStreptococcus bacteria normally live within the intestines of

chickens, in-fecting birds only if their resistance is low — usually due to infection by someother disease. S.faecalis is one of the causes of omphalitis, in which embryosdie in the shell and chicks die soon after hatching. S. zooepidemicus can causesudden death in mature birds. S. equisimilis causes wounds to fill with pus.Avoid strep infections by minimizing stress and practicing good sanitation.

PasteurellosisPasteurellosis is a group of illnesses caused by 125 species of

pasteureilabacteria. The only significant disease of chickens in this group is cholera,caused by Pasteureila multocida, a bacterium that both causes damage andgenerates toxins.

Fowl cholera can be either acute or chronic. Although the two forms arequite different, symptoms may overlap, since survivors of the acute form oftenbecome chronic. Mature chickens are more susceptible than young ones.

P. multocida bacteria survive at least 1 month in droppings, 3 months indecaying dead birds, and 2 to 3 months in moist soil. T hey are spread


primarilythrough mucus discharged from the mouth, nose, and eyes of infected birds(including wild species), wild animals (rodents, raccoons, opossums), live-stock (particularly pigs), pets, and humans. They may be eaten incontaminated feed or water and may be spread on contaminated equipmentand shoes. They are not transmitted through hatching eggs.

Antibiotic treatment sometimes reduces the rate of death, but die diseaseusually returns when medication is withdrawn. At one time, cholera was verycommon. Today it is controlled through good management, which entails notbringing in older birds that might be carriers and not mixing birds of different ages.

TuberculosisAvian tuberculosis, one of die first poultry diseases ever investigated,

iscaused by Mycobacterium avium, bacteria that infect all species of birds, but


more often chickens and captive exotic birds than other domestic poultry orv\ild species. The bacteria also infect pigs and rabbits, and to some extentpeople (aldiough a different bacterium is usually responsible for human TB).

Avian tuberculosis is more likely to be found in the northcentral statesthan in the West or South. It spreads through contact widi the droppings ofinfected birds. The bacteria survive in soil for up to 4 years. The concentrationof bacteria in soil depends on how long infected birds have been housed thereand on how crowded they are.

Since die disease requires a long period of exposure to get established, itaffects primarily older birds. Symptoms are not dramatic. An infected chickenis less active than usual and gradually loses weight, even though it continues toeat well. Eventually its breast muscles shrivel, causing its keel to stick out. Itmay live for months or years, depending on how extensively the disease in-vades its body.

Prevention entails replacing each year's breeding or laying flock withyoung birds, keeping birds away from housing or range that formerly held aninfected flock, not mixing birds of different ages, and preventing chickens frompicking in their droppings.

The disease may be controlled by blood-testing or skin-testing a flock andremoving positive reactors. If just one infected bird is overlooked, however, diedisease will continue to spread. Since contaminated premises are difficult todecontaminate, the best approach is to dispose of an infected flock and estab-lish a new flock in a new environment.


Uncommon Bacterial DiseasesSome bacteria commonly found in the poultry environment infect

chick-ens only if their resistance has been reduced by some other disease orcondition. Once chickens become infected, the bacteria multiply within thebirds' bodies, become more numerous in the environment, and continue tocause disease. Among diese opportunistic infections are two diat are signifi-cant in their ability to infect humans as well as chickens.

Listeria monocytogenes bacteria are common in the soil and intestines ofbirds and other animals living in temperate climates. They cause listeriosis, adisease to which most chickens are resistant. The bacteria primarily infect achicken's heart and brain (encephalitic form), but may get into the blood-stream (septicemic form) and cause death.

Pseiidomonas aeruginosa bacteria live in soil, water, and other humid en-vironments. Infection may occur in chickens treated with a vaccine orantibiotic that has been handled in an unhygienic manner. Pseudomonasspreads from breeders to chicks through hatching eggs, causing death tochicks during late incubation or early hatch.


Viral DiseasesCompared to bacteria, viruses are simpler in structure and are much smaller.They are, in fact, the smallest patiiogens known — so tiny they can be seenonly through a microscope that magnifies them to 100,000 dines. Like bacte-ria, not all viruses cause disease and the diseases they do cause range frommild to fatal.

Viruses differ from bacteria in being more host specific. They are more dif-ficult to control than bacteria because they

• break down die defenses of a healthy bird,• do not respond readily to drugs,• survive well in nature,• are readily transmitted from one location to another.Since t hey are so small, millions of viruses can travel on one speck

of dust,lust think how many can be carried on the hair of a fly, a rat's foot, a feather, thesole of a man's shoe, or a used chicken crate.

Outside the cells of another living organism, a virus has no life — it neitherbreathes nor eats. Its only known activity is to take over the cell of another lifeform for the purpose of making copies of itself.

Pathogenic viruses usually get into a chicken's body by being inhaled orswallowed, but they may also enter through an eye or a wound (including aninjection puncture). Sometimes viruses invade a cell and hide there formontiis or years before becoming active. Sometimes they take over cells neartheir point of entry, causing a skin disease such as pox. Other times they travelto another preferred site, most often the respiratory system (infectious bron-chitis) or the nervous system (Marek's disease). Sometimes they travel throughthe bird's body, producing plague-like infections such as exotic Newcastle dis-ease and lethal forms of avian influenza.


Vinises cause disease in five ways, by• disrupting or destroying cells;• invading or disrupting the immune system;• activating the immune system, causing fatigue or fever;• triggering development of antibodies that lead to inflammation ortissue damage;• interacting with chromosomes to cause a minor.Usually when a bird is attacked by a virus, its immune system

mobilizes tofight off the virus, which may take a few days to a few weeks. In die process, thebird's body becomes sensitized to the virus, and it is thereafter immune to thedisease caused by that virus. The bird may, however, continue to shed the virusand infect birds that haven't yet been exposed.


Chart 7-2 Viruses Infecting Chickens

Chicken DiseasePrevalence

infectious anemia

egg drop syndr


Virus Family*

Adenovirus

rarevery rare

ome

infectious bursal disease

common

infectious bronchitis

infectious laryngotracheitis commonMarek's disease very common

influenza

Newcasde disease (mild)Newcastle disease (exotic)


Birnavirus

Coronaviruscommon

Herpesvirus

Orthomyxovirus

Picornavirus

rare

commonvery rare

rare

commonpoxPoxvirus

epidemic tremor


Chicken Disease

arthritisinfectious stunting syndrome rare

rotaviral enteritis

* Illustrations are drawn to scale.

Some viruses, on the other hand, attack so fast the bird's body cannot re-spond before serious damage or death occurs. Other viruses weaken theimmune system, leaving the bird open to attack by an


PrevalenceVirus Family

Reovirus

rare

lymphoid leukosisosteopetrosisrunting syndrome

Retrovirus

commoncommonvery rare

Rotavirus

opportunistic or sec-ondary infection (which may cause the bird's death). If a chicken has a viralinfection when it is vaccinated against some other disease, the virus may inter-fere with the vaccine's ability to trigger immunity.

Viruses are classified into families according to their size and shape. Eachfamily includes numerous members, and new families are constantly beingdiscovered.


Adenovirus Syndromes

Viruses in the adenovirus family are not yet well understood. They appar-endy cause a variety of infections, often in combination with other organisms.They may be the cause of infectious anemia, a fatal disease of broiler chicksintensively raised on used litter. The viruses enter a chicken's body through thedigestive system and spread slowly by means of contaminated body dis-charges,


especially droppings. Their main method of transmission is throughhatching eggs laid by infected hens or placed in contaminated cartons. Iodinedisinfectant slows the spread of disease. Chicks are protected by maternal an-tibodies for their first 2 or 3 weeks of life.

Egg drop syndrome is caused by a waterfowl adenovirus introduced tochickens either through vaccine derived from infected duck eggs or throughcontact widi


common

infected waterfowl or drinking water contaminated by them. The


virus remains quiet and undetected until hens approach their peak of produc-tion. Eggs laid by infected hens may have thin gritty shells, soft shells, or noshells. The first sign in brown-egg layers is pale eggs. Although die virus hasbeen found in numerous ducks and geese in North America, and has infectedchickens elsewhere, so far no chickens have experienced egg drop syndrome


in North America.

ArthritisViral

arthrids, caused by the avian reovims, is quite similar in appearanceto infectious synovitis caused by mycoplasma bacteria. The main symptomsare swollen hocks and lameness, primarily in intensively raised broilers 4 to 8weeks old. Aside from vaccination, the only known way to prevent viral arthri-ds is to avoid overcrowding.


BronchitisInfectiou

s bronchitis, the most contagious disease of chickens, is a respi-ratory illness caused by a coronavirus and characterized by coughing,sneezing, and ratding sounds in the throat. It starts suddenly, spreads rapidly,and can travel through the air to a second dock more than 1,000 yards away.Deaths occur primarily in chicks. Pullets that survive may have permanentovary damage and


may not lay eggs as mature hens.

Vaccination is not foolproof, since it bestows immunity only against thestrains contained in the vaccine, and new strains keep popping up. Survivorsare carriers, so the only sure way to get rid of infectious bronchitis is to get rid ofyour flock, clean up, disinfect, and start over. Because the disease is not usuallytransmitted through hatching eggs, you can get clean chicks from an


infectedflock, but be sure to carefully clean up die environment and avoid introducinginfected birds in die future.

Bursal Disease

Infectious bursal disease occurs when a birnavirus invades lymph tissue,particularly tissue of the cloacal bursa. The disease is sometimes called"Gumboro disease" because it was first studied in Gumboro, Delaware. Itcauses atrophy of the cloacal bursa, resulting in


suppressed immunity andgreater susceptibility to future infections, particularly colibacillosis and ne-crotic dermatitis. Another result of suppressed immunity is failure to developan immune response to vaccines.

The disease appears suddenly, usually in large flocks of broilers, and in-volves most birds in the flock. The first symptoms are watery or whitish


diarrhea that sticks to vent feathers, causing birds to pick at their own vents.Deaths, when they occur, peak within a week and survivors recover rapidlythereafter. A subsequent infection in die same housing may be so mild youdon't notice it.

IBD virus is not egg-transmitted and survivors are not carriers, but the dis-ease is highly contagious and difficult to get rid of in housing


that once held aninfected flock. Chicks exposed to die virus before tiiey are 2 weeks old developnatural immunity. Vaccines are also available.

Viral Diarrhea

Enteritis, characterized by inflamed intestines and diarrhea, has many vi-ral causes, some of which have yet to be discovered. Viral enteritis in chickensis becoming more common dian ever, and can be divided into three maingroups:


Bluecomb— cause unknown. The disease affects pullets just coming intoproduction. It is similar to bluecomb in turkeys, caused by a coronavirus towhich chickens are resistant.

Infectious stunting syndrome—cause unknown, but likely involves one ormore reoviruses. This disease primarily infects intensively raised broilers.

Rotaviral enteritis—rotaviruses are common in the poultry environment


and do not always cause disease. When infection does occur, massive amountsof new viruses are released in the droppings of infected birds, causing the dis-ease to spread.

Avoid viral diarrhea through good sanitation and not crowding birds.Thoroughly clean up and disinfect between flocks, and don't reuse old litter.

Epidemic Tremor

Avian encephalom


yelitis is a relatively rare infectious disease of chickscaused by a picornavirus. Its chief symptoms are loss of coordination andrapid trembling of the head and neck, giving the disease its common name,epidemic tremor. The disease is transmitted from breeders to chicks throughhatching eggs. An adult outbreak is so mild it is likely to go unnoticed, lasts lessthan a month, and leaves birds immune


without making them carriers. Survi-vors of a chick outbreak should be culled, since they rarely develop into goodlayers or breeders.

InfluenzaAvian

influenza was among the first diseases known to be caused by a vi-rus. It is caused by several different orthomyxoviruses and conies in many


forms, ranging from mild to rapidly fatal. Symptoms vary widely and mayrelate to respiration (coughing, sneezing), digestion (appetite loss, diarrhea),reproduction (reduced fertility, soft-shelled eggs), or nerves (twisted neck,wing paralysis). Sometimes the first symptom is numerous sudden deathsof apparently healthy birds.

In North America, outbreaks among


chickens are rare and widespreadin both time and place, and primarily affect operations where large numbersof chickens are concentrated. If avian influenza occurs in your area, stayaway from infected flocks and their handlers. If possible, keep your flockindoors, away from wild birds that can spread the disease. In the event of aserious outbreak, you may be advised to vaccinate your flock to help locallycontain the disease.


Laryngotracheitis

Infectious laryngotracheitis, or "laryngo," is a highly contagiousrespiratory disease caused by a virus in the herpes family. Its chief symptomsare moist respiratory sounds (gurgling, choking, rattling, whistling, or"cawing") and coughing up bloody mucus. In a serious case, a largepercentage of birds die.

Vaccination keeps the disease from spreading, but causes birds tobecome carriers. Vaccinating


therefore doesn't make sense unless laryngois prevalent in your area. Vaccination is usually recommended for thosewho show or who regularly bring in adult birds, but since vaccinated birdsare carriers, if you vaccinate, you run the risk of having your birds infectany unvaccinated birds they come into contact with. (In the old days, flockswere immunized by bring in an infected bird - survivors of the ensuinginfection became immune.)


The virus does not live long off birds and is not spread through hatchingeggs. You can safely start a new flock from infected breeders if, and only if,you dispose of the old flock and carefully clean and disinfect housing beforemoving the young birds in.

Newcastle Disease

Newcastle disease gets its name from the British town of Newcastle-upon-Tyne, one of the first places where it was studied. The disease comesin many different


forms, ranging from mild to devastating. Mild forms arequitecommon, not particularly serious, and can be controlled by vaccinationwhere the virus is prevalent. Virulent or so-called "exotic" forms will infecteven a properly vaccinated flock, but fort unately are relatively rare.

Vaccination in the face of an exotic outbreak slows the spread of diseaseand reduces the number of deaths, but won't keep birds from getting


thedisease. Furthermore, vaccinated survivors are likely to be carriers.

Exotic Newcastle is usually introduced by illegally imported cage birds


that have not gone through official quarantine. It is spread by contaminateddroppings on used equipment and the shoes of humans, and causes a rapid,high number of deaths. The disease can easily be confused with other seriousrespiratory infections.

Symptoms include a sharp drop in laying accompanied by breathing diffi-


culties, soon followed by muscular tremors, twisted neck, and wing or legparalysis, and sometimes wateiy, greenish diarrhea. If an exotic infection oc-curs in your area, stay away from infected birds and keep their handlers awayfrom your flock until the outbreak has been controlled.

Chart 7-3Forms of Newcastle Disease


Characteristic

mild:Beaudettes

affects all ages,

mild respiratory

infe

ct's

s,dr


Formal Name

SymptomsForm

laying,slight wheezing,few deathswheezing,

some deathsmesogentcNewcastle disease

lentogenicNewcastle dise

as


affects all ages,

acute, lethal,

nervous

&

respiratory

infection

affects all ages,acute, le

thalnervous,respiratory &intestinal infectionappears suddenly,

gas


enteric asymptomatic -enteric lentogenicNewcastle disease

mild intestinalinfection

EXOTIC:Beach's

Doyle's

none

ping & coughing,

drop in laying,

wing or leg par

alysis,

100% affected,

up to 50% adults die,

up

to 90% young diesudden death orlistlessness, rapidbreathing, drop inlayin


g, watery greenishdiarrhea, 100% affected,nearly 100

% die, bloodydigestive tractneurotropicvelogenic New

castledisease

viscerotropicvelogenic Newcastledisease


PoxPox in chickens (not at ail the same as chicken pox in humans) occurs

when the pox virus gets into wounds caused by insect bites, dubbing, fighting,cannibalism, or injury on poorly designed equipment. Fowl pox appears intwo forms: diy pox affecting the skin (cutaneous form) and wet pox affectingthe upper respiratory tract (diphtheric fonn).

Dry pox causes clear or whitish bumps on the comb, wattles, and otiierunfeathered portions of the body. The bumps eventually come together toform scabs, fall off, and leave scars. Wet pox causes yellowish bumps in diemouth, throat, and windpipe, sometimes affecting the bird's ability to breatheso that it dies from suffocation. In either case, survivors recover in 4 to 5 weeks.

In pox-prone areas, disease may be controlled through vaccination and bycontrolling mites and mosquitoes.

Viral TumorsSome viruses are nearly identical to die growth-promoting

chromosomesin a chicken's cells, and have the ability to invade cells and modify those chro-mosomes. The resulting mutation induces die cells to multiply out of control,causing a tumor.

Tumors can occur in any part of a chicken's body. They may be benign(starting and developing in one place) or malignant (spreading to other partsof the body). External benign tumors may be removed surgically (assuming thebird is worth the cost); malignant tumors usually come back after surgery. In-terior tumors, whether benign or malignant, are rarely discovered until afterthe bird dies.

In veterinary jargon, a tumor is called a neoplasm (from neo meaning new


and plasm meaning shape). Miscellaneous viruses occasionally cause neo-plasms in a hen's ovary or oviduct (most often in hens over one year old) oralong the backs and thighs of broilers (appearing as crater-like ulcers that mayclump togedier).

By far the most important tumors in chickens are in the avian leukosiscomplex, an interrelated group of viral diseases diat affect few other birds (oranimals) besides chickens and that fall into two categories based on theircauses:

• Marek's disease, caused by six different herpesvimses that primarilyaffect the nerves of growing birds;

• the leukosis/sarcoma group (leukosis means "whitening," sarcomabeing a malignant tumor), caused by retroviruses diat primarily affectolder birds.


Marek's DiseaseThe Marek's virus killsmore chickens than anyother disease. It's so com-mon, you can safely assumeyour flock is infected, even ifyour chickens don't showany symptoms. Stress due tocrowding, moving, or eventhe natural process of ma-turing can weaken a flock simmunity, causing an out-break of the dormant virus.The virus attacks variousparts of a chicken's body, re-sulting in an array ofsymptoms — droopy wing,paralyzed leg, head held low,twisted neck, blindness, sud-den death.

The virus is not transmitted by means of hatching eggs. In fact, a newlyhatched chick is briefly protected if its dam transmits a high antibody levelthrough her eggs. Chicks should be brooded away from adult birds, however,since the first few weeks of life are the most critical time for infection. Chicksthat are isolated until the age of 5 months develop a natural immunity thathelps them overcome exposure to Marek's virus as adults. Some chickenstrains are genetically more resistant dian otiiers.

Turkeys carry a non-tumor-forming vims that prevents the Marek's virusfrom developing tumors. Chickens that are run with turkeys therefore developsome measure of immunity (altiiough keeping the two together creates otherproblems, such as the possibility of the turkeys getting blackhead from diechickens).

Marek's vaccine for chicks is derived from the turkey virus, making it one


vaccine that does not cause a mild case of disease in order for birds to build upantibodies. To become immune, chicks must be exposed to the turkey virusbefore they are exposed to Marek's vims. Vaccination should therefore occuras soon after hatch as possible and chicks should be isolated until immunitydevelops in about a week. A single vaccination confers lifelong immunity, butis not 100 percent foolproof — about 5 percent of all vaccinated chickens getthe disease anyway.

Marek's disease in chickens has been used as a model for studying cancerin humans, and Marek's vaccine has become a model for developing a human

Chart 7-4Forms of Marek's Disease

FormCharacteristicsCutaneous (skin

form)

Neural (nerve form)

enlarged featherfolliclesprogressive paralysisweight lossanemialabored breathingdiarrheafew or insignificantpostmortem findingsgraying, shrunken irisirregular-shaped pupilemaciationdiarrheablindnessdeathtumors in ovary, heart,lung, and other organs

Ocular (eye form)

Visceral(internal organs.)


cancer vaccine. There is no evidence, however, diat the Marek's virus causescancer in humans.

LeukosisLike Marek's disease, the neoplasms in the leukosis/sarcoma group

infectall chickens by die time they reach maturity. Rarely, however, do they causedisease.

The viruses in til is group are most likely to cause lymphoid leukosis, occa-sionally osteopetrosis (thickening of the leg bones that affects primarilycockerels and cocks), only rarely erythroid leukosis (causing enlarged, brightred liver and spleen) or myeloid leukosis (causing chalky white internal tumorsalong the spinal column and beneath the keel). The latter two are so infrequentthat they warrant only brief mention.

Lymphoid leukosis usually strikes chickens just reaching maturity. Thesymptoms are not particularly dramatic and are so similar to those of Marek'sdisease that the two are easily confused. Unlike Marek's disease, lymphoidleukosis cannot be prevented by vaccination.

Chart 7-5Differences Between Lymphoid Leukosis and Marek's

Disease

Lymphoid Marek'sCharacteristic Leukosis Disease

Incubation period 14 weeks 2 weeksEarliest age 14 weeks 4 weeksUsual age over 6

monthsunder 6 months

Peak age 4 to 10 months

2 to 7 months

Peak age for deaths

24 to 40 weeks

10 to 20 weeks

Paralysis no yesEye tumors no possibleSkin tumors rare possible


Nerve tumors 110 yesLiver tumors yes yesHeart tumors yes yesIntestinal tumors yes yesBursal tumors yes noMuscle tumors rare possible


Runting SyndromeRunting syndrome, like lymphoid leukosis, is caused by a retrovirus

andcan be easily mistaken for Marek's disease. The virus that causes runting syn-drome seems to be more prevalent than the disease, but since it doesn't alwaysproduce symptoms, it's considered relatively rare and not much is knownabout it. In North America, it is most likely to occur in southeastern states, es-pecially Florida, Mississippi, and North Carolina.

Fungal DiseasesFungi are parasitic plants that lack chlorophyll and live on decaying organicmatter. They include molds, mildews, yeasts, mushrooms, and toadstools. Ofmore than 100,000 different species, most are either beneficial or harmless.Two kinds of fungi cause disease — yeast-like and mold-like. They cause dis-ease of four types:

• allergic reaction to inhaled spores in moldy litter;• poisoning due to toxins released by fruiting bodies fi.e. poisonousmushrooms and toadstools);• poisoning due to toxins generated through invasion of stored feed (e.g.aflatoxicosis or ergotism) — this type of poisoning is called"mycotoxicosis" (discussed on page 140);• infection due to invasion of skin, lungs, or other body tissue (e.g. favusor thrush) — this type of infection is called a "mycotic disease" or a"mycosis."

MycosesMycoses are grouped according to whether they are:

• superficial — affecting the skin or mucous membranes (e.g. favus);• deep — affecting internal organs, usually the lungs (e.g. aspergillosis,dactylariosis, histoplasmosis, thrush). Deep infections are opportunis-


tic, taking advantage of a chicken's low resistance due to stress or thepresence of some otiier disease.Fungal infections have gotten more common since the use of

antibioticsbecame widespread, because antibiotics destroy normal body flora, making iteasier for pathogenic fungi to take over. Still, mycoses are rare enough in chick-ens that methods for their control and treatment remain less advanced thanthose for bacterial and viral diseases.


Chart 7-6Fungal Diseases

Disease Cause PrevalenceAspergillosis Aspergillus spp rareDactylariosis Dactylaria gallopava very rareFavus Microsporum

gallinaerare

Histoplasmosis Histoplasma capsulatum

very rare

Thrush Candida albicans common

AspergillosisAspergillosis refers to any disease caused by the spores of

Aspergillus sppfungus commonly found in die environment, especially in soil, grains, and de-caying vegetative matter including litter. These molds are capable of infectingall birds, more commonly turkeys than chickens. They produce a form ofpneumonia diat is acute in chicks and chronic in mature birds.

Infection is rare in North America and may easily be prevented throughgood sanitation (especially in the incubator and brooder), avoiding moldygrain and litter, periodically moving feeders and waterers or placing them ondroppings boards, providing good ventilation to minimize dust, and keepingstress to a minimum.

ThrushCandida albicans causes thrush or candidiasis in many species of

birdsand animals, including humans. Thrush probably occurs among chickensmore often than we know, since its symptoms are not particularly distinctive.Thrush is primarily a disease of chicks and growing birds. It can be preventedby controlling coccidiosis and by avoiding the overuse of antibiotics.

Rare Mycoses


Uncommon fungi that occasionally invade chickens include:Microsporum gallinae that causes a superficial infection called

"favus," inwhich the comb of a mature cock looks like it's been sprinkled with flour;

Dactylaria gallopava in moldy sawdust used as litter, causing a brain dis-ease called "dactylariosis" diat makes chicks tremble and walk in circles;

Histoplasma capsulatum, a fungus that causes histoplasmosis, a rare butpotentially fated disease chickens share with other buds and with humans liv-ing along the Mississippi, Missouri, and Ohio rivers.


SyndromesA syndrome is a group of symptoms that occur in combinat ion and appear as aparticular disease. In most cases, the disease is poorly defined — its symptomsare not always the same and/or its cause is not yet known. These diseases areso poorly defined that one disease may have several names (malabsorptionsyndrome, pale bird syndrome, infectious stunting syndrome) or the samename may be applied to more than one disease (e.g. runting syndrome). Thediseases in this group are described more fully in chapter 15:

• air-sac syndrome (air-sac disease)• egg drop syndrome• fatty liver syndrome• infectious anemia• infectious stunting syndrome• runting syndrome• star-gazing syndrome (epidemic tremor)• sudden death syndrome• swollen head syndrome

Diseases of Unknown CauseSyndromes are not alone among diseases for which we've not yet found acause, despite all our modem technology. The following conditions (describedin chapter 15) have unknown causes:

• bluecomb• broiler ascites• crop impaction• gout (visceral)• round heart disease• twisted leg


Environment-RelatedProblems

THE ENVIRONMENT CANNOT BE OVERLOOKED as a source of health prob-lems for chickens. Extremely cold weather can lead to frostbite. Steamyweather can cause heat stress. Crowded conditions often lead to cannibalism.Unsafe chemicals or vegetation cause poisoning. Rodents spread diseasesand, on occasion, attack chickens. Happily, each of diese problems can beavoided through awareness and good management.

FrostbiteAll chickens can tolerate quite a bit of cold weather, provided you see diat theirdrinking water doesn't freeze and their housing is neither drafty nor damp.Draftiness removes warm air trapped by ruffled feathers. Moisture in the airmakes chickens cold by absorbing body heat. Combs and wattles are thereforemore likely to freeze in damp housing tiian in dry housing.

315

Since cocks don't sleep with their heads tucked under a wing, as hens do,cocks are more likely than hens to have their combs and wattles frozen whentemperatures dip during the night. Cocks with large combs are more likelythan others to be frostbitten.Frozen combs and watdes look pale. If you discover the condition while


Hecwily feathered birds likethese New Hampshiresadapt better to winterweather than lightlyfeathered birds.the part is still frozen, apply a damp, warm cloth (105°F, 40.5°C) to the frozenpart for 15 minutes or until it thaws. Do not rub. After the part has thawed,gently apply an antiseptic ointment such as Neosporin. Isolate the bird andkeep an eye on it to see that the comb heals properly.

Frozen combs and wattles are more likely to be discovered after they havethawed and become red, hot, swollen, and painful. The bird doesn't feel likemoving, is listless, and loses interest in eating. If the part has already thawed,warming it is no longer necessary. Gently coat the part with Neosporin andisolate the bird.

After the swelling goes down, the skin may peel, the part may itch, and itmay be sensitive to cold for a while. It may turn scabby, develop pus, and even-tually fall off. The suffering cock will continue to lose weight and may becomeinfertile.

If the comb or wattles were seriously frozen, instead of swelling they mayremain cold, begin to shrivel, and eventually die back. Other chickens maypeck at die affected part, making matters worse.

If a comb or wattle turns black, the affected tissue has died and gangrenehas set in — the comb or wattle is no longer receiving a blood supply and mustbe surgically removed.

ENVIRONMENT-RELATED PROBLEMS 317

Dubbing and Cropping

Surgical removal of the comb (dubbing) and wattles (cropping) is done forone of several reasons:

• to remove injured or infected tissue

• to keep combs and wattles from freezing

• to increase egg production and reduce feed costs


• to minimize blood loss in fighting cocks• because show regulations require itModem and Old English game cocks must be dubbed and cropped in

or-der to avoid disqualification from some shows (other breeds may bedisqualified if tiiey flredubbed or cropped). Fighting cocks are dubbed to mini -mize blood loss due to injuries. In cold climates, large-combed hens may bedubbed to minimize heat loss, thereby reducing feed costs and improving eggproduction; cocks are dubbed to avoid frostbitten combs and wattles that in-terfere widi fertility.

Dubbing and cropping are stressful and should be avoided immediatelybefore or after birds are vaccinated. Neither should breeders be dubbed beforeor during hatching season, or low fertility may result. Birds can be dubbed atany age after their combs and watdes develop, but those in the 8- to 12-week-old bracket bleed less than older birds.

Regardless of a bird's age, it can bleed to death as a result of improper dub-bing. Feeding each bird a vitamin K tablet daily for 5 days preceding theoperadon aids clotting. The surgery is painful and should be done under vet-erinary supervision so an anesthetic can be used.

Use small tin snips or 6-inch (12 cm) curved surgical scissors, availablefrom a medical supplier, and heat the instrument to destroy any bacteria thatmight be present. Snip off the comb Vz inch (1 cm) above the head. Cauterizethe surface by searing it widi a hot iron to minimize bleeding. If the wattles areto be cropped at the same time, snip diem off and coat them with an astringentsuch as iron subsulfate.

To prevent infection, either inject Vi cc penicillin into the bird's breastmuscle daily for 10 days or add 1 teaspoon (5 ml) tetracycline or bacitracin per


gallon to die drinking water for 10 days. The comb and wattles should healwithin 30 days.

Heat StressLightly feathered breeds like Leghorns, Hamburgs, and Minorcas suffer less inwarm weather than heavily feadiered breeds like Brahmas, Cochins, Rocks,and Reds. Laying hens are more susceptible to heat stress than birds not inproduction. Closed nests make matters worse. Avoid using trapnests duringhot weather. If hens must be trapnested, check nests frequentiy and releasehens before they suffocate in the close confines of a too-hot nest. Outdoors,while birds are less subject to heat stroke than dark birds because they reflectsunlight better.

Any chicken's body operates most efficiendy when die outside tempera-ture is 70-75°F (21-24°C). Chickens cannot sweat to keep cool. Instead, they


hold their wings away from their bodies and pant. Holding the wings awayfrom the body exposes more skin surface under the wings, thereby increasingevaporation and radiational cooling. Panting releases heat through evapora-tion from the lungs.

A mature chicken starts panting when the temperature reaches 85°F(29.5"C). A chick pants when die temperature is 1()0°F (38°C) or more. Pantingcauses a chicken to exhale large quantities of carbon dioxide, which raises itsblood pH. The resulting changes in physiology cause stress. The chicken stopseating and lays fewer and smaller eggs with thinner shells. A young bird stopsgrowing.

When the temperature reaches 104 "F (40°C), even panting is not enoughand deaths may occur. Cool things down by increasing air cir culation — opendoors and windows or install a fan. Among the least expensive fans is a vari-able-speed paddle or Casablanca fan. Be sure the coop is properly vented sohot air doesn't get trapped against the ceiling.

Hosing down the outside walls and roof improves cooling dirough evapo-ration, as does occasionally misting or fogging chickens. Take care not to mistso much that water puddles on the floor. Mist only adult chickens and onlywhen the temperature is above 95"F (35"C) and the humidity is below 75 per-cent. Cooling won't occur if the air is already so humid that no more water canevaporate. Mist only when the fan is running or air circulation is otherwise suf-ficient to dry the birds.

Chickens eat less when they're hot. To ensure adequate nutrition, feedonly fresh radons. Chickens also drink more in hot weadier so they can


expelextra moisture in their droppings as an additional cooling mechanism (caus-ing droppings to be looser in hot weather). Encourage drinking by supplyingcool water and extra watering stations. If the water supply remains die samewhen a flock's water requirements go up, water deprivation may result (see"Dehydration," page 40).

Walking among your birds will encourage them to move, stimulatingdrinking, but don't disturb them at peak heat periods, which only increasesstress. Symptoms of serious heal stress include drinking excessive amounts ofwater, labored breathing, and weakness. If a heat-stressed bird becomes pros-trate, but is still alive, move it into the shade. Dunk it in cool water and use aplastic tube attached to a funnel to fill its crop with cool water. If the bird sur-vives, it may remain weak for several days.

CannibalismLight, high-strung laying breeds, especially Leghorns and other Mediter-raneans, ate more likely to engage in cannibalism than the heavier Americanand Asiatic breeds. Within a breed, some strains are more cannibalistic than


others. Birds of die same strain may be cannibalistic when raised in one placebut not anodier, proving diat you can discourage cannibalism by providing aproper environment.

The problem has many causes, often working in combination. Conditionsdiat can trigger cannibalism include:

• heat without adequate ventilation• nests not dark enough• bright lights in the brooder house (lights on all night or sunlightcoming through windows)• crowding (especially in fast-growing chicks that quickly fill the avail-able space and can't get away from each other)• boredom or lack of exercise (more likely in caged or housed birds thanin free-ranged flocks)• feed and water troughs too few or too close together (failure to increasethe number of feed and water stations as chicks grow)» feed too high in calories and too low in fiber (chickens quickly satisfytheir nutritional needs and get bored)• external parasites (a chicken pulls out its own feathers, drawing bloodthat attracts other birds to pick)• injury or bleeding (e.g. from an injured comb or a broken feadier

quill)

Toe PickingCannibalism often starts with toe picking, a common problem

amongchicks, especially those reared on paper to prevent litter eating. Toe pickingcan also occur in chicks brooded on wire — sharp wire edges cut their toes andthe bleeding attracts toe pickers. Toe picking may start when chicks can't find


anything else to eat because die feeder is poorly designed, is too high, is too fat-away, or is too small for the number of chicks involved.

To get chicks picking at feed instead of feet, sprinkle a little starter rationon paper, or place shallow containers of starter close to the heat source wherethe chicks can easily find it. If toes are injured from picking, light the brooderwith a red light so chicks can't easily delect blood while the toes heal.

Head PickingHead picking generally occurs in older birds, especially when combs

orwattles bleed due to fighting or frostbite. Cocks or hens housed in adjoiningcages may pick each other's heads, even if the birds have been debeaked.When possible, space cages far enough apart to prevent picking. Cardboard orpaper feed sacks wedged between cages are not the answer, since a solid bar-


rier reduces air circulation, causing caged birds to suffer in warm weather. Iso-late any bleeding bird until the wound heals.

Feather PickingEvidence of feather picking is dull, broken leathers and bare patches

on abird's neck, breast, back, and below the vent. Tail-feather picking is especiallycommon in growing birds, when new feathers filled with blood attract pickersbefore enough plumage grows to cover the area. But it can start at any time,triggered by crowding, lack of exercise, irritation due to parasites, or low-protein diet and other nutritional deficiencies. Picked birds must continuallygrow new feathers, causing the same stress reactions associated with molting,including a drop in laying.

Feather loss doesn't necessarily indicate feather picking. Layers often havebroken or missing feathers, especially on their necks and tails, rubbed off onfeeders and nests. Mating cocks frequently wear the feathers off a hen's back.The annual molt also causes feather loss. Some birds drop and replace theirfeathers gradually, others lose many feathers at a time. During the molt, en-courage feather growth and discourage feather picking by increasing dietaryprotein.

Vent PickingVent picking is the worst form of cannibalism because it escalates

quicklyand often ends in death. It can start if nests are too light, so that a hen's ventgets picked while she's laying. But it is most likely to occur among pullets justcoming into lay, usually alter one tears tissue or prolapses while passing


anunusually large egg (see "Prolapsed Oviduct," page 53).

Egg EatingEgg eating occurs when not enough nests are provided, nests are too

light,housing is too light in general, or hens are crowded and bored. Egg eating isalso encouraged by anything that causes egg breakage — eggs aren't collectedoften enough, have soft or thin shells, or become cracked due to insufficientnesting material. Once chickens find out how good eggs taste, they will breakeggs on purpose to eat diem.

A nutritional deficiency, especially vitamin D or calcium, can cause softshells that lead to egg eating. A laying hen's calcium needs are increased bywarm weather and by age. Appropriate nutritional supplements include free-choice feeding of limestone or ground oyster shell, or adding vitamin AD&Epowder to drinking water three times a week.


Toxic seeds are sometimes accidentally harvested along with feed grains.Such seeds include:

• coffee weed (Cassia obtusejblia) in corn and soybeans, causing a dropin egg production, diarrhea, paralysis, and death;

• gossypol in cottonseed meal, causing bluish combs and wattles,emaciation, low egg production, and low egg quality;

• crotalaria seeds and stems, causing bright yellowish-green droppingsand inactivity;

• sorghum seed, causing depressed growth and leg deformity;• lye seed, causing poor growth, pasting, soft bones, and lameness.

Other naturally occurring toxins in the environment cause selenium poi-soning (see page 32), blue-green algae poisoning (see "Algae Poisoning," page246), botulism (see "Clostridial Diseases," page 111), and mycotoxicosis.

Mycotoxicosisl Jnlike infectious fungal diseases, which occur when fungi or their

sporesinvade body tissue, fungal poisoning occurs when chickens consume toxic by-products generated by mold growing in feed. A number of poisons ormycotoxins are produced by molds that grow naturally in grains, and somemolds generate more than one kind of poison.

Aspergillus flavus, the same fungus that causes aspergillosis, also causesallatoxicosis, a disease that increases a bird's susceptibility to heat stress andinfection. In the United States, aflatoxins are the only feed-borne mycotoxinsregulated by law.

Fusarium sporotrichioides, along with other species of Fusarium, causes


fusariotoxicosis, a digestive disorder that interferes with egg production,growth, and feathering.

Claviceps purpurea produces a highly toxic alkaloid that causes ergotism,the oldest known mycotoxicosis. It is characterized by shriveled combs, soreson legs, convulsions, and death.

Aspergillus spp and other fungi generate ochratoxin, one of the most poi-sonous of all mycotoxins. The fungi that cause ochratoxicosis prefer hightemperatures and so, in contrast to ergot and fusarium molds, they tiirive inpelleted feed (which is manufactured under intense heat) unless it containsmold inhibitors.

All mycotoxicoses increase a chicken's need for vitamins, trace elements(especially selenium), and protein. Poisoning is difficult to identify and diag-nose, in part because one feed source may contain more than one kind ofmycotoxin. A positive diagnosis usually requires analysis of die feed to identify


any fungi present. Since smalJ-flock owners generally buy feed in small quanti-ties, it's likely that a given batch will be used up before anyone thinks ofanalyzing it. Once the contaminated feed is removed, chickens usually re-cover.

Fungal poisoning can be avoided by using commercially prepared feedscontaining mold inhibitors and by storing feeds away from humid conditions.Use plastic storage cans rather than metal ones, which generate moisture bysweating. Never give chickens feed that has gone moldy. Ifyou buy moldy feed,take it back and insist on a refund.

Chart 8-1Fungal Poisoning

Grain Source

Aflatoxicosis

ErgotismFusariotoxicosis

OchratoxicosisAspergillus flavus and otherfungiClaviceps purpureaFusarium sporotrichioides andothersAspergillus ochraceous

andother fungiall grains

wheat, rye, cereal grainscorn, wheat, barley, millet,safflower seedbarley, com. sorghum, wheat


Caused ByDisease

Antifreeze Poisoning

Nearly all animals are attracted LO ethylene-glycol because it tastes sweetand it doesn't freeze, thereby becoming the only "water" available to drink incold weather. Poisoning is most likely to occur due to antifreeze spillage in fell,winter, and early spring. The lethal dose is 0.1 ounce per pound (8 ml/kg) ofbody weight, or about 3 tablespoons of antifreeze per mature chicken.

Antifreeze destroys a bird's liver and kidneys. The bird appears drowsyand uncoordinated, twists its head back, has trouble breathing, and has waterydroppings. It ruffles its feathers, lies down, and dies. Few people would recog-nize antifreeze poisoning unless they actually'saw the bird drinking antifreeze.

Chick PoisoningChicks are especially susceptible to certain toxins, including:

• carbon monoxide, from being transported in the poorly ventilatedtrunk of a car (chicks die);


Rats are active at night. If you see a rat in the daytime, you have a bad ratproblem — the rats have overpopulated and the dominant ones are keepingthe weaker ones away from feed, forcing them to eat during the day.

Feed loss is one of the worse consequences of an infestation. Eight rats eat1 pound (2.2 kg) of feed each day. One pair of rats produces four to seven litterseach year. Even though not all of the offspring reach breeding age, within ayear one pair can easily become 1,500 rats.

MiceChickens are die natural enemies of mice, but die agile little rodents

aregood at scurrying away. Mice reproduce even faster than rats — each pair hasfive to eight litters per year. Mice are most active at dusk and dawn, but theyfeed all day long. It takes 305 mice to chowdownon 1 pound (2.2kg) offeed per day.

Rodent ControlDespite all our modern technology, we still haven't found a better

mouse-trap. The best way to discourage rodents is to make the chicken houseunattractive to them. Since rats and mice shun open areas, keep the landaround your coop clear of weeds and trash. If die floor is raised, make sure it'sat least 1 foot (30 cm) above ground so rodents don't feel protected. Use liang-

/

Norway rat

House mouse


r


ing feeders that are difficult for rodents to reach, store feed in containers withtight-fitting lids, and avoid spillage.

Keep a cat. A cat's advantage for rodent patrol far outweighs any disadvan-tages it may have as a potential disease carrier.

If yon have a serious rodent problem, set traps. Use spring traps, placed atright angles to the wall with the trigger and bait close to wall. Since mice runalong sills, rafters, and other high places, set traps high as well as on theground. As cliched as it may sound, Swiss cheese is still the best trap bait.

Identify tunnels and fill them in. Place poisoned bait near tunnels that arereopened within a day or so (the unopened tunnels have become inactive).After a course of baiting (which varies with the type of bait you use), reclose theactive tunnels. Rebait any that are opened again. Continue until tunnels are nolonger reopened.

Rodent BaitThe most common rodent poison contains an anticoagulant that com-

petes with vitamin K and thereby interferes with blood clotting. Amultiple-dose anticoagulant must be eaten several times to be effective. A

Rodent bait stationt3----- PtASTIC CAP

- - -THREAD WIRE THROUGH HOLE

AND AFFIX TO WALL

2 FT.(61 CM|

2 IN. t(5 CM) -l<INTERNAL BAFFLE TOCONTAIN BAIT


single-dose anticoagulant kills afteronly one feeding.

Since a multiple-dose bait requiresseveral days to take effect, be sure to putout enough bait to accomplish yourpurpose. Keep the bait out until nomore is eaten. Multiple-dose bait isrelatively safe for pets and other ani-mals, since a single dose is ineffective.

Single-dose anticoagulants are alsorelatively safe for otiier animals,

since alarge dose is needed to be lethal to ani-mals larger than a rodent. Even though single-dose anticoagulants requireonly one feeding, leave the bait out for at least 2 days to make sure all rodentsconsume some.

Not till baits are anticoagulants. Some contain vitamin D3, which causesdeath through an imbalance of blood-calcium levels. This type of bait is fairlysafe to animals other than rodents, since they must eat a large amount tobe affected. Single-dose bait that attacks the nervous system is toxic to allanimals.

Regardless of a bail's level of safety, take care when putting it out so thatchickens, pets, and children can't get into it. Never just scatter bait around ordrop it into tunnels — rodents may kick it out where chickens or other animalswill find it and eat it. No bait is effective if an abundance of otiier feed is avail-able, so carefully clean up spilled grain before putting out bait.

Chart 8-4Rodenticides

Multiple-Dose Single-Dose

BrodifacoumBroraadiolonBromethalin*Cholecalciferol

ChlorophacinoneDiphacinonePivalWarfarin

Unlike other baits (which are relativelysafe), Bromethalin affects the centralnervous system and is fairly toxic to allanimals.


Diagnostic Guides

TRYING TO FIGURE OUT WHAT DISEASE your chickens have, or diagnosingthe disease, involves four basic steps:

• examining flock history• considering the symptoms• conducting a postmortem examination• performing laboratory proceduresHome laboratory procedures are pretty much limited to investigating

in-ternal parasites, as described in chapter 5. Postmortem examination isdiscussed in detail in die next chapter, as is die process of submitting speci-mens to a pathology laboratory. Consider enlisting the help of your state lab if,after going through the first three steps, you're still not sure what diseaseyou're dealing with.

148

Flock HistoryWhen you experience a problem, suddenly all those little details you dioughtyou'd never forget, but now can't quite remember, become immensely impor-tant. You'll be happy you took a few moments to write down events as theyoccurred. If you neglected to keep accurate records as you went along, try toreconstruct your flock's history based on the accompanying chart.

DIAGNOSTIC GUIDES 149

Chart 9-1

Flock History

Can Help You Determine This:Diseases prevalent in your areaDisease-causing agents already present on your propertyDiseases possibly transmitted by carrier chickens, visitors,

dirtv equipment, etc.Diagnosis based on age group involved (approximation only)


This:Other diseased flocksPrevious diseasesContacts

Flock ageTime of yearFeed changesDuration of diseaseRate of spreadPast vaccinationsMedications usedPercentage involvedMortality rate

Relationship to weather or to carriers such as mosquitoesDiseases due to improper nutrition or toxins in feedDiagnosis based on how long symptoms lastDiagnosis based on how fast symptoms spreadDiseases not likely to be involvedDiagnosis based on flock response to drugsDiagnosis based on percentage of sick birdsDiagnosis based on percentage


of dead birds

Symptoms

Chart 9-2

Signs of Health

Body Part AppearanceComb & wattles

bright, full, waxy

Eyes bright, shinyalert

Nostrils clean, no rasping

Head & tail held highBreast full & plumpAbdomen firm but not

hardPosture erect, active,

alertFeadiers smooth & cleanVent clean, slig

moistDroppings firm, gray-brown

with white caps

Symptoms are visible signs of disease.

In order to readily recognize symp-toms, you need to be thoroughlyfamiliar with how a healdiy flock looks,acts, and smel


ls. Be observant whenyou tend your flock. Each time you en-ter your coop, stand quietly for amoment and watch.

Any change

you detect, including achange in the amount of feed yourbirds eat, the amount of water theydrink, their posture, their droppings,and the condition of their plumage


mayall be first signs of disease.


Signs of Disease

If you notice anything unusual in your flock, follow these steps in checkingfor signs of disease.

1. Watch from a distance to see what each bird is doing, how it moves, and


Taking Blood Samples

Your veterinarian or pathol ogist may askyou to bring in blood samples from livebirds. Blood samples are usually taken from a main wing vein or brachial. Beginby pulling a few feathers from the depression in the upper


part of the undersideof the wing to expose the main vein. Disinfect the skin with 70 percent alcohol.

In one hand, hold both wings over the chicken's back so it can't flap. Inserta sharp 20-gauge needle (%-inch for chicks, 2-inch for mature birds) into thevein with the needlepointingawayfromthechicken'sbodyand toward the wingtip. Starting with the plunger pulled back slightly to allow an initial air space inthe syringe, slowly but steadily pull back on the plunger until


the syringecontains at least 2 ml of blood.

Take care to neither go through the vein nor nick the vein at the top, bothof which will prevent you from drawinga sample. The first time you need a bloodsample, try to get a veterinarian or other experienced person to show you how.

When you withdraw the needle, if the bird bleeds internally, press the spotwith your thumb for a few moments. Unless the chicken has a clotting problem,drawing blood should pose


no threat to its health.

Without jostling or rotating the syringe, place it in a clean container whereit will remain horizontal. Do not refrigerate or freeze it, but take the sample tothe lab for analysis the same day it was drawn. If the lab needs a whole bloodsample (rather than one in which water-like serum separates from the blood)your veterinarian or pathologist will give you an anticoagul ant to keep the bloodfrom separating.


how it stands when still. Check droppings on the ground. Note unusual smells.Listen for unusual sounds: if you whistle, the birds will stop their activities tolisten, and you can more easily hear respiratory sounds.

2. Count die number of affected birds. Come back a few hours later andcount again. How fast the illness sweeps or creeps through a flock can providean important clue as to what die


disease might be. Since different diseasesprogress at different rates, if more dian one disease is involved, liow fast indi-vidual symptoms move through a flock can be especially important.

3. Keep track of the number of birds diat die. Note how and where dieydie, and how soon they die after they first show symptoms.

4. For a closer look, catch birds with a minimum of fuss. Symptoms canchange


when you pick up a bird, especially if die bird had to be chased to becaught. Check body openings for unusual excretions: discharge from themoudi, clogged nostrils, sticky eyes, diarrhea. Note any unusual smell comingfrom these discharges.

5. Check for wounds, swellings, blindness, and external parasites. (Seechapter 4 for instructions on checking for parasites.) To check for blindness,


move a finger toward die bird's eye. If the bird blinks, it is not blind. Don't waveyour hand, or air movement may make the bird blink.

6. If symptoms lead you to suspect a disease that involves a change inbody temperature, take the bird's temperature: shake down die thermometer,insert it into the bird's vent, and hold it there for 3 minutes or until the ther-mometer beeps if its electronic. The normal


temperature for an adult bird is103°F (40"C); normal body temperature for a chick is 106.7°F (42°C).

7. Use the diagnostic charts in this chapter to help you identify die dis-ease. Then look up each possibility in die alphabetic list in chapter 15 (or, inthe case of parasites, chapters 4-6) and find the condition whose combinationof symptoms most closely matches those of your flock.


Matching Symptoms to Diseases

General symptoms appear in nearly any illness, whether it results from aninfection, parasitic invasion, nutritional deficiency, or poisoning. Generalsymptoms include droopiness, ruffled feathers, weight loss, and reduced eggproduction.

Each disease group has its own set of general symptoms as well. Coughing,sneezing, and labored breadiing are general


symptoms of respiratory diseases.Diarrhea, increased thirst, and dehydration are general symptoms of intestinaldiseases. Inability to stand or walk are general symptoms of muscular or skel-etal disorders. Twitching, trembling, and convulsions are general symptoms ofdiseases that attack the nervous system.

Specific symptoms are produced by specific diseases. Facial swelling


with reddish, bad smelling nasal discharge is specific to infectious coryza.An inflamed foot with a hard, swollen abscess is specific to bumblefoot. Dis-tended abdomen and an unhealed or mushy navel in a newly hatched chick isspecific to omphalitis.

Your chickens may not have all the symptoms listed in chapter 15 underthe disease you suspect, or your flock may have


symptoms in addition to thoselisted. Some diseases are caused by different strains of the same pathogen, af-fecting different birds in different ways. Some pathogens affect different birdsin different parts of their bodies. Diseases may occur in combinations of two ormore, causing a confusing array of symptoms.

Veterinarians arrive at a probable diagnosis (otherwise known as an edu-cated


guess) in part by considering the accumulat ion of symptoms. The rest ofus are more likely to work by the process of elimination — decide what theproblem is not, and you may eventually determine what it probably is.

Start with the obvious. Consider management errors causingyour birds torun out of feed or water, get too hot or too cold, become injured, or be attackedby a predator. If your chickens


seem a little droopy or they aren't growing well,they most likely have worms, external parasites, or coccidiosis. Before you startconsidering rare diseases, eliminate common diseases as the probable cause.

ScatologyTo some

extent, diseases can be diagnosed by the appearance of a bird'sdroppings. But remember, variations in droppings are quite normal. Lightbrown (or sometimes


copper green), pasty droppings, usually bad smell-ing, are normal cecal droppings deposited by each chicken two or threetimes a day.

Chickens don't usually produce liquid urine, as humans do. Instead, theyexpel solid urine in the form of salts or urates that look like chalky white capson top of their droppings. An excessive amount of urates can be a sign that thekidneys are not functioning


properly, perhaps because the chicken isn't get-ting enough to drink or has a kidney disease.

Watery droppings are a sign of increased urine output. They often appearas a pool of liquid surrounding solid matter that's slightly greenish in color,and can occur when chickens eat lots of succulent spring grass or drink extrawater during warm weather. Watery droppings can also be a sign of diseasecaused by


such things as kidney failure and fever.

Intestinal diseases often cause diarrhea. Based on the specific disease in-volved, the diarrhea may be foamy, bloody, sticky, pasty, mucousy,off-colored, smelly, or any combination thereof.


152 The Chicken Health Handbook

Chart 9-3Diseases Causing a Change in Droppings

Characteristics

0-10 days ven t pasting0-3 weeks vent pasting

diarrhea0- 4 weeks watery diarrhea

white or greenish browndiarrhea

1- 6 weeks diarrhea with undigestedfeed

2- 6 weeks diarrhea

3- 14 weeks diarrhea

3- 18 weeks whitish or water diarrhea,may be bloody

4- 6 weeks bloody diarrhea4-12 weeks diarrhea (may be bloody)

white-capped greenishdroppings

pasted ventarizonosisomphalitiscampylobacteriosispullorum

infectious stuntingsyndromenecrotic enteritisinfectious anemiainfectious bursaldisease

blackhead

ulcerative enteritisinfectious synovitis

Age Disease Prevalencecommon

rarecommoncommonrare

common

rare

not

common

common

rarecommonnot common

12 weeks +

diarrhea typhoid rare

up to 5 weeks

watery diarrhea with pasting

paratyphoid common

chicks and bloody diarrhea coccidiosis (cecal) common

growing diarrhea listeriosis rareprofuse, watery diarrhea rotaviral enteritis comm

onwhite droppings, sometimes

toxoplasmosis rare

diarrheaGrowing greenish yellow diarrhea erysipelas rarecockerelsGrowing watery, mucousy, pasty,

tancoccidiosis comm

onor bloody diarrhea (intestinal)green diarrhea leucocytozoonosis rarediarrhea, sour crop thntsh comm

onGrowing & mucousy, bloody

diarrheacampylobacteriosis

common

mature yellowish droppings chronic respiratory

common

disease


6 months +

lymphoid leukosis

commonloose white or greendroppings

Cha meter is tics Maturing greenish, watery, pastypullets

diarrheaMaturing diarrhea, first watery and& mature white then greenish yellowMature hens diarrhea

Mature

watery, greenish,

blood-stained diarrheayellow, watery, foamydiarrheayellowish or greenish-yellow diarrheayellow diarrheagreen diarrhea

2 years +

persistent diarrheaAny

greenish-yellow diarrhea

greenish-yellow


Age Disease Prevalence

diarrheacapped with whitechalky whitegreenish diarrheafoamy diarrheablue or green fluorescentdroppingsbright yellow greendroppingspastingdiarrhea

diarrheadiarrheadiarr

heawatery diarrheabrown, pasty, smellydroppingsloose, watery droppings

colibacillosisochratoxicosisstreptococcosispull

orumtuberculosischlamydiosisspirochetosis


oviduct flukesinfluenzawormsmoldy graincrotalaria seedpoisoningrye seed poisoningcoffee-weed seedpoisoningergotismhistoplasmosispseudomonasantifreeze poisoningnone — normal cecaldischarge

none — coolingmechanism in hotweathercommonsporadic

not commonrarecommonrarerare

rarerarevery


bluecomb

cholera (acute)

commonnot common

rarerarerare

rare

rare

rarenot commoncommon

common


rare

not common

fatty liver syndrome not commonNewcastle (exotic) very rare

Chart 9-4 Diseases Interfering with Movement

Characteristics

uncoordinated, circlinginability to standdroopy wings,

draggy legsleg paralysis, twisted neckjerky movements, fallingoverlost balance,outstretched legsflapping wings, Hippi


Prevalence

DiseaseAge

ngonto back, deathsquatting, feet up, weighton hockslameness, incoordinationincoordination

dege

nerated leg muscleslamenessparalysislameness, swollen hocksand feetweight on keel,reluctant to movedactylariosisfatty liver syndromeNewcastle (exotic)


At hatchChicks

0- 3weeks

1- 3

weeks

1-8

weeks

1-12

weeks

3-6

weeks

3-20

weeks3- 18

weeks

4 weeks4- 8

weeks4-10 weeks4-12 weeks

'1-17 weeks

arizonosisepidemic tremor

encephalomalacia rare

sudden deathsyndromekinky back

necrotic dermatitisinfectious bu

rsaldiseasewhite

muscle disease not commonviral arthritisrunting syndromeinfectious synovitis

ciyptosporidiosis not common


common

not

common

rarecommon

backward somersaulting congenital tremor rarerarerarevery rarerarerare

rarerarenot common

6 weeks + lameness, swollen joints cholera (chronic) not common

lameness, weaknesscircling, twisted neckunable to stand, twisted legs ricketsand wingscircling, head twisted back toxoplasmosisone or both legs bent

twisted legoutward

lameness, swollen joints erysipelas


Chicks &growing

leucocytozoonosislisteriosis

rarerarerare

rarecommonGro

wingcockerels

rare

Age Characteristics Disease Prevalence

Growing droopy wing, draggy leg,lasted necktwisted legs with swollenjoints

Newcasde

slipped tendon

common

common

Maturingcockerels

abscess on foot pad bumblefoot common

Maturingpullets

inability to standinability to stand

cage fatiguerickets

not commonnot common

Maturing

wing or leg paralysis Marek's disease common

Young ormature

lameness, stilted gait,thick leg boneslameness, swollen hocksand feetstilted gait, thickened legsweakness, paralysisparalysis

osteopetrosis

pseudomonas

scaly leg mitetapewormfowl tick

common

rarevery commonnot commonrare

Mature tremors, twisted neck,paralyzed wing or leglameness, head tremors

Newcasde

(exotic)

streptococcosis

very rare

not

commonAny convulsions, paralysis algae poisoning

progressive flaccid botulismparalysisswollen joints staphylococcic

arthritisswollen, white foot joints gout (articular)

rarerare

common

not common


weak legs, lost coordination spirochetosisleg deformity sorghum seed

poisoninglameness rye seed poisoningincoordination, twisted neck antifreeze poisoning

rare

rarerare

not common


186 Tin-: CHICKEN HEALTH HANDBOOK

Chart 9-5Diseases and Conditions Affecting Egg Production

Other characteristics

aflatoxicosis

campylobacteriosischolera (chronic)chronic respiratorydiseasecoccidiosis (intestinal)egg drop syndromeencephalomalaciaepidemic tremorerysipelasfatty liver syndrome

fusariotoxicosisinfectious coryzainfectiouslaryngotracheitisinfluenzalymphoid leukosisNewcasdeparatyphoidpox (dry)swollen head syndrome

tuberculosiswater deprivation

infectious bronchitisNewcastle (exotic)

Newcastle (exotic)cholera (chronic)

cholera (chronic)heredity

vitamin A deficiencySmaller aflatoxicosis

salt deficiencythin breast, weak legsin brown-egg layers15-30% drop for 2 weekstemporary drop70% dropsudden drop

sudden drastic dropwater)' eyes, swollen facetemporary drop

sudden drop, broodinesstumors in ovarytemporary dropoften no other symptomsbumps on combs & wattlesswollen head & wattles

Changein Eggs

Prevalence

Disease Fewer

WaterywhitesBlood-stainedyolksBloodspots

prominent, deformed keeldehydrationvery low productionvery low production

very low productionwrinkled, off-color yolks

low productionno other symptomsclutches tardier apartdrop in productiondrop in production

commonverycommonvery rarenot common

not commoncommonnot commonrarenot common

small eggs, low hatchability rare35% dropincrease in blood spotscoughing, weight loss

commonnot commoncommon

rarerarerarerarerarenotcommonrarecommoncommon

rarecommoncommoncommonnot commonrarecommon


DI AG NOSTIC G UIDES 157

Changein Eggs

Disease Other characteristics Prevalence

Misshapenshells

Newcastle (exotic)infectious bronchitis

very low productionvery low production

very rarecommon

Pale shells

egg drop syndrome

low production rare

Pimpledshells

vitamin D excess leave holes if scraped off

not common

Ridgedshells


very low production common

Soft shells

egg drop syndrome

low production rare



infectiouslaryngotracheitis

low production common

influenza low production rarevitamin D deficiency

cycles of low production

not common

Thin shells

cage fatigue soon stop laying not common

egg drop syndrome

shells are gritty rare

fusariotoxicosis high death rate rareinfectious bronchitis


ochratoxicosis yellow diarrhea sporadicNo shells

egg drop syndrome

egg eating rare

influenza low production rare

No eggs

cage fatigue followed by paralysis, death

nor common

colibacillosis no other symptoms or death

common

Newcastle (exotic)

drop within 3 days very rare

gout (visceral) soon followed by death commoninfectious bronchitis

gasping, coughing common

158 The Chicken Health Handbook

Chart 9-6Diseases Causing Breathing Difficulties

Age Characteristics Disease Prevalencechicks gasping, sneezing,

"chirping"labored breathing, droopyhead

Newcastle (exotic)typhoid

very rarerare

0-1 week

gasping, swollen eyes aspergillosis rare

0-4 weeks

gasping pullorum rare

1-7 weeks

swollen eyes and sinuses

roup (nutritional)

rare

4 weeks +

nasal discharge, swollen face

infectious coryza

common

4-12 weeks

slight rattling infectious synovitis

notcommon

4-17 weeks

coughing, extending neck

crvptosporidiosis

notcommon

5-12 weeks

rattling air-sac disease common

6 weeks +

sneezing, rattling, nasaldischarge

cholera (chronic)

notcommon

Young rapid labored breathing leucocytozoonosis

rare

Growingcockerels

breathing difficulty,nasal discharge

erysipelas rare

Growing &mature

rapid breathing, mucusdischarge mouth and nosegasping, ratding, coughing,bloody mucus, nasaldischarge

cholera (acute)

infectiouslaryngotracheitis

not

common

common

Mature gasping, coughingdifficult breathing, nervoussigns

aspergillosisNewcastle (exotic)

rarevery rare

Any nasal dischargegasping, rattling, wet eyescoughing, sneezing, rattlingsneezing, progressive swellingof head and wattles

chlamydiosisinfectious bronchitisinfluenzaswollen headsyndrome

rarecommonrarerare



Chart 9-7 Diseases Causing Discoloration

Characteristics Chicks &

growing

Over t> months

Growi

ng &mature cocksGrowing &mature

Maturi

ngpulletsMaturingMaturing &MatureMature

Mature Hens

2 years +darkened headpale, shr

PrevalenceDiseaseAge

iveled comb

black feathers in red or buff

breedpal

e, shriveled, sometimesbluish combgrayish white patcheson c

ombdarkened headpale headbluish comb

pale skinpale head

blackish, swollen eyesdraining straw-colored fluidpurplish head,



comb

, wattles

pale, shriveled c

ombb

luish combpale, swollen comb and

wattles

darkened head and shankspale or bluish comb andwattlesexudative diathesisinfec

1-4 weeks greenish blue breast and legs1-6 weeks pale skin

3-12 weeks reddish black skin patches3- 14 weeks pale comb, wattles, skin, legs

4- 6 weeks dark face

4-12 weeks bluish comb

4-17 weeks pale skin

6 weeks + bluish, hot comb

tious stuntingsyndromenecrotic dermatitisinfec

tious anemia

blackheadinfectious synovitis

cryptosporidiosis

cholera (chronic)

cankertoxoplasmosisrickets

lymp

hoid

leuk

osis

com

mon

favu

s

rarechronic respiratorydiseasecholerabluecomb

Marek's diseasecholera (acute)

Newcastle (exotic)


common

rarerare

commonnotcommonvery rare


paratyphoid

commonpullorum

rareaspergillosis (chronic

) rarefatty liver syndrome not

commongout (visceral)

commontuberculosis

common

(chart conove

rarecommon

rarenotcommonrarenotcommonnotcommonnotcommonrarerarerare

Diseases Causing Discoloration (cont.)Characteristics Disease Prevalence

bluish, wilted, cold combbluish comb and wattles

pale comb, skin, shankspale headdarkened head, comb, andwattleswhite bumps on comb andwattlespale or purplish combergotismgossypol seedpoisoningcoccidiosis(intestinal)worms/lice/mites

influenza

pox (dry)

spirochetosis


AgeAny rare

rare

commo

n

verycommonrare

notcommonrare


Chart 9-8 Diseases Causing Off Odors

Characteristics smelly unabsorbed yolk sac omphalitis commonsmelly mouth discharge canker rare

distended, sour crop thrush raresour crop bluecomb rareHatched chicksChicks &growingGrowingMaturing pulletsGrowing &mature cocksGrowing &matureMaturemoldy smelling, scabby comb favus rare

smelly nasal discharge infectious coryza common

smelly droppings on ventsour-smelling, distended crop crop impaction rare

Prevalence

DiseaseAge

pasted vent notcommon

Chart 9-9 Diseases Affecting the Eyes

Characteristics

0-1week

1-3

weeks

1-8 weeks

4 weeks +Up to 5 weeks

6

w

e

e

k

s

+

G

r

o

w

i

n

g


Disease PrevalenceAge


Growing &

matureMaturing

pulletsMaturing &

m

ature

Mature

Anyswollen with yellow cheesymatterdull eyesone or both eyes blindon

e or both eyes swollen shutone or both eyes swollen orblind

s

w

oll

en

,

s

t

i

c

k

y

e

y

e

s

w

a

t

e

r

y

eye

sswollen eyelids with sticky orcheesy dischargeblindness

frot

hy

eye

s

sun

ke

n

eye

s

mu

co

us

y

ey

es

w

at

er

y,

s

w

oll

en

ey

esclear eye becomes blind



cloudy eyecloudy eye, sunlight avoidance

wate

ry eyeswatery and/or swollen eyescloudy grayish, dilated,irregular pupil; distortedor blinded eyeblackish eyes drainingstr

aw-colored fluidred swollen eyes

swollen, inflamed, wateryepidemic tremor

encephalomalacia

infectious coryz

a

paratyphoid

cholera (chronic)

cankerroup (nutritional)

toxoplasmosischronic respiratorydisease

bluecomb

cholera (acute)

infectiouslaryngotracheitiscolibacillosisNewcastleconjunctivitisinfectious bronchitis



influenzaMarek's disease

Newcastle (exotic)

swolle

n head

syndrome

eve worm

aspergillosis (acute) rare

rarerarecommoncommon

notcommonrarerare

rare

commo

n

rare

notcommoncommon

commoncommoncommoncommonrarecommon

commo

n

very

rare

notcommon

Chart 9-10

Diseases Causing Sores in the Mouth

Chicks &

white or yellow sores canker rare

growingGrowing whitish yellow sores roup

(nutritional)rare

grayish white circular sores

thrush common

Any yellow patches on roof Newcastle (exotic)

very rare

sores at corners of mouth

fusariotoxicosis

very rare

white, yellow, or pox rare



brownpatchessores in roof of mouth red mites rare

Chart 9-11Diseases Causing Temperature Changes

Characteristics 3-18weeks

4-12

weeks

6 weeks +12 weeks +

Young or

mature

GrowingMaturing

cockere

Age

Characteristics

Disease

Prevalence

Age PrevalenceDisease

lsMaturing

pulletsMaturing &

matureMature

Anyfever

, then drop to belownormalhot, swollen legs and feethot, bluish comb1-5 °F (1-3°

C) above normalwarm, puffy legs

fever, weaknesshot, infla

med foot

body feels cold

feverfever, purplish headhot swoll


*The normal body temperature for adult chickens is 103"F (39.5'C); for chicks(41.5'C).


en joints

fever, weight loss

fever, sneezing, ra

tdingfever, dropping to belownormal just before deathfever, pale head, diarrheainfectious bursaldise

aseinfectious synovitischolera (chronic)choleraosteopetrosis

leucocytoz

oonosisbumblefoot

bluecomb

cholera (

acute)par

fever, depression, weight loss streptococcosis

atyphoid

staphylococcic arthritis

aspergillos

isinfluenzaspirochetosis

typhoidcommon

not commonnot commonrare

c

o

m

m

o

n

r

a

r

e

c

o

m

m

o

n

r

a

r

enot common

not commoncommoncommon

rare

rare

rare

rareit's 106.7"F



Chart 9-12Diseases Causing a High Rate of Death

Age Symptoms Disease Prevalence

0-3 weeks rapid deaths carbon monoxidepoisoning

not common

diarrhea, leg paralysis arizonosis rarediarrhea, gasping pullorum rare

1-3 weeks jerky movements, falling over

epidemic tremor

rare

3-18 weeks

diarrhea, vent picking infectious bursaldisease

common

Over 3 weeks

growing thin while eating well

Marek's disease

common

2-6 weeks reluctant to move, diarrhea

necrotic enteritis

rare

3-6 weeks can't walk, dehydration kink)' back not common

3-20 weeks

huddling, ruffled feathers

infectious anemia

not common

lameness, loose feathers & skin

necrotic dermatitis rare

4-6 weeks no symptoms or droopiness

blackhead rare

4-17 weeks

reluctant to move ciyptosporidiosis

not common

Up to 5 weeks

droopy, thirsty, huddling paratyphoid common

Young & bloody diarrhea coccidiosus (cecal) common

growing gasping, watery nose and eyes

infectiousbronchitis

common

weakness, rapid deaths leucocytozoonosis rarediarrhea, inflamed vent rotaviral

enteritiscommon

emaciation, incoordination

toxoplasmosis rare

Growing diarrhea, nasal discharge,

erysipelas rare

cockerels lamenessGrowing slow growth, diarrhea coccidiosus

(intestinal)common

diarrhea, sour crop thrush rareBroiler mffled feathers, slow

growthbroiler ascites

common

CockerelsMaturing sour crop, diarrhea bluecomb rarepulletsMaturing & rapid death cholera

(acute)not common

mature coughing, gasping infectiouslaryngotracheitis

common

Mature thin-shelled eggs fusariotoxicosis

very rare

depression, weight loss streptococcosis

not common

Any convulsions, paralysis algae poisoning

rare

progressive flaccid paralysis

botulism rare

ruffled feathers, no appetite

typhoid rare

(chart continues over)



Diseases Causing a High Rate of Death (cont.) Symptoms sudden deathcoughing, huddlingrespiratory problems &/orparalysis &/or suddendeathsbumps or scabs 011 face, mouth pox (wet)lameness, diarrhea, rapid deaths pseudomonasdiarrhea, weakness, convulsions spirochetosis

Chart 9-13

Diseases Causing Sudden DeathAge Disease PrevalenceAt hatch typhoid rare1-12 weeks sudden death syndrome common0-4 weeks pullorum rare3-14 weeks infectious anemia not common3-20 weeks necrotic dermatitis rare2-6 weeks necrotic enteritis rare4-12 weeks ulcerative enteritis common4-8 months round heart disease very rareOver 6 months lymphoid leukosis commonGrowing aflatoxicosis rareBroiler cockerels broiler ascites commonMaturing pullets bluecomb rareGrowing & mature

campylobacteriosis common

colibacillosis commonMature hens fatty liver syndrome not commonMature streptococcosis not commonAny malaria rare

botulism not commoncholera not commonerysipelas raregout (visceral) common

PrevalenceDiseaseAge gout (visceral) not commoninfluenza rareNewcastle (exotic) very rare

Any (cont.)

rarerarerare

influenza very rarelisteriosis rareMarek's disease commonNewcastle (exotic) very rarechoking (too rapid eating)

not common

pesticide poisoning not commonanaphylactic shock rare


Postmortem Examination

MANY DISEASES, in addition to causing easily observable symptoms, causeless obvious changes inside the body. Studying the insides of a bird for signs ofdisease is called postmortem examination ("post" meaning after and"mortem" meaning death).

Conducting a postmortem is sometimes called "posting," or more scien-tifically, "necropsy" (the animal equivalent of an autopsy). Posting gives youclues to help you determine the cause of a disease outbreak.

Laboratory AnalysisIf you have a sudden, severe disease outbreak, or you find several dead birds ina short time, the best way to get a rapid, positive diagnosis is to have a few birdsposted at your state poultry pathology laboratory (you'll find a list of state labsin the appendix). Since the pathologist will want to know the disease's progres-sion, submit eitiier three live birds in various stages of illness or one bird thathas recently died, one that is veiy sick, and one just beginning to show

214

symp-toms.

When you bring live birds to the lab, be prepared to leave them behind.The pathologist will no t help you try to save any birds you bring in for examina-tion. Taking chickens to the lab is a one-way street for two reasons:

• A pathologist's job is to examine a bird's innards, which means die birdmust be dead before the examination can proceed.

POSTMOR TEM EXAMINATION 215


• You wouldn't want to return a bird to your flock after it has beenexposed to all the disease-causing organisms floating around theaverage lab, some of which may be worse than what your chickensalready have.

Submitting SpecimensWhen you plan to submit a dead bird for examination, as soon as

you findone dead, wet its feathers with cold water and a little detergent, taking care notto get any into die mouth or nose. Bag the bird in plastic and refrigerate it untilyou're ready to leave for the lab. Whether you're submitting dead or live birds,identify each with a numbered leg band (or wrap a piece of tape several timesaround its leg and write a number on it with an indelible marker).

Write a detailed history of the disease, how it affected each bird you aresubmitting, and anything else about your chickens you think might be impor-tant. The lab will provide a form for you to fill out. Attach your history to theform.

If the lab is far from your home, you may wish to ship your birds. Call firstfor shipping instructions. It's a good idea to call ahead, anyway, instead of just

Disease HistoryWhen you submit a sample to a diagnostic laboratory, provide thisinformation:• your name, address, and phone number• housing type (cage, floor, range)• feed used (sources and types)• breed of your birds• number in your flock• birds'age(s)• where you got them

• symptoms you have observed• date symptoms started• approximate number sick• number that have died• when, where, and how they died• approximate days from first symptoms to death• any medications you have tried• recent changes (new rations, new chickens brought in, toxic spray-ing in your area, etc.)• additional history (vaccinations, nearby flocks, previous diseaseproblems, etc.)



showing up with sick or dead chickens. You may be asked to consult your vet-erinarian and get a referral to the lab. If there are no veterinarians nearby, oryour vet is not willing to examine chickens, say so.

Unfortunately, most veterinarians know little about chickens. Even ifyou're lucky enough to find one with poultry experience, the fee you will becharged may be more than the cost of buying new, healthy birds. State poultrypathology laboratories, on the other hand, charge little or nothing for an initialexamination.

What to ExpectWithin a few days, the pathologist should call you with a preliminary

re-port, then follow up with a written report. Don't be bashful about askingquestions if you don't understand something — pathologists tend to usewords only a veterinarian or other trained person can understand. If you sub-mit your birds under a veterinarian's referral, your vet will explain the report toyou.

Not all path labs are equipped to diagnose all poultry diseases. If the initialreport is inconclusive, the pathologist may take an educated guess as to whatthe problem might be and ask if you want the diagnosis confirmed by furtherlaboratory tests such as tissue examination, bacterial cultures, virus isolation,or sensitivity tests (to determine which drug, if any, will kill the particularpathogen in question). These tests can be time-consuming and expensive.

Even if the diagnosis is certain, the pathologist is unlikely to suggest a spe-cific treatment. The job of a pathologist is to identify diseases, not recommendtreatments. You should, however, be given enough information to obtain de-tails on treatment options from your veterinarian, your state Extension

poultryveterinarian, or your state Extension poultry specialist. Aimed with this infor-mation, you can decide whetiier to treat the remainder of your chickens or getrid of diem and start over.

Do-It-Yourself PostingRunning to the path lab with every dead bird you find is neidier feasible noreven necessary. A 5 percent death rate is considered normal in any flock. Still,it's a good idea to examine dead birds and record the results in your flock his-tory. You may see an emerging pattern diat can help you discover and treat adisease in its early stages of development.

Eveiy flock includes weak birds that have lower resistance than others todisease as a result of stress, genetic factors, or insufficient nourishment due tobeing far down in the peck order. These weaker birds become indicators ofimpending problems. If you do find signs of a disease in progress, you can take



future samples to a qualified pathologist for a con-firmed diagnosis.

Another reason to do your own posting is that, ifthe lab is particularly busy, the pathologist may notget back to you for several days or even weeks.Meanwhile, if your chickens are getting sicker or aredying fast, you might tentatively identify the prob-lem yourself and take appropriate action. The labreport, when it comes, will then serve as a confirm-ing diagnosis.

Posting a chicken makes sense only if you knowwhat the insides of a healthy bird look like — some-thing you can easily learn by paying attention whenyou butcher chickens for eating. The more oftenyou post chickens, the more observant you will be-come. To help sharpen your skills, get a good reference book of color photos,such as Color Atlas of Diseases and Disorders of the Domestic Fowl cmd Turkeyor the less expensive Solvay Manual of Poultry Diseases (both books are listedin Recommended Reading, page 333).

Preparing the SpecimenYour goal is to find abnormalities such as abscesses, tumors, inflamma-

tion, fluid accumulation, foreign materials, changes in muscle or bonecondition, and irregularity in the size, shape, or color of internal organs.

Exam-ine not just dead birds but at

least one bird that recently be-gan showing symptoms and onein which the disease is quite far

along.

Examining birds in variousstages of illness shows liovv thisparticular disease progresses,which may help you determinewhat the disease might be.Checking more than one birdalso helps you determine whichsigns are specific to individuals(therefore possibly insignificant)and which are flock-wide occur-rences (likely signs of disease).Kill a bird for posting by stretching its neck.

When a bird is not already

CautionIf you suspect achicken of havingchlamydiosis or anyotiier disease diat iscontagious to hu-mans (see chapter14) do not post ityourself. Take it tothe state pathologylaboratory.



dead, you will have to kill it. If that sounds like a drastic measure, rememberyou're doing it out of concern for the rest of your chickens. If a serious illness isgripping your Hock, this and other birds may die anyway. Your goal is to deter-mine the cause so you can prevent additional deaths.

The best way to kill a chicken for posting is to stretch its neck, which pain-lessly breaks the neck and spinal cord. With one hand, hold the bird's feet.Grasp the bird's head with the other hand, your thumb behind its comb andyour little finger beneath its beak. Tilt the head back and pull steadily until thehead is separated from the neck.

Continue to bold the head up until the bird stops struggling. Otherwise, itmay spit up and inhale crop contents, leaving the false impression that thedisease caused the respiratory system to till widi foreign matter.

Wait a few minutes while blood collects and clots beneath the neck skin,and the body tissues firm up. Meantime, examine external openings and runyour hands over feathered areas to find lumps

or other

irregularities.

WINDPIPE(TRACHEA)crop

\ BRONCHIAL TUBESi \

LUNGS

KIDNEYovaryUPPER

LARYNX •ESOPHAGUS -

OVIDUCT

SMALL INTESTINEDUODENAL LOOP GIZZARD'

PANCREAS

Position of interna! organs - Horizontal


HEART

CLOACALARGE INTESTINE

STOMACH(PROVENTRICUtUS)

GAlt BLADDER

spieen


Opening the Bird

Conduct your postmortem outdoors or in a garage or carport, using a tableor the tailgate of a pickup truck as your work surface. (Posting a diseased birdin a kitchen where food is prepared is not a sensible idea.) Cover your worksurface with clean paper. Wear rubber gloves and an apron.

Use water and detergent in a spray bottle, or a wet cloth, to dampen diebird's feathers so they won't blow around. Lay the bird on its back. Holdingone leg away from the body, cut the skin between the leg and the abdomen. Dothe same on the other leg.

Stabilize the bird by bending the legs back, one at a dme, until die jointssnap to let the legs lay flat against the table. Cut the skin from the vent to thethroat. Note any bloody spots or streaks in the breast or thigh muscles.

WINDPIPE(TRACHEA)

MOUTH

UPPER LARYNX

ESOPHAGUS

GIZZARD

PANCREASDUODENALLOOP

CECA

CLOACAVENTSMALL INTESTINE

CROPHE

ART

Position of internal organs - Vertical

OVARYSPLEENKIDNEYSGALL BLADDERLARGE INTESTINEOVIDUCT

STOMACH(PROVENTRICULUS)

LIVER

About halfway from the vent to the keel, cut through the abdomen wallcrosswise from one leg joint to the other. Use a pair of heavy scissors, kitchenshears, or tin snips to cut upward on one side, through the rib cage and otherbones, taking care not to cut into or disturb the internal organs. Stop cuttingjust short of the wing joint. Make a similar cut on the other side, only this timecut all the way through the wing joint. Note how easy or difficult it is to cut thebones — an indication of their condition.

Use scissors to cut through the abdominal wall just behind the point of the keel.



Lift the breast and rotate it on the uncut joint as if it were a hinged cover.Now you can see the internal organs in their natural position.

Examining the Organs

Take hold of the gizzard in the palm of one hand, your thumb and forefin-ger grasping the stomach (proventriculus), and make a cut between thestomach and the crop. With one hand, lift the stomach away. With the otherhand, loosen and remove the gizzard, liver, spleen, and intestine. Set them

aside, leaving the intestine attached to the vent. Examine the heart, lungs, re-productive organs, kidneys, and nerves still in place.

To examine the contents of the digestive system, use your shears to cutlongways through the stomach, gizzard, intestine, and ceca. Note any para-sites present. Also note any unusual odor, especially related to the crop orintestines.

To examine the respiratory system, cut through the corner of the mouth

Carefully separate thegizzard from the stomach(proventriculus).



Examine the digestive systemby cutting longways throughthe stomach, gizzard,intestine, and ceca.

and expose the throat and crop. Then cut down the windpipe from the back ofthe mouth to the lungs.

To examine the head, cut across the face, half-way between the nostrilsand the eye. Note any unusual odor coming from the nose area.

If the bird was lame or paralyzed, cut through the ligaments of one hockjoint and twist the leg until the joint pops open. Break the leg bone, both toexamine the marrow cavity and to test the bone's strength. A healthy bonemakes a snapping sound when it breaks.

InterpretationWithout using a microscope and staining techniques to examine

tissue,you will not be able to observe minute changes caused by illness. There are,however, plenty of obvious changes to look for.

In technical terminology, easily observable changes are called "gross le-sions" ("gross" meaning large and "lesion" being medical jargon foralteration). A gross lesion is any visible change in the color, size, shape, or

Digestive tract infected with large roundworms (Ascaridia galli)



structure of an organ. Examples of lesions are: tumors, inflammations, accu-mulations of fluid, dead tissue, and enlarged organs.

Pay attention to:• the location of the lesion (note specific organs)• the nature of the lesion (its size, shape, color, and consistency)• the possibility that the lesion killed the bird (by blocking airways orintestines, through extensive bleeding, by destroying a vital organ, bycausing paralysis)

Try to determine the possible cause of the lesion — infection, nutritionaldeficiency, poisoning, injury, or whatever. Determining the cause often re-quires microscopic analysis, but some causes are fairly obvious, such asworms or injury due to cannibalism.

Lesions, like symptoms, may be general or specific. A general lesion can becaused by any of several diseases. A specific lesion is characteristic of a particu-

Chart 10-1Postmortem Findings

Body Part

Finding Age/Sex

Possible Cause

Bones fragile, thin, soft hen cage fatiguesoft, rubbery young ricketsthickened all osteopetrosis

Bone tumors in marrow 2 years

tuberculosis

marrow

all lymphoid leukosis

fatty marrow broiler

infectious anemia

Body broken yolk pullets

bluecomb, cholera,

cavity colibacillosis, infectiousbronchitis, pullorum

Breasl dried out chicks infectious bursal disease

young ulcerative enteritishens gout (visceral)2 years

tuberculosis

blood spotted all erysipelaswhite streaks chicks white muscle

diseasepullets

bluecomb

Ceca cheesy core chicks arizonosis, blackhead,coccidiosis, salmonellosis

bloody chicks coccidiosisyellow nodules young ulcerative enteritis



all erysipelasyellowish, water,' young rotaviral enteritis

Cloacal swollen, cheesy chicks infectious bursal disease

bursa shriveled young infectious anemiayoung runting syndrome

tumors any lymphoid leukosisCrop empty or foul

fluidyoung canker

sour growing

thrush

pullets

bluecomb

mature

crop impaction

maggots all botulismsticky mucus matur

echolera

Turkish-towel look

growing

thrush

Age/Sex Possible Cause

Heartfilm covered

discolored

pale, yellowish

pale, enlarged

yel

low, enlargedspotted, enlargedenlarged right side

Body Part Finding



surrounded with fluid

tumors

Intestine mucus fil

led

greenish mucuswatery mucussticky mucusbloody mucusb

loody

foul brown fluid

yellowish buttons

yellowish, w

ateryinflamed, slimyinflamed

spotted

pale, distendedfeed-filled



yellow or gray knobsKidneys grayish dotsspotted, paleswollen

swollen, spotted

swollen, dark

swollen, pale

young

air-sac diseaseall

chronic

respiratory diseasechicks

arizonosisall

fatty liver syndromeyoung

listeriosismature

streptococcosisall

spirochetosisgrowing

round heart diseasechicks

pullorumgrowing

broiler ascitesall

choleraall

lymphoid leukosisyoung

infectious bursal diseasepullets

bluecomball

ochratoxicosis

all

spirochetosisall

campylobacteriosismature

choleraall

colibacillosischicks

coccidiosisall

leucocytozoonosisyoung

necrotic enteritisyoung

ulcerative enteritisyoung

rotaviral enteritisall

typhoidall

ergotismall

paratyphoidchicks

coccidiosisall

pullorumyoung

infectious

stunting syndromeyoung

sudden death syndrome2 years

tuberculosisall

colibacillosisgrowing

infectious synovitischicks

salmonellosismantre

lymphoid leukosisall

paratyphoid,typhoid, erysipelas

growing

Marek's diseaseall

pseudomonaspullets

bluecombchicks



infectious bursal diseaseall

gout (visceral), infectious

bronchitis, ochractoxicosis,spirochetosis(chart

continues, over)

Kidneys blood-tilled

(cont.) (umors

shriveled or enlarged

Liver film-

c

o

v

er

ed

sw

oll

en

swollen, mottled, yellow

swollen, discolo



red

swollen, gray spots

swollen, gray areas

swolle

n, bronze or green

swollen, greenish

swollen, red

swollen, red streaks/white dotsswollen, white or gray nodulesswollen, spotted

patchypatchy red or pale

mottle

d with yellow

mushymushy, yellowdarkgreenishgreenish with red spots



yellow "stars"

needle-like crystals

tumors

gray or yellow nodules

Lungs g

reen, furry ballsgrayishgrayish yellowyellow "pearls"brownishred, bloatedbloodygrowing

infectious an

Chart 10-1

Body Pari

emia

mature

lymphoid leukosis

mature

gout (visceral)

all air-sac disease, ch

ronicrespiratory disease

young

necrotic dermatitis

mature

lymphoid leukosis

all

alga



e poisoning, erysipelas

chicks

arizonosis

growing

broiler ascites

all

chl

amydiosis

all

cholera

all

Marek's disease

mature

typhoid

growing

infectious synovitis

chicks

typhoid

chicks

paratyphoid

chicks

pullorum

young

toxoplasmosis

all

och

ratoxicosis, pseudo-

monas, spirochetosis

young

infectious anem



ia, blackhead,listeriosis

mature

streptococcosis

young

ulcerative e

nteritis

all

histoplasmosis

all

fatty liver syndrome

pullets

bluecomb

all

colibacill

osis

growing

infectious anemia

pullet

campylobacteriosis

chicks

gout (visc

eral)

growing

Marek's disease

mature

lymphoid leukosis

2 years

tuberculosis

all

aspergi



llosis

chicks

salmonellosis

chicks

aspergillosis

all

aspergillosis

all

ty

phoid

all

sudden death syndrome

young

toxoplasmosis

growing

broiler ascites

mature

cholera


Postmortem Findings (cont.)Finding Age/Sex Possible Cause

Finding Age/Sex

Possible Cause

white or gray nodules

chicks pullorum

mature

lymphoid leukosis

solidified mature

Marek s disease

gray or white nodules

2 years

tuberculosis

gray white tumors growing

Marek's disease

swollen chicks pullorumall erysipelas,

leucocytoswollen, red young typhoidswollen, dark, soft all chlamydiosisswollen, spotted young ulcerative enteritis,

infectiousbursal disease

all colibacillosisall pseudomonas

swollen, patchy all Marek's disease, spirochetosis

all histoplasmosisshriveled growi

nginfectious anemia

mature

lymphoid leukosis

gray or yellow nodules

2 years

tuberculosis

gray white tumors growing

Marek's disease

swollen, bloody young infectious stunting syndrome

crystals mature

infectious bronchitis,

gout (visceral)


lar disease. Few lesions are specific; most are general, testing your power ofobservation.

Sometimes you can identify a disease by the organ on which a lesion oc-curs. Other times you might idenufy a disease by the combination of lesionsyou find. When more than one disease is involved, as is often the case, thecombination of lesions they produce can be confusing.

As a starting place, look up any lesion you find in the charts in this chapter.Then look up die indicated disease in the alphabetic list in chapter 15 to see ifdie overall description of diat disease matches the condition of your birds.

DocumentationEach time you post a

chicken, write down your findings in your flock his-tory, even if you aren't sure what disease the bird might have. The informationmay become helpful later on, especially if a serious disease is progressingthrough your flock.

Veterinarian Arthur A. Bickford, a poultry pathologist in California, sug-

gests that you not worry about trying to use proper technical jargon. lust write



down what you see. If you're not sure what you're looking at, but you knowsomething isn't right, jot down the location and describe it as "abnormal." Ifyou don't know whether you're looking at a tumor or an abscess, write "lump."Getting too specific when you're not sure may cause confusion if you later sub-mit your notes to a diagnostic lab.

Tissue SamplesIfyou find similar

lesions in several birds, you might send tissue samples tothe path lab for examination. Sending samples is particularly handy if the lab isnot close enough for you to conveniently drop off whole birds. As with submit-ting whole birds, call the lab in advance to make sure you include everythingthe pathologist will need.

To make a tissue sample of the organ involved, take a slice at least Vt inch(1 cm) thick. Include healthy-looking tissue as well as abnormal tissue. Place

the sample in a clean, unbreakable container and cover the sample with 10percent formaldehyde solution. (If you can't get formaldehyde from yourdruggist or veterinarian, you might get a little from a local high school or col-lege biology lab or from a funeral home. Call first, and bring your owncontainer — tiiese sources are not in the business of distributing formaldehyde.)

Be sure the container holding the sample is sealed well so it won't leak.Pack it in a carton surrounded by plastic peanuts or an ample amount of otherpacking material. Include the same detailed history of the disease you wouldprepare ifyou were submitting whole birds.

InflammationAn inflammation or

swelling is only one kind of lesion, but the most com-mon one. Inflamed conditions are identified by die suffix "itis" following dietechnical name for the body part that's inflamed. If it all sounds like Greek toyou, that's because it is — the medical terms for various body parts are



derivedfrom the Greek language.

Words ending in "itis" are not necessarily diseases, but are often caused byseveral different diseases. It's helpful to know the names of the various "itises"when you're trying to understand a pathology report or a disease descriptionin a technical poultry manual. (See next page for a list of inflamed conditions.)

Diagnosing Nutritional Deficiencies

Like infectious diseases, nutritional deficiencies may cause gross lesionsthat, together widi other symptoms, can be used to identify the cause. Sincenutritional deficiencies are no longer common, their characteristic lesions are

listed separately here, along with additional symptoms as a diagnostic aid.For a fuller description of nutritional problems, see the section on nutritionaldiseases in chapter 2.

Chart 10-2Inflamed Conditions

Condition Body Part

air sacs

joints

("arthr

on")

eye

lining

("conjun

ctiva")


Common Cause


Encephalitis

b

r

a

i

n

(

"

e

n

k

e

p

h

a

l

o

s

"

)

intestine

("entero

n")

liver

("hepato

s")

kidney ("nephros")

Pericarditis membrane surrounding abdominalorgans ("peritoneum")nasal passage lining ("rhinos")

Salpingitis oviduct ("salpinx")

Septicemia blood ("septikos" = putrefaction;"hamia" = blood)

sinus cavities

membranes lining joints("synovium")

chlamydiosiscolibacillosismycoplasmosiscolibacillosismycoplasmosissalmonellosisstaphylococcosisviruses

ammonia fumes

eye wormencephalomalacia

listeriosis



colibacillosissalmonellosisblackheadcampylobacteriosisinfectious anemiacolibacillosisgout (visceral)virusescolibacillosischolerastreptococcosisEscherichia coliEscherichia colipasteurellosissalmonellosisstreptococcosisMycoplasmagallisepticum

Escherichia coli

mycoplasmosis

salmonellosisStreptobacillus moniliformisviruses

Chart 10-3 Nutritionally Related Findings Additional Symptoms Deficiency

chicks swollen

hip nerve.

toes curved inwardblue green gelatinousfluid under skinsoft, swollen

, greenishyellow brain; or bluish greenfluid under skin and bloodspots in leg and breast muscles;or light stre


Age/Sex Finding


aks in breast muscles

growing blood spots Ln muscles, slowblood clotting, pale marrow

hen broken yolks in body cavity

all swollen kidney

, crystals inureterwhite sores in mouth

and throatsoft keel, collapsed ribs

walking on hocks

riboflavin

bluish breast and legsseleniumretracted head, prostra-

vitamin Etion, death

pale comb, bleeding vitamin Kwattles, bleeding eyeshrunken, bluish combs, waterwattles, promi

nent legtendons on back of egsoff-color droppings, watershrunken muscleswatery diarrhea, sticky vitamin Aeyes and noseweak legs, soft beak vitamin D



Disposing of Dead Birds

Before you dispose of a dead bird, check local laws. Legal methods for dispos-ing of animal bodies vary from place to place. For public health reasons,depositing them in a dumpster or local landfill is illegal nearly everywhere.

When the bodies are those of diseased

birds, find a disposal method thatprevents the spread of infectious agents or toxins. Do not bury them in a com-post pile — the warm, moist environment may provide perfect conditions forpadiogens to keep multiplying, and flies and rodents may spread the disease.

The two best disposal methods are burial and burning. Bury bodies deeplyso they can't be dug up by dogs or wild animals. Find a spot far from wells,streams, and other water sources. While you're at it, bury all contaminated



lit-ter, feed, and droppings associated with die diseased birds.

Burning may be necessary where the water table is high, the soil is rocky orfrozen, or burying is prohibited by law but burning is not. You'll need a heap ofcombustible materials — scrap wood or tree prunings, along vvidi diy straw fora hot blaze. Make sure die carcasses are fully burned, then bury the ashes.

Therapy

SOME CHICKEN DISEASES CAN BE CURED if treatment starts early. Othersare irreversible or fatal. By the time chickens show obvious signs of illness, thedisease is usually pretty far along. Recognizing a disease as soon as it starts isthe first step toward curing the ones that are temporary and dealing effectivelywith those that are permanent or irreversible. The longer you wait before youtake action, the more difficult treatment or control becomes, and the morelosses you may incur.

Treating Sick BirdsAttempting to treat a flock without knowing what's wrong can be costly, mayresult in continuing losses, and could make the disease worse. For example, ifyou treat chickens with a drug that's appropriate for coccidiosis when in factthey have infectious anemia (a disease with similar symptoms), you will makematters significantly worse.

265

Once you identify the problem, you have three choices:• cull the affected birds• wait until the disease goes away• embark on a course of dierapy


THERAPY 267

In this context, cull means kill. When a condition is serious, sometimes theonly humane approach is to put the birds out of their misery. Some seriousdiseases should not be cured because recovered birds will be carriers, continu-ing to spread disease intermittently or continuously, for die rest of their lives.Other diseases are so contagious that the only way to keep them from spread-ing is to destroy the diseased flock.

If you are raising chickens to get healthful meat, you may prefer to culldiseased birds and start over, rather than run the risk of eating meat containingdrug residue or disease-causing microbes — some of which can harm hu-mans. By contrast, a commercial producer tries to bring as many birds aspossible to market with a minimum of downgraded or condemned carcasses.

If you're raising an endangered or exhibition breed, you'll likely wish topreserve the gene pool by keeping breeders going until you can hatch enougheggs to peipetuate the flock — an approach that works only if die disease doesnot spread through hatching eggs. You must, of course, raise the new chicksaway from diseased adults, cull the diseased breeder flock as soon as possible,and meticulously clean up their housing with an appropriate disinfectant.

Waiting until the problem goes away works only if the disease is self-limiting, meaning it naturally runs its course in a short time and birds recoveron their own. Few diseases fall into that category. A good number of diseaseslie somewhere between serious and self-limiting, and can be effectivelytreated with drugs.

Drug UseMany non-prescription datgs are available from farm and feed stores andthrough mail-order catalogs. Such over-die-counter drugs are considered safewhen they are used according to directions on the label. Whetiier you obtain adrug over the counter or by a veterinarian's prescription, it will be effective

only if you have selected the right drug for the disease and know when to use it,how to use it, how often to use it, and how much to use. In addition:

• Avoid out-of-date drugs.• Store drugs at 35 to 55°F (1.5-12.5°C), away from sunlight.• Administer a drug only as directed — If it's supposed to be given

bymouth, for example, it may be toxic as an injection.

• Observe the safe dosage level —The drug won't be effective in anamount less than the label specifies, and may be toxic in greateramounts.

• Observe the withdrawal time when treating meat birds or laying hens.• Do not combine drugs or use more than one at a time, unless such

acombination is approved by a veterinarian.


THERAPY 269

Administering DrugsFor a drug to be effective, it must reach the infectious microbes in suffi-

cient quantity and remain in contact long enough to do the job. Most drugsshould be administered for at least 3 days, or for 2 days after the symptomsdisappear, whichever is longest. As a general rule, ifyou do not see some im-provement within 2 days, you are using the wrong drug.

How you administer a drug depends on the drug you use, the diseaseyou're treating, the number of birds involved, their condition, and the lengthof time the dmg must be administered. Drugs can be applied:

• topically• orally• by inhalation• by injectionTopical or local medicat ions are applied directly to the skin, eyes,

nose, orother external organs. Examples of topical drugs are antibiotic powders orointments used to prevent infection of wounds, and liquids applied to an in-fected eye.

Oral medications are given by mouth. They work either by controlling mi-crobes in the intestine or by being absorbedthrough the intestine to be distributed to otherparts of the body. Oral drugs take effect slowly,usually in 4 to 12 hours, depending on the chugused, the bird's metabolic rate, and the amountof feed in its crop. Oral drugs are convenient andsafe, but can be unpredictable in dieir absorpdonrates, especially when a bird has diarrhea. Ex-amples of oral medications are tablets, capsules,feed or water additives, and drenches.

Inhaled medications work against microbesin die respiratory system or are absorbed throughthe respiratory system to be carried to other partsof the body. Such a drug may be a liquid solutionapplied by means of a fine mist or a dust puffedinto the air. Specialized equipment is needed toput particles of just the right size and density into the air, making the use ofinhaled drugs impractical for small llocks.

Injected medications, which take effect rapidly, are inserted with a needleand syringe into one of three places: beneath the skin, into the muscle, or intothe bloodstream.

Shots, tablets, and drenches are suitable for treating individual chickens.

DrenchingA liquid medication,or "drench," is in-serted into a chicken'smouth by means of asyringe fitted with ashort piece of plastictubing that lets yousquirt the liquid intothe bird 's throat—tak-ing care not to get anyinto the windpipe.


THERAPY 271

They ensure that each bird gets an adequate dose, but administering them istime-consuming and handling each bird can increase stress and aggravate thedisease.

Drugs administered by feed, water, or through the air are suitable where alarge number of birds are involved or the drug must be administered over along period of time. Although flock administration saves time, you can neverbe sure eacli bird gets an adequate dose.

Feed and Water AdditivesWhen medications are added to feed or water, low birds in the peck

ordermay not spend enough time at the trough to obtain a sufficient dose. Further-more, there's always the danger that birds won't eat or drink at all, or will eat ordrink to excess and overdose.

If a medication must be administered by means of feed or water, adding itto water is preferable for two reasons:

• many diseases cause appetite loss and increased thirst;• on a small scale, diluting a drug in water is easier than trying to stir itevenly into feed.Some small-scale flock owners medicate feed or drinking water either

rou-tinely or during times of stress as a precaution against disease. The practice isnot only expensive but counterproductive, since it lias little or no effect in pre-venting disease, and can cause resistant strains of microbes to develop so thatdrugs won't work if a disease does strike.

Commercial growers add low levels of drugs to rations to improve egg pro-

Diluting Medications

When a drug label calls for medicating feed at a level of 200 parts per million(ppm), an equivalent amount in drinking water would be 400 milligrams pergallon (assuming chickens consume twice as much water as feed).When instructions call for diluting a drug 1:2000 in water, combine:

drug with water2 tablespoons (1 ounce) 16 gallons1 tablespoon ('/2 ounce) 8 gallonsV2 tablespoon* ('/< ounce) 4 gallons1 teaspoon 2V2 gallonsVi teaspoon 5 quarts

'You can find a '/> tablespoon measure with the canning and freezing supplies at mostdiscount department stores. An equivalent measure is Vfr teaspoons.


THERAPY 273

duction and to stimulate the growth rate and feed-conversion efficiency ofbroilers. For unknown reasons, antibiotics cause a bird's intestinal wall to thin,improving nutrient absorption. But the routine non-medicinal use of antibioticsin food-producing flocks leads to antibiotic resistance in humans as well as inthe chickens (see "Andbiotic Residues," page 191).

InjectionsWhenever you administer a drug by injection, use a fresh or sterile

needleand syringe. To sterilize a used needle and syringe, separate them, boil them inclean water for 15 minutes, dry them on a clean paper towel, and store them ina clean, dust-free place.

If you use the same needle to inject more than one bird, before refilling thesyringe between birds, dip the needle in alcohol (unless you are applying alive-virus vaccine), or pass the needle through a match flame. Keep extraneedles on hand in case the one you're using gets too dull to pierce easily.

Use a 20-gauge needle, % inch (.75 cm) long for chicks, 2-inches (5 cm)long for mature birds. Syringes are marked off in cubic centimeters (cc) andportions thereof. Drug dosages are specified either in ccs or in ccs per pound ofweight. To determine how many ccs you need, multiply the bird's weight bythe number of ccs per pound. Sometimes dosages are given in milliliters (ml).Since 1 ml equals 1.000027 cc, for practical purposes they are the same. Use asyringe large enough to hold the entire dose in one shot.

Subcutaneous injections (SC or SQ) are given directly under the skin, usu-ally at the breast or the nape of the neck where the skin is loose. Pick up a pinchof skin and insert the needle at an angle. If you're injecting chicks, take care notto push the needle all the way through die skinand squirt the drug out the other side (or intoyour thumb). A subcutaneous injection is easyand safe to administer and lasts a long time —

up to 2 days. On the other hand, the drug takeseffect slowly because it requires a long rime tomigrate to the bloodstream for distributionthroughout the body.

intramuscular injections (IM) go into themeaty portion of the breast. They take effectfast — in about an hour — and last about 8hours, but you must take care not to touch abone or nerve, or deposit the dntg into fat or thebloodstream. Insert the needle straight into thebreast muscle, at a right angle. Before injectingthe drug, pull back on the plunger. If blood ap-

SYRINGE

PLUNGER


THERAPY 275

pears in the syringe, move the needle to another spot. Otherwise, you may killthe bird by inserting the drug directly into its bloodstream.

Intravenous injections (IV) insert medication directly into the bloodstream,where it takes effect almost immediately. They are the trickiest shots to giveand should be used only for drugs designed for IV administration, and only ona bird that's comatose, paralyzed, or otherwise in imminent danger of dying—IV administration of C. Botulinum antitoxin, for example, might be used on avaluable breeder that's been paralyzed by botulism.

An IV injection goes into the main wing vein or brachial (see the box onpage 149). First, pull a few feathers from the depression in the upper part of theunderside of one wing, so you can better see the main vein. Insert the needleinto the vein, pointed toward the wing tip (away from the chicken's body) anddepress the plunger to release the drug very slowly.

AntibioticsAll drugs derived from fungi or bacteria and used against other living organ-isms are called antibiotics [anti meaning against and biotic referring to livingorganisms), or sometimes antimicrobials. The use of antibiotics and otherchemicals is controlled by the FDA (Food and Drug Administration), USDA(United Stales Department of Agriculture), and EPA (Environmental Protec-tion Agency). With all these agencies involved, it's not surprising thatregulations change constantly. Ifyou want to know the current status of anydrug to be used on chickens, consult the Code of Federal Regulations, The Fed-eral Register, and die Feed Additives Compendium (all listed in the appendix).

Antibiotics fall into six basic categories:• anthelmintic — against worms (discussed in chapter 5)• anti-protozoal — against protozoa (see chapter 6)• antiviral — against viruses

• anti-fungal — against mold and fungi• antibacterial — against bacteria

Antiviral AgentsViruses are difficult to treat with drugs, and to date no safe, broad-spec-

trum antiviral drug has been discovered. A virus in the environment neithereats nor breathes, and is therefore impervious. Once a virus attaches itself to acell in a chicken's body, any drug that harms the virus tends also to harm theinfected cell. Treatment of viral diseases largely involves alleviating symptoms(in a respiratory infection, for example, using a product such as Vicks or VetRxto open up blocked airways) and keeping the bird as comfortable as possible


THERAPY 277

while its immune system fights the virus.Antiviral drugs may soon become available diat either keep viruses

frominvading cells or interfere with their replication within a cell. The most promis-ing of these is interferon. When a vims attacks a cell, the cell produces thenatural protein, interferon, that keeps the virus from multiplying and infectingadditional cells. The problem is that insufficient amounts of interferon arewitiiin the body produced to stop an especially vimlent virus.

Interferon can be artificially produced and has successfully been used inmassive doses to treat a variety of viral diseases, including influenza andNewcasde. It may also be combined with vaccines to provide temporary pro-tection while immunity is developing. Interferon may soon become lessexpensive and more readily available.

Anti-fungal AgentsFungal diseases, like viral diseases, do not respond well to drug

treatment.Not only are fungi somewhat impervious to drugs, but drugs interfere with achicken's natural microflora, making room for fungi to run rampant — the rea-son fungal infections commonly follow the use of antibiotics in treating otherdiseases.

Copper sulfate (CuS04), also known as "powdered bluestone," is toxic tofungi and can be used to prevent or control many fungal diseases. Clean feed-ers, waterers, and other equipment with an 0.5 percent solution. Treat birdswidi a 1:2000 concentration in drinking water (Vz teaspoon per gallon) everyother day for a week. Take care— a concentration of 1:500 or greater is toxic tochickens. Due to the possibility of a chemical reaction between copper sulfateand galvanized metal, do not use a metal waterer.

Superficial mycotic infections are treated with topical medications such asamphotericin B (trade name Fungizone), gentian violet, iodine, and nystatin(trade name Mycostatin, among others). Any drug used to treat a fungal infec-

tion (ringworm, athlete's foot, etc.) of pets or humans can be tried on achicken. You can't tell in advance what will work, since fungi are resistant tomany drugs. Furthermore successful treatment requires persistence, since achicken with a superficial fungal disease infects other birds and reinfects itself.

AntibacterialsMost antibiotics are antibacterials, and some antibacterials work

againstfungi and protozoa as well as bacteria, so die two words are often consideredsynonymous. A narrow-spectrum antibacterial is effective against a specificbacteria or group of bacteria. A broad-spectrum antibacterial is effectiveagainst numerous kinds.


THERAPY 279

Whether an antibacterial is narrow-spectrum or broad-spectrum, its ef-fectiveness will be reduced in a bird that has been infected for a long time orwhose immunity has been weakened due to poor sanitation, malnutrition, orthe presence of a viral infection. Although andbacterials have no effect againstviruses, they are often used in treating viral diseases to keep weakened birdsfrom getting a secondary bacterial infection.

Andbacterials that destroy bacteria are called "bactericidal." Andbacteri-als that retard the growth of bacteria, thereby giving the immune system timeto produce antibodies and otherwise rally its own defenses, are called "bacte-riostatic."

Sulfonam ides ox sulfa drugs were introduced in the 1930s as the first medi-cations used to treat infection. Originally they were effective against a widerange of bacteria. Many bacteria have since become resistant, particularly sta-phylococci, Clostridia, and pseudomonas. Nevertheless, sulfa drugs are stillused today because of their low cost relative to their effectiveness. They shouldnot, however, be used to treat laying hens.

The sulfonamide group includes several related drugs, easily identifiedbecause their names almost always start with "sulfa." They fall into two cat-egories:

• rapidly absorbed and rapidly excreted, requiring treatment one to fourtimes a day;

• rapidly absorbed and slowly excreted, allowing treatment only onceevery second or third day.

Most sulfonamides are bacteriostatic, but some can be bactericidal, de-pending on the drug, the dose, and the bacteria involved. Sometimes threedifferent sulfonamides are combined to create a more effecuve tablet or liquidmedication called "triple sulfa."

Sulfa drugs are added to drinking water for the treatment of bumblefoot,toxoplasmosis, a variety of respiratory infections, systemic colibacillosis

(oftenin combination with penicillin G), and coccidiosis (see "Drugs Used to TreatCoccidiosis," page 103). The sulfas work best when treatment starts in the earlystages of infection. A chicken usually shows improvement within 3 days, butshould be treated for an additional 2 days after symptoms disappear.

In any case, sulfa treatment should not go on longer than 7 days or theresult may be kidney damage and/or vitamin K deficiency (interfering withblood clotting). In addition, if a chicken does not drink enough water duringtreatment, its pH balance becomes too acidic. If prolonged treatment is neces-sary, add 1 tablespoon of sodium bicarbonate (baking soda) per gallon to thedrinking water.

The penicillins are a large group of antibiotics derived from mold andidentified by names ending in "cillin." The first penicillin was discovered in


THERAPY 281

1928 by a bacteriologist named Fleming who wanted to know why bacteria donot grow in die presence of mold. When penicillin was first used in 1941, it wasconsidered a miracle drug and was administered so indiscriminately thatmany strains of bacteria have become resistant .

The penicillins may be bactericidal or bacteriostatic — depending on thesensitivity or resistance of the bacteria involved — and are used to treat a vari-ety of acute infections. They fall into two types:

• Natural penicillin (such as penicillin G) works against a narrow spec-trum of bacteria, including some strains of staphylococci, streptococci,and E. coli. It is sensitive to light and heat, so is usually mixed justbefore it is used. Natural penicillin is poorly absorbed by the intestine,and so must be administered by intramuscular injection.

• Semi-synthetic derivatives (such as ampicillin and amoxicillin) absorbbetter than natural penicillins and can be given orally. They workagainst a broader spectrum of bacteria that have become resistant tonatural penicillins, including most strains of E. coli and Salmonella.Tetracyclines, the first broad-spectrum antibiotics, all have names

endingin "cycline." There are three naturally occurring tetracyclines and a number oftheir derivatives, all bacteriostatic against the same kinds of microbe — somechlamydia, staphylococci, streptococci, mycoplasmas, and a few other groups(but not most strains of E. coli).

The tetracycline most often used for chickens is oxytetracycline (tradename Terramycin), which conies both in injectable form and in a powder to beadded to drinking water. Since it works best in an acidic environment, its ab-sorption rate can be improved by adding 1 cup of cranberry juice, Vz cup ofvinegar, or 2 teaspoons of citric acid (from the canning department of a gro-cery store) to each gallon of drinking water. To further increase the drug'seffectiveness, discontinue calcium supplements during treatment. Despitethe broad spectrum of tetracyclines, diey work rather poorly and are used

inindustry primarily as growth promoters.

Aminoglycosides get tiieir name from the fact that each contains at leastone sugar (glycoside) attached to one or more amino groups. They kill bacteriathat multiply rapidly — such as those causing enteric and septicemic diseases— after only brief contact, but die drugs have no lasting effect. The group includes:

• Gentamicin (trade name Garasol), a very broad spectrum antibacterialadministered as an intramuscular or subcutaneous injection to treatsystemic infections, particularly those caused by E. coli.

• Neomycin, used for staphylococcal skin infections such as bumblefootand infected breast blister. As a topical antibiotic, neomycin comes inpowder form (trade name Neo-Predef) or as an ointment (trade name


THERAPY 283

Neosporin, among others). Neomycin sulfate is used orally to treatdiarrhea caused by susceptible B. coli and Salmonella.

• Streptomycin, given as an intramuscular or subcutaneous injection,works against a fairly narrow range of susceptible E. coli, Pasteureila,Salmonella, and staphylococci.

Aminoglycosides are often combined with penicillin to create synergism— a phenomenon whereby two drugs applied together have a greater total ef-fect than the sum of their individual effects. An example of a synergisticcombination is penicillin and streptomycin (trade name Combiotic, amongothers).

Erythromycin (trade name GaJlimycin) belongs to a group of broad-spectrum drugs called "macrolides". It is so similar to penicillin that it is oftenconsidered an alternative. It is basically a bacteriostat, but in large doses can bebacteriocidal. Erythromycin is used to treat superficial staphylococcal andstreptococcal infections, as well as chlamydiosis, mycoplasmosis, andsalmonellosis. It is usually given orally, but absorption is poor unless the stom-ach is empty. An intramuscular injection absorbs more rapidly, but causesswelling and pain.

Bacitracin (trade name Solu-tracin 50) is similar in range to penicillin G,but does not absorb well in the intestine and is relatively toxic when given as aninjection. It is mainly used topically to treat staphylococcal and streptococcalinfections of the skin and mucous membranes. (It is also used in industry as agrowth promoter.) Besides being bacteriocidal, bacitracin is also bothfungistatic and fungicidal. Combined with neomycin, it's sold as the antibac-terial ointment, Neosporin.

Antibiotic ReactionsAntibiotics can cause reactions that are as bad as, or worse than, the

dis-ease they're used to treat. For starters, they upset the balance of normalmicroflora in a chicken's body, particularly in its digestive tract, paving the

wayfor entry by additional disease-causing bacteria and fungi. A classic symptomis diarrhea, which can be fatal if the drug is not discontinued.

Long-term use of sulfa drugs can cause vitamin K deficiency due to inhibi-tion of the microflora that normally synthesize this important vitaminresponsible for normal blood clotting. Infectious anemia may result unless thedrug is either discontinued or supplemented with vitamin K.

Anaphylactic shock, a violent allergic reaction, may result from repeatedantibiotic injections. Symptoms are paleness and rapid loss of consciousness.Swelling within the respiratory system may cause death through asphyxiation.


THERAPY 285

Antibiotic ResistanceThe routine use by commercial growers of low levels of antibiotics, par-

ticularly penicillin and tetracycline, has caused more and more bacteria tobecome resistant to these drugs. The drug-resistant strains are spread throughdie use of slaughterhouse wastes as protein in rations. Since slaughterhousewastes also contain antibiotic residues, feeding a flock rations that containthem encourages die further mutation of drug-resistant strains.

When a diseased flock is treated with a drug, strains that are sensitive tothat drug are destroyed, while resistant strains survive. As a result, bacterialdiseases, particularly cholera, colibacillosis, pseudomonas, salmonellosis, andstaphylococcosis, are becoming more difficult to treat. Successful treatmentrequires a sensitivity test to determine which drug will work against the straincausing the disease.

Antibiotic ResiduesWhen you medicate birds raised for meat or eggs, take special care to

ob-serve any precautions highlighted with die double Arrow Universal WarningSymbol. One important piece of information you'll find in the "warning" sec-tion of die label is the drug's withdrawal time.

Special precautions are highlighted by thisdouble Arrow Universal Warning SymbolIP^E^r in the "Warning" section of a drug label.

When a drug is absorbed, it is first distributed throughout the chicken'sbody dssue and fluid, and then is gradually eliminated through the filteringprocesses of the kidneys and liver. Different drugs are eliminated at differentrates.

The wididrawal time on a drug label tells you die drug's elimination rate,

or the number of days that must pass between the time you discontinue thedrug and the time you butcher the birds for food. Remember, the withdrawaltime is die minimum required by law — it doesn't hurt to err on die side ofcaution and add a few extra days. Before you start collecting eggs to eat, add 10days to any withdrawal time specified for meat birds, since substances can bedeposited in an egg as long as 10 days before it is laid.

Antibiotic residues in meat and eggs are harmful to humans in at leastthree ways:


THERAPY 287

1. They disturb the natural balance of microflora in the intestines andelsewhere.

2. They may cause microbes to become resistant to drugs prescribed by aphysician.

3. They can cause a severe reaction in people who are allergic to penicillinor sulfa drugs.

FlushesWhen a chicken suffers from an intestinal disease or from food poisoning, youcan hasten its recovery by flushing its system with a laxative that absorbs toxinsand removes them from the body. Although Epsom salts make the best flush,chickens must be handled individually, since they don't like the taste of anEpsom-salt solution and won't readily drink it. When a number of birds areinvolved, or handling the birds would cause undue stress, use molasses in aHock flush. Flush only adult birds, never chicks.

Epsom-salt flush: 1 teaspoon Epsom salts (magnesium sulfate) in Yz cupwater, poured or squirted down the bird's throat twice daily for 2 or 3 days, oruntif the bird recovers.

Molasses flush: I pint molasses per 5 gallons water, given for no longerthan 8 hours.

Supportive TherapyAnytime you treat diseased birds, isolate them away from the rest of the flock.After they have been moved, avoid moving them again to minimize stress.When you tend your flock, take care of healthy birds first, so you won't spreaddisease from the sick ones to the healthy ones.

Be sure the sick birds get plenty of clean water and fresh feed. Since manydiseases cause a chicken to eat less, feed often to stimulate appedtes. If neces-

sary, move feed and water troughs so they'll be easier for the birds to reach.Increase the number of waterers so the birds won't run out of water during theday, and so those crowded around a waterer won't discourage others fromdrinking. Encourage drinking by providing cool water in summer and warmwater in winter.

Provide good ventilation so the chickens won't keep breathing the samestale air, but avoid cold drafts that cause chilling. In cool weather, supply addi-tional heat, especially if the birds are young. Pay special attention to sanitationso the population of pathogens can't build up and reduce the birds' resistanceeven further — drain puddles from the yard, keep droppings out of feed andwater, and make sure litter is deep and clean.


THERAPY 289

Vitamin TherapyBoost a flock's ability to liglit disease, and minimize the chance of a

sec-ondary infection, by adding a vitamin supplement to the drinking water. Avitamin supplement can also be used to guard against disease in times ofstress, such as during a move, before and after a show, during breeding season,or when the weather is particularly unpleasant. Chicks will get a healthy start ifyou treat them to a vitamin supplement throughout their first 3 weeks of life.

ElectrolytesDehydration caused by diarrhea, worms, and other conditions depletes

body fluids of certain minerals known as "electrolytes." They are called elec-trolytes because, when dissolved in water, they split into electrically chargedparticles (ions) that transmit electrical impulses. The electrolytes — calcium,chloride, magnesium, phosphorus, potassium, and sodium — play a vital rolein regulating body processes and in maintaining both hydration and thebody's acid/base balance.

Any time a chicken has diarrhea, or otherwise suffers from dehydration,help its body replace and retain fluids by adding an electrolyte supplement(brand name Vita-Tone, among others) to its drinking water at die rate of 1teaspoon per gallon for at least a week.

Homemade Electrolyte SolutionIf you do not have an electrolyte supplement on hand, this homemade versionwill get you through in a pinch.

Ingredient Source'/3 teaspoon potassium chloride salt substituteVz teaspoon sodium bicarbonate baking soda1 teaspoon sodium chloride table salt2 quarts water

Use this solution in place of drinking water for 4 to 6 hours per day for

1 week, offering fresh water for the remainder of each day.

Competitive ExclusionAntibiotics disrupt the microflora that normally live in a chicken's intes-

tines and work in cooperation with the bird's immune system. To restore thebalance of microflora following drug treatment, feed each chicken a heapingtablespoon of plain active-culture yogurt every day for a week. The process of


THERAPY 291

controlling beneficial microflora to help fend off disease is called "competitiveexclusion" — the beneficial microflora provide stiff competition that excludespathogens.

A relatively new idea in the poultry world is the use of competitive exclu-sion to minimize bacterial diseases by feeding newly hatched chicks the kindof bacteria that naturally live in the digestive tract of an adult chicken. The ben-eficial immunity-enhancing microflora then have a chance to get establishedbefore die chicks come into contact with pathogens. You can give chicks aboost in the right direction by occasionally feeding them a tiny amount ofyogurt, but take care — it doesn't take much yogurt to cause diarrhea.

Treating WoundsAny injury in a poultry flock must be treated promptly, or it will attract pickingthat quickly becomes cannibalism. Wounds can be caused by faulty equip-ment, nails protruding from walls, serious fighting, and even mating. Cocks,usually of the heavier breeds, sometimes rub the protective feathers from ahen's back during successive matings until no feathers are left to keep thecock's claws from cutting through the hen's skin.

As soon as you discover an injured bird, isolate it. Clean broken tissue fromthe wound by pouring hydrogen peroxide over it. As the hydrogen peroxidebubbles up, it lifts organic matter so it can be rinsed away with more hydrogenperoxide. If the injury is serious, remove feathers from around the edges sothey can't stick in the wound and hinder healing.

When the wound is clean, coat it with neomycin in the form of Neo-Predefpowder (for an oozing wound) or Neosporin ointment (for a diy wound). If theinjury is on the bird's foot or is quite large, wrap it in a gauze bandage and tapethe bandage in place. To keep pus from forming and giving bacteria a place togrow, change the dressing daily, clean the injury with hydrogen peroxide,

andreapply neomycin.

Treating ShockShock is a condition brought on by a serious wound or other severe stress, suchas an allergic reaction to antibiotics or being chased and caught by a dog andshaken in the dog's mouth. Shock causes pale skin, reduced circulation, rapidweak pulse, rapid breathing, subnormal body temperature, weakness, andsometimes prostration and death. If the bird is valuable enough to warrant theexpense, and a vet is close enough at hand, the bird may recover after veteri-nary treatment with steroids and fluids. Otherwise, all you can do is keep thebird warm and calm until it either recovers or dies.


THERAPY 293

SurgerySurge 17 is rarely performed on chickens, due to their relatively low economicvalue. On those rare occasions when surgery is performed, it is done to:

• caponize broiler cocks (no longer necessary, with today's improvedstrains that grow bigger and faster on less feed);• decrow a valuable breeder cock (requires the services of a skilledveterinarian);• debeak birds to prevent cannibalism (see "Debeaking," page 138);• dub and crop fighting cocks and chickens raised in cold climates (see"Dubbing and Cropping," page 133);• clean out an impacted crop (see "Crop Impaction," page 264).Following surgery, treat the surgical wound as you would any other

wound, as described above.

What Went Wrong?If, despite your best efforts, sick chickens don't get better, one or more of thefollowing may be the cause.

•The diagnosis was wrong.•The organism causing the disease is resistant to the drug used.• An inadequate dose of the drug was used.•The drug was administered improperly (reread die label).•The drug's expiration date has long since passed (try a fresh batch).•An incompatible combination of drugs was used.•The drug caused adverse side effects.•The bird was reinfected (medication was discontinued too soon).•An inflammation, abscess, or other condition interfered with drug action.•The bird has more than one infection and not all of them were treated.• Disease was caused by a nutritional deficiency that was not corrected.•The bird's defense mechanism is too low (due to the disease, drug use, orpoor nutrition).•Supportive therapy was inadequate.• Biosecurity breach was not corrected (look for ways to improvemanagement).

Reportable DiseasesSome diseases are so serious they must be reported either to the federalAnimal and Plant Health Inspection Service or to your state pathologylaboratory. Each state has its own regulations as to which diseases arereportable. Diseases that are designated as reportable are a serious threateither to the poultry industry or to public (human) health. If your flockexperiences a sudden, high death rate (over 50 percent in a short time), youwould do well to report it to your state veterinarian.

If a veterinary or pathology lab diagnoses a reportable disease inyour flock, they are bound by law to report it. The immediate result willbe quarantine of your flock to keep the disease from spreading. In somecases, you may be allowed to treat your birds under strict supervision. Inother cases, you may be required to depopulate — a polite way of sayingyour entire flock will be destroyed. If you keep chickens for commercialpurposes, you may be reimbursed for your loss.

Even when your flock is not involved, if a reportable disease occursin your area, the movement of all birds may be restricted. Restriction ofmovement does not occur as often with birds as it does with larger livestock,especially cattle, horses, and hogs. Exactly how a particular reportabledisease is handled depends on the nature and scope of the outbreak and onthe virulence and contagiousness of the pathogen involved.

C hart 1 1 - 1Reportable Diseases


THERAPY 295

Governing Body

Disease Threat To

Federal* chlamydiosis public healthNewcastle (exotic) poultry

industryinfluenza (lethal form) public healthparatyphoid public health(Salmonella en teritidis)spirochetosis poultry

industryMost states pullorum poultry

industrytyphoid poultry

industryMany states chronic respiratory

diseasepoultry industry

infectious laryngotracheitis

poultry industry

*United States Department of Agriculture, Animal and Plant HealthInspection Service, Federal Building, Hyattsville, MD 20782

Enhancing Immunity

IMMUNITY IS THE ABILITY OF THE BODY TO RESIST INFECTION. Anotherword for immunity is resistance; the opposite of immunity is susceptibility. Achick hatches with a certain amount of innate immunity and acquires new im-munities as it grows, but may need your help to develop additional immunityagainst diseases in its environment.

ImmunityImmunity can be broken down into two categories:

1. Inherited — which may be:a. complete (all chickens are resistant)b. partial (some breeds, strains, or individuals are resistant)2. Acquired — which may be:a. passive, in which antibodies are transferred:

• naturally, from hen to chick• artificially, by an antitoxin

b. active, in which the production of andbodies is stimulated:• naturally, by disease• artificially, by vaccinadon

296

ENHANCING IMMUNITY 297

Inherited ImmunityChickens are immune to some diseases due to inherited or genetically

controlled factors. When the entire species is resistant, immunity is "com-plete." Chickens have complete immunity to a long list of diseases that infectother birds or animals but never infect chickens.

As a species, chickens are immune to some pathogens they commonlycarry in dieir bodies, but that make them sick if their resistance is brokendown. The protozoan Histomonas meleagridis is a classic example. It com-monly lives in the poultry environment, causing chickens to get blackheadonly when their resistance is drastically reduced by a massive Infestation. (Tur-keys, on the other hand, are highly susceptible to blackhead and often get itfrom chickens that carry the protozoa without being infected.)

When only certain breeds, strains, or individuals are resistant to a disease,immunity is "partial." Chickens have partial immunity to Marek's disease,since some strains never succumb to the otherwise common killer. In nearlyevery disease outbreak, some individuals do not become infected due to in-herited immunity. Those are the birds you'll want in your breeder flock if youwish to breed for resistance, as described in chapter 1.

Passive Acquired ImmunityAcquired immunity is any resistance to disease that is not inherited, but

instead is conferred by antibodies. Passive acquired immunity is resistancedue to antibodies produced in the body of one bird or animal and passed on tothe body of another. Passive immunity provides immediate but temporary re-sistance — since the antibodies are not produced within the chicken's ownbody, immunity is short-term, lasting only about 4 weeks.

Passive immunity may be acquired naturally or artificially. Natural passiveimmunity is acquired by a chick from a hen via the egg. The source of maternalantibodies is immaterial — they may result from a disease the hen once had orfrom a vaccination designed specifically to build up her antibodies so she

canpass immunity along to her chicks.

Artificial passive immunity is acquired by a chicken when it is given aninjection containing antibodies against toxin-producing bacteria. Botulism isan example of a disease caused by bacteria that produce toxins. An antibodythat fights a toxin is called an "antitoxin." Fluid taken from the blood of ananimal that has been immunized and therefore has antitoxins against a dis-ease such as botulism is also called "antitoxin." An injection of antitoxinconfers immediate immunity, and can therefore be used to treat disease. Theimmunity is only temporary, however, since it is passively acquired.

298 THF. CHICKEN HEALTI I HANDBOOK


Active Acquired ImmunityActive immunity differs from passive immunity in three important ways:

• It is caused by antibodies produced within a bird's own body.• It is not immediate but takes time, usually measured in weeks.• It is long-term.

Although active immunity is always longer term than passive immunity, itmay be temporary (as in the case of staphylococcal and streptococcal infec-tions), it may be permanent (as in the case of typhoid), or it may be permanentunless stress weakens the bird's resistance. As a general rule, immunity to vi-ruses is absolute and long lasting, while immunity to bacteria is relative(dependent on stress avoidance) and usually temporary.

Like passive immunity, active immunity can be acquired naturally or arti-ficially. Natural acquired active immunity occurs when a chicken's bodyproduces antibodies to fight a particular disease (see "Immune System," page44). If the chicken recovers, its body continues to contain antibodies specific tothat disease — they confer immunity only to that one disease. A bird can ac-quire active immunity as an embryo during incubadon or at any point after ithatches.

active

natural artificial

invasion bybacteria or virus

vaccination

Artificial active immunity is acquired from a vaccination containing anti-gens that cause a chicken's body to produce antibodies against thoseparticular antigens. Active immunity resulting from vaccination takes about 2weeks to develop and can be renewed through one or more booster shots tokeep the level of antibodies high enough to ward off disease. The booster dose,

passive

exposure to bacteria or virus

immune system stimulated toform antibodies that cause

future immunity

which is usually smaller than the original vaccination dose, must be adminis-tered at a specified time following die original vaccination.

Acquired Immunity



VaccinesAlthough vaccines, like antibiotics, are used to control disease, they differ fromantibiot ics in two important ways.

• They are used to prevent rather than treat disease.• They do not cause resistant strains of microbes to develop.

Since viral diseases have defied a cure, vaccines were originally developedto trigger immunity against viruses. Although most bacterial diseases can besuccessfully treated with antibiotics, some are so devastating that bacterialvaccines, called "bacterins", have also been developed. Few people make anydistinction between vaccines and bacterins, but call them all "vaccines."

Successful vaccines against some diseases have not yet been developedbecause the viruses keep changing (as in the case with influenza), too manydifferent viruses cause the disease (as in infectious bronchitis), or the viruscausing the disease hasn't yet been identified (as in infectious anemia).

In addition, not all vaccines are created equal. Some trigger a good im-mune response, others confer only a low level of immunity. Some produce areaction that can be as serious as the disease itself. Live virus vaccines and con-taminated vaccines sometimes actually transmit disease.

A good vaccine has these five properties:• It contains enough antigens to protect chickens against infection by aspecific pathogen.• It contains antigens from all strains of the pathogen that cause thedisease.• It is not contaminated with additional antigens.• It is not too toxic to chickens (therefore causes no serious reaction).• It will not cause disease.Some state governments would like to restrict the use of vaccines to li-

censed veterinarians and others who hold a permit. Their reasons are thatmishandled vaccines lose effectiveness and that bootleg vaccines occasionallyappear having little or no effect to begin with. Purchase vaccines only fromlicensed, registered manufacutrers, as evidenced by an assigned code

numberstamped on the bottle.

Vaccine TypesA vaccine derived from viruses or bacteria is used to trigger a chicken's

immune response against the viruses or bacteria from which it was derived.When a vaccine is administered, a chicken's body responds by producing anti-bodies just as it would in a natural infection by the virus or bacteria.



The difference between an infection and a vaccination is that the patho-gens in a vaccine either cause a mild case of disease or have been intentionallyaltered so they cannot cause disease at all. A chicken's antibody-producing tis-sue cannot tell the difference between the three basic vaccine forms:

• live• modified live• inactivatedLive vaccines are the most effective. They are used to induce

infection, butto be safe they must be made from harmless microbes closely related to patho-genic microbes. Live vaccines are relatively inexpensive and easy to use,especially for mass application to large flocks, and can be applied to birds at ayounger age than can inactivated vaccines. They cause immunity to developrapidly and to spread via shedding of live viruses from successfully vaccinatedbirds to unsuccessfully vaccinated birds.

A live vaccine has several disadvantages. It can be easily killed by heat andchemicals (such as alcohol usedto sterilize a needle). It may becontaminated with other virusesduring manufacture, spreadingunintended diseases. Just as thevirus can spread from success-fully to unsuccessfully vaccinatedbirds, so can it spread to suscep-tible nearby unvaccinated flocks.The vaccine produces some of thesymptoms of the disease beingvaccinated against and, if chick-ens are stressed or infected withsome other microbe, it can causeserious disease.

Because of these dangers,only mild viruses are used in a livevaccine, and multiple application is required. Live vaccines should be usedonly to prevent a serious disease already present in die yard that cannot be

controlled any other way. Live virus vaccines are available against epidemictremor, infectious bronchitis, infectious bursal disease, infectiouslaryngotracheitis, Marek's disease, Newcastle, pox, and viral arthritis.

Modified live vaccines contain pathogenic organisms that have been ge-netically altered to make diem less infectious so they can no longer causedisease, but can continue to replicate and trigger the production of antibodies.The process of genetically altering pathogens is called "attenuation," and

Live Virus DangerVaccines containing live viruses aresupposed to give birds a mild case ofdisease, but they can cause serious dis-ease if they are not used properly. Thedisease will remain mild if:• the vaccinated birds are healthy• they are the right age for vaccination• the vaccine is properly administered• the birds are kept warm• their housing is clean and dry• weather conditions remain steady



modified live vaccines are sometimes called "attenuated" vaccines.A modified live vaccine is more potent than a live vaccine and is

thereforecheaper to use, since you need less per dose. Like a live vaccine, a modified livevaccine must be handled carefully to avoid killing the viruses or bacteria, thusdestroying their ability to trigger immunity.

Like live vaccines, modified live vaccines cause shedding to unvaccinatedbirds. In addition, if attenuation is incorrectly done, the vaccine may causedisease rather than immunity. Even if attenuation is correct, the vaccinemay cause disease as a result of contamination with other pathogens or byinterfering with the bird's immune response (making it susceptible toother diseases).

Inactivated vaccines contain bacteria or viruses that have been killed bychemicals or heat. While most virus vaccines are live or modified live,bacterins are always inactivated. Inactivated vaccines are both expensive toproduce and time-consuming to administer, since they require multiple dosesand must be injected. Unlike other vaccines, some inactivated vaccines have a21 -day withdrawal lime. In addition, they may confer only short-term, low-level immunity. To produce a higher, more uniform response, birds are oftenprimed with live vaccine first.

On the other hand, inactivated vaccines are the easiest to store and safestto use. They do not cause disease in stressed or infected birds, as live andmodified live vaccines can. They produce few adverse reactions — most com-monly stress due to handling and/or a lump at the site of injection, caused bythe fluid in which the killed pathogens are suspended.

New technologies under investigation that may one day offer terrificbreakthroughs in disease control include biogenetically engineered recombi-nant DNA vaccine, for which large quantities of pure viruses can be producedat a relatively low cost, and synthetic vaccines that eliminate the risks inherent

in working with genetically modified microorganisms (such as the possibilitythat genetically altered pathogens may mutate and cause new diseases).

Vaccination ProcedureVaccines come in bottles containing enough for 500 or 1,000 birds.

Even ifyou can't use it all, the cost is usually still low in relation to the cost of losingbirds in a disease outbreak.

Some vaccines (such as tiiose against Marek's disease and pox) come intwo vials, one filled with powder and one with liquid. Once the two are mixedtogether, the vaccine is good for only about an hour, so you can't save it. De-stroy unused vaccine and empty containers by burning or deep burial.

The age at which birds should be vaccinated and the precise vaccination



procedure you use depend on your purpose in keeping chickens and the dis-ease you are vaccinating against. Vaccines against some diseases come inmore than one form and can therefore be administered by more than onemethod. Some methods of application are more suitable for flock-wide appli-cation involving large numbers of birds, others require handling individualbirds to ensure that each gets an even dose.

Water vaccination is die most popularmass method. It involves withholdingdrinking water overnight, then addingvaccine to the water in a measuredamount calculated to deliver an adequatedose, based on die amount of water an av-erage bird drinks within a 3-hour period.Since water consumption varies with age,feed, and weather, determine the exactamount of wateryour flock needs by mea-suring how much your birds drink the daybefore.

A vaccine may be inactivated if thetemperature is high or the water containsimpurities, including sanitizers such aschlorine used to control bacteria or fungi.Do not use water sanitizers within 48hours of vaccinating. Clean waterers andrinse them well, leaving no disinfectantresidue to inactivate the vaccine.

The vaccine can be somewhat stabilized by adding powdered milk to thewater. Milk protein neutralizes sanitizers and protects a vaccine from theshock of dilution. Before adding die vaccine, stir in skim milk powder at therate of 50 grams or % cup per 5 gallons (45 g/20 liter) of cool water. (You canfind a '/a cup measure in the canning section of nearly any discount depart-ment store; an equivalent measure to Va cup is 10 tablespoons.)

Remove drinking water the night before vaccinating. Provide vaccine-laden water in the morning, right after mixing it. If you're treating a large flock,

ensure that birds low in peck order get a drink by adding only half the vaccineto as much water as the flock will drink in about 2 hours. Then add the otherhalf to as much water as die flock will drink in another 2 hours.

Coated, pelleted feed containing vaccine, designed in Australia, is used intropical countries, where high water temperatures inactivate vaccines.

Spray or aerosol vaccination offers an easy way to vaccinate large numbersof birds in a short time. It is most commonly used for infectious bronchitis and

Methods of VaccineApplication

Flock applicationdrinking waterfeed additiveaerosol (dust or spray)

Individual applicationbeak dipdrop in eye (intraocular)drop in nose (intranasal)injection (intramuscular

or subcutaneous)vent brushwing-web stab



infectious bursal vaccines, to give boosters, and to prime a flock with live vac-cine prior to administering an inactivated vaccine.

Aerosol vaccination is tricky because it can induce a severe vaccine reac-tion and because it requires special equipment to get the droplets just the rightsize. A line mist penetrates deeply into the respiratory tract, a coarse spray notso deeply. A fine mist is used for adult birds, while a coarse spray is used toinduce a milder reaction in chicks.

Since birds must be confined to a small area for the aerosol method towork, it is most often applied in brooder housing. A hand pump may be usedfor occasional application; a coarse-sprav cabinet is used by those who regu-larly vaccinate large numbers of chicks.

Applying a vaccine dust by aerosol is similar, except that the powder ispuffed dry rather than diluted and sprayed as a liquid.

Wing-web vaccination involves the use of a two-prong stabber. Thestabber is dipped into vaccine, then used to pierce the unfeathered skin of thewing-web, or the chicken's "armpit." When vaccinating chickens of variousages, start with the oldest birds, then break off one prong to immunize chicks.

The wing-web method won't work ifyou stab feathers instead of skin, or ifthe stabber isn't adequately immersed in vaccine. When you use a live virusvaccine, you can tell if die vaccination takes by watching for slight swelling andscabbing in 1 to 2 weeks.

Injected vaccines may be administered intramuscularly (into the muscle ofthe breast) or subcutaneously (under loose skin of the breast or neck). Somevaccines can be applied either way. Others (such as those against cholera anderysipelas) can only be administered by subcutaneous injection; a serious re-action will occur if they are injected into the muscle or bone. Followinstructions carefully as to needle size and injection site.

Subcutaneous injection is currently the only way to administer Marek'svaccine to newly hatched chicks. Take a pinch of skin from the back of thechick's neck between your thumb and forefinger. Stick the needle into the skinand inject the vaccine, taking care to neither poke the needle out the other sidenor stab your fingers.

Hye or intraocular vaccination comes in a kit with a viaJ of vaccine and avial of dyed mixing solution, called diluent, with an eye dropper in the cap.Colored diluent is used to verify proper vaccine placement in the eye — colorappears on a bird's tongue when die procedure is correct.

Beak dip vaccines are administered by dipping each chick's beak into thevaccine.

Vent brush vaccination requires the use of a brush to apply vaccine to themucous membrane of the cloaca. This was once a standard vaccinationmethod, but because it involves application of especially virulent viruses, it isno longer legal in most states.



Chart 12-1Vaccination Methods*

METHODS VACCINE TYPESDE = drop in eye L - live vaccineDW = drinking water M = modified live vaccineIM = intramuscular injectionI = inactivated vaccineSC = subcutaneous injectionS = sprayWW = wing web

Vaccination ProgramsYour veterinarian or state poultry specialist can help you work out a

vacci-nation program based on disease problems occurring in your area and yourpurpose in keeping chickens. For each vaccine you consider, take into ac-count:

• its availability• its cost in relation to the worth of your birds• the size of your flock• your flock's expected lifespan• maternal immunity your chicks may inherit from your breeder flock• the presence of infection in your flock, your yard, and your area

Disease DE

DW

IM

SC

S WW

Cholera IChronic respiratory disease

I I

Coccidiosis LEpidemic tremor L LErysipelas IInfectious bronchitis L L I I LInfectious bursal disease M I IInfectious coryza I IInfectious laryngotracheitis

M

Infectious synovitis I IMarek's disease L LNewcastle L L I I LPox L/MViral arthritis I M

/IM

*Age of birds at application, method of application, and need for repeat application depends

on the vaccine source and form — follow instructions on label.

• your need for other vaccines• your flock's past vaccination history• state laws



Establish a vaccination program only to solve specific problems — pastproblems your flock has experienced or the serious threat of a new problem.Vaccinate against diseases your flock has a reasonable risk of getting. Do notvaccinate against diseases diat do not endanger your flock. If you show yourbirds, if serious diseases have occurred on your place (in your own flock or inthe previous owner's llock), or il'serious diseases infect nearby flocks (particu-larly if you live near a high concentration of commercial chickens), you mayhave good reason to vaccinate. To learn about diseases that occur in your area,ask your veterinarian, county Extension agent, state poultry specialist, or theavian pathologist at your state diagnostic lab. In some states, it is illegal to usecertain live virus vaccines or to introduce viruses by bringing in birds from an-other state that have been vaccinated with a live virus vaccine.

Several vaccines come in combinations that trigger immunity againstmore than one disease at a time. If your vaccination plan requires the use ofseveral vaccines, a combination vaccine may save you time and money. On theother hand, sometimes a chicken's response to one vaccine interferes withdevelopment of immunity to anodier. Furthermore, if your birds have an ad-verse reaction, you may have trouble determining which vaccine in thecombination caused the reaction. Whenever you use a vaccine, record thevaccine's name, manufacturer, and serial number in your flock history.

Vaccine FailuresVaccine failures usually result from improperly storing or handling a

vac-cine or from using improper vaccinating procedures. Whenever you use avaccine, read and follow instructions regarding storage and handling, methodof application, dosage, recommended age of birds at the time of first vaccina-tion, and the timing of revaccinations (boosters). All these factors affect thelevel, quality, and duration of immunity.

If your birds are in poor health, the results of vaccinating may be worsethan not vaccinating at all. Unless you deliberately use vaccine to slow thespread of pox or infectious laryngotracheitis, do not vaccinate chickens thathave symptoms of the disease you're vaccinating against.

Some diseases, including infectious bursal disease, reduce resistance toother diseases. Chicks that hatch with a good level of maternal antibodiesagainst infectious bursal disease arc protected against early damage to theirimmune system, but the same antibodies that confer immunity also interferewith the desired immune response to vaccines.

If vaccination fails, consider these possible causes:• Vaccine was not stored in the refrigerator or odierwise as

directed(improperly stored vaccines decay rapidly).



• Vaccine's expiration date long since passed.• Vaccine was not handled in a hygienic manner.• Wrong vaccine was used (not all vaccines protect against all strains).• Wrong dosage was used (underdosing is more common than

overdosing).• Vaccine was administered incorrecdy.• Housing sanitation is poor.• Flock was exposed to pathogens before immunity took effect.• Flock's immune response was suppressed (due to heat stress,

feedcontaminated with mycotoxins, poor health, etc.).

No vaccine will protect your flock 100 percent — every vaccine has at leasta 5 percent failure rate. In addition, disease can occur if you bring in new birdsthat are not on the same vaccination program as your old ones (a vaccine maycause your old birds or your new birds to shed pathogens). Then, too, younever know what disease may turn up next. Good management with an eyetoward disease prevention remains your best defense.

Natural VaccinationBefore commercial vaccines became widely available, farmers practiced natu-ral immunization by mixing young birds with older ones, thus exposing theyoungones to any diseases theolder ones were exposed to. Genetically resistantflocks were developed by culling birds that did not lully recover and keeping(immunized) survivors as breeders.

Chicks may be naturally vaccinated for a variety of respiratory diseases,most notably infectious bronchitis and mild Newcastle disease. Signs thatnatural vaccination may be occurring includc mild wheezing and watery eyes.Cull birds that do not recover within a week so they don't have a chance toreproduce more weaklings.

Other diseases for which natural vaccination commonly occurs throughgradual exposure include chronic respiratory disease, infectious coryza, andinfectious bursal disease. Chicks exposed to infectious bursal disease (IBD)before the age of 14 days rarely develop noticeable symptoms.

Natural vaccination can backfire if chicks are exposed to massive amountsof microbes before immunity iscomplete. In at least onedisease, Marek's, thereis an alternative to gradual exposure — raise a few turkeys with your chickens.Turkeys carry a related though harmless virus that keeps the Marek's virus

fromcausing tumors.


Incubation and Brooding

CHICKENS ARE MORE LIKELY TO REMAIN HEALTHY if they have a healthystart from the time they hatch. Modern practices of selective breeding and arti-ficial incubation have minimized some problems that occurred in the past, butalong the way new ones have been introduced. Good hatchability and strong,healthy chicks result from:

• proper egg collection and storage• correct operation of incubator• good incubator sanitation• healthy, well conditioned breeders• proper feeding of breeders► hereditary vigor

Hatching Egg CareCollect hatching eggs several times a day so they will neither heat nor chil l. Tohelp you track hereditary and/or egg-transmitted problems, identify the eggsfrom each breeder or breeder group by writing a code on each egg with agrease pencil or China marker. If you trapnest hens to identify their eggs, check

317

nests often, especially in warm weather. Hens can suffer from being enclosedin a small, hot space, and may soil their eggs if confined in the nest too long.Eggs laid in floor litter have twenty to thirty times more bacteria on their


INCUBATION AND BROODING 319

shells than eggs laid in cages. The eggs of floor-reared hens are dierefore 3 per-cent lower in hatchability and result in more rough red navels in newlyhatched chicks. In addition, contaminated eggs may explode during incuba-tion, contaminating other eggs and causing diem to subsequently explode.

Bacteria on the shell, from feces or contaminated dust and nest litter, ismore likely to get into the egg if the shell is porous. Older hens lay eggs that aremore porous than pullets' eggs. Vitamin or mineral deficiency or imbalance indie breeder flock, or a respiratory virus, can also cause shells to be more porousthan otherwise.

Manage your flock so that eggs will be clean when you collect diem, whichincludes keeping litter dry so hens won't track mud into nests. Minimize bac-terial contamination by dry cleaning slightly soiled eggs with fine sandpaper.Avoid saving heavily soiled eggs for hatching. If valuable eggs become soiledand must be washed, use water warmer than the eggs (but not over 140°F,60"Q, otherwise bacteria may be forced through the shell.

Household detergent combined widi a dash of chlorine bleach (Clorox)serves as both sanitizer and cleaning agent. Other ways to thoroughly sanitizeeggs: dip diem for 1 minute in a chlorine compound, quaternary ammoniaproduct (such as Germex), I percent iodine solution, or other sanitizer de-signed specifically for use on hatching eggs.

Store eggs in clean cartons to avoid introducing contamination duringstorage.

Egg StorageHatching problems can occur due to storing eggs for too long or at the

wrong storage temperature. The storage temperature must be below "physi-ological zero," the temperature above which development (however erratic)begins to take place. The optimum storage temperature for batching eggs is

55°F (13"C). The storage area should have low enough humidity not to attractmold, but should not be so dry diat moisture is rapidly drawn from the eggs.

The less moisture that evaporates from eggs during storage, the greatertheir hatching rate will be. Speed of evaporation varies from one strain to an-other. Small eggs, such as those laid by bantams and jungle fowl, have arelatively large surface-to-volume ratio, so they evaporate more quickly thanlarge eggs. Early season eggs of any size evaporate more slowly than latesummer eggs.

Eggs have a built-in ability to remain hatchable after several days of stor-age, otherwise a hen could not collect a batch of eggs to hatch all at one time.Even under the best storage conditions, hatchability drops after 6 days. Youcan increase storage time to as long as 3 weeks, while maintaining reasonablehatchability, by wrapping each egg in plastic wrap.



IncubationTemperature, rtiaiive humidity, ventilation, and turning during incubation allaffect the hatch. Eggs must be turned at least three times a day at regularlyspaced intervals, as close to 8 hours apart as possible. Fairly inexpensive incu-bators are available that improve the hatching rate by automatically turningeggs every hour.

Ventilation is necessary to bring in oxygen and remove carbon dioxidegenerated by developing embryos. Most incubators have either adjustablevents you can open or plugs you can remove as the hatch progresses.

Operating an incubator at the correct temperature can be tricky. Unlessthe incubator is extremely well insulated, temperature fluctuations in theroom where the incubator is set up can affect the hatch. Sunlight falling on theincubator can cause its temperature to rise. A thermometer diat isn't properlypositioned according to the incubator manufacturer's instructions can give afalse temperature reading. Even if the thermometer is properly placed, incuba-tion temperature can't be accurately set if the numbers are too close together,as is often die case. The thermometer itself may be inaccurate — it's alwayswise to check a new thermometer against a second or even third thermometerwhose accuracy you are sure of.

When incubation temperature is too low, chicks lake longer than 21 daysto hatch. They will tend to be big and soft with unhealed navels, crooked toes,and thin legs. They may grow slowly or may not learn to eat and drink at all.

When the temperature is too high, chicks hatch before 21 days. They tendto have splayed legs and can't properly walk, a problem that does not improveas the chicks grow. These chicks should be culled.

No matter what combination of temperature and humidity is suggested bythe manufacturer, you'll have to make minor adjustments depending on yourlocation and the eggs you hatch. Keep accurate records as you make adjust-

ments, and after a few hatches you will hit on die optimum combination foryour particular situation.

Whether your incubator is still-air (no fan) or a forced-air (has a fan), itsoptimum temperature and humidity are interrelated. As the temperature goesdown, relative humidity must go up to maintain die same hatching rate. Hereare some likely combinations:still-air: 102"F (38.9"C) at 58 percent forced-air: 99°F (37.2"C) at 56 percent

100°F (37.8-C) at 61 percent 98°F (36.7°C) at 70 percentFor a successful hatch, moisture must evaporate from eggs at just the

rightrate. Small eggs, such as those laid by bantams and jungle fowl, evaporatemore rapidly than larger eggs. Small eggs therefore hatch better at a higherhumidity or lower temperature than regular-sized eggs.



Incorrect humidity can cause embryos to die in the shell or chicks to besmall. Too-high humidity can lead to omphalitis, otherwise known as "mushychick disease." In high humidity the yolk sac does not absorb completely andthe navel therefore cannot heal properly. Bacteria in the incubator invadethrough the unhealed navels, causing deaths for up to 14 days after the hatch.

Incubator SanitationBringing eggs together from various sources is a sure way to introduce disease-causing organisms into your incubator. For healthier chicks, hatch only yourown eggs. If you must bring in eggs from other sources, fumigate them (seepage 213). Ifyou sell hatching eggs to a custom hatchery, do not bring chickshome from one.

Good incubator sanitation improves hatching success and gives chicksa healthy start in life. It also offers an important way to break the diseasecycle in a flock. Another way to break the disease cycle is to avoid hatchingyear-round.

Good incubatorsanitation ensures a

healthy hatch.

>zo>2mo

Hatching itself is a major source of incubator contamination. By the timethe hatch is over, die incubator is littered with organic debris that provides anideal environment for disease-causing organisms. If you pracdce continuoushatching (continuously adding new settings of eggs as previous settingshatch), keep a separate small incubator to use for hatching. Thoroughly cleanthe hatcher after each hatch.

Begin by vacuuming out loose down. Then wipe out hatching debris with adamp sponge, or the debris will protect disease-causing organisms from thedisinfectant. Scrub the hatcher with detergent and hot water, followed by agood disinfectant such as Germex or chlorine bleach (Vi cup bleach per gallonof hot water, or 30 ml/1). If possible, let the incubator dry in the sun.



Clean your hatcher at the end of eachhatching season. Cleaning and disinfect-ing does not destroy all disease-causingorganisms, but it does make the environ-ment less favorable for the survival of anymicroorganisms that remain. If you letcleanup go until the beginning of the nextseason, you'll have more microbes to con-tend with, harbored all that time in fluffand droppings.

FumigationCommercial and custom hatcheries

routinely fumigate their incubators tominimize the spread of salmonella andother bacteria. Small home incubatorsrarely need fumigation, except after a serious disease outbreak. Fumigationrids an incubator of disease-causing organisms by means of gas that pen-etrates cracks and other areas you can't reach with a brush or spray. Prior tofumigation, thoroughly clean hatching debris from the incubator.

For the fumigant, you will need formaldehyde (CFl.,0), the most effectivedisinfectant against viruses, but one drat works only in an enclosed space. It isa toxic, volatile chemical that has a strong odor, is caustic, and irritates theeyes. A common brand name is Formalin, formaldehyde mixed with water in a40 percent solution (37 percent by weight). You will also need potassium per-manganate (KMnOj), a poison that comes in the form of a dry powder.

These two chemicals are available from drugstores and veterinarians, buttheir safe use requires knowledge and care. Wear plastic gloves while handlingdiem. If you get any on yourself, flush your skin with plenty of water. If younormally keep your incubator in the house, move it to an outbuilding for fumi-gation. Due to the danger of inhaling the gas, this is not a safe procedure tocarry out in your living room.

For mixing the chemicals, you'll need a tall earthenware or enamel con-tainer. Do not use metal — the chemicals may eat right through it. Do not useglass unless it's Pyrex — the chemical reaction will generate heat that mightcrack regular glass. Use a container ten times larger than the combined vol-ume of the chemicals, so none can splash out during the chemical reactionthat will cause the mixture to bubble up.

Close all vents to make the incubator airtight. Holding your breath to avoidinhaling poisonous gas, combine the chemicals in die earthenware or enamelcontainer and place the container in die incubator, off the floor somewhere

Styrofoam IncubatorsAlthough no one has formallystudied the difficulty of clean-ing styrofoam incubators,people using them have expe-rienced hatching difficultiesin successive years in spite ofsanitation practices thatwould be adequate for awooden incubator. Since dis-infectants may no I adequatelypenetrate the porous styro-foam, fumigation may be theonly option.



near the center. Quickly close the in-cubator door.

Run the incubator at normaltemperature and humidity for atleast 30 minutes, preferably over-night. At die end of the fumigationperiod, open the incubator and allthe vents to let the gas escape. Alsoventilate the room or outbuilding inwhich the incubator is located.

Fumigating EggsFumigation of hatching eggs is

an effective method of controllingdiseases when eggs are brought to-gether from varying sources (acommon way to spread disease fromflock to flock) or where valuablehatching eggs become dirty.

Fumigating eggs before hatching destroys organisms on the outside of theshell. The procedure is the same as for fumigating an empty incubator. If youare making only one setting at a time, you can place the eggs in the incubatorand fumigate both at die same time. Ifyou make weekly settings, fumigate eggsbefore placing them in the incubator, which means keeping a separate incuba-tor just for fumigation. If you use a separate hatcher, time your settings so youcan fumigate new eggs right after die previous hatch.

If you fumigate eggs during incubation, do so eitiier within 12 hours altersetting diem or after the fourth day. Otherwise, the fumigant may harm em-bryos during the early days of development. Commercial and customhatcheries often fumigate again after moving eggs to die hatching incubator(but never after eggs have pipped, or chicks may be injured). Fumigate eggs for20 minutes using 0.8 cc Formalin and 0.4 g potassium permanganate per cubic

foot (26 cc Formalin and 13 g potassium permanganate per cubic meter).

FertilityDuring incubation, remove eggs that are not developing properly to eliminatea potential source of incubator contamination. The first eggs that can be iden-tified as developing improperly are infertiles, which look clear during candling.

The cause of infertility may be easy or difficult to identify. Sometimes thegerminal disc or "zygote" dies between the time an egg leaves a hen's ovary

Determining ChemicalAmounts for Fumigation

To figure out how much of eachchemical you need, determine thecubic footage of your incubator bymultiplying its length times itswidth times its height. As a generalrule, use twice as much Formalin byliquid measure (ml or cc) as potas-sium permanganate in dry measure(g). For each cubic foot, measureout 1.2 cc Formalin and 0.6 g potas-sium permanganate (per cubicmeter, 40 cc Formalin and 20 gpotassium permanganate). Do notmix them together until you'reready to fumigate.



and the time incubation begins — a phenomenon known as "weak fertility."Since weak fertility is indistinguishable from infertility, die cause is impossibleto trace.

One cause of infertility may be an incorrect ratio of cocks to hens. The op-timum mating ratio for lightweight laying breeds is one cock for up to onedozen hens; the optimum ratio for heavier meat breeds is one cock per eighthens. More hens than diat, and the cocks may not get around to all of them;more cocks than that, and the cocks will be so busy fighting among themselvesthat they won't have time to get around to all the hens.

Even if the mating ratio is right, fertility will be low in a breeding flock that'stoo closely confined. In a small Hock with only one cock, the cock may prefersome hens and ignore the others. Hens that are high in the peck order tend tobe mated less often dian hens lower in peck order. The answer is to either dis-rupt the order by rotating cocks or identify and artificially inseminating theinfertile hens.

A cock that's loo old or too fat may have fertility problems. Frozen combsand wattles can also cause infertility (see "Frostbite," page 132). A cock widi aleg or foot injury may have trouble breeding. Never catch a rooster by one leg,or you may permanently damage a joint. Excessively showing breeders, cocksor hens, can cause stress that leads to infertility. During hatching season, keepvaluable show birds in the breeding pen.

Nutrition can affect fertility. Vitamin E deficiency causes a cock's testes todegenerate, resulting in reduced fertility or even sterility. Vitamin A deficiencyalso causes reduced fertility in cocks. Cocks with large combs that interfere atthe feed trough may have low fertility. Eggs laid by hens that are

underweightor overweight may be infertile. Supplementing lay ration with grains duringthe breeding season interferes with vitamin, mineral, and protein balance.

Diseases diat affect fertility include chronic respiratory disease, infectiouscoryza, infectious bronchitis, and Newcastle. Eggs from breeders that have re-covered from any of these diseases may be infertile. Marek's disease can causepermanent ovary damage that leads to infertility. Parasite problems, internalor external, can interfere with fertility.

Infertility problems may be breed-related. A classic example is low fertilitycaused by the abnormal semen of white Wyandotte cocks with rose or peacombs. Heavily feathered breeds such as Brahma, Cochin, Orpington, andWyandotte may have fertility problems unless the feathers are clipped fromaround their vents. Cocks with crests, such as Houdan or Polish, may not seewell enough to catch wily hens unless dieir crests are clipped back.

Season can affect fertility, which tends to be low during times of year whendaylight hours are fewer dian 14. Just as lighting keeps hens laying during shortwinter days, it aJso improves the fertility of cocks. Fertility is highest in springand drops during the heat of summer.



HatchabilityJust because a fertile egg contains a sperm cell, making it potentially capable ofdevelopment during incubation, doesn't mean the egg will survive die 21 daysof incubation and hatch into a healthy chick. Many things can happen to affectthe egg's hatchability.

On average, even a hen hatches only 89 percent of her fertile eggs. Notmany years ago, 60 percent was considered a reasonable rate for artificial incu-bation. Today's improved incubators average 85 percent. By conventionaldefinition, anything more than 75 percent of fertiles hatched is considered ahigh rate; less than 50 percent is low.

If you are hatching in die mid to high range, you can probably improveyour rate by fine-tuning die way you run your incubator. If your hatches fall inthe low range, look for odier causes.

The age of your hens may be a factor. The small eggs with small yolks laidby pullets are low in hatchability and produce a high percentage of deformedembryos. Hatchability rises as eggs reach full size, but drops again by 3 to 4percent between a hen's first and second year. Whether hatchability continuesto drop thereafter is a matter of contention, but hatchability is certainly likelyto go down in hens that are out of condition, parasitized, or diseased. Hatch-ability is especially affected by salmonellosis, which is transmitted through dieegg and causes embryo or early chick death.

Salmonellosis and odier diseases are transmitted from infected breedersto their offspring through hatching eggs in one of two ways:

• The infectious organism may enter the egg as it is being formed withinan infected hen.

• Bacteria may get on the shell as the egg is laid or when it lands in acontaminated nest. Bacteria then enter the egg through die shell,which occurs more readily if the shell cracks or gets wet (for example,during improper washing).

Diseases Transmitted Through Hatching Eggs

Colibacillosis Infectious stunting Runting syndromeAir-sac disease syndrome SalmonellosisChronic respiratory Infectious synovitis Arizonosis

disease Lymphoid/Sarcoma ParatyphoidOmphalitis Lymphoid leukosis PullorumEgg drop syndrome Osteopetrosis TyphoidEpidemic tremor Pseudomonas Viral arthritisInfectious anemia Rotaviral enteritis



Diseases then spread from infected chicks to healthy chicks in the incuba-tor (often inhaled in fluff) or in the brooder (usually through ingesteddroppings in feed or water).

Hatchability and NutritionNutritional deficiency is one of the most common causes of poor hatch-

ability. Lay ration contains less protein, vitamins, and minerals than a breederflock needs, affecting egg composition and resulting in poor hatchability. Theolder the breeders are, the worse the problem becomes.

In some areas, feed stores carry breeder ration. In other areas, the closestthing is gamebird ration. If you can find neither, feed your flock a handful ofdry catfood two or three times a week and either add a vitamin/mineralsupplement to the drinking water or give each bird Vz cc vitamin AD&E inject-able every 3 weeks. Start this regime 6 weeks before you plan to start collectinghatching eggs.

An embryo's appearance, combined with the day on which it died, pro-vides a clue regarding which nutrient might be lacking. For example, in

Egg-transmitted Disease Cycle

riboflavin deficiency, deadis peak at three points: the fourth, tenth, and four-teenth day of incubation. Embryos may be dwarfed, have beaks that look like aparrot's, have unusually short wings and legs, and have clubbed down — acondition, seen most often in black breeds, in which the down is clumpy, andcurls in a characteristic way because the down sheaths fail to rupture.



Chart 13-1Nutrition-Related Hatching Problems

Symptom Deficiency Symptom DeficiencyDay of Death: Embryonic Appearance

(cont.):Early incubation vitamin A Bones/beak soft vitamin D1-7th day biotin & rubbery4th day riboflavin Clubbed down riboflavin

vitamin E Eyes pale vitamins A & D

10th day riboflavin small zinc10th-21st day magnesium Feathers,

abnormalpantothenic acid

14 th day riboflavin black in ermine vitamin D17th day vitamin B12 pattern18th- 19th day vitamin D Fluid in body vitamin B1219th-21st day biotin Growth, dwarfed riboflavin20th & 21st day manganese stunted vitamin DLate incubation folic acid

pantothenic acid

Legs/feet/wingstwisted

biotin

vitamin E Legs, bowed vitamins A & D

vitamin K short riboflavinselenium excess

manganese

At pipping folic acid undeveloped vitamin B12selenium excess

missing zinc

Soon after hatch vitamin E Perosis vitamin B12Embryonic Appea

ranee: Navel not closed manganeseiodine

Beak/head zinc Skull deformed biotinabnormal manganese

Beak, short vitamin B12 Spine poorly zincupper/lower beak vitamin D developed

short Incubation time iodinecrooked (parrot riboflavin loo long

beak) manganese

InbreedingInbreeding is a sure way to reduce hatchability. Continuous, close in-

breeding causes a phenomenon known as "inbreeding depression," for whichlow hatchability is usually the first sign. Later signs are fewer and fewer eggslaid, and chicks lacking in "constitutional vigor," meaning diey're droopy

andunthrifty, and may or may not die soon after hatching.

Inbreeding is unavoidable ifyou raise an exhibition strain or you're tryingto preserve one of the fast-disappearing classic breeds. For every 10 percentincrease in inbreeding, however, you can expect a 2.6 percent reduction inhatchability. A flock that reaches 30 percent hatchability is nearing extinction



Chart 13-2 Incubation Trouble-Shooting

Solution

Eggs:

infertile

blood ring

gre

en appearance

Embryos:die day 1-2

d

i

e

d

a

y

1

-

7

d

i

e

a

t

1

ProblemCause

2

-

1

8

d

a

y

s

die at 19-21 days

(yellowish b

rown

fluid in eggs)die at 21 days

(without pipping)

die at 21 days

(pipped)too many or too few cocks

cock too oldcock too fatcocks hav



e foot/leg injuries

frozen combs and wattles

excessive

showing of breeders

eggs stored loo long

wrong storage

temperaturehens too fat or too thinllock too closely confinedbreeder flock unhealth

y

breeder ration low in vitamins

eggs chilled or heat

ed

improper fumigation

irregular incubator temper

atureaspergillosis

eggs stored too longirregular incubator temperatureim



proper turning

deficient breeder rations

inbreedingaflat

oxicosis

temperature too high or low

poor ventilation

incor

rect breeder ration

colibacillosis

eggs not turned properlyhereditary weaknesswrong temper

ature

pseudomonashumidity too low

temperature too low

temporary temperature surgeI cock/12 light breed hens1 cock/8 h

eavy breed hensuse younger cockcondition cocktreat injuriestreat for frostbitekeep breeders homestore 6 days or lessstore eggs at 55



"F(13"C)condition hensgive breeders more roomcheck for parasit

es and diseasesfeed alfalfa meal and cod liveroilcollect hatching eggs oft

endo not fumigate between 12thand 9fith hour

control temperaturedo

not ha

tch eggs with

cracked or poor shells; clean

and disinfect in

cubator

between hatches

store 6 days or lesscontrol temperatur

eturn eggs at 8-hour intervalsvitamin-mineral supplementobtain new cockavoid feeding breeders moldyg

rain

contro



l temperature

open vents or remove plug

feed milk,

yellow corn, alfalfa

meal, cod liver oilh

atch only

clean, sanitizedeggs

turn at least 3 times/dayuse slock with high hatchabilitycontrol hatching temperature

improve incubator sanitationincrease humidityincrease tempera

turecontrol temperature



Problem Cause Solution

Embryos (cont.):die at 21 days(pipped andunpipped)

omphalitisparatyphoid

hatch only clean, sanitized eggshatch eggs only from typhoid-clean breeders

die at 21 days(pipped, hut chickstoo big to work outof shell)

poor hatching ventilation open vents or remove plug

Hatch:early

high incubation temperature

decrease temperature Vz°

slow low incubation temperature

increase temperature V*'

late temperature too lowpower outage

eggs stored too long

increase temperaturecover incubator during poweroutagesstore 6 days or less

Chicks:can't get free ofshell

hatching humidity too lowhatching temperature too high

too much hatching ventilation

increase hatching humiditydecrease temperature athatching timereduce vent openings

stick)', shellsclinging

hatching humidity too low increase hatching humidity-

sticky, smearedwith yolk

hatching temperature too lowhatching humidity too high

increase hatching temperatureopen vents or remove plug

rough navels hatching temperature too hightemperature fluctuationhatching humidity too low

decrease hatching temperaturecheck wafer in incubatorincrease hatching humidity

small eggs too smallhumidity too lowtemperature too high

hatch only normal-sized eggsincrease humiditydecrease temperature

short down temperature too highhumidity too low

decrease temperatureincrease humidity

splayed legs temperature too high decrease temperaturecrooked toes temperature too low increase temperaturebig, soft, weak temperature too low

poor ventilationincrease temperatureopen vents or remove plug

unabsorbed yolksac

hatching humidity too high decrease humidity

mushy and smellbad

omphalitis sanitize incubator

crossed beaks hereditary cull breeders



due to failure to reproduce. A flock can become extinct after only six to eightgenerations of brother-sister matings.

Inbreeding depression has two distinct causes: concentration of geneticfactors and the inbreeding itself. You can iherefore slow die decline and im-prove reproduction in two ways. First, by selecting and culling for number ofeggs laid, hatchability of the eggs, and vigor of the resulting offspring. Second,by using less close matings that result in more gradual inbreeding — makingFifty birds the minimum size for fin inbred (lock.

Better yet, occasionally introduce birds from a different strain. Matingbirds from different strains invariably results in hybrid vigor. The opposite ofinbreeding depression, hybrid vigor causes more rapid growth, larger size, in-creased viability, and improved productivity.

Lethal GenesOne result of inbreeding is concentration of lethal genes — recessive

genesthat show up only when two birds with the same trait are mated. Many lethalsare related to specific breeds.

Japanese chickens carry the most widely studied lethal, the creeper gene, atrait that was once valued in broody hens because it causes short legs andtherefore keeps the hen's body close to her chicks. When a creeper hen ismated to a cock carrying the creeper gene, one-quarter of the chicks die duringthe first week of incubation.

Dark Cornish carry a similar short-leg gene that causes death at the time ofhatch. Signs of "Cornish lethal" include short beaks and wings, and bulgingeyes.

New Hampshires carry a lethal that causes death in the twentieth andtwenty-first day of hatch. Signs are crooked necks, short upper beaks,

andshriveled leg muscles.

The silver gray Dorking has a letiial that causes death in the ninth day ofincubation. Embryos have short necks and beaks.

A Barnvelder lethal causes "Donald Duck syndrome," in which the upperbeak curls upward, the lower beak curls downward, and death occurs in thelast days of incubation.

Congenital tremor is a ledial gene found in a number of breeds includingAncona, Plymouth Rock, Rhode Island Red, white Leghorn, and white Wyan-dotte. Chicks hatch but can't control their neck muscles. When a chick tries tostand, its head falls over and the bird falls down. Unable to eat or drink, it diessoon after hatching.

This is by no means a complete list of all the possible lethal genes. Amongother lethals are those found in die black Minorca (short legs widi extra toes),Rhode Island Red (short legs, wings, and beaks), white Leghorn (short legs and



parroi-like beaks), and white Wyandotte (early embryonic death). Two com-mon genetic factors that don't qualify as lethal genes, but that do reducehatchability, are frizzledness and rumplessness.

One way to avoid the effects of lethal genes is to avoid mating closely re-lated birds. Another way is to deliberately mate related birds and tiy to ferretout and cull breeders carrying lethal genes.

Genetic DefectsTwo common hereditary defects, wry neck and wry tail, are caused

by re-cessive genes, meaning they show up only when two birds are mated that carrythe same gene.

Wry or twisted neck, resulting from curvature of the spine or "scoliosis,"occurs as birds grow, and is particularly common among brown Leghorns. Itusually happens to a group of related birds and does not affect their ability todrink.

Wiy or twisted tail is a condition in which the tail feathers lean or twist toone side due to weakness in the vertebrae that hold the tail. Wry tail usuallyshows up as the tail feathers grow and become heavy.

Do not use birds wit h either of these defects as breeders. Cull breeders youcan identify as carrying these recessive genes.

Chick IdentificationYou can't identify problem breeders unless you have some way to track theiroffspring. Chicks can be tracked in one of two ways: embryo dyeing and toe-punching. Embryo dyeing works best on chicks with white or light-coloreddown, and wears off as soon as the chicks grow their first feathers. Toe-punching works for all chicks and is permanent. You might want to

combinethe two techniques, dyeing embryos so you can toe-punch chicks diat getmixed up during the hatch.

Embryo DyeingInjecting dye into eggs before they hatch lets you color-identify

chicksfrom different matings. Dyeing in no way affects a chick's healdi or growthrate, provided you handle the eggs carefully and use only clean materials.

You will need a 20-gauge, 1-inch (25mm) long hypodermic needle, a sharpsewing needle of the same size or a little bit bigger, and a set of food dyes in 2 or3 percent concentration (sold at most grocery stores). Among the primary col-ors, red, green, and blue show up best. Purple, made by combining red andblue, also works well. Yellow and orange don't show up well at all, since chick



down is often yellowish to start widi.Embryos dye best during the eleventh to fourteenth day of

incubation. Toavoid chilling the eggs, remove no more eggs from the incubator than you candye within 30 minutes.

About V2 inch (13 mm) from ihe pointed end, disinfect an area about the

size of a quarter by wiping it with 95

percent rubbing alcohol or 2 percent

tincture of iodine. Dip the sharpneedle into the alcohol or iodine.Cushioning die egg in one hand, makea tiny hole in the center of the disin-fected area by pressing against it withthe needle, twisting the needle backand forth until it just penetrates theshell and membranes. Take care tomake only a tiny hole that does not go

deeper than necessary to pierce theinside membrane (110 more than '/binch or 3mm).

Dip the hypodermic needle intothe alcohol or iodine and fill it with V2 cc of dye. Insert it into the hole so die tipis just beneath the inner shell membrane. Very slowly depress the plunger torelease the dye without letting it overflow. To avoid mixing two colors, use aclean needle if you change dyes.

Seal the hole with a drop of melted paraffin or a tiny piece of adhesive ban-dage (Sheer Strip sdcks best). Return the eggs to the incubator.

Toe-PunchingA toe-punch, available from many poultry supply catalogs, is about

die

ALBUMENDyeing an embryo

size of fingernail clippers. It functions like a paper-hole punch and is used toremove the web between the toes of a newly hatched chick. As the chick grows,you can identify its parentage by the pattern of its punched-out webs.

When chicks are dry and ready to come out of the incubator, hold eachgently but securely in one hand with one foot extended. Carefully posidon thepunch over die web. With one firm stroke, punch away the web. Don't justpunch a hole through the web, or the web may eventually grow back.

The pattern of removed webs lets you identify chicks from up to sixteendifferent matings. Here's how it works: on each foot, a chick has three maintoes and therefore two webs—the outer web (between die middle and outsidetoe) and the inner web (between die middle and inside toe).

Starting at the chick's left side, the first web (left outer) stands for 1; the



next web (left inner) stands for 2; the nextweb (right inner) stands for 4; the far right-hand web (right outer) stands for 8. Assigneach mating a number bom 1 to 15 andidentify chicks from each mating by add-ing up the numbers corresponding to thepunched webs. (For a sixteenth mating,leave the chicks unpunched.)Chicks in batch number 1 have the leftouter web punched. Chicks in batch num-ber 2 have the left inner web punched.Chicks in batch number 3 have both theleft outer and left inner webs punched (1 +2 = 3). Chicks in batch number 5 have theleft outer and right inner webs punched (1+ 4 = 5). And so forth.Toe-punching works only ifyou knowwhen you open the incubator whichchicks came from which mating. You canidentify chicks by:• dyeing embryos• hatching different matings atdifferent times• keeping eggs fiom differentmatings on different hatching trays• enclosing small groups of eggs inupside-down baskets (pedigreebaskets) such as plasdc pint-size fruitbaskets.

BroodingThe typical death rate among chicks is 5 percent or less during the first 7 weeks,up to half of which usually occurs during the first 2 weeks. As distressing asoccasional deaths among chicks can be, they're nothing to be concernedabout.

Left Foot

Right Foot

\o| / 1 \ /

Toe punch patterns

\ |o/ 2 \ /\o|o/ 3 \ /\ ! / 4 \

o/

\ o j / 5 \o

/\ \ o / 6 \

o/

\o|o/ 7 \o

/

\ ! / 8 \ o/

\o| / 9 \ o/

\ \ o / 10

\ o/

\ o j o / 11

\ o/

\ ! / 12

\o

o/

\ ° ! / 13

\o

O/

\ j o / 14

\o

o/

\o 1 o/ 15

\o

o/

\ 1 / 16

\ /On the other hand, stress caused by chilling, overheating,

dehydration, orstarvation, or any combination diereof, can drastically reduce die immunity ofnewly hatched chicks, making diem susceptible to diseases they might other-wise resist. As soon as you remove chicks from the incubator, place them in aclean carton or disinfected brooder.



Chilling or overheating can occur if the brooder is too cool or too warm.You can tell chicks are comfortable when they are evenly distributed in thebrooder. If they crowd to the corners, they are too warm. If they crowd beneaththe heat source, they are cold. Brooding chicks at too cool a temperature in-creases their susceptibility to salmonella infections. Start the broodingtemperature at approximately 95°F (35°C) and reduce it 5"F (3°C) each weekuntil you reach room temperature.

Smothering cm occur if chicks don't get enough heat or are placed in adraft, causing them to pile on lop of each other to slay warm. As a result, thechicks on the bottom may be smothered. Smothering due to drafts or insuffi-cient heat usually occurs at night. It can be prevented by placing a cardboardring around the chicks during their first week of life, which keeps them near thesource of heat and out of corners. Smothering also occurs when chicks aretransported in stacked boxes with too few ventilation holes, or in the trunk of acar where air circulation is poor. In older chicks, piling may be caused by fright,especially if they've been moved to unfamiliar housing. When you move chicksto new housing, keep on dim lights and check the chicks often during the firstfew nights.

Crowding causes litter to become hard-packed and caked with droppings.Pads of litter and droppings may stick to the chicks' feet, causing cripplingand/or infection. In crowded conditions, litter may have a strong odor, usuallyof ammonia. Severe ammonia fumes cause chicks to sit around with their eyesclosed. If crowding is not corrected, chicks' eyes may become inflamed.

Feather- and toe-picking may result from crowding or from a diet too lowin protein. Commercial chick starter usually contains enough protein to pre-vent picking. For more details, see "Cannibalism," page 135.

Brooder DiseasesDisease is usually not a problem in newly hatched chicks unless

eitherthey contract an egg-transmitted disease during incubation or the brooder en-vironment is contaminated. The brooder may become contaminated eitherbecause it was not diorouglily cleaned after the last batch of chicks or becausedisease-causing organisms are being shed by chicks with an egg-transmitteddisease, passing the disease on to other chicks in the brooder.

Since adult birds are reservoirs of infection (whether or not the adult birdsthemselves are sick), brood chicks away from older birds to give diem time todevelop natural immunities. Natural immunity is die result of gradual expo-sure to infectious organisms, rather than exposure to a high concentration thatcan cause disease instead of immunity.

The age at which chicks first show symptoms gives you a clue as to whatdisease might be involved. The diagnostic charts in chapter 9 list diseases by



age group. If your chicks get sick, look for a disease in their age group that mostclosely matches their symptoms. If you can't find a good match, consider dis-eases that are common in chicks slightly younger or older than yours.

The most common brooder disease, especially in warm humid weather, iscoccidiosis. If you brood chicks in a temperate climate, or you hatch late in theseason, prevent coccidiosis by using medicated starter ration containing acoccidiostat from day 1 to 16 weeks.

Brooder NutritionSlow growth in chicks can result from nutritional deficiencies that are

alltoo common in breeder-flock diets. General signs of deficiency are poorgrowth and lack of vigor. All chicks up to 3 weeks old, especially chicks thathave been shipped, benefit from the addition of a vitamin supplement in

Chicks up tothree weeks oldbenefit front avitamin supple-ment in theirdrinking water.

theirdrinking water.

Starve-OutStarvation or "starve-out" results when chicks don't start eating

within 2 to3 days of hatch, causing them to get too weak to act ively seek food. Starve-outcan occur when shipped chicks are in transit for too long, so that they becomeweak before they are offered feed. It can also be caused by feeders that areplaced where chicks can't find them or by feeders that are so high chicks can'treach them.

Other causes are excessive heat over feeders that drives chicks away, andusing sand or sawdust as litter for newly hatched chicks. To keep chicks fromeating litter instead of feed, cover the litter with paper toweling or burlap untilchicks start eating well.



DehydrationChicks will die if they do not start drinking by the time they are 4

days old.Chicks that can't find water don't grow at the proper rate, develop bluishbeaks, and stop peeping. Deaths start occurring on the fourth day and con-tinue until the sixth day. If water is available, but some chicks can't find it, theones surviving after the sixth day are those that found the water.

If chicks have been shipped, make sure they know where to find water bydipping each beak into the fount as you transfer birds from the shipping cartonto the brooder. Do not place the waterer on a platform where chicks can'treach it. If you switch from one waterer to another, leave the old waterer inplace for a few days until the chicks get used to the new one. Stick your fingerinto the water to make sure a bad electrical connection isn't causing chicks toget a shock each time they try to drink.

Slipped Tendon

Healthychicks arebriglit-eyedand perky.

Slipped tendon, properly known as "perosis," may result from broodingchicks on paper or other slick surfaces. It occurs most often in heavy and last-growing breeds, and may be caused either by hereditary factors or impropernutrition. If the cause is manganese deficiency, the problem should clear upafter 1 month of feeding the chicks a supplement containing manganese.(Slipped tendon is described more fully in chapter 15).

Crooked ToesA chick with crooked toes walks on the sides of its feet, causing the

toes toaccumulate manure clumps and/or develop sores. Chicks can have crookedtoes if humidity was low during incubation or the brooder floor is cold. Forunknown reasons, crooked toes have been associated with infrared brooding



and wire floors. They may also be hereditary, occurring most often in heavybreeds, especially in males. If you can't identify a cause, don't keep crooked-toed chickens as breeders.Crooked toes can be easily distinguishedfrom curled-toe paralysis caused by riboflavindeficiency. In the former condition, toes twistto the side but the chick can still walk fine. Incurled-toe paralysis, the toes curl under, caus-ing the chick to walk on the tops of its toes.Because walking is difficult, the chick spends alot of time resting on its hocks.Curled-toe paralysis can occur wherebreeder hens are fed unsupplemented lay ra-tion. The chicks grow slowly and may havediarrhea during their first week or two of life.In a severe case, the toes curl completely back and the legs become so weak thechicks walk on their hocks. Deaths occur after about 3 weeks.

If the starter ration (rather than breeder ration) lacks sufficient riboflavin,symptoms will occur when chicks are 10 to 14 days old. An early warning sign isalert chicks that can't stand up. If you supply a multivitamin supplement in thechicks' water before their feet are permanently damaged, they should recoverin 2 to 3 days.

Crooked toes can also be caused by flexing of the toes due to vitamin Edeficiency, a condition known as "encephalomalacia" (sometimes called"crazy chick disease"), described fully in chapter 15.

Brooding DeficienciesWhen vitamin A is deficient in the chicks' ration, the birds won't

grow andwill appear drowsy, weak, uncoordinated, and emaciated. They will haveruffled feathers, will stumble and stagger when they try to walk, and may havedry, dull eyes.

Thiamin (vitamin B1) deficiency in starter ration shows up suddenly whenchicks are 2 weeks old and lose dieir appetites. As they lose weight, their feath-ers ruffle, they develop weak legs, and they become unsteady on their feet.Progressive paralysis starts at the feet and works upward, until chicks sit backon their hocks with their heads pointed upward (the so-called "star gazing"posture). Chicks given an oral thiamin supplement may recover.

In riboflavin (vitamin B2) deficiency, chicks continue to have good appe-tites but grow slowly and become weak and emaciated. They may havediarrhea, droopy wings, and dry skin. They are reluctant to move, doing so bywalking on tiieir hocks with the help of their wings.

Pyridoxine (vitamin B6) deficiency causes chicks to walk with jerky move-

Cliick with curled toe paralysis



Chart 13-3 Nutritional Problems in Chicks

Beak, crusty

Blood,hemorrhage

clots slowlyBones

, soft

(rickets)

Breast, muscles,

dege

nerated

(white muscle

disease)Droppings,

soft

Eyes, dry/dullscabby or crustystuck to

Deficiency/Imbalance

DeficiencyIImbalance

Sign Sign

gether

pointed

upward

(stargazing)Feathers, black

i

n brown or red

breed

lack color

long or uneven

rough

and

frizzled

ruffled

Feet, bottoms

rough and

cracked

scalytoes curl

biotinpantothenic acidcoppervitamin Kvitamin BI2vitamin Kcalcium

phosphorus

v



itamin Dselenium &vitamin £•

biotin

niacin

riboflavinvitamin

A

biotinpantothenic acid

vitamin A

thiamin

vitamin

L)

copperfolic acidironamino acidproteinfolic acidniacinpantothenic acidzinc

vitamin Athiaminbiotinpantothenic acidniacinriboflavinzincLegs, short/thick

twisted

(slipped

tendo

n)

hocks enlarged

musclesdegenerated(white muscledise

ase)

paralyzed

weak

Mouth, inflamed

(black tongue)

Nervous

disorders,excessive fr ight

jerky movements

trembling(encephalomalacia)uncoordinated

Parasites,(coccidia,roundworm)Skin, drypale



greenish fluidbeneathWings, droopy

manganesezincbiotincholinefolic a

cidmanganesenicotinic acidpyridoxinezincniacinzinc

selenium & vitamin E

thiaminthiamin

chloride

pyridoxinevitamin E

vitamin Avi

tamin Evitamin A

riboflavinfolic acidcopperironpyridoxine

sel

eni

um

&

vit

ami

n E

rib

ofla

vin

ments. I'hey may run around flapping their wings, then fall onto their sides orbacks, jerking their heads and legs. Pyridoxine deficiency is similar loencepbalomalacia, except that here the nervous activity is much more intenseand ends in exhaustion and death.

Folic acid deficiency causes poor growth, anemia (skin appears pale), andslipped tendon. It can cause lack of feather color in Rhode Island Red andblack Leghorn chicks and poor feathering in any breed.

Vitamin E deficiency causes chicks to stumble and stagger when they



walk. A serious deficiency may result in encephalomalacia, exudativediathesis, or white muscle disease (till described in chapter 15).

Vitamin /^deficiency causes a chick's blood to clot slowly, so the chick maybleed to death from a relatively minor wound. Chicks will be deficient in vita-min K if the breeder-flock diet was deficient.

Chickens and Human Health

THE CHANCE THAT YOU WILL GET A DISEASE from your chickens is prettyslim, especially if you practice common sense hygiene that includes washingyour hands after working in or around your hen house. Many of the organismsthat cause the diseases described in this chapter are fairly common in the hit-man environment, whether or not that environment includes chickens.Ordinarily, those organisms cause no problems. Exceptions are in people withimpaired immune systems or low resistance due to systemic therapy (immu-nosuppressive or antibacterial therapy, for example), pregnancy, obesity,diabetes, or some disease unrelated to chickens.

The low risk of getting any of these diseases is no consolation to those few

372

CHICKENS AND HUMAN HL-AI.TII 373

who might be infected. This chapter, then, is offered in die spirit of helpfulness— physicians tend to overlook or misdiagnose diseases they don't often see. Ifyou visit your doctor about a condition you suspect might be related to yourchickens, mention your concern to your doctor.

Although many of these diseases have sources other than the poultry envi-ronment, the focus here is on dieir relationship with chickens. Diseases thathumans can get, directly or indirectly, from chickens can be broken down intofour categories: environmental, parasitic, zoonotic, and toxic.

Chart 14-1 Poultry-Related Human Diseases

Risk of Human Infection

ENVIR

ONMENTALAspergillosisCandidiasisCryptococcosisFarmer's LungHen Worker's LungHistoplasmosisPs

eudomonas

PARASITIC

Mites

Ticks

Toxoplasmosis


Chicken Disease

Category


Worms

ZOONOTICChlamydiosisConjunctivitisErysipeloidListeriosisCampylobacter

Clostridium

Colitis

Salmonella

Staph poisoning

AspergillosisThrushnonenonenoneHistoplasmosisPseudomonas

Mites

TicksToxoplasmosis

Worms

C

hlamydiosis

Newcast

le

Erysipelas

ListeriosisCampy

lobacteriosisBotulismNecrotic enteritisColibacillosisParatyphoid (E. enteritidis)Staphylococcosis


MEAT/EGG-BORNE TOXINS

lowmoderatevery lowlowlowvery lowextremely low

lowlowextremely lowextremely low

lowmoderatelowextremely low

moderateextremely lowmoderatemoderatemoderateextremely low


Environmental Diseases

It is possible for humans to contract some infections from die same sources aschickens, the result of environmental exposure rather than inter-species con-tagion. Most human diseases caused by the poultry environment are mycosesor fungal infections.

Aspergillosis

Aspergillusfumigatusfungus is quite common in both poultry and humanenvironments, but infection is more common in chickens than in humans.Humans get infected by inhaling spores from decaying litter. It is a rare disease



that affects primarily people with low resistance or compromised immunesystems, in whom the infection can be serious and occasionally fatal. In others,the usual result is allergic bronchitis (a respiratory disease characterized bycoughing), usually successfully treated with anti-asthmatic drugs.

Aspergillus fleams, found in moldy grains, peanuts, and manioc (fed toboth chickens

and humans), produces a poison that has been implicated asthe cause of human liver cancer in tropical Africa and Asia, where the fungus iscommon.

CandidiasisCandida

albicans yeast commonly lives in the bowels of humans, chick-ens, and many other animals. Infection is transmitted by direct contact withyeast in droppings and is usually superficial, except in people with low resis-tance or compromised immunity. Infection may involve the mouth (children),



the genitals (adults), or the skin under fingernails (all ages), resulting in anitchy rash that eventually swells with pus. It can be treated with an anti-fungalpowder or cream (such as nystatin) and corticosteroid cream (such as hydro-cortisone).

Cryptococcosis

Cryptococcocus neoformans is a fungus found worldwide in bird environ-ments (more commonly birds otiier than chickens). The fungus is not knownto infect chickens, but on rate

occasions does cause infection in humans. Itinflicts primarily men between the ages of 40 and 60, particularly those whouse steroids, have I lodgkin's disease, or otherwise have suppressed immunesystems.

Infection can be acute or chronic and may affect the brain or lungs, or be-come systemic and affect the entire body. The most likely result of inhaling thefungus is meningitis or inflammation of the brain covering. Symptoms includeheadache, stiff neck, blurred



vision, and confusion, leading to coma and deathif not treated with anti-fungal drugs. Inhaling the fungus may cause growths inthe lungs. Symptoms of lung infection are chest pain and coughing, some-times involving phlegm. Lung cases usually clear up on their own.

Hen Worker's Lung

Hen worker's lung is an allergic reaction to blood protein and droppingsinhaled in poultry dust. Few people develop this disorder, which usually re-quires prolonged

exposure such as a professional poultry worker mightexperience. Symptoms may come on suddenly, approximately 6 hours after



exposure. They include difficult or painful breathing, cough, fever, chills, andsometimes loss of appetite, nausea, and vomiting. The symptoms, easily mis-taken for flu, may last several hours or up to 2 days, although completerecovery may take weeks.

The allergy sometimes develops gradually, starling with bouts of breath-ing difficulties and coughing that increase in frequency and severity.

Theallergy occasionally takes a chronic form, resulting in difficult or painfulbreathing brought on by physical activity, accompanied by the coughing up ofphlegm, extreme fatigue, and gradual weight loss. If corrective measures arenot taken, the end result may be respiratory failure.

I bis disease is difficult to diagnose. The primary clue is the relationship ofsymptoms to exposure — for example, professional workers who experiencerelief during their days off.



Backyard keepers may experience symptoms 4 to 8hours after exposure, something that can be hard to determine ifyou visit yourcoop two or more times a day. Although frequent attacks reduce the lung'selasticity and eventually cause scar tissue, an early chest x-ray may appear nor-mal, leading to a possible misdiagnosis of heart condition.

Hen worker's lung can usually be cleared up by avoiding the poultry envi-ronment. Complete recovery is possible if avoidance

occurs before lung tissuebecomes scarred. Whether or not you suffer from hen worker's lung, it makesgood health sense to wear a dust mask when you work in the coop, particularlyduring cleanup, and to install a fan to remove floating dust particles from theair.

Farmer's Lung

Farmer's lung is an allergic reaction similar to hen worker's lung, butcaused by the spores of Micropolyspora faeni or Thermoactinomyc.es vulgarisinhaled from



moldy grains or litter. The allergy typically occurs in areas of highrainfall, usually toward the end of winter following a wet summer. Symptomsare nearly identical to those of hen worker's lung. Prevention involves wearinga face mask when working in dusty areas and avoiding die storage of moistlitter or grain over winter.

Histoplasmosis

Inhaled Histoplasma capsulatum spores from old, dry chicken droppingswhile cleaning or dismantling an old chicken house (or

while working in in-fected garden soil) can cause a rare though potentially serious infectiousfungal disease. Histoplasmosis occurs mainly in the Ohio and central Missis-sippi river valleys where the altitude is low, rainfall is 35 to 50 inches a year, andtemperatures remain even. Infection does not spread from birds to humans, h



usually occurs only in someone who inhales large numbers of spores or whohas an immunodeficiency disorder.

Histoplasmosis settles first in the respiratory system and may produce nosymptoms (other than an abnormal chest x-ray) or may cause symptomsvirtually identical to those of llu — fever, coughing, joint pains, and generaldiscomfort. In patients with suppressed immunity, the disease may spreadthroughout the body, requiring treatment with anti-

fungal drugs to prevent afatal outcome.

Most cases require no treatment — the disease usually clears up on itsown. Avoid infection by misting litter to control dust before cleaningyour coopand by wearing a respirator or a dampened handkerchief over your mouth andnose while you work.

Pseudomonas

Pseudomonas aeruginosa bacteria are commonly found in soil, particu-larly in humid environments. In the rare case where chickens becomeinfected, their contaminated



meat decays rapidly. Human infection is ex-tremely rare and most likely to occur through an open wound or a deeppuncture, typically to the foot. The puncture turns purplish-black toward the cen-ter widi a reddened area around the outside, and requires antibiotic treaunent.

Parasitic Diseases

Parasitic diseases are among the most unlikely diseases a human can get froma chicken.

Mites and Ticks

Mites may crawl onto your body if you handle infested chickens, but theyusually won't stay long. Minimize discomfort by taking a shower and washingyour clothing.

A tick can also get 011 you from a chicken. If the tick bites, it might possiblytransmit a disease such as tick paralysis (characterized by loss of appetite,weakness, lack of coordination, and gradual paralysis) or Rocky Mountainspotted fever (characterized by severe headache, chills, muscle



pains, andprostration).

If you find a tick trying to burrow into your skin, grasp it with a pair oftweezers and pull until it releases its hold — pull gently but firmly so you nei-ther crush the tick nor break its body away while its head remains in your skin.Disinfect the bite with rubbing alcohol. See your doctor if you experience anysymptoms of a tick-borne disease.

WormsYou aren't

likely to get infested by worms from your chickens, sincemost worms that prefer poultry do not invade humans. You can, however,accidentally ingest worm eggs if you eat without washing your hands afterhandling contaminated soil or litter. Such an infestation causes few or nosymptoms and is easy to treat with an appropriate anthelmintic.

Toxoplasmosis

Toxoplasma gondii protozoa rarely infect chickens and even more rarelyinfect humans.



Toxoplasmosis results from eating raw or undercooked meatof infected chickens (or other animals). Infection usually causes no ill effect,except in people with immunodeficiency disorders and in unborn children.One-third of the pregnant women who get toxoplasmosis during pregnancypass it to their unborn children, resulting in serious damage (such as blindnessor retardation), miscarriage, or stillbirth.

The most common symptoms of toxoplasmosis are fatigue, low fever, and

muscle pains. The disease is self-limiting and usually goes away on its own.Extremely rare are serious cases involving vital organs (eye, brain, or heart),which may be diagnosed through blood tests and treated with antimalarialand sulfa drugs.

ZoonosesMany diseases are species specific, meaning they affect only one species,whedier it be chickens, humans, or some other animal. A few diseases, called"zoonoses," are shared by animals and humans. Some chicken diseases arecaused by



zoonotic organisms — creatures so flexible diat they can adapt tothe human species. Don't be too quick to suspect you have a zoonosis unlessyour chickens have been positively diagnosed as having the disease.

Chlamydiosis

Humans can contract chlamydiosis, a rare form of pneumonia, by inhal-ing dust from feathers or dried droppings of infected birds. The disease wasfirst recognized in psittacine birds (parrots), and so was called "psittacosis" or"parrot

fever." The same disease, when transmitted from chickens to humans,is sometimes called "ornithosis."

Virulent strains appear in cyclic fashion, but not every avian outbreakcauses human illness. The two most likely causes of chlamydiosis in humansare heavy exposure while dressing birds, more often turkeys than chickens (so-



lution: wet leathers before plucking), and exposure to dusty, crowded facilities(improve ventilation and wear a dust mask and gloves).

The incubation period (time between exposure and first symptoms) is 1 to2 weeks. Symptoms include loss of appetite, fever, chills, severe headache, drycough, constipation, muscle stiffness, and sensitivity to light; sometimes rash,diarrhea, and vomiting. Early symptoms may be easily confused with llu orother forms of pneumonia. Left untreated, chlamydiosis can be fated, espe-cially in those over the age of 50, but usually clears up after 10 days of antibiotictreatment.

Conjunctivitis1 Iumans who handle vaccine for Newcastle disease often suffer from

conjunctivitis (eye inflammation) within 1 to 4 days. Conjunctivitis can alsooccur in those who butcher infected birds and, much less likely, those whotreat sick chickens. The virulence of Newcastle disease in chickens has nobearing on whether or not humans become infected. Symptoms are itchy, red,watery, sometimes swollen eye (usually only one). No treatment is known. Re-covery is spontaneous and complete, usually in 4 days, but may take as long as3 weeks.

ErysipeloidErysipeloid is a bacterial skin infection that invades through a cut or

otherwound on a person who handles or slaughters infected birds. Infection usuallyappears within a week as an itchy, burning, raised and hardened purplish-redpatch on the hand that may gradually grow larger.

Infection is most likely to occur in butchers, kitchen workers, veterinar-

ians, and artificial inseminators — more often those handling fish, pork, andturkey than chickens. The infection is self-limiting. Treated with penicillin, itusually clears up within 2 to 3 weeks.

ListeriosisListeriosis is more common in animals other than chickens, and is

evenrarer in humans. It is, however, life threatening to senior citizens over the ageof 70 and to unborn children infected through their mother's blood. The dis-ease spreads to humans who handle or butcher infected birds or who eatimproperly cooked infected meat.

Symptoms range from mild skin irritation, to fever and muscle aches, tomeningitis (inflammation of the brain covering) or blood poisoning. The mostlikely result of infection in humans, primarily those who process the meat of



infected birds, is conjunctivitis (eye inflammation).Diagnosis requires blood tests — be sure to tell your doctor you

suspectlisteriosis, or the lab won't think of looking for Listeria. The disease is easilytreated with antibiotics.

Meat and Egg ContaminationOne of the reasons people raise their own chickens, even though doingso costsmore than purchasing store-bought meat and eggs, is due to concerns aboutpesticide and herbicide residues, bacterial contaminants, and antibiotics incommercial poultry products. Sadly, no one is seriously guarding the safety ofour meat and egg supply. Even the physician who oversees the food-borne-diseases branch of the Centers for Disease Control and Prevention, Dr. lamesHughes, has been quoted as saying, "We've got the most rudimentary surveil-lance of food-borne diseases you can imagine." The CDC tracks and reportson food-borne illnesses, but does little to control them.

Pesticides and herbicides are used on most feed crops that make upchicken rations. Unless you have a source of so-called organic rations, youreggs and chicken meat will contain no less residue from pesticides and herbi-cides than commercial meat, which in any case is extremely low.

Antibiotics at low levels, along with growth-promoting hormones, areused commercially to make chickens reach market weights faster and withlower feed costs. You can easily avoid antibiotics and hormones in home-grown meat by not making them part of your management routine and byobserving the withdrawal period for any drug you use for therapeutic pur-poses.

Bacteria pose die greatest threat among contaminants in poultry meat oreggs, especially those diat are commercially produced, since large-scale

pro-duction lends itself to unsanitary practices. Homegrown meat birds, bycontrast, are usually killed and cleaned individually, are rinsed under a run-ning faucet (rather than in a vat of rapidly contaminated water), and arerefrigerated promptly; similarly, homegrown eggs are exposed to fewersources of contamination. Nonetheless, remaining aware of the dangers ofbacterial contamination is the first step toward avoiding them.

Food-Borne BacteriaIf meat or eggs are held at room temperature for loo long, any

bacteriapresent will proliferate. Some multiply more rapidly than others. Since there'sno way to tell whether or not bacteria are present, you can't go wrong if youalways handle meat and eggs as if they are contaminated.

In a healthy adult, bacterial food poisoning is usually little more than an



annoyance. In the very young, theaged, or someone with a weakenedimmune system, however, bacterialfood poisoning can be serious or evenfatal. General symptoms are loss ofappetite, nausea, vomiting, abdomi-nal cramps, and diarrhea diat comeson suddenly. In many cases, illnessstrikes a group of people who haveshared a tainted meed.

Most cases are resolved with bedrest and plenty of fluids. For most people, the most serious consequence is lossof body fluids and salts (electrolytes). Since symptoms resemble the flu, mostcases go untreated and end in spontaneous recovery. Unless die illness is com-plicated by other factors, antibiotics may be of little help and may actuallymake matters worse.

The most common causes of bacterial food poisoning are Campylobacter,E. coli, and Salmonella. Some food-borne bacteria are infective— they causedisease by invading the intestine wall. Others produce toxins that inhibit nutri-ent absorption. Some work both ways.

Egg SanitationA freshly laid egg is warm and moist, and therefore attracts bacteria

andmolds that exist in the poultry environment. After leaving a hen's warm body,the egg immediately starts to cool. As its contents contract, a vacuum is createdthat can draw bacteria and molds through the (->,000-pi us pores in the shell,potentially causing egg spoilage and human illness.

Eggs produced at home in a clean environment, collected often andpromptly placed under refrigeration (after cracked or seriously soiled eggs arediscarded), rarely pose a health problem. Eggs diat are slighdy soiled widi dirt

or dried droppings should be dry cleaned with fine sandpaper. Improperlywashing them can do more harm than good.

Eggs produced in a not-so-clean environment and those destined for mar-ket may need to be washed. Market eggs are often subjected to storagetemperatures that are higher than desirable (causing bacteria and mold on theshell to multiply) and to repeated

warming and cooling (drawing more micro-organisms dirough die shell each time).

Ifyou wash eggs, use water that is 20'F (11 "C) warmer than the eggs are,otherwise vacuum action may draw microorganisms through the shell or tinycracks may develop in the shell that expose eggs to invasion by bacteria andmolds. Wash eggs with detergent (not soap) to remove soil. Rinse them in wa-ter of the same temperature as the wash water, adding a sanitizer to reduce the

Chart 14-2Food-Borne Bacteria

Infective Toxic

Campylobacter jejuni xClostridium botulinum xC. perfringens xEscherichia coli x xSalmonella enteritidis xStaphyloccus aureus x


C L I K 'khns and human htaltii 239

number of microorganisms on the shell (the sanitizer won't eliminate all bac-teria and mold). If you wash a large number of eggs, change the wash and rinsesolution often, since both rapidly become contaminated.

Sanitizers that will not introduce off odors, colors, or flavors include chlo-rine solution (such as Clorox bleach) and quaternary ammonium compoundsor "quats," used at the rate of 100 to 200 parts per million. Don't get carriedaway and combine chlorine and a quat, or they'll counteract each other.

Diy eggs dioroughly before placing them in cartons, since wet shells morereadily pick up bacteria.

SalmonellosisSalmonella bacteria can be found almost everywhere. You would

have ahard time finding meat, eggs, or any other food that did not harbor one of the2,200 salmonella strains. An estimated 3 to 4 million cases of salmonellosis oc-cur each year. No one knows the exact number, since not all cases are reported.Only about 5 percent of all cases can be traced to chickens.

Over 150 different salmonella strains that produce paratyphoid infectionsin chickens cause serious illness in humans. In the 1960s, outbreaks of salmo-nella poisoning from bacteria in eggs resulted in institution of the Egg ProductsInspection Act in the United States. Among other things, the Act removed sub-standard non-Grade A (cracked or "check") eggs from the marketplace. For atime, fewer incidence of salmonellosis in humans were reported.

Since the 1960s, however, an especially virulent, antibiotic-resistant strainof S. enteriridis has appeared in commercial poultry flocks, and incidents ofsalmonella poisoning have doubled.

Until a few years ago, experts believed that S. enteriridis infected an eggthrough die shell, after the egg was laid, and that frequent egg collection anddisinfection would minimize contamination. In the 1980s, a new outbreak ofsalmonellosis in the Northeast led to the discovery of salmonella bacteria inhens' ovaries, infecting eggs before they were laid. The bacteria have sincespread to regions outside the Northeast and are becoming antibiotic resistant,possibly due to drug overuse by commercial producers.

An infected hen won't always lay salmonella-contaminated eggs, and ahen that usually lays normal eggs may occasionally produce a contaminatedegg. According to the Centers for Disease Control, only about 1 in 5,000 to10,000 eggs is contaminated. The problem is compounded, however, whenone contaminated egg is added to a recipe along widi several good eggs, orfoods are served that contain raw eggs. The concentration of bacteria increaseswhen egg-rich foods — quiche, homemade eggnog or mayonnaise, custardpie, hollandaise and bernaise sauce, and the like — are held at room tempera-ture before they are served.

Despite all the press coverage of salmonella poisoning, experts claim your



chance of getting salmonellosis from eggs is only about 1 in 2 million. In ahealthy person, poisoning requires eating a large number of bacteria. Mostcases occur not in homes but in restaurants, schools, hospitals, and other insti-tutions where fresli eggs may not be cooked long enough or may sit on acounter too long, allowing any bacteria present to rapidly multiply. Most of the500 deaths per year occur in nursing homes.

Salmonella bacteria, when present, are concentrated in an egg's yolk,since the white has antibacterial properties. They may also be present inundercooked meat. Although salmonella poisoning from eating chicken gets alot of publicity, rare beef is a mare common cause, since most people cooktheir chicken thoroughly. Chicken is thoroughly cooked at 180°F (82°C); sal-monella bacteria are killed at any temperature above 142°F (61 °C).

Chart 14-3Bacterial Food Poisoning Quick-Check

Symptoms

Bacteria Incubation

DurationCampylobacter jejuni 2-5 days 2-7 dayscramps

diarrheafeverheadachedifficulty:breathingseeingspeakingswallowingconstipationno feverdiarrheagas painsno fevercrampswatery or bloodydiarrheano or low feverdiarrheafevervomitingdiarrheavomitingheadachefever

Clostridium botulinum 18-36 hours

fatalwithoutcare

24 hoursC. perfringens

H-24 hours

1 -8 days

Escherichia coli

3-4 days

2-7 davsSalmonella spp.

12-72 hours

3-6 hoursStaphylococcus aureus 2-8 hours

Many people who have salmonellosis never know it, believing instead thatthey have an upset stomach or a mild case of flu. The illness usually runs itscourse in a week or less. Symptoms begin 12 to 72 hours after eating contami-nated food, which tastes and smells normal. Symptoms include nausea, fever,abdominal cramps, and diarrhea.

A serious infection can spread from the intestines to the bloodstream andother body sites, causing death, especially among: infants, the elderly, anyonewith an impaired immune system, a patient undergoing treatment with anti-biotics (which remove beneficial bacteria from the intestines, clearing the wayfor disease-causing bacteria), an ulcer patient taking antacids (which reducebacteria-killing stomach acids).

Most infections are relatively mild and most people recover without treat-ment, as long as they avoid dehydration by drinking lots of fluids.Hospitalization and antibiotic treatment are needed if symptoms persistor the diarrhea is severe and/or accompanied by high fever, weakness, ordisorientation.

CampylobacteriosisAlthough campylobacteriosis gets less press dian salmonellosis, it is

theworld's leading food-borne pathogen, the most common cause of diarrhealillness in humans, and of growing concern to chicken keepers because of itsprevalence in commercially produced poultry. Of the three species that causehuman disease, Campylobacter jejuni— which causes campylobacteriosis inchickens — has been identified more than 90 percent of the time.

Campylobacteriosis is an occupational hazard in poultry processingplants. Humans become infected by handling infected birds or by eatingundercooked infected poultry. (Unlike salmonellosis, campylobacteriosisdoes not infect humans through raw or undercooked eggs.)

The bacteria produce a toxin that irritates the lining of the intestine, caus-ing abdominal pain and watery, sometimes bloody diarrhea, occasionallyaccompanied by a fever ranging from 100° to 104°F (38-40°C). Campylo-



bacteriosis can be prevented by observing the same precautions that preventsalmonellosis, as outlined on page 242.

Clostridium PoisoningClostridium petfringens is called the "buffet germ" because it

proliferatesand creates toxins in slowly cooling foods and in foods kept at low holdingtemperatures. Prevent it by keeping cooked meat and eggs at 140°F (60°C) orby cooling them quickly to less than 40°F (5°C). When you cook for a crowd,divide large amounts of food to speed cooling. Separate chicken from gravy orstuffing before you store them in the refrigerator. Most strains of C. petfringenscause a mild, self-limiting illness, but some can be serious to fatal. See a doctor

Cooking PoultryFollow these precautions whenever you handle poultry meat and eggs.Handling PoultryWhen you butcher chickens, avoid feather and fecal contamination; rinse

meat thoroughly in clear water.Thaw frozen poultry dioroughly before cooking it.Thaw raw meat in the refrigerator (or in a plastic bag under cold running

water), never on the counter top.Wash hands, knife, cutting board, and other utensils after contact with rawmeat.Sanitize counters by wiping them with 2 teaspoons of chlorine bleach in a

quart of warm water.Wipe counters with either paper towels or a dish cloth washed in soap and

chlorine bleach after each use.Don't let cooked meat (such as chicken barbecue) come into contact with

raw meat or the plate it was carried on.Before storing cooked meat, cool it quickly to slow the multiplication of bacteria.Cooking PoultryHeat poultry meat to 185T (85"C).Reheat leftovers to 165T (74'C).Cook casseroles and other combination foods to 16CTF (71°C).Barbecue until no red shows at the joints.Hold cooked poultry above 140"F (60"C,) for no longer than 2 hours.Handling EggsCollect eggs often and refrigerate them promptly.Don't use cracked or dirty eggs.Wash hands and utensils after contact with raw eggs.Don't serve foods containing uncooked eggs.Don't hold foods prepared wirh raw or undercooked eggs at room

temperature.Promptly refrigerate leftovers.Cooking EggsHeat eggs and egg-rich foods to 160°F (71"C).Poach eggs for 5 minutes in boiling water.Boil eggs in shells for 7 minutes.Fry eggs (in an electric frying pan set at 250"F, 121"C) as follows:

Scrambled, 1 minute;Sunnyside up, uncovered, 7 minutes;Sunnyside, covered or basted, 4 minutes;Over easy, 3 minutes one side, then 2 minutes.Hold cooked eggs between 40° and 140 "F (5-60°C) for no longer than 2 hours.When in Doubt: Call the toll-free USDA meat and poultry hotline:

1-800-535-4555



if you experience cramps, severe diarrhea, and bloating gas.Clostridium botulinum is usually associated with improperly canned

low-acid foods. Home-canned vegetables are the most common source, butunconfirmed reports have implicated canned chicken meat. Botulinum-ladenfood may or may not appear cloudy, contents may swell causing jars to crackor lids to become loose. Do not use any canned food that smells improper orthat sprays out when you open the container. Never test suspect foods by tast-ing them. Cook home-canned chicken to 176°F (80°C) for at least 30 minutes— the toxin is readily destroyed by heat.

The botulinum toxin affects the nervous system, causing double vision,slurred speech, and difficulty breathing and swallowing. Symptoms may occurany time from 4 hours to 8 days after eating poisoned food, but usually appearwithin 18 to 36 hours. Botulism affects everyone who shares a poisoned meal.If you suspect botulism poisoning, get immediate medical attention. Nervedamage is irreversible. Untreated botulism poisoning can cause death due toparalysis of the respiratory system.

ColitisE. coli from poultry droppings may contaminate meat during

butchering,although avian strains are not a significant cause of infection in humans. Of the3 percent of commercial meat contaminated with E. coli, beef is more likelythan chicken to carry it. Coliform bacteria invade the intestine wall and alsoproduce toxins, causing severe cramps and wateiy diarrhea that soon turnsbloody. Prevention and treatment is the same as for salmonellosis.

Staphylococcal Food PoisoningStaphylococcus aureus bacteria are present wherever there are

chickens.About 50 percent of the strains generate toxins that cause food poisoning inmishandled poultry meat. Symptoms are nausea, vomiting, cramps, diarrhea,and sometimes headache, fever, and prostration. Recovery is usually

sponta-neous and occurs in about a day. Typically, several people get ill after sharing ameal together. Staph bacteria can't be destroyed by heat, making sanitaiybutchering especially important.

Humans can potentially get a superficial staph infection (impetigo) whiletreating chickens for bumblefoot or an infected breast blister. Although therehas never been a proven case of a chicken infecting a person, wear plasticgloves during treatment and thoroughly wash your hands afterward.

414

Diseases and DisordersThis alphabetic listing is designed to seme as a quick reference to llie most criticalinformation surrounding common diseases and disorders. The information isorganized and cross-referenced for easy retrieval. Unless otherwise noted, crossreferences are found within this chapter. Tallowing are explanations of the categoriesused in each disease and disorder entry.

Sample ListingCommon Name

ALSO CALLED — alternative names, scientific names (lor ihe benefit of specialistsand readers who consult technical works), and names no longer in vogue (forreaders who peruse old poultry books)INCIDENCE — how common ihe disease is and die geographic area in which i( islikely to be foundSYSTEM/ORGAN AFFECTED — primary body part or system the disease affectsINCUBATION PERIOD — amount of time from exposure to the first sign of infection(helps diagnose the disease based on past contacts or identify the source ofinfection once the disease has been diagnosed)PROGRESSION — how hard the disease hits a flock, how fast it spreads, and whether

it is acute (short-term, ending in recovery or death) or chronic (long-term)SYMPTOMS — most likely symptoms or combinations of symptoms; since no twocases are ever exactly alike, not all symptoms will always appear; age groupsare approximations onlyPERCENTAGE AFFECTED — proportion of an affected tlock likely to be involvedMORTALITY — percentage of affected birds likely to die from the diseasePOSTMORTEM FINDINGS — changes that occur within a diseased bird's body (for

details on postmortem examination, see chapter 10)RESEMBLES — diseases with similar symptoms and, when possible, how to tellthem apartDIAGNOSIS— best way to identify the disease through a combination of flockhistory, symptoms, and postmortem findings; some diseases are so similar toothers that laboratory tests are required for a positive diagnosis, some can onlybe identified by laboratory tests (for diagnostic guidelines, see chapter 9)CAUSE — primary cause of the disease (for information on the causes of infectious

diseases, see chapter 7)TRANSMISSION — how the disease spreadsPREVENTION — steps for preventing the disease (for information on immunity,

seechapter 12)

TREATMENT — approaches toward dealing with the diseases (for information on

therapy, see chapter 1 1 )HUMAN HEALTH RISK — any potential risk this disease poses for humans (addi-tional information can be found in chapter 14)

416

A-avitaminosis 245

- A -A-avitaminosis. See Roup (nutritional)Acariasis. See"Mites," page 67Acute Death Syndrome. See Sudden Death SyndromeAcute Heart Failure. See Sudden Death SyndromeAdenoviral Infection. See Infectious AnemiaAE. See Epidemic TremorAflatoxicosisALSO CALLED — aspergillus toxicosis, x diseaseINCIDENCE — rare but increasingly more common worldwideSystem/Organ Affected — ENTIRE BODYINCUBATION PERIOD — up to 2 weeks, depending on amount of toxin ingestedPROGRESSION — usually acute, sometimes chronicSYMPTOMS— in incubated eggs from poisoned hens: embryo death

during firstweek— in young birds: loss of appetite, slow growth, weakness, increasedsusceptibility to bruising and heat stress, sudden death— in hens: reduced egg production, smaller eggs with decreased hatchabil-ity, increased susceptibility to infection (especially cecal coccidiosis andMarek's disease)— in cocks: weight loss, reduced fertility

PERCENTAGE AFFECTED — 100 percent of those consuming contaminated feedMORTALITY'— none in adult chickensPOSTMORTEM FINOINGS — none or light-colored muscles; sometimes swollen

kidneys and enlarged liver with pale yellowish areas that are white at the centerRESEMBLES— fatty liver syndrome, lymphoid leukosis; infectious anemia, except

that infectious anemia affects only growing birdsDIAGNOSIS— difficult: symptoms, feed analysis, microscopic examination of livertissueCAUSE— toxins produced by Aspergillusflavus, A. parasiticus, and

Penicilliumpuberulum mold in litter and in corn and other grain (especially grain that'sinsect damaged, drought stressed, or broken into pieces); increases suscepti-bility to infectious diseases and often found in combination with infectiousanemia and/or fatty liver syndromeTRANSMISSION — eating moldy grain

PREVENTION — avoid moldy grain; use only fresh feed (most commercial feedscontain mold inhibitors); store feed in plastic bin (metal sweats) in cool, dryplace

TREATMENT — remove and deeply bury moldy grain; minimize stress; boost dietaryenergy and protein and offer a vitamin supplement until recovery

HUMAN HEALTH RISK — alia toxin (a poison and a carcinogen) is rapidly excreted indroppings so there is little danger of residue in meat: residue may appear inyolks of eggs up to 10 days after contaminated rations are withdrawn; humansmay get food poisoning from eating moldy grainAl. See InfluenzaAirsacculitis. See Air-Sac Disease

418

419 Air-Sac Disease

Air-Sac DiseaseALSO CALLED — airsacculitis, air-sac infection, air-sac syndrome (one form of

colibacillosis and/or mycoplasmosis)INCIDENCE — common worldwideSYSTEM/ORGAN AFFECTED — respiratoryINCUBATION PERIOD — 6 to 21 daysPROGRESSION — acute to chronicSYMPTOMS — in young birds, 5 to 12 weeks old (most commonly 6 to 9 weeks old):coughing, rattling, nasal discharge, breathing difficulty, loss of appetite, rapidweight loss, standing around with eyes closed, stunted growthPERCENTAGE AFFECTED — 100 percentMORTALITY — up to 30 percentPOSTMORTEM FINDINGS — thick mucus in nasal passages and throat; cloudy air sacs

containing cheesy material; transparent film covering liver and heartRESEMBLES — chronic respiratory disease, except that CRD affects older birds andis usually milder

DIAGNOSIS— flock history, symptoms, postmortem findings, confirmed bylaboratory identification of bacteria

CAUSE— Escherichia coli and Mycoplasma gallisepticum (sometimes M. synoviae)bacteria; often occurs in combination with or following vaccination for chronicrespiratory disease, infectious bronchitis, infectious laryngotracheitis,Newcastle

TRANSMISSION— contact with infected or carrier birds; inhaling contaminated dustor respiratory droplets; spread from breeders to chicks through hatching

eggsPREVENTION — avoid dusty litter; provide good ventilation; avoid chilling

and otherforms of stress; buy mycoplasma-free birds

TREATMENT— keep birds warm and well fed with high protein rations and avitamin E supplement; treatment with antibiotics such as tylosin (trade nameTylan) or erythromycin (trade name Gallimycin) is effective (/started early andbacteria are identified so ineffective drugs can be avoided, otherwise resultsmay he variable and disappointing; survivors continue to earn,' and transmitM. gallisepticumHUMAN HEALTH RISK— none knownAlgae Poisoning

INCIDENCE — West and Midwest, rare in chickens

420 Arthritis, Staphylococcic

SYSTEM/ORGAN AFFECTED — nervous system or liver and other internal organsINCUBATION PERIOD— minutesPROGRESSION — acuteSYMPTOMS — in all ages: weakness, staggering, collapse, convulsions, lying onbreast with legs extended toward rear, neck extended and curved backwarduntil head almost touches back, paralysis, rapid deathPERCENTAGE AFFECTED — 100 percent of those drinking toxic waterMORTALHY — 100 percentPOSTMORTEM FINDINGS — swollen liverRESEMBLES — botulism

Arizonosis 421

DIAGNOSIS — identification of toxins in water (turns dark green, bluish green, orbrownish green)

CAUSE — two different kinds of toxins in "bloom" or "waterbloom" produced byblue green algae (cyanobacteria) growing in shallow inland lakes, ponds, orsloughs in warm (72-80 "F, 22-27"C), dry, low-wind days of summer and fallTRANSMISSION — drinking surface water containing concentrated toxinsPREVENTION — keep chickens away from shallow inland water; apply 3/4 pound(12 ounces) copper sulfate (powdered bluestone) per acre of water as bloom isforming, repeal even,' 2 to 3 weeks throughout bloom seasonTREATMENT— restrict birds' activity; offer vitamin-electrolyte supplementHUMAN HEALTH RISK — noneAmmonia Blindness. SeeConjunctivitisAnaphylactic Shock. See "Antibiotic Reactions," page 190.Aplastic Anemia. See Infectious AnemiaArizona Infection. See ArizonosisArizonosis

ALSO CALLED — avian arizonosis, AA, Arizona infection, paracolon (one form of

salmonellosis)INCIDENCE— worldwide but rare in chickensSYSTEM/ORGAN AFFECTED — digestiveINCUBATION PERIOD—5 daysPROGRESSION — acute in chicks, chronic in mature birdsSYMPTOMS — in chicks up to 3 weeks old: droopiness, closed eyes, diarrhea withvent pasting, weakness, twisted neck, resting on hocks, difficulty walking, legparalysis, blindness; sometimes tremblingPERCENTAGE AFFECTED — 100 percentMORTALITY — up to 50 percent, starting at 1 week of agePOSTMORTEM FINDINGS — retained yolk sac; yellowish, mottled, swollen liver;

discolored heart; ceca or abdominal cavity filled with cheesy materialRF.SEMBI.ES — paratyphoid: nervous symptoms resemble those of Newcastle and

other nerve diseasesDIAGNOSIS — laboratory identification of bacteriaCAUSE — Salmonella arizonae bacteria that persist in the environment for months

and affect turkey poults more often than chicksTRANSMISSION — contaminated droppings in soil, litter, feed, or water; contami-nated feathers, dust, hatchery fluff; spread from infected breeders


to chicksthrough hatching eggs (eggs can blow up during incubation, further spreadingbacteria); spread by infected eggs and chicks in incubator and brooder; spreadon dirty equipment, boots, feet of insects and rodents, droppings of infectedreptiles (especially lizards), rodents, and other animalsPREVENTION — keep breeders on wire flooring; collect hatching eggs often: hatchonly eggs from S arizonae-free breeders; hatch only clean eggs; clean anddisinfect incubator and brooder after each hatch; in chicks, minimize chilling,overheating, parasitism, withholding of water or feed; keep water free ofdroppings; control reptiles, rodents, cockroaches, beetles, fleas, and Hies

Arizonosis 423

TREATMENT — none effective, survivors are carriersHUMAN HHAI.TII RISK — diarrhea may result from lack of sanitation after

handlinginfected chicksArthritis, Staphylococcic. See Staphylococcic ArthritisArthritis/synovitis. See Staphylococcic ArlhritisArthritis, Viral. Sec Viral ArthritisAscaridiasis. See "Large Roundworm," page 83Ascites. See Broiler AscitesAsiatic Newcastle Disease. Set'Newcastle Disease (exotic)Aspergillosis (acute)

ALSO CALLED — Aspergillus infection, brooder pneumonia, mycotic pneumonia,

pneumomycosis, pulmonary aspergillosisINCIDENCE—worldwide but rareSYSTEM/ORGAN AFFECTED — respiratory; sometimes liver or brainINCUBATION PERIOD— up to 2 weeksPROGRESSION — acuteSYMPTOMS — in hatching eggs: green appearance when candled

— in chicks, usually under 3 weeks of age: gasping, sleepiness, swollen eyes,yellow cheesy material in eye, loss of appetite; sometimes nasal discharge,diarrhea, twisted neck, paralysis; convulsions, deathPERCENTAGE AFFECTED—highMORTALITY — up to 10 percentPOSTMORTEM FINDINGS — grayish yellow lungsRESEMBLES — dactylariosis; infectious bronchitis, infectious laryngotracheitis, and

Newcastle, except that acutc aspergillosis seldom infects chicks over 40 days oldDIAGNOSIS — flock history, symptoms, postmortem findingsCAUSE — spores of Aspergillus Jumigaius fungus and other molds commonlyfound in the poultry environment that multiply readily at normal incubationtemperature and humidityTRANSMISSION — through the shells of hatching eggs, spreads in incubator if

infected eggs break; inhaled from contaminated air, feed, or brooder litterPREVENTION — do not hatch eggs with cracked or poor shells; thoroughly clean anddisinfect incubator and brooder between hatches; clean and disinfect feedersand waterers daily; avoid stress, moldy lifter, moldy feed, dusty conditionsTREATMENT— none, cull (try thiabendazole at die rale of 10 mg/lb or 22 mg/kgevery 12 hours); prevent reinfection by replacing litter and disinfecting


incubator and brooder with copper sulfate (powdered bluestone)I IUMAN HEALTH RISK— the same fungus that affects chicks can affect a humanwith reduced resistance; see "Aspergillosis," page 231Aspergillosis (chronic)

ALSO CALLED —Aspergillus infection, mycotic pneumonia, pneumomycosis.pulmonary aspergillosis

Incidence — worldwide but rareSystem/Organ Affected — respiratory; sometimes liver or brainINCUBATION PERIOD — 2 weeks or morePROGRESSION — chronic

Avian Leukosis 249

SYMPTOMS — in mature birds: gasping, coughing, bluish comb, loss of appetite,

rapid weight lossPERCENTAGE AFFECTED—few at a timeMORTALITY — few (higher in confined than in free-ranged birds; highest

after birdshave been handled, especially carried by legs)

POSTMORTEM FINDINGS — numerous small, yellowish or cream-colored pearl-shaped cheesy nodules in lungs (nodules turn green and furry in advancedstages); circular, yellow, dished-out nodules attached to air sacs in chest andabdomenRESEMBLES — infectious bronchitis, infectious laryn go tracheitis, and Newcastle,except that aspergillosis usually does not cause gurgling, rattling, or otherrespiratory soundsDIAGNOSIS— flock history, symptoms, postmortem findingsCAUSE — spores of Aspergillus fumigatus fungus and other molds found in theenvironment of all poultry, especially in areas surrounding feeders andwaterers (appear blue green and can easily be seen while growing); infectsconfined llocks (especially in winter) where stress is high, nutrition is poor,immunity has been reduced by another disease, and/or exposure is heavyfrom seriously moldy litter or grainTRANSMISSION — inhaled from contaminated air, feed, or litter, particularly where

temperature and humidity are highPREVENTION — avoid alternating conditions of wet (when fungi multiply) and diy(when fungi spread by blowing in dust); avoid stress, damp or moldy litter,moldy feed, dusty conditions; periodically move feeders and waterers or placethem on platforms; spray litter with copper sulfate (powdered bluestone);control humidity and dust by providing good ventilation (opened windowswork better than fans)TREATMENT — none, cull; control spread of disease by adding '/2 teaspoon coppersulfate (powdered bluestone) per gallon of drinking water served in a non-metal waterer for 5 days; prevent reinfection by cleaning facilities,

426 Avian Malaria

disinfectingwith copper sulfate solution ('/a teaspoon per gallon of water), and replacinglitter

HUMAN HEALTH RISK — the same fungus that affects chickens can affect humanswith reduced resistance; see "Aspergillosis," page 231Aspergillus Infection. See Aspergillosis (acute); Aspergillosis (chronic)Aspergillus Toxicosis. See AflatoxicosisAvian Arizonosis. See ArizonosisAvian Chlamydiosis. See ChlamydiosisAvian Cholera. See Cholera (acute), Cholera (chronic)Avian Diphtheria. See Infectious LaryngotracheitisAvian Distemper. See Newcastle DiseaseAvian Encephalomyelitis. See Epidemic TremorAvian Hemorrhagic Septicemia. See Cholera (acute)Avian Infectious Bronchitis. See Infectious BronchitisAvian Influenza. See InfluenzaAvian Leukosis. See Lymphoid Leukosis, Marek's Disease, Osteopelrosis

Botulism 427

Avian Malaria. See MalariaAvian Malignant Edema. See Necrotic DermatitisAvian Monocytosis. See BluecombAvian Pasteurellosis. See Cholera (acute), Cholera (chronic)Avian Plasmodia. See MalariaAvian Pox. See Pox (dry), Pox (wet)Avian Tuberculosis. See TuberculosisAvian Vibrionic Hepatitis. See Campylobacteriosis

- B -Bacillary White Diarrhea. See PullorumBig Liver Disease. See Lymphoid LeukosisBlackhead

ALSO CALLED —histomoniasis, infectious enterohepatitisINCIDENCE—throughout North American but rare in chickensSYSTEM/ORGAN AFFECTED — ceca and liverINCUBATION PERIOD — 7 to 12 daysPROGRESSION — acute or chronicSYMPTOMS — in young birds 4 to 6 weeks old: no symptoms or droopiness,

drowsiness, weakness, ruffled feathers, increased thirst, loss of appetite, weightloss, darkened face; sometimes bloody cecal dischargePERCENTAGE AFFECTED — 25 to 50 percentMORTALITY — limited to exceeding 30 percent, peaks at 17 days,

subsides by 28th dayPOSTMORTEM FINDINGS — thickened ceca filled with grayish yellow cheesy, some-times blood-tinged, material adhering to the lining; sometimes liver mottledwith circular, dished-out spots, dark at the center and grayish white oryellowish green at the rim (differing from spots due to leukosis, mycosis,trichomoniasis, and tuberculosis, which are raised and yellowish gray)RESEMBLES — cecal coccidiosis. salmonellosis

DIAGNOSIS — symptoms, postmortem findings (spots on liver), laboratory identi-fication of protozoa required when postmortem findings are insignificantCAUSE— Histomotuis meleagridis protozoan present wherever poultry occurexcept where soil is dry, loose, and sandy; free-living forms do not live long,but may survive for years in cecal worm eggs; tends to affect turkeys moreoften than chickens

TRANSMISSION — eating droppings from infected chickens, earthworms containing

428 Avian Malaria

infective cecal worm eggs, or protozoa attached to flies, sowbugs, grasshoppers, orcrickets; carried by cecal worms (Heterakis gallinarum); spread by wild birdsPREVENTION — easy, with good management and sanitation; worm regularlyagainst cecal worms; place feeders and waterers on wire platforms; low-leveldrugs in feed may be the only preventive in contaminated housing (due tolongevity of infectious cecal worm eggs, range rotation of free-ranged flocks isineffective)

TREATMENT — none effective; recovered birds are carriersHUMAN HEALTH RISK — none known

Botulism 429

BluecombALSO CALLED — avian monocytosis, the greens, mud fever, new wheat disease,nonspecific infectious enteritis, pullet disease, summer disease, X diseaseINCIDENCE —rare in chickensSYSTEM/ORGAN AFFECTED — digestiveINCUBATION PERIOD — unknownPROGRESSION — spreads extremely slowlySYMPTOMS — in pullets approaching maturity: depression, hunching up, loss ofappetite, weight loss, distended sour-smelling crop, bluish comb, greenishwatery or pasty bad-smelling diarrhea, dehydration, sunken eyes, shriveledshanks, cold-feeling bodyPERCENTAGE AFFECTED—LOWMORTALITY — up to 50 percent „POSTMORTEM FINDINGS — white streaks in breast muscles; sometimes yolk in

abdominal cavity, mucus-tilled intestines, dark liver, swollen kidneysRESEMBLES — any acute septicemiaDIAGNOSIS — difficultCAUSE— unknown (chickens are resistant to the coronavirus that causes

bluecomb in turkeys), possibly a virus combined with stress induced by hot orrainy weather, lack of drinking water, lack of shade, or change in feed; some-times follows the feeding of immature oat or wheat grainsTRANSMISSION—unknownPREVENTION — practice good sanitation; breed for resistance

TREATMENT — none known, cull; affected birds may respond to molasses flush (seepage 192) or Vz teaspoon copper sulfate (powdered bluestone) per gallon ofdrinking water served in a non-metal waterer for 2 daysHUMAN HEALTH RISK — none knownBotulism

ALSO CALLED— food poisoning, limberneck, toxicoinfection, Western duck sicknessINCIDENCE —rareSystem/Organ Affected — NERVESINCUBATION PERIOD — high dose of toxin produces symptoms within hours,

lowdose takes up to 2

daysPROGRESSION — acuteSYMPTOMS — in birds of all ages: sudden death or leg weakness and

drowsinessfollowed by progressive flaccid (not rigid) paralysis of legs, wings, and neck,

430 Avian Malaria

difficulty swallowing, mffled, loose feathers (raised hackles on cocks), lying onside with outstretched neck and eyes partly closed; sometimes trembling,diarrhea; coma and death due to heart and/or respiratory paralysisPERCENTAGE AFFECTED — depends on how many eat the toxinMORTALITY— usually less than 100 percent, depending on amount of toxinconsumed

POSTMORTEM FINDINGS — none obvious; sometimes mouth fills with mucus and

dirt, or crop and intestines contain suspicious organic matter or maggotsRESEMBLES — castor-bean poisoning (see page 142); tick paralysis (see "Soli

Ticks,"page 73); lameness caused by mild botulism resembles Marek's disease

431 Breast Blister

(pseudo-botulism form), except that in pseudo-botulism birds recover quickly,usually within 24 hoursDIAGNOSIS — flock history (birds ate rotted organic matter), symptoms (progres-sive flaccid paralysis, loose feathers, mucus and dirt in mouth), absence ofpostmortem findings, laboratory identification of bacteria (if Vlarek's diseaseor castor-bean poisoning is suspected)CAUSE— Clostridium botulinum, soil-borne bacteria commonly found in thepoultry environment that produce toxins when they multiply in warm, moist,decaying vegetable or animal matter (including dead chickens)TRANSMISSION — consuming decayed organic matter, maggots feeding on rottinganimal tissue, or beetles (in litter) that contain toxin; drinkingwatercontainingcontaminated organic matterPREVENTION — do not feed spoile F food to chickens; burn or deeply bury deadrodents, chickens, or other animal carcasses, and rolling, solid vegetables suchas cabbages; control flies; acidity soil with ammonium sulfate fertilizer; avoidwet spots in litter; keep birds away from marshy or swampy areas wherevegetation rots in water; keep chickens from scratching in compost piles;immunize flock with type C toxoidTREATMENT— remove source of poisoning from yard: move bird to cool environ-ment; squirt cool water into crop twice daily; flush with molasses or Epsomsalts (see "Flushes," page 192); inject intravenously with antitoxin (expensive, ifavailable); remove contaminated litter and disinfect widi calcium hypochloriteor iodine-based disinfectantHUMAN HEALTH RISK — humans are poisoned by toxin types A, B, E, and F;chickens are poisoned by type C, rarely by types A and E; chickens andhumans can be poisoned by the same contaminated food or water; reports ofhuman poisoning from eating contaminated chicken meat are unconfirmed(see "Clostridium Poisoning," page 241)Breast Blister

ALSO CALLED — keel cyst, keel bursitis, sternal bursitisINCIDENCE —commonSYSTEM/ORGAN AFFECTED — keelPROGRESSION — chronic

432 Broiler Runting Syndrome

SYMPTOMS — in growing or mature cocks, particularly of the heavy breeds: largeblister on keel that eventually becomes a callus or

thick scarPERCENTAGE AFFECTED— up to 10 percentMORTALITY—lowRESEMBLES — infectious synovitis except an uninfected blister is filled with

clearor bloody fluid, an infected blister contains creamy or

cheesy materialDIAGNOSIS — flock history (breed and sex), symptomsCAUSE— irritation and inflammation due to pressure of breast bone

against roostor wire floor

TRANSMISSION — not contagious; occurs in birds with weak legs or with poorfeather development offering no breast protection; most likely where floor iswire, roosts have sharp corners, or litter is wet or hard-packed

PREVENTION — wrap roosts in something soft to cushion the breast bone or do not

provide a roost for cocksTREATMENT — open and drain blister, clean with iodine, and pack with Neosporin;antibiotic treatment in drinking water or by injection may be necessary ifblister becomes infected with Mycoplasma synoviae (infectious synovitis) orStaphylococcus aureus (necrotic dermatitis)HUMAN HEALTH RISK — none, as long as blister is not infectedBroiler Ascites

ALSO CALLED — ascites with right ventral failure, ARVF, dropsy, water bellyINCIDENCE — common worldwide, especially in winter at high altitudesSYSTEM/ORGAN AFFECTED — heartINCUBATION PERIOD — unknownPROGRESSION — acuteSYMPTOMS — in male broilers 4 to 7 weeks old: ruffled feathers, slow growth,

reluctance to move; sometimes sudden deathPERCENTAGE AFFECTED—lowMORTALITY — up to 30 percentPOSTMORTEM FINDINGS — dark red muscles; thick, straw-colored fluid in abdominalcavity; liver swollen, discolored, and sometimes mottled or pimpled (earlystage) or small and pale with rounded edges (later stage); bloody lungs;distended right side of heartRESEMBLES — stilt poisoning (see page 31)DIAGNOSIS — symptoms, postmortem findingsCAUSE — unknown, may be due to genetically inadequate respiratory systemfailing to draw in enough oxygen; may be nutritionally related (e.g., excess saltin rations); in newly hatched chicks, may be caused by putting chicks intobrooder too soon after using volatile disinfectantTRANSMISSION — unknown

Breast blister


PREVENTION — none known; may help to provide good air circulation and avoid

ammonia fumesTREATMENT—none knownHUMAN HEALTH RISK — none known

Broiler Ascites 253

Broiler Runting Syndrome. See Infectious Stunting SyndromeBronchitis. See Infectious BronchitisBrooder Pneumonia. See Aspergillosis (acute); Aspergillosis (chronic)Bumblefoot

ALSO CALLED — staphylococcosis, plantar pododermatitisINCIDENCE — commonSYSTEM/ORGAN AFFECTED — foot padPROGRESSION — chronicSYMPTOMS — in maturing birds, especially in males of heavy breeds: lameness,reluctance to walk, inflamed foot (one or both), hot, hard, swollen, or pus-filledabscess or dark black scab on bottom of foot, resting on hocks; sometimessores appear on hocks and bottoms of toesPERCENTAGE AFFECTED — 1 to 2 percentMORTALI TY — usually low; up to 50 percent if untreatedPOSTMORTEM FINDINGS — pus or cheesy material in foot pad; sometimes hock

joints filled with grayish white fluidDIAGNOSIS — symptoms (abscess in foot pad)CAUSE — Staphylococcus aureus bacteria, present wherever there are chickensTRANSMISSION — contaminated hatching eggs; bacteria enters foot through injurycaused by splinters, sharp roosts, jumping from roost on to hard or rockyground, housing on wire, irritation due to improper litter managementPREVENTION — practice good sanitation; provide deep, dry litter that does notpack; avoid high perches; round off edges of perch and sand off splinters; feedvitamin supplement (especially vitamin A); do not breed susceptible chickensto avoid getting more of the sameTREATMENT — difficult to cure; inject swollen area with Vz cc penicillin/streptomy-

cin (Combiotic); if abscess is large, wash foot, cut open abscess, squeeze outcheesy core, rinse well with hydrogen peroxide, pack with Neosporin, wrapfoot with gauze bandage or strip of clean cloth, and tape; confine bird on deeplitter and dress foot every


2 or 3 daysHUMAN HEALTH RISK — superficial skin infection (impetigo); wear plastic gloveswhen treating a bird, wash hands afterward, gather blister contents in papertowel and dispose by burning or deep burial

Healthy foot (left) compared tobumblefoot (right).

Campylobacteriosis 255

-c -Cage Fatigue

ALSO CALLED — cage layer fatigue, cage layer osteoporosis, cage layer paralysis,osteoporosis

INCIDENCE— no longer commonSYSTEM/ORGAN AITECTED— bonesPROGRESSION — usually chronic but can be acuteSYMPTOMS — in caged pullets, usually high-production commercial

strains insummer: weakness, squatting, inability to stand (but will continue to eat anddrink if feed and water are within reach)

— in laying hens: thin-shelled eggs with low hatchability followed bycessation of laying, paralysis, death due to dehydration

PERCENTAGE AFFECTED — depends on duration of dietary deficiencyMORTALITY' — depends on duration of dietary deficiencyPOSTMORTEM FINDINGS — deformed or collapsed rib cage; soft, thin, or fragile

bones that break easilyRESEMBLES — Marek's disease and other paralytic conditions; ricketsDIAGNOSIS — flock history (age, sex, and housing method), symptoms, postmor-tem findings

CAUSE — low calcium or phosphorus diet or disturbance in the metabolism ofdietary minerals, particularly calcium (causing hen to draw calcium from herown bones)

TRANSMISSION — nutritional, does not spread from bird to birdPREVENTION — house hens on litter; feed properly balanced diet

supplementedwith ground oyster shell or limestone; allow birds out into the

sunshineTREATMENT — calcium phosphate supplement; if hen can't get up, give I gramcalcium carbonate in a gelatin capsule daily for 1 week, covcr wire cage bottomwith solid boards or move pullets to floor, pullets should recover within a weekHUMAN HEALTH RISK — noneCage Layer Fatigue/Osteoporosis/Paralysis. See Cage FatigueCampylobacteriosis

ALSO CALLED — avian vibrionic hepatitis, Campylobacter hepatitis, entericcampylobacteriosis, infectious hepatitis, liver disease

INCIDENCE — common worldwide, especially in floor-reared llocks


SYSTEM/ORGAN AFFECTED — intestinesINCUBATION PERIOD — 24 hoursPROGRESSION — sometimes acute, usually chronic, spreads slowlySYMPTOMS — in chicks up to 4 weeks old: depression, watery diarrhea, slow growth(chronic), death (acute)

— in growing or mature birds: sudden death of apparently healthy birds(acute) or listlessness, scaly shntnken comb, weight loss, unthriftiness,sometimes mucousy, bloody diarrhea (chronic)

— in hens: 35 percent drop in egg production (may be only sign)PERCENTAGE AFFECTED — few at a time totaling 30 to 100 percentMORTALITY— 10 to 15 percentPOSTMORTEM FINDINGS —intestine filled with mucus and watery fluid; pale,

watery

439 Candidiasis

bone marrow; sometimes green- or brown-stained liver with characteristicyellow star-shaped patchesRESEMBLES— blackhead, bluecomb, infectious anemia, cholera, typhoid, lym-phoid leukosis, pullorum, ulcerative enteritisDIAGNOSIS— symptoms (thin birds), postmortem findings (stars on liver, whenpresent), laboratory fecal examination to identify bacteria (sinceCampylobacters are sensitive to drying, ask veterinarian or pathologist for asuitable collection container)CAUSE — Campylobacter fetus jejuni bacteria that among birds affect onlychickens, survive well in the environment, and resist disinfectants; oftenoccurs in combination with another infection such as Marek's disease, pox, orparasitesTRANSMISSION — droppings of infected or carrier birds in feed or water;

spread byIlies, cockroaches, and rodents; spread on contaminated equipment and solesof shoes; may spread from breeders to chicks through hatching eggsPREVENTION — good management and sanitation; do not combine birds fromdifferent sources; keep birds free of internal parasites, coccidia, and odierstress-inducing infections; house chickens on wire to keep them from pickingin droppings; control (lies, cockroaches, rodents; cull weak, unthrifty birds;remove infected flock, disinfect, and leave housing vacant for 4 weeks beforeintroducing new birdsTREATMENT — none effective

HUMAN HEALTH RISK — eating undercooked meat of infected birds can causeserious diarrhea, see "Campylobacteriosis," page 241Candidiasis. See ThrushCanker

ALSO CALLED — roup, trichomoniasisINCIDENCE — worldwide, especially in warm climates or during warm weather, but

rare in chickensSYSTEM/ORGAN AFFECTED — mouth, throat, and cropINCURSION PERIOD — 2 weeksPROGRESSION — acute or chronic

440 Cholera (acute)

SYMPTOMS — usually in young or growing birds: loss of appetite, rapid weight loss,weakness, darkened head, extended neck, frequent swallowing, sunken breast(due to empty crop), watery eyes, foul-smelling discharge from mouth, whiteor yellow sores in mouth and throat, inability to close mouth or swallow due tomassive soresPERCENTAGE AFFECTED — high

MORTALITY — limited, usually within 8 to 10 days due to suffocationPOSTMORTEM FINDINGS — cheesy white or yellowish raised buttons on throat walls;

sometimes crop filled with foul-smelling fluidRESEMBLES — capillary worms (see page 84), thrush, pox (wet)DIAGNOSIS — flock history (drinking from stagnant water), symptoms, laboratory

identification of protozoa from throat scrapingsCAUSE — Trichomonas gallinae protozoan parasite that infects a variety of birds,primarily pigeons

Chlamydiosis 257

TRANSMISSION — stagnant drinking water or feed contaminated with discharge

from infected bird's mouth; spread by wild birds and pigeonsPREVENTION — good sanitation; keep pigeons away from chickens; avoid bringing

in new birds that may be carriersTREATMENT — move unaffected birds to sanitary surroundings; isolate infectedbirds; combine 1 pound copper sulfate (powdered Milestone) with 1 cupvinegar and 1 gallon water, mix well, add 1 tablespoon ('/z ounce) solution pergallon drinking water for 4 to 7 days, served in a non-metal waterer; non-meatbirds may be treated with metronidazole (trade name l-'lagyl) injections or pillsor with carnidazole (Spartrix) pills for 5 days; recovered birds are carriersHUMAN HEALTH RISK — none known; not the same as trichomoniasis in humansCannibalism. .Seepage 135Capillariasis. See "Capillary Worm," page 84Cauliflower Gut. See Necrotic EnteritisCestodiasis. See "Tapeworm," page 89Chicken Anemia Agent Infection. See Infectious AnemiaChicken Pox. See Pox (dry)Chlamydiosis

ALSO CALLED — avian chlamydiosis, AC, ornithosis, parrot fever, psittacosisINCIDENCE — worldwide but rare in chickensSYSTEM/ORGAN AFFECTED — respiratory, entire bodyINCUBATION PERIOD — 5 to 9 daysPROGRESSION — acute or chronic, spreads slowlySYMPTOMS — in all ages: no recognizable symptoms or droopiness. nasal

dis-charge, greenish yellow diarrhea, loss of appetite, weakness, weight lossPERCENTAGE AFFECTED— 100 percentMORTALITY— mostly in younger birdsPOSTMORTEM FINDINGS — not always obvious; enlargeddiscolored liver; dark, soft, enlarged spleen;sometimes enlarged heartRESEMBLES — aspergillosis, cholera, colibacillosis,

influenza, mycoplasmosis, pasteurellosisDIAGNOSIS — history (contact with infected birds), symptoms, postmortem

findings, laboratory identification of chlamydiaCAUSE— Chlamydia psittaci, a bacteria-like organism that affects many species ofbird but cannot survive long off birds; often found in combination withsalmonellosis

442 Cholera (acute)

TRANSMISSION — contagious; contact with infected birds and their droppings or

inhaled dust; spread by wild birdsPREVENTION — control wild birds; blood test periodically and cull reactors whereoutbreaks occur; keep chickens away from ponds, lakes, and other surfacewater frequented by wild birds; after an outbreak, disinfect with quaternaryammonium compound or an alcohol-iodine solutionTREATMENT— none effective, relapse is likely, survivors may be carriers; this is a

reportable disease, see "Reportable Diseases" page 196HUMAN HEALTH RISK —high chance of lung infection, see "Chlamydiosis," page 235

Do not post birdsyou suspect have

chlamydiosis

Cholera (acute)Aiso CALLED — avian cholera, avian hemorrhagic septicemia, avian

pasteurellosis,fowl cholera

INCIDENCE— relatively common worldwide; more likely in warm climates and infree-ranged birds; more prevalent in late summer, fall,

and winterSYSTEM/ORGAN AFFECTED — entire body (septicemic)INCUBATION PERIOD — 4 to 9 daysPROGRESSION — acute, spreads rapidly, kills quicklySYMPTOMS — in mature birds or those approaching maturity: sudden

death (hensdead in nests) or fever, loss of appetite, increased thirst, depression, drowsi-ness, ruffled feathers, head pale and drawn back, increased respiratory rate,mucous discharge from mouth and nose, watery white diarrhea laier becom-ing thick and greenish yellow, bluish comb and wattles, death within hours offirst symptoms; survivors may recover and either eventually die from emacia-tion and dehydration or develop chronic choleraPERCENTAGE AFFECTED — high

MORTALITY — 10 to 20 percent among mature birds, can be as high as 45 percent;rare in birds under 16 weeks oldPOSTMORTEM FINDINGS — none in case of sudden death, otherwise blood in lungsand in fatty tissue of abdomen; heart surrounded by fluid containing cheesyflakes; swollen, grayish liver (looks cooked) with small grayish white spots(resembles cornmeal); sticky mucus in digestive tract, especially in the cropand intestine

— in hens: yolk in abdominal cavityRESEMBLES — erysipelas, septicemic colibacillosis, poisoning (see page 139),typhoidDIAGNOSIS — symptoms, postmortem findings, laboratory identification

ofbacteria

CAUSE— Pasteurella multocida bacteria that affect a variety of birds and increasein virulence as disease spreads; bacteria survive for 1 month in manure, 3months in moist soil; destroyed in 10 minutes by sunlight, also easily destroyedby disinfectants, drying, heat

444 Cholera (acute)

TRANSMISSION — contagious; contact with mucus from the nose, mouth, or eyes ofbirds or animals with chronic infection; mucus contaminating feed or drinkingwater; mucus on feed sacks, shoes, and used equipment; picking at carcassesof dead birds

PREVENTION — vaccination is not effective; purchase only cholera-free birds; avoidpurchasing growing or mature birds, which may be carriers; avoid stress due toheat, rough handling, parasites, abrupt change in rations, poor nutrition, andpoor sanitation; provide clean, safe drinking water; do not mix birds ofdifferent ages; control wild birds, rodents, and other animals; keep pets awayfrom chickens; burn or deeply bury carcasses of dead chickensTREATMENT — none effective, disease recurs when medication is discontinued andsurvivors maybe carriers: isolate and dispose of infected flock, thoroughlydisinfect and dry housing, leave it vacant at least 3 months before introducingnew birds

Cholera (chronic) 259

HUMAN HEALTH RISK — in poorly ventilated housing, possible upper respiratorytract infection (which can in turn infect chickens through mucus dischargedfrom human's mouth or nose); wear protective maskCholera (chronic)

ALSO CALLED — avian cholera, avian pasteurellosis, endemic fowl cholera, roupINCIDENCE — worldwide but less common than acute choleraSYSTEM/ORGAN AFFECTED — primarily respiratoryINCUBATION PERIOD — weeks to monthsPROGRESSION — chronicSYMPTOMS — in birds at least 6 weeks old: cheesy nasal discharge, loss of

appetite,rapid weight loss, increased thirst; lameness or swelling of leg joints, wingjoints, foot pads, wattles, and sinuses; swollen, sticky eyes; sometimes bluish,hot comb; sometimes breathing difficulties, rattling, and sneezing

— in hens: drop in egg production, increased blood spotting in eggs— in cocks: loss of aggressive behavior and desire to crow

PERCENTAGE AFFECTED—limitedMortality—LIMITEDPOSTMORTEM FINDINGS — sinuses filled with yellow cheesy material; white

cheesymatter along breast bone; wrinkled, bloody and/or off-colored yolks

RESEMBLES — bluecomb, which is even less common than chronic cholera;infectious coryza, except that coryza is associated with a foul odor;

Newcastle,except that Newcastle often includes nervous symptomsDIAGNOSIS — symptoms, postmortem findings, laboratory identification ofbacteriaCAUSE— Pasteurella multocida (also called P. septica) bacteria oflow

virulence orlingering after an acute cholera infectionTRANSMISSION — contagious; contact with mucus from the nose, mouth, or eyes ofcarriers, including wild birds, wild animals (opossums, rodents, raccoons),domestic animals (dogs, pigs); feed or drinking water contaminated withmucus; mucus on feed sacks, shoes, and used equipment; picking at thecarcasses of dead birds

1Face swollen with

cholera

446 Chondrodystrophy

PREVENTION — same as for acute choleraTREATMENT — same as for acute choleraHUMAN HEALTH RISK — same as for acute choleraChondrodystrophy. SeeSIipped TendonChronic Respiratory Disease

Atso CALLED — CRD, MG, PPLO (pleuropneumonialike organism) infection, stressdisease (one form of mycoplasmosis) (the same disease in turkeys is called"infectious sinusitis")INCIDENCE — common worldwide, primarily in winter in large commercial flocksSYSTEM/ORGAN AFFECTED — respiratory, sometimes ent ire bodyINCUBATION PERIOD—6 to 21 days

PROGRESSION — chronic, spreads slowly, lasts longer in colder weatherSYMPTOMS — in broilers, 3 to 8 weeks old: drop in feed consumption, slow growth— in growing or mature birds: no symptoms or droopiness, coughing,sneezing, rattling, gurgling, swollen face, nasal discharge, ruffled leathers,frothy eyes, squeaky crow, drop in laying; sometimes darkened head, loss ofappetite, weight loss, yellowish droppingsPERCENTAGE AFFECTED —nearly 100 percentMORTALITY— usually low except in young birds

POSTMORTEM FINDINGS — thick mucus in nasal passages and throat; cheesymaterial in air sacs; thickened heart sac; transparent film covering liver

RESEMBLES — other respiratory diseases (infectious coryza, cholera, infectious

bronchitis, Newcastle), except that CRD spreads more slowly than mostDIAGNOSIS — flock history (time of year, age, potential contact with carriers),symptoms (respiratory distress, weight loss, drop in laying), postmortemfindings, laboratory identification of bacteriaCAUSE — Mycoplasma gallisepticum bacteria, often aided by Escherichia coli and/or a reovirus; often seen in combination with cholera, infectious bronchitis,infectious coryza, Newcastle; often follows vaccination for infectious bronchi-tis or Newcasde

TRANSMISSION — contagious; contact with infected or carrier birds and theirrespiratory discharges; inhaling contaminated dust; spread from breedersthrough hatching eggs; spreads on shoes, crates, etc.PREVENTION — purchase mycoplasma-free stock; minimize stress due to suddenweather changes, feed changes, drafts, chilling, crowding, transporting,

showing, worming, vaccinating, dust, and ammonia fumes; vaccinate; afteroutbreak, clean and disinfect housing and leave empty for a few weeksTREATMENT — none effective; tylosin (Tylan) or erythromycin (Gallimycin) willreduce death rate but survivors are carriers; this is a reportable disease inmany states, see "Reportable Diseases" page 196HUMAN HEALTH RISK— none knownCircling Disease. See ListeriosisCloacitis. See Pasted VentClostridial Dermatomyositis. See Necrotic Dermatitis

448 Coccidiosis (respiratory)

Coccidiosis (intestinal) 261

Coccidiosis (cecal)ALSO CALLED — cocci (coxy)INCIDENCE— common worldwide, especially in warm, humid weatherSYSTEM/ORGAN AFFECTED — cecumINCUBATION PERIOD — 5 to 6 daysPROGRESSION — usually acute, spreads rapidly, survivors recover in 10 to 14 daysSYMPTOMS — in chicks or young birds: droopiness, huddling with ruffled feathers.

loss of appetite, retarded growth, bloody diarrhea in early stagesPERCENTAGE AFFECTED—80 to 100 percentMORTAIJTY — highPOSTMORTEM FINDINGS — pale breast muscles, swollen cecal pouches filled

withbloody or cheesy material

RESEMBLES — blackhead, necrotic enteritis, salmonellosisDIAGNOSIS — flock history, postmortem findings, fecal test (see page 92)CAUSE — Eimeria tenella coccidial protozoan parasitesTRANSMISSION — contact with droppings of infected birds; spread on

used equip-ment, feed sacks, feet of humans and wild birds, etc.PREVENTION — defies good sanitation; breed for resistance; hatch and brood chicksearly in the season; raise chicks on clean, dry litter to expose (hem graduallyand let them develop resistance; avoid crowded, damp conditions; in warm,damp weather, treat chicks to 16 weeks of age with medicated starter orcoccidiostat in drinking water, according to directions on label (excessive use ofcoccidiostat can be toxic); most adults are immuneTREATMENT— 1 teaspoon amprolium (20 percent) per gallon drinking water for 5days; antibiotic treatment guards against secondary infection; follow treat-ment with a vitamin supplement (especially A and K); survivors are immune,but may never be as productive as uninfected birdsHUMAN HEALTH RISK — none knownCoccidiosis (intestinal)ALSO CALLED — cocci (coxy"'

INCIDENCE — common worldwide, especially in warm, humid weatherSYSTEM/ORGAN AFFECTED — intestinal tractINCUBATION PERIOD — 5 daysPROGRESSION — usually chronic

SYMPTOMS— in growing or semi-mature birds: droopiness, huddling with ruffledfeathers, loss of interest in water and feed, retarded growth or weight loss,watery, mucousy, or pasty, tan or blood-iinged diarrhea (see chart 6-2 page100); sometimes emaciation and dehydration

— in mature birds: thin breast, weak legs, drop in laying; sometimesdiarrhea

—in yellow-skinned breeds of all ages: pale comb, skin, and shanksPERCENTAGE AFFECTED — 80 to 100 percentMORTALITY— limited to highPOSTMORTEM FINDINGS —vary with Eimeria species (see chart 6-2 page

100)RESEMBLES— infectious anemia, ulcerative enteritis, salmonellosis, worms, andother enteritic diseases


DIAGNOSIS— flock history (exposure to large number of oocysts), symptoms,postmortem findings, fecal test (see page 92)

CAUSE — several different species of coccidial protozoan parasites (see chart 6-2page 100) that flourish in warm, humid environments and survive for longperiods outside a bird's body; more than one species may infect a bird at onetime; the presence of coccidia does not always cause infectionTRANSMISSION — droppings of infected birds; spread on used equipment, feed

sacks, feet of humans and wild birds, etc.PREVENTION — same as for cecal coccidiosis; not all coccidiostats are effective

against all coccidial speciesTREATMENT — same as for cecal coccidiosis (axcept that choice of drugs dependson identification of species involved); survivors are immune to the coccidialspecies causing die infection, but may not be as productive as uninfected birdsHUMAN HEALTH RISK— none knownCoccidiosis (respiratory). See CryptosporidiosisCold. See Infectious Coryza, Infectious BronchitisColibacillosis. [See also Air-Sac Disease, Chronic Respiratory Disease, InfectiousSynovitis, Omphalitis, Swollen Head Disease)ALSO CALLED — coliform infection, E. coli infectionINCIDENCE— common worldwideSYSTEM/ORGAN AFFECTED — various

PROGRESSION — severe and acute to mild and chronic; spreads rapidlySYMPTOMS — in incubated eggs: dead embryos late in incubation with wateryyellowish brown yolk sacs, instead of normal thick yellowish green (yolk sacinfection)

— in newly hatched chicks: swollen, inflamed navel, deadi within 6 days ofhatching (omphalitis)

— in growing birds: lameness, listlessness, ruffled feathers, fever, swollenjoints, recovery in about a week or emaciation (infectious synovitis)

— in growing or mature birds: sudden numerous deatiis of apparentlyhealthy birds with full crops (acute septicemia)

— in mature birds: clear eye that becomes blind, swollen leg joint filled withgolden-colored fluid (infectious synovitis), yellow, watery, or foamy diarrhea(enteritis)

— in hens: cessation of laying, upright penguin-like posture, death within 6months (salpingitis)

Percentage Affected—VARIESMortality— VARIESPOSTMORTEM FINDINGS — vary with location of infection, may include:

dehydration;greenish liver; swollen liver, spleen, and kidneys with grayish dots; cheesy orfibrous material covering heart; thick, inflamed intestines filled with mucusand blood

— in hens: yellowish fluid or yolk-like material in body cavity or distendedoviduct filled with whitish curdy or yellowish cheesy material (salpingitis, seepage 53)


Conjunctivitis 263

RESEMBLES — many other diseases; acute septicemia resembles cholera andtyphoid

DIAGNOSIS — flock history, symptoms, postmortem findings, laboratory identifica-tion of bacteria

CAUSE — many strains of Escherichia coli bacteria commonly found in the poultry

environment that infect birds with impaired resistance; often occurs as asecondary infection to chronic respiratory disease or infectious coryza

TRANSMISSION — ingested droppings of infected birds or mammals in feed orwater; spread by infected breeders to chicks through hatching

eggsPREVENTION — good sanitation and ventilation; avoid stress; keep drinking waterfree of droppings; control rodents; practice good incubator sanitation andhatch only clean eggsTREATMENT— keep birds warm and well fed with high protein rations and a

vitamin E supplement; antibiotic treatment is effective only if started early andE. coli strain is identified in order to avoid ineffective drugs, otherwise resultsof treatment can be variable and disappointingHUMAN HEALTH RISK— minimal (see "Escherichia Coli", page 243)Coliform Infection. See ColibacillosisCongenital Loco. See Congenital TremorCongenital Tremor

ALSO CALLED — congenital loco, jittery chicks, crazy chick disease (not the same as

encephalomalacia, which is also called crazy chick disease)INCIDENCE — rareSystem/Organ Affected— NERVOUS SYSTEMSYMPTOMS — in newly hatched chicks: uncontrolled movements, head tremors,sagging of head until beak touches floor, standing only a short time beforefalling over backward (somersaulting), death due to inability to eat or drinkPERCENTAGE AFFECTED — lowMORTALITY —100 percentPOSTMORTEM FINDINGS — irregularities in muscle, bone, and/or brainRESEMBLES — epidemic, tremor and encephalomalacia, except that congenital

tremor starts at the time of hatchDIAGNOSIS — symptoms

CAUSE — injur)' during hatching or hereditary defect caused by a recessive genetic-trait

TRANSMISSION — does not spreadPREVENTION — cull breeders whose chicks are affectedTREATMENT— none; cullHUMAN HEALTH RISK— noneConjunctivitis

ALSO CALLED—ammonia blindness, keratoconjunctivitisINCIDENCE — common in Hocks raised on deep litter, especially in winterSystem/Organ Affected — EYESIncubation Period — HOURSProgression — ACUTE

454 Contagious Catarrh

SYMPTOMS — in all ages: rubbing eyes with wings, reluctance to move, avoidingsunlight, one or botli eyes cloudy (in case of vitamin A deficiency, nose andeyes water, later become encrusted with white cheesy material), blindnessPERCENTAGE AFFECTED — 80 to 100 percentMORTALITY — variesPOSTMORTEM FINDINGS — none significantRESEMBLES — any mild respiratory diseaseDIAGNOSIS — history (detection of ammonia fumes), symptoms (eye

and eyeliddamage)

CAUSE— ammonia fumes from accumulated droppings, vitamin A deficiency,infection

TRANSMISSION — environmental, does not spread from bird to birdPREVENTION — provide proper nutrition and good ventilation; avoid wet litterTREATMENT — replacing wet litter or correcting vitamin A deficiency in early stages

leads to recovery in about 2 months, but won't reverse blindnessHUMAN HEALTH RISK — squinting in ammonia fumes is no less unpleasant forhumans than it is for chickensContagious Catarrh. See Infectious CoryzaCoryza. See Infectious CoryzaCrazy Chick Disease. SeeEncephalomalacia, Congenital TremorCRD. See Chronic Respirators' DiseaseCrooked Legs. See Twisted LegCrop Binding. See Crop ImpactionCrop Impaction

AI.so CALLED — crop binding, pendulous cropINCIDENCE — rareSYSTEM/ORGAN AITECTED — cropSYMPTOMS — in mature birds: distended, sour-smelling crop filled with feed

androughage (crop feels hard when pressed between fingers),

emaciationPERCENTAGE AFFECTED — up to 5 percentMOR TALITY — limited, deaths due to impaired digestionPOSTMORTEM FINDINGS — sometimes sores in crop liningRESEMBLES — thrush, except that in crop impaction birds appear otherwise healthyDIAGNOSIS — symptomsCAUSE— unknown, possibly genetic susceptibility, injury, fungal infection,

improper fermentation of crop contents, or insufficient rations forcing birds toeat litter or fibrous vegetation that pack the crop until it loses muscle tone and

Dactylariosis 455

cannot empty itselfTRANSMISSION — does not spread from bird to bird

PREVENTION — provide proper rations and plenty of clean, fresh water; if feed iswithheld preparatory to worming, offer a moistened ration 1 hour afterworming

TREATMENT— disinfect skin, slit through skin with very sharp blade, pull skin asideand slit through crop, clean out crop, isolate bird and keep wound clean until itheals

Human Health Risk — NONE

456 Dikkop

Crop Mycosis. See ThrushCrud. See Necrotic EnteritisCryptosporidiostsALSO CALLED — coccidiosisINCIDENCE — not commonSYSTEM/ORGAN AFFECTED— respirator,' (lungs, air sacs), cloaca, cloacal bursaPROGRESSION — acute (lasting 2 to 3 weeks) or chronicSYMPTOMS — in birds 4 to 17 weeks old: no symptoms or pale skin, coughing,sneezing, swollen sinuses, nose and eye discharge, extending neck to breath,silting widi weight on keel, reluctance to move, slow growth; sometimesdiarrheaPercentage Affected—5 TO 25 PERCENTMortality—HIGHPOSTMORTEM FINDINGS — air sacs contain clear, foamy, white, or gray fluid or thick,

white, cheesy material; ceca filled with foamy fluidRESEMBLES — any mild respiratory disease

DIAGNOSIS — laboratory identification of oocysts from moist cotton swab vigor-ously rubbed against windpipeCAUSE — Cryptosporidium baileyi protozoa; usually infect in combination withother respiratory diseases including cholera, chronic respiratory disease,infectious bronchitis, Newcasde, and othersTRANSMISSION— inhaled oocysts from res pirn ton,' discharges and droppings ofinfected birds

PREVENTION — none known other than meticulous sanitationTREATMENT— none known; reduce mortality with supportive therapy (see page

192) and treatment of concurrent infection(s); survivors tire immuneHUMAN HEALTH RISK—none knownCurled-Toe Paralysis. See "Crooked Toes," page 226Cutaneous Pox. See Pox (dry)

- D -DactylariosisAlso Called — DACTYLARIAIncidence—RARESystem/Organ Affected— BRAIN, LUNGSIncubation Period — 6 TO 10 DAYSProgression — ACUTESYMPTOMS — in chicks 1 to 6 weeks of age: tremors, circling, incoordination

Dactylariosis 457

Percentage Affected — UP TO 5 PERCENTMORTALITY— up to 100 percentPOSTMORTEM FINDINGS — granular tumors in brainRESEMBLES — aspergillosis, encephalomalaciaDIAGNOSIS — flock history (age of birds, litter derived from wood), symptoms,

postmortem findingsCAUSE — Dactylaria gallopava fungus contaminating sawdust or shredded treebark used as litter

458 Dikkop

TRANSMISSION — inhaled from moldy litterPREVENTION — avoid moldy litterTREATMENT — cull affected birds and replace litterHUMAN HEALTH RISK—none knownDikkop. See Swollen Head SyndromeDiphtheritic Pox. See Pox (wet)Dermatitis, Necrotic. .See Necrotic DermatitisDermatitis, Vesicular. See ErgotismDropsy. See Broiler Ascites

- E -Egg Binding. Seepage 54Egg Drop Syndrome

Also Called — EDSINCIDENCE — sporadic worldwide, except in North AmericaSYSTEM/ORGAN AFFECTED—reproductiveINCUBATION PERIOD — 7 to 17 claysPROGRESSION — spreads slowly, lasts 4 to 10 weeksSYMPTOMS — in mature hens, especially broiler-breeders and brown-egg

layers:gradual drop in laying up to 40 percent lasting 4 to 10 weeks, eggs with paleshells, thin gritty shells, soft shells, or no shells (hens may eat eggs, making itlook like they are laying less than they actually are)PERCENTAGE AFFECTED—varies greatlyMORTALITY—low

POSTMORTEM FINDINGS — none obvious; inactive ovary and atrophied oviductRESEMBLES — Newcastle and influenza in loss of egg quality, except that in EDSbirds do not appear sick; infectious bronchitis, except bronchitis does notinvolve soft-shelled or shell-less eggsDIAGNOSIS — symptoms (pale-shelled, thin-shelled, soft-shelled, and shell-lesseggs Hearing peak of production); laboratory identification of virus throughblood testing

CAUSE—adenovirus (originally introduced into chicken flocks through Marek'svaccine grown in a medium derived from duck embryos); the virus is primarilycarried by ducks and geese bui does not infect themTRANSMISSION — contact with infected waterfowl or surface water

Dactylariosis 459

contaminatedby them; spread from breeders to chicks through hatching eggs; contact withinfected chickens and their body discharges, especially droppings; contactwith contaminated equipment, particularly cartons for hatching egg storagePREVENTION — good sanitation; breed for resistance; vaccinate birds at 14 to 16weeks of age; avoid flockwide injections or vaccinations using one needle;scrupulous sanitation limits the virus's spreadTREATMENT — none; discard obviously affected eggs; force molt hens to renew

productionHUMAN HEALTH RISK — none known

Encephalomalacia 267

EmphysemaAlso Called — VVINDPUFFIncidence—RARESystem/Organ Affected — RESPIRATORY

SYMPTOMS — bird grows large and round without associated weight gainPercen tage Affected—INDIVIDUAL BIRDS

MORTALITY— only among severely affected birdsPOSTMORTEM FINDINGS — accumulation of air beneath the skinRESEMBLES — no other diseaseDIAGNOSIS — symptoms, postmortem findings

CAUSE— ruptured air sac due to a defect in the respiratory tract or injury due torough handling, caponizing, crash landing while flying, heavy coughing causedby respiratory infectionTRANSMISSION — unknown; often follows brooder house firesPREVENTION — unknown

TREATMENT — release air by puncturing skin with a large hypodermic needle orother sharp instrument

HUMAN HEALTH RISK — none knownEncephalomalaciaAiso CALLED— crazy chick diseaseINCIDENCE — rareSYSTEM/ORGAN AFFECTED — brainPROGRESSION — acute

SYMPTOMS — in chicks 1 to 8 weeks (most commonly 2 to <1 weeks) old: sudden lossof balance with legs outstretched, toes flexed, head pulled in or bent back.Happing wings and falling over, circling, moving head from side to side;sometimes trembling head and legs; paralysis, death— in hens: 15 to 30 percent drop in laying for up to 2

weeksPERCENTAGE AFFECTED— 1 to 10 percentMORTALITY—100 percent in chicks

POSTMORTEM FINDINGS — none or softened, swollen, deteriorated brain with red,brown, or greenish yellow discoloration

Erysipelas 461

Chick stifferingfrom encephalomalacia

462 Encephalomyelitis

RESEMBLES — curled-toe paralysis, except that in curled-toe paralysis toes curlinstead of flex and chicks tend lo walk on their hocks (see "Crooked Toes,"page 226); pyridoxine deficiency, except that in pyridoxine deficiency thenervous activity is much more intense and often ends in death (see "BroodingDeficiencies," page 227)DIAGNOSIS — symptoms, postmortem findings, ration evaluationCAUSE — vitamin E deficiency, often related to selenium deficiencyTRANSMISSION — nutritional, does not spread from bird to birdPREVENTION — use only fresh feed, fortified with vitamin E and containing anti-oxidants; store feed in cool dry place, use within 2 weeks of purchase; do notuse expired vitamin supplementsTREATMENT— successful only if begun before brain is seriously damaged; forchicks: V2 teaspoon vitamin AD&E powder per gallon of water until symptomsdisappear; for older birds: '/1 cc AD&E injected into breast (intramuscular) inaddition to vitamin powder in drinking water; recovered birds may be blind inone or both eyesHUMAN HEALTH RISK— noneEncephalomyelitis. See Epidemic TremorEndemic Fowl Cholera. See Cholera (chronic)Endemic Newcastle. See Newcastle DiseaseEnlarged Hock Disease. See Infectious SynovitisEnteric Campylobacteriosis. See CampylobacteriosisEnteritis. See Bluecomb. Colibacillosis, Infectious Stunting Syndrome, Necrotic

Enteritis, Rotaviral Enteritis, Ulcerative EnteritisEnterohepatitis. See BlackheadEnterotoxemia. SeeNecrotic EnteritisEpidemic Tremor

At.so CALLED — avian encephalomyelitis, AF., encephalomyelitis, infectious avian

encephalomyelitis, New England disease, star-gazing syndromeINCIDENCE — worldwide but rare; more often in large commercial flocks in winter

and springSYSTEM/ORGAN AFFECTED — nervous systemINCUBATION PERIOD — 5 to 40 days [9 to 21 average)PROGRESSION — rapid, lasts 21 to 3D days in mature birdsSYMPTOMS — in I - to 3-week-old chicks: dull eyes followed by lost coordination,jerky or irregular gait, inability to stand, sitting 011 hocks, falling over

Erysipelas 463

withoutstretched wing, weak peeping; sometimes periodic vibration of the headand neck and "buzzing" sound when chick is held; death due to inability to eator to being trampled hv other chicks

— in mature hens (symptoms easily go unnoticed): 5 to 10 percent drop inegg production for 2 weeks, poor hatchability of eggs, poor livability of chicksPERCENTAGE AFFECTED — 40 to 60 percentMORTALITY— in chicks: 25 percent average, may be as high as 90 percent

inmature birds: none

POSTMORTEM FINDINGS — none obviousRESEMBLES — congenital tremor, except that congenital tremor affects

chicks from

464 Encephalomyelitis

the time of hatch; encephalomala-cia, except that encephalomalacia

usually affects older chicks; Marek'sdisease, except that Marek's usuallyaffects much older birds; Newcastle,encephalitis (bacterial, fungal, ormycoplasmal), rickets, deficiency ofriboflavin or vitamin A or E, salt orpesticide poisoning (see "Poisoning,page 139)DIAGNOSIS — history (age of birds),

symptoms, confirmed by laboratory, Chick dead Irom epidemic tremorprocedures J

CAUSE — picornavirus that survives for up to 4 weeks in droppings

TRANSMISSION — contact with infected birds or their droppings; spread frominfected breeders through hatching eggs; spread by turkeys, pheasants,coturnix quail; spreads on used equipment; spread by ticksPREVENTION — cull breeders whose chicks are affected; vaccinate breeder pulletsover 8 weeks of age, but at least 4 weeks before production startsTREATMENT— none; chicks may survive but should be culled since they will neverbe good layers or breeders; survivors of an adult outbreak becomc immuneand are not carriersHuman Health Risk — NONE KNOWN

ErgotismALSO CALLED — sod disease, vesicular dermatitisINCIDENCE — worldwide but rareSYSTEM/ORGAN AEEECTED — endocrine, nervous, blood vesselsSYMPTOMS — in all ages: listlessness; loss of appetite; increased thirst; diarrhea;convulsions; bluish, wilted, cold comb that eventually shrivels: abnormalfeadiering; sores on legs, shanks, and tops of toes; slow growth; low eggproductionPERCENTAGE AFFECTED — lowMORTALITY — 25 percentPOSTMORTEM FINDINGS — inflamed intestinesRESEMBLES — mycotoxicosis resulting from trichothecene poisons generated byFusarium spp in corn, barley, brewer's grains, oats, sorghum, and safflowerseedDIAGNOSIS — flock history (fed moldy grains), symptoms, feed analysisCAUSE — toxic alkaloids produced by Clautcepspurpurea fungus in stored wheat,rye, and other cereal grainsTRANSMISSION — contaminated grain and grass seed, particularly ryePREVENTION — use commercially prepared, pelleted feedsTREATMENT— replace contaminated feedHUMAN HEALTH RISK — humans may be poisoned by eating contaminated

grainErysipelas

ALSO CALLED — Erysipelothrix infection

465 Erysipelothrix Infection

INCIDENCE — worldwide but rare in chickens; most likely to occur in cool monthsSYSTEM/ORGAN AFFECTED — entire body (septicemic)INCUBATION PERIOD — shortPROGRESSION — acute, sometimes followed by chronic infection

SYMPTOMS — usually in growing free-ranged cocks: listlessness, loss of appetite,greenish-yellow diarrhea; sometimes nasal discharge and/or breathingdifficulties, lameness due to swollen joints, purple blotches on skin; suddendeath

— in cocks: reduced fertility— in hens: up to 70 percent drop in egg

productionPERCENTAGE AFFECTED—up to 40 percentMORTALITY — nearly 100 percentPOSTMORTEM FINDINGS — none significant or small blood spots in almost

any tissueor organ; swollen liver, kidney, spleen; yellow nodules in ceca; pus surround-ing swollen joints

RESEMBLES — cholera, except that cholera does not cause enlarged spleen;

chlamydiosis, colibacillosis, Newcastle, salmonellosis, streptococcosisDIAGNOSIS — flock history (age and sex, presence of wounds, birds ranged on landthat once held turkeys, pigs, or sheep), symptoms (sudden losses amongapparently healthy cockerels), postmortem findings (blood-spotted breastmuscle), confirmed by laboratory identification of bacteriaCAUSE — Erysipelothrix rhusiopathiae bacteria that survives for many years inalkaline soil and is resistant to disinfectants; affects turkeys more often thanchickens; often follows stress due to overcrowding, dampness, bad weather,poor sanitation, ration change, vaccinationTRANSMISSION — bacteria in soil from droppings of infected chickens (or turkeys,pigs, or sheep) enters through wounds caused by fighting, cannibalism, orpoorly designed equipment; bacteria ingested from soil, water, or meat(cannibalism)PREVENTION— breed for genetic resistance; in erysipelas-prone areas,

keepchickens away from range previously occupied by turkeys, pigs, or sheep;avoid crowding; control rodents

466 Favus

TREATMENT — since disease poses human health risk, eliminate infected Hock andstart over on fresh ground; otherwise, move birds to clean environment (willcontrol losses but contaminate new ground); add sodium or potassiumpenicillin to drinking water at the rate of 1,000,000 IU per gallon for 5 days;survivors are resistant to future infection, but may be carriersHUMAN HEALTH RISK — painful infection that can be serious to fatal withoutmedical attention; see "Erysipeloid," page 230Erysipelothrix Infection. See ErysipelasEscherichia coli Infections. See Air-Sac Disease. Chronic Respiratory Disease,

Colibacillosis, Omphalitis, Swollen Head DiseaseEuropean Fowl Pest. See InfluenzaExotic Newcastle Disease. See Newcastle Disease (exotic)Exudative Diathesis

ALSO CALLED — exudate diathesis

Fatly Liver Syndrome 271

Incidence—RARESYSTEM/ORGAN AFFECTED—skin and muscle tissueSYMPTOMS — in chicks 1 to 4 weeks old: breast and legs look greenish

blue, chicksstand with legs far apart due to fluid under skin,

paralysisPERCENTAGE AFFECTED— L to 5 percentMORTALITY —100 percentPOSTMORTEM FINDINGS — yellow or bluish green gelatinous fluid under skin;

bloodspots in breast and leg muscles

DIAGNOSIS— symptoms, postmortem Findings, ration evaluationCAUSE — vitamin E deficiency, usually related to selenium deficiency; sometimes

occurs in combination with white muscle diseaseTRANSMISSION — nutritional problem, does not spread from bird to birdPREVENTION — use only fresh feed fortified with vitamin E and selenium; store feed

in cool dry place and use within 2 weeks of purchaseTREATMENT—vitamin F. and selenium supplement in feed or orally (300IU per

bird); replace old feedHUMAN HEALTH RISK — none

- F -Facial Cellulitis. See Swollen I lead SyndromeFalse Botulism. See Marek's DiseaseFata) Syncope. See Sudden Death SyndromeFatty Liver Syndrome

ALSO CALLED — fatly liver and kidney syndrome, FLKS, pink diseaseINCIDENCE— sporadic worldwideSYSTEM/ORGAN AFFECTED — liverPROGRESSION — chronicSYMPTOMS — in commercial broiler chicks: depression, ruffled feathers,

inability tostand

— in mature hens, particularly in warm weather: sudden death (sometimesafter puncture from cock's toenails) or sudden drop in laying to about 50percent, diarrhea; sometimes overweight (25 to 35 percent above normal);enlarged, pale combs and wattlesPERCENTAGE AFFECTED — 1 to 5 percent, depending on dietMORTALITY — less than 5 percent (dead birds have pale heads)POSTMORTEM FINDINGS — excess body fat, often pink; mushy yellow, greasy liver;pale, yellowish heart; dark, smelly matter in small intestine; sometimes

468 Favus

largeblood clots in abdomen (called "fatly liver-hemorrhagic syndrome" or "FLHS")RESEMBLES — campylobacteriosisDIAGNOSIS — flock history, symptoms, postmortem findings

CAUSE — unknown; may be genetic; may be caused by molds in feed or water thatdamage liver; may be caused by high stress due to heat, high egg production,inapparent disease; may be due to biotin deficiency, perhaps caused bydisease thai increases biotin requirement; often associated with high-energyfeeds combined with inactivityTRANSMISSION — nutritional, does not spread from bird to bird

PREVENTION — avoid moldy or high-energy feeds (consisting mostly of grains),raise birds on litter with room for activity; provide good ventilation to preventheat stress

TREATMENT— none effective; restrict feed consumption; substitute wheat bran forpart of corn; feed brewer's yeast, dried molasses, or alfalfa and other greenleafy plants; oral or injectable biotin supplementHUMAN HEALTH RISK — noneFavus

Also Called — WHITE COMBIncidence— RARE IN NORTH AMERICASystem/Organ Affected — COMBProgression — SPREADS SLOWLYSYMPTOMS — in growing and mature cocks with well-developed combs,

usually olthe Asiatic breeds: grayish white patches 011 comb that scale off (comb looksdusted with flour), ihicken, and join to form a wrinkled crust that smellsmoldy; sometimes crust spreads to unfeathered areas creating honeycombappearance where feathers are lost, soon followed by depression, weakness,emaciation, and deathMORTALITY — rare

POSTMORTEM FINDINGS — spots, nodules, and yellowish cheesy deposits in diges-tive and upper respiratory tractsRESEMBLES — mites, skin disorders due to poor nutritionDIAGNOSIS — symptomsCAUSE— Microsporum gallinae fungus

TRANSMISSION — contact with infected birds or sloughed-off scalesPREVENTION — improve nutrition and sanitation; breed for resistanceTREATMENT— most birds recover in a few months without treatment; recoverymay be hastened with daily liberal applications of anti-fungal or mangemedication (for pels) until symptoms disappearHUMAN HEALTH RISK — scalp infectionFlip-Over Disease. See Sudden Death SyndromeFood Poisoning. See BotulismFowl Cholera. See Cholera (acute), Cholera (chronic)Fowl Diphtheria. See Pox (wet)Fowl Pest. See InfluenzaFowl Plague. See InfluenzaFowl Pox. See Pox (dry)Fowl Spirochetosis. See SpirochetosisFowl Typhoid. See TyphoidFusariotoxicosis

470 Favus

ALSO CALLED — trichothene mycotoxicosisINCIDENCE — worldwide in temperate zones, but rareSYSTEM/ORGAN AFFECTED — digestive system and skinINCUBATION PERIOD — accumulativePROGRESSION—acuteSYMPTOMS— in birds of all ages: refusal to eat, slow growth, abnormal feathering,

Gout (visceral) 273

depression, bloody diarrhea, sores at corners ol month and on skin, reducedresistance to respiratory diseases— in hens: sudden drastic drop in egg production, thin

shellsPERCENTAGE AFFECTED — highMORTALITY — low

POSTMORTEM FINDINGS — sores in upper digestive tract, reddening throughoutdigestive tract, mottled liver, shriveled

spleenDIAGNOSIS — symptoms and feed analysisCAUSE — trichothecene (type T-2) toxins produced by Fiiscniuin sporoirichioides

and other fungi in wheat, rye, millet, barley, corn, safflower seedsTRANSMISSION — poisoning clue to eating contaminated feed; burning of skin

coming into contact with caustic toxinsPREVENTION — use commercially prepared pelleted feedTREATMENT — replace moldy feedHUMAN HEALTH RISK — serious diarrhea from eating same contaminated

grainsthat poison chickens

- G -Gangrenous Cellulitis/Dermatitis/Dermatomyositis. See Necrotic Dermatitis

Gapes. See "Gapeworm," page 88Gas Edema Disease. See Necrotic DermatitisGout (articular)

INCIDENCE — sporadicSystem/Organ Affected — EXCRETORY SYSTEMIncubation Period — LONGProgression — CHRONICSYMPTOMS — in all ages: enlarged foot joints with pasty while urate deposits easily

seen through the skinPERCENTAGE AFFECTED — individual birds onlyMORTALITY — nonePOSTMORTEM FINDINGS — white tissue surrounding joints, white semi-fluid

deposits within jointsRESEMBLES — no other diseaseDIAGNOSIS — symptoms, postmortem findingsCAUSE — abnormal accumulation of urates in the body due to kidney

damage,excessive protein in diet, or hereditary

susceptibilityTRANSMISSION — genetic and/or related to nutritionPREVENTION—none known

472 Favus

TREATMENT— none knownHUMAN HEALTH RISK — noneGout (visceral)

ALSO CALLED — acute gout, nephrosis, renal failure, renal gout, gout (visceral),

visceral urate depositionINCIDENCE — not common in North AmericaSYSTEM/ORGAN AFFECTED — kidneysINCUBATION PERIOD— 14 days or more

473 Gray Eye

Progression — ACUTESYMPTOMS — in chicks: flockwide deaths soon after hatch

— in mature birds: sudden death or depression, weight loss, darkened headand shanks, white pasty diarrhea, cessation of laying, attempting to hidePERCENTAGE AFFECTED — 1 to 5 percentMORTALITY — 2 to 4 percent per month, usually totaling no more than 50

percentbut can be up to 100 percent

POSTMORTEM FINDINGS — diy, shrunken breast muscles; both kidneys shriveled orone shriveled and one pale and swollen; chalky white needle-like crystals inkidneys and on surfaces of liver, abdominal fat, keel, and in jointsRESEMBLES — any inflammation of the kidneysDIAGNOSIS — symptoms, postmortem findingsCAUSE— kidney failure due to inability to excrete urates for unknown

reasons;possibly due to genetic defect, kidney damage from disease, water deprivation,fungal toxins, excessive dietary protein (30 to 40 percent), excess calcium (3percent or more), excess sodium-bicarbonate, calcium-phosphorus imbal-ance, vitamin A deficiency; sometimes follows bluecomb; often follows kidneydamage due to infectious bronchitisTRANSMISSION — does not spread from bird to bird

PREVENTION — provide plenty of pure drinking water, cool in summer and warm inwinter; feed balanced, commercially prepared rations; avoid excessively highprotein rations

TREATMENT— none if problem is genetic, otherwise improve nutritionHUMAN HEALTH RISK— noneGray Eye. See Marek's DiseaseThe Greens. See BluecombGumboro Disease. See Infectious Bursal Disease

- H -Heart Attack. See Sudden Death SyndromeHelicopter Syndrome. See Infectious Stunting SyndromeHelminthiasis. See "Internal Parasites: Worms" (chapter 5)Hemophilus Infection. See Infectious CoryzaHemorrhagic Anemia Syndrome. See Infectious AnemiaHepatitis. See Blackhead. Campylobacteriosis. Infectious AnemiaHistomoniasis. See BlackheadHistoplasmosis

474 Infectious Avian Encephalomyelitis

INCIDENCE — worldwide but rare, in North America found only along Mississippi,

Missouri, and Ohio riversSYSTEM/ORGAN AFFECT ED — entire bodyINCUBATION PERIOD — 2 weeksPROGRESSION — acute or chronicSYMPTOMS — all ages: emaciation, sometimes diarrheaPERCENTAGE AFFECTED — lowMORTALITY —100 percentPOSTMORTEM FINDINGS — mushy liver and spleen

Infectious Anemia 275

DIAGNOSIS — laboratory identification of fungusCAUSE — Histoplasma capsulatum fungus that proliferates in soil rich with the

droppings of chickens and other birdsTRANSMISSION — inhaled fungiPREVENTION — keep area free of dry accumulations of droppings from starlings

and other birdsTREATMENT —

noneHUMAN HEALTH RISK — possible respiratory infection from inhaled dust, see

"Histoplasmosis," page 233

-1 -IBD. See Infectious Bursal DiseaseInclusion Body Hepatitis. See Infectious AnemiaInfectious Anemia

ALSO CALLED — adenoviral infection, aplastic anemia, chicken anemia agentinfection, CAA infection, hemorrhagic anemia syndrome, HAS, hemorrhagicdisease, hemorrhagic syndrome, inclusion body hepatitis, IBMINCIDENCE — common in major chicken-producing countries, especially in

commercial broiler flocks raised on reused litterSYSTEM/ORGAN AFFECTED — bloodINCUBATION PERIOD — 3 daysPROGRESSION — acute, sudden onset with rapidly increasing deaths;

lasts about 3weeks

SYMPTOMS — in growing broilers, 3 to 20 weeks old (most often 5 to 9 weeks):sudden deaths of apparently healthy birds or depression, huddling, ruffledfeathers, drawn-in head, pale comb, wattles, skin, and legs; sometimesdiarrhea (may be bloody); death or recoveiy within 2 daysPERCENTAGE AFFECTED — usual ly lowMORTALITY — 5 to 10 percent average, may be up to 40 percent during first 5 daysPOSTMORTEM FINDINGS — enlarged, pale, dull greenish, yellow, or tan liver mottledwith red spots; bright red, watery blood; pale, yellow, fatty bone marrow;swollen, blood-filled kidneys tinged with yellow; pale muscles with pinpoint-sized bloody spots in muscles and organs; shriveled spleen and cloacal bursa


RESEMBLES — coccidiosis, infectious bursal disease, ulcerative enteritis, poisoning;aflatoxicosis, except that chickens are unlikely to be exposed to high enoughdoses of aflatoxin to produce these symptomsDIAGNOSIS — flock history, symptoms (sudden deaths without symptoms),postmortem findings (fatty bone marrow, liver appearance), microscopicexamination of liverCAUSE — unknown, possibly an adenovirus and/or a parvovirus called "chickenanemia agent;" may be related to vitamin K deficiency and/or drug toxicity(especially sulfa drugs); often found in combination Willi or following infec-tious bursal disease and/or secondary bacterial or fungal infectionsTRANSMISSION — ingesting bacteria from droppings of infected birds; spreads frombreeders to chicks through hatching eggs; contaminated litter or equipment(especially hatching-egg cartons)

PREVENTION — healthy birds in clean surroundings develop natural immunity afterabout 3 weeks of age; do not hatch eggs from breeders whose previous chickshad infectious anemia; vaccinate breeder flock for infectious bursal disease;avoid chilling, vaccinating, or prolonged use of sulfonamides in young birds;thoroughly clean contaminated facilities with disinfectant containing iodineTREATMENT— none other than supportive therapy (see page 192) including asupplement containing trace minerals and vitamins B and K; avoid coccid-iostats, which increase the disease's severity; treatment with antibiotics orsulfa drugs may worsen the diseaseHUMAN HEALTH RISK — none knownInfectious Avian Encephalomyelitis. See Epidemic TremorInfectious Bronchitis

ALSO CALLED — avian infectious bronchitis, IB, mild coldINCIDENCE — common worldwideSYSTEM/ORGAN AFFECTED — respiratoryINCUBATION PERIOD — 18 to 36 hoursPROGRESSION — acute, starts suddenly, spreads rapidly, runs through flock

in 24 to48 hours, individuals recover in 2 to 3 weeks

SYMPTOMS — in birds of all ages: gasping, coughing, sneezing, rattling, wet eyes,nasal discharge

— in young and growing birds: watery nasal discharge, huddling near heal,loss of appetite, slow growth; sometimes swollen sinuses

— in maturing birds: sometimes swollen wattles— in hens: sharp drop in laying to near zero, eggs with soft, thin,

mis-shapen, rough, or ridged shells and watery whites

Percentage Affected—100 PERCENTMORTALITY — limited in older birds; 25 percent in chicks, but can be

up to 90percent, especially in cold weather and/or in the presence of a secondarybacterial infection

POSTMORTEM FINDINGS — in chicks: yellowish cheesy plugs in lliroat; swollen, palekidneys

— in growing and mature birds: swollen, pale kidneys; urate crystals intubes leading from kidneys; fluid yolk or whole eggs in abdominal cavity ofhens


RESEMBLES — infectious laryngotracheitis, except that laryngo spreads less rapidlyand is more severe; Newcastle, except that Newcastle is more severe, producesa greater drop in egg production, and can cause nervous symptoms; infectiouscoryza, except that coryza often has a foul odor and produces facial swelling(bronchitis rarely does): egg drop syndrome, except that EDS does not causerunny egg whites; nutritional roup, except that roup does not affect egg whitesor shells

DIAGNOSIS — difficult; symptoms, laboratory identification of virusCAUSE — several strains of coronavirus that survive no more than one week offchickens and are easily destroyed by disinfectants; infects only chickens,which vary in susceptibility among breeds and strainsTRANSMISSION — the most contagious poultry disease; spreads by contact with

Infectious Bursal Disease 111

infected birds or their respiratory discharges; spreads on contaminatedequipment; travels over 1.000 yards through airPREVENTION — defies good management; avoid mixing birds of different ages orfrom different sources; vaccinate with strain(s) of virus found locally (infec-tious bronchitis may still occur due to a different or new strain of virus); beprepared to treat with broad-spectrum antibiotic if signs of air-sac diseasefollow vaccination; hens that have a strong reaction to vaccine may never lay wellTREATMENI —electrolytes in drinking water (see page 193); keep birds warm andwell fed; avoid crowding; watch for secondary bacterial infection, particularlyair sac disease; survivors are permanently immune but become carriers (hensreturn to production in 6 to 8 weeks, but may never produce the same eggquality or quantity as before due to permanent ovary damage)HUMAN HEAI.TU RISK— none known, a different virus causes bronchitis in humansInfectious Bursal DiseaseALSO CALLED — Gumboro disease, 1BD

INCIDENCE—common worldwide (except in New Zealand), primarily in largellocks

SYSTEM/ORGAN AFFECTED— lymph tissue, especially cloacal bursaINCUBATION PERIOD — 1 to 3 daysPROGRESSION — acute, appears suddenly, spreads rapidly, runs through

flock in 1to 2 weeks

SYMPTOMS — in young birds 3 to 18 weeks old (most often broilers 3 to 6 weeksold): droopiness, ruffled feathers, vent picking (bird picks at own vent),straining while trying to eliminate, whitish or watery (sometimes blood-tinged)diarrhea staining feathers below vent (making litter sticky), slight trembling,loss of appetite, dehydration, incoordination, fever followed by drop in bodytemperature lo below normal, prostration, deathPERCENTAGE AFFECTED — nearly 100 percent

MORTALITY — 0 to 30 percent, peaking within a week; greater in Leghorns than inheavy breeds, in chicks fed 24 percent protein starter, and in birds infected

Infectious Bursal Disease 111

with bronchitis, Newcastle, or cecal coccidiosisPOSTMORTEM FINDINGS — none significant or dark, shriveled breast muscles fleckedwitli bloody streaks; mucus-filled intestine; cloacal bursa may be yellow, pink,red, or black, swollen, oblong-shaped, filled with creamy or cheesy material,and surrounded by gelatinous film (as the disease progresses, the bursareturns to normal size, then shrinks and shrivels up); swollen spleen coveredwith gray dots; birds that die from infection have swollen, pale kidneysRESEMBLES — coccidiosis, except that cocci does not cause bloody flecks inmuscles or swelling of cloacal bursa

DIAGNOSIS — flock history (age of birds, rapid onset, number of birds involved),symptoms (white or watery diarrhea, birds picking own vents, deaths peakingwithin a week, rapid rec overy), postmortem findings (swollen or shriveledcloacal bursa)

CAUSE — birnavirus that affects primarily chickens and is common in every majorpoultry-producing area; survives in feed, water, and droppings for weeks andin housing for at leasl 4 months after removal of infected birds

278 Infectious Catarrh

TRANSMISSION — highly contagious; spread from infected birds through theirdroppings in contaminated litter and dust in air, and on equipment, feed,shoes, insects, rodents, and wild birds; may be spread by darkling beetle, orlesser mealworm (Alphitobius diaperinus) found in litterPREVENTION — good sanitation helps but virus defies good management and isdifficult to eradicate; vaccinated breeders pass temporary immunity to theirchicks; natural immunity develops in chicks exposed to infection before theage of 2 weeks; vaccinate only where disease is prevalentTREATMENT— none; keep birds warm and well ventilated and provide plenty ofdrinking water; recovered chickens are more susceptible to other diseases andmay not develop immune response to vaccines, especially Marek'sHUMAN HEALTH RISK — none knownInfectious Catarrh. See Infectious CoryzaInfectious Coryza

ALSO CALLED — cold, contagious catarrh, coryza, hemophilus infection, infectiouscatarrh, IC, roup

INCIDENCE — common worldwide, particularly in fall and winter in tropical andtemperate climates (southeastern United States and

California)SYSTEM/ORGAN AFFECTED — respiratoryINCUBATION PERIOD — 1 to 3 daysPROGRESSION — acute and spreads rapidly or chronic and spreads slowly

SYMPTOMS — in chicks at least 4 weeks old: depression, nasal discharge, facialswelling, one or both eyes closed, death

— in growing and mature birds (most likely group affected): watery eyeswith eyelids stuck together, reddish foul-smelling discharge from nose, drop infeed and water consumption, drop in egg production, swollen face, eyes, andsinuses; sometimes diarrhea, rales or wheezingPERCENTAGE AFFECTED — high (more in an acute outbreak than in a chronic

outbreak)MORTALITY — lowPOSTMORTEM FINDINGS — thick, grayish fluid, or yellowish solid material in

nasalpassages

Face swollen with infectious coryza

280 Infectious Leukemia

Infectious Laryngotracheitis 279

RESEMBLES — cholera, except that coryza causes facial swelling; chronic respiratorydisease, infectious laryngo tracheitis, Newcastle, nutritional roup, infectiousbronchitis, influenza, except that coryza produces a characteristic odorDIAGNOSIS — symptoms (facial swelling, characteristic odor], laboratory identifica-tion of bacteriaCAUSE — Haemophilus paragallinarum bacteria that do not survive long in theenvironment and are easily destroyed by disinfectants; often found in combi-nation with chronic respiratory disease, cholera, pox, infectious bronchitis, orinfectious laryngotracheitisTRANSMISSION — contagious; contact with infected or carrier birds and their nasal

or respiratory discharges in dust, drinking water, or feedPREVENTION — avoid combining birds from different flocks and of different agegroups; remove infected birds, disinfect, and leave housing vacant for3 weeksbefore bringing in new birds; vaccinate only if the disease has been positivelyidentified; vaccinated breeders pass temporary immunity to their offspring;after an outbreak, clean and disinfect housing and leave vacant for a few daysTREATMENT — erythromycin (Gallimycin), streptomycin IVetstrep), sulfadimeth-oxine; disease may recur after treatment is discontinued; culling is preferablesince survivors (including all birds in the flock) may be carriersHUMAN HEALTH RISK — none knownInfectious Enterohepatitis. See BlackheadInfectious Hepatitis. See CampylobacteriosisInfectious Laryngotracheitis

A1.S0 CALLED — avian diphtheria, ILT, laryngo, LTINCIDENCE — common worldwideSYSTEM/ORGAN AFFECTED — upper respiratory tractINCUBATION PERIOD — 6 to 12 daysPROGRESSION — acute, spreads slowly, most birds die or recover within 2

weeks,runs through flock in 2 to 6 weeks

SYMPTOMS — in maturing or mature birds (mild infection): watery inflamed eyes,swollen sinuses, nasal discharge, drop in egg production, unthriftiness

— in maturing or mature birds (acute infection): nasal discharge, coughing(sometimes producing bloody mucus that gets on face or featilers), headshaking, breathing through mouth, gasping (neck extended during inhale,head on breast during exhale), choking, gurgling, rattling, whistling, or"cawing," swollen sinuses and wattles, watety eyes, drop in egg production,soft-shelled eggs

PERCENTAGE AFFECTED—5 percent in mild case, 90 to 100 percent in acute infectionMORTALITY — 10 to 20 percent average, can be up to 70 percent in acute infection;

least in young birds during wann weather, greatest in layers during winterPOSTMORTEM FINDINGS — swollen windpipe clogged with bloody mucus or a cheesyplug

RESEMBLES — infectious bronchitis, except that laryngo spreads less rapidly and ismore severe; Newcastle, except that laryngo does not cause nervous symp-toms; pox (wet), except that laryngo does not produce facial sores; swallowedfeed-sack string wrapped around tongue, except that string affects only one

282 Infectious Leukemia

bird at a time; gapeworm, except that in laryngo birds die more quickly with noworms in throat

DIAGNOSIS — flock history, symptoms (coughing up blood, high death rate),

postmortem findings, confirmed by laboratory proceduresG\USE— a herpes virus that affects primarily chickens and pheasants and does

not live long off the birdTRANSMISSION — highly contagious; inhaled virus from infected or carrier birds orcontaminated litter; can be spread on equipment or the feet of rodents, dogs,and humansPREVENTION — flock isolation and scrupulous sanitation; do not mix

vaccinated orrecovered birds with others; vaccinate //laryngo is common in your area, youshow your chickens in areas where it is common, you regularly bring in newadult birds, or you frequently visit with chicken-keepers from laryngo-prevalent areas

TREATMENT — none, cull; vaccination keeps disease from spreading and survivorsare immune, but survivors (and vaccinated birds) are carriers; disinfecthousing and leave it empty for 6 weeks; this is a reportable disease in manystates, see "Reportable Diseases" page 196HUMAN HEALTH RISK—none knownInfectious Leukemia. See TyphoidInfectious Sinusitis. See Chronic Respiratory DiseaseInfectious Stunting Syndrome

ALSO CALLED — broiler runting syndrome, ISS, malabsoiption syndrome, pale bird

syndrome, split-wing syndrome, stunting syndrome, helicopter syndromeINCIDENCE — increasingly more common in die United States, Europe, and AustraliaSYSTEM/ORGAN AFFECTED — digestiveINCUBATION PERIOD — 1 to 13 daysPROGRESSION — chronicSYMPTOMS — in 1 - to 6-week-old birds (primarily intensively raised

broilers):uneven or seriously stunted growth (chicks reach only half their normal size by4 weeks of age), pale skin, slow feather development; sometimes protrudingabdomen, undigested feed in droppings, diarrhea, increased thirst; lamenessand/or reluctance to walk (when disease occurs in combination

with viralarthritis or osteoporosis)PERCENTAGE AFFECTED — 5 to 20 percentMORTALITY — less than 6 percent, peaking early

POSTMORTEM FINDINGS — enlarged, sometimes bloody stomach (proventriculus);pale, distended intestines; small intestine filled with poorly digested feed;sometimes thin, white, fibrous pancreasRESEMBLES — infectious anemia, runting syndromeDIAGNOSIS — symptoms, postmortem findings

GUISE — unknown, possibly due to a combination including one or morercoviruses and/or bacteria and/or fungal toxins; may occur in combinationwith encephalomalaciaTRANSMISSION — unknown; possibly transmitted by inhaling or ingesting virus gen-erated by infected birds; or spread from infected breeders through hatching eggs

284 Influenza

Infectious Synovitis 281

PREVENTION — unknown; avoid crowd-ing and practice good sanitationTREATMENT — unknown; following anoutbreak, thoroughly clean anddisinfect housing with lye or0.5percent organic iodine solutionHUMAN HEALTH RISK — none knownInfectious Synovitis. See alsoColibacillosisALSO CALLED — enlarged hock disease,Mycoplasma synoviae infection, MS(one form of mycoplasmosis)INCIDENCE—worldwide but notcommon except in large commercialflocks, especially in cold, damp weatherSYSTEM/ORGAN AFFECTED— joints, sometimes upper respiratory tractINCUBATION PERIOD — II to 21 days

PROGRESSION — usually acute with slow recovery in young birds, chronic in older

birds (survivors of acute form become chronic)SYMPTOMS — in growing broilers, 4 to 12 weeks old: no signs or slow growth,lameness, pale comb, followed by depression, ruffled feathers, shrunkencomb, hunkering around feeders and waterers, emaciation; sometimesswollen hocks, shanks, and foot pads (swollen areas feel hot), breast blisterfrom squatting on floor, slight rales, bluish comb, green droppings cappedwith large amounts of white urate depositsPERCENT AFFECTED—usually 100 percent, bu t only 15 to 20 percent have symptomsMORTALITY — up to 10 percent (usually due to secondary infection)POSTMORTEM FINDINGS — creamy yellowish or grayish fluid (acute) or thick orangeyellow matter (chronic) in joints, keel, and fool pad; swollen, mottled, palekidneys; enlarged, greenish liverRESEMBI.ES — staphylococcic or viral arthritis, except that infectious synovitis

more often involves wing joints and produces breast blistersDIAGNOSIS — flock history, symptoms, postmortem findings, blood tests, labora-tory identification of bacteriaCAUSE — Mycoplasma synoviae bacteria, often infecting following stress due toNewcastle or infectious bronchitis; may be caused by Escherichia coli, in whichcase some birds recover in about a week, others remain infected

and becomeemaciated

TRANSMISSION — inhaling bacteria from infected or carrier birds; spread by

breeders through hatching eggsPREVENTION — keep litter dry; do not combine birds from different sources;

acquire only MS-free stock; hatch eggs only from MS-free breeders; blood testand remove positive reactors; vaccinate where infection is prevalent (expensive)TREATMENT — none effective; aureomycin or terramycin in water or streptomycin

by intramuscular injection may help, but survivors may be carriersHUMAN HEALTH RISK — none known

Leg swollen with infectious synovitis

286 Influenza

InfluenzaALSO CALLED— avian flu, avian influenza, AI, bird flu, European fowl pest,

fowl plagueINCIDENCE — worldwide, but serious outbreaks are rareSYSTEM/ORGAN AFFECTED — primarily respiratory, sometimes involves diges-tive and nervous systemsINCUBATION PERIOD — a few hours to 3 daysPROGRESSION — acute, spreads rapidly, runs through flock in 1 to 3 daysSYMPTOMS — in birds of all ages: sudden death without signs, or severe de-pression, droopiness, coughing, sneezing, rattling, watery eyes, huddling,ruffled feathers, loss of appetite, weight loss, reduced fertility, suddendrop in egg production, increased broodiness, eggs with soft or no shells,skin hemorrhages, fever; sometimes bloody nasal discharge, greenishdiarrhea, darkened head, comb, wattles, and/or swollen eyes, comb, andwattles; sometimes twisted neck, loss of coordination, paralysis of legs orwings, swollen hock joints, purplish shanks; rapid deathsPERCENTAGE AFFECTED — 100 percentMORTALITY — 0 to 100 percent, usually lowPOSTMORTEM FINDINGS — none obvious; mild form: cheesy plugs in

sinuses,throat, air sacs, oviduct— severe form: large and small reddish brown spots or blotches (hemor-rhages) along the interior of the upper and lower digestive tract, on theovaries, and over the fat of the abdomen; straw-colored fluid beneath skinof face; enlarged blood vessels; loose gizzard lining

RESEMBLES — mild form: infectious bronchitis, chlamydiosis, chronic respira-tory disease, Newcastle— severe form: acute cholera, exotic Newcastle, infectious

laryngotracheitisDIAGNOSIS — symptoms (high rate of rapid deaths), confirmed by laboratory

identification of virusCAUSE — several strains of type A influenza orthomyxoviruses, some mild,some lethal, that affect a wide variety of bird species but do not survivelong in the environment; often infect in combination with a bacterial ormycoplasmal diseaseTRANSMISSION — highly contagious; contact with infected birds (either do-mestic or wild) and their body discharges, especially droppings; spreadsihrough improper disposal of infected birds and their manure, on con-

taminated equipment and the feet of insects, rodents, and humansPREVENTION — during a local outbreak do not visit flocks or let people visityour flock; keep chickens indoors away from wild birds and water fre-quented by wild waterfowl; consult your vet about the availability of avaccine against the virus responsible for the outbreakTREATMENT — mild form: antibiotic to prevent secondary bacterial or my-coplasmal infection; survivors are immune for several months but arecarriers

— severe form: this is a reportable disease, see page 196HUMAN HEALTH RISK— the severe (highly pathogenic) form has the

potentialfor causing infection in humans and other mammals, but rarely does

288 Influenza

Leucocytozoonosis 283

Iritis. See Marek's Disease

- I -Jittery Chicks. See Congenital Tremor

- K -Keel Bursitis. See Breast BlisterKeel Cyst. See Breast BlisterKeratoconjunctivitis. See

ConjunctivitisKinky BackALSO CALLED — spondylolisthesisINCIDENCE— common in broiler

llocks Broiler with kinky backSYSTEM/ORGAN AFFECTED — joints or

vertebraeSYMPTOMS — in broilers 3 to 6 weeks of age: arched back, extended neck, squattingwith weight on hocks and tail, feet off the ground, struggling backward onbocks to move around (backpedaling), sometimes falling over with inability toget up, paralysisPERCENTAGE AFFECTED — 2 percentMORTAIJTY—100 percent (due to dehydration)POSTMORTEM FINDINGS — deformed spinal columnRESEMBLES — any crippling condition including infection that causes

swelling andpressure to the spinal cord

DIAGNOSIS — symptoms (few birds involved at once)CAUSE — unknown, possibly hereditary; rapid growth causes vertebrae to

twistand pinch the spinal cord

TRANSMISSION — genetic and/or feed related, does not spread from bird to birdPREVENTION — breed for resistance; do not feed for rapid growthTREATMENT— none, cullHUMAN HEALTH RISK — none

Laryngotracheitis. See Infectious LaryngotracheitisLeucocytozoonosisALSO CALLED— Leucocytozoon diseaseINCIDENCE — only in areas where biting midges (Cuiicoides) and

blackflies(Simuliidae) are prevalent, especially during summer and fall; in NorthAmerica occurs in southeastern states, Minnesota, and Wisconsin

System/Organ Affected — BLOOD

PROGRESSION — sudden onset, spreads rapidly, acute in young birds, chronic inmature birds

SYMPTOMS — in young birds (particularly those carrying heavy loads of internalparasites): droopiness, weakness, lameness, fever, loss of appetite, emaciation,

290 Leukosis/Sarcoma

increased thirst, vomiting, increased excitability, rapid labored breathing,sometimes green diarrhea; birds recover or die within 3 days

— in older birds: no symptoms but may remain carriers for monthsPERCENTAGE AFFECTED — highMortality—10 TO 80 PERCENTPOSTMORTEM FINDINGS — enlarged spleen, pale muscles and other tissues; some-times flabby, yellow llesh; often upper intestine filled with bloodRESEMBLES — malariaDIAGNOSIS— requires laboratory procedure (blood smear)CAUSE — Leucocytozoon spp protozoan parasites that infect many other kinds of

birds more often than chickensTRANSMISSION — spread by biting midges from infected or carrier birds; does not

spread through direct contact wiLh infected birdsPREVENTION — control blackflies and midges (see page 62) or do not raise chickensin areas where they are abundant; isolate brooding chicks from infected adults;dispose of breeder (lock each year to eliminate carriers; continuous drugtreatment (pyrimethamine in feed plus sulfadimethoxine or sulfaquinoxalinein feed or water) is a preventative but not a cureTREATMENT — ineffective; recovered birds are carriers, may be stunted, and willnever lay well

HUMAN HEALTH RISK — none knownLeukosis/Sarcoma. See Lymphoid Leukosis, OsteopetrosisLimberneck. See BotulismListeriosis

ALSO CALLED — circling diseaseINCIDENCE — worldwide in temperate areas, but rare (chickens are resistant)SYSTEM/ORGAN AFFECTED — brain and heart (encephalitic) or entire body

(septicemic)INCUBATION PERIOD — 5 to 15 daysPROGRESSION — acute, moves dirough flock slowlySYMPTOMS — in young birds: walking in circles with misted neck

(encephaliticform); diarrhea, gradual weight loss, death (septicemic form)

—in mature birds: sudden death (septicemic)PERCENTAGE AFFECTED — lowMORTALITY— usually low but can reach 40 percentPOSTMORTEM FINDINGS — patchy spots on liver; pale, inflamed heart

RESEMBLES — encephalitic form: encephalomalacia, epidemic tremor, exoticNewcastle

—septicemic form: any acute septicemiaDIAGNOSIS — difficult; laboratory identification of bacteriaCAUSE — Listeria monocytogenes bacteria commonly found in soil and the bowels

of birds and other animalsTRANSMISSION — inhaling or ingesting bacteria; bacterial contamination of awoundPREVENTION — good sanitationTREATMENT—none, cull

Lymphoid Leukosis 285

HUMAN HEALTH RISK — conjunctivitis and listeric abortion from contact withinfected or carrier birds; see "Listeriosis," page 236Liver Disease. See CampylobacteriosisLong-Bone Distortion. See Twisted LegLymphoid Leukosis

Ai.so CAI.U;O — big liver disease, LL, lymphatic leukosis, visceral lymphoma (one

disease in the leukosis/sarcoma group)INCIDENCE—common worldwideSYSTEM/ORGAN ABFECTED — entire bodyINCUBATION PERIOD— 14 weeksPROGRESSION — usually chronicSYMPTOMS — in birds 16 weeks or older (especially those nearing

maturity):depression, death

— in birds over 6 months old: death without symptoms or pale shriveledcomb, loss of appetite, diarrhea, emaciation, weakness; sometimes bluishcomb, vent feathers spotted with white (urates) or green (bile); sometimes youcan feel enlarged kidney, cloacal bursa, liver, or nodular tumors through skin

— in hens: reduced egg production, enlarged abdomen, loose droppingsPERCENTAGE AFFECTED — sporadicMORTALITY — up to 25 percent (rapidly following first symptoms)

POSTMORTEM FINDINGS — in birds 16 weeks or older: large and numerous soft,smooth, shiny white or gray tumors in liver, spleen, and cloacal bursa; some-times swollen grayish crumbly or gritty liver, enlarged joints, tumors in kidney,lungs, heart, bone marrow, testes or ovaryRESEMBLES — Marek's disease (see chart page 128), blackhead, pullorum, tuber-culosis

DIAGNOSIS — flock history (birds' age), symptoms (progression and mortality),

postmortem findings (especially involvement of cloacal bursa)CAUSE — a group of retroviruses that primarily infect chickens and do not live longoff a bird's bodyTRANSMISSION — contact with infected birds; spreads from infected

breedersthrough hatching eggs (main source of transmission) or by infected chicks to

292 Malabsorption Syndrome

non-infected chicks through droppings; mechanically by blood-suckingparasites or unhygienic vaccination methodPREVENTION — defies good management but can be controlled by: buying andbreeding resistant strains (heavier meat breeds are more resistant that lighterlaying breeds); identifying and eliminating breeders that produce infectedchicks (requires testing for reactors); not reusing chick boxes; raising chicks onwire; not combining chickens of different ages or from different sources;thoroughly cleaning facilities before introducing new birds; thoroughlycleaning and disinfecting incubator and brooder between hatches; controllingblood-sucking parasites; avoiding use of same needle for flockwide injectionsor vaccinationsTREATMENT — none, cull; clean up and disinfectHUMAN HEALTH RISK— none known

- M -

Malahsorption Syndrome. See Infectious Stunting SyndromeMalariaALSO CALLED — avian plasmodia, Plasmodium infectionINCIDENCE — worldwide in temperate climatesSystem/Organ Affected— BLOODINCUBATION PERIOD — 5 to 7 daysPROGRESSION — acute to chronicSYMPTOMS — in all ages: none to deathPERCENTAGE AFFECTED — 5 to 20 percentMortality — 0 TO 90 PERCENTPostmortem Findings — ANEMIARESEMBLES — leucocytozoonosisDIAGNOSIS — laboratory testing (blood smear)CAUSE — Plasmodium spp protozoan parasitesTRANSMISSION — mosquito bilesPREVENTION — control mosquitoes; isolate chickens in mosquito-proof housingTREATMENT — noneHUMAN HEALTH RISK — none knownMarble Bone. See OsteopetrosisMarek's DiseaseALSO CALLED — MD, neuritis, neurolymphomatosis, range paralysis (eye form:

gray eye. iritis, ocular lymphomatosis, uveitis)INCIDENCE — very common worldwide (more so in large breeds than in bantams)SYSTEM/ORGAN AFFECTED — organs (liver, lungs, and others), nerves, or skin; see

page 127 for chart describing forms of Marek's diseaseINCUBATION PERIOD — 2 weeksPROGRESSION — often acuteSYMPTOMS — in chicks over 3 weeks old (most commonly 12 to 30

weeks): growingthin while eating well (most common form), deaths starting at 8 to 10 weeksand persisting until 20 to 25 weeks— in maturing birds (6 to 9 months old): enlarged, reddened featherfollicles or white bumps (tumors) on skin that scab over with a brown crust(skin form); stilted gait or lack of coordination, pale skin, wing or leg paralysis(involves nerve); when both legs are paralyzed, one points forward and dieother points back under body; sometimes rapid weight loss, gaping or gasping,transient paralysis lasting 1 to 2 days (pseudo-botulism form), dehydration,emaciation, coma; death due to inability to get to food and water

294 Malabsorption Syndrome

or tramplingby other chickens— in breeds with reddish bay eyes: cloudy grayish, dilated, irregular pupil("gray eye," involves optic nerve); distorted or blinded eye— in all ages: sudden death of apparently healthy birds

PERCENTAGE AFFECTED — 30 to 50 percent in unvaccinated flocks, less than 5

percent in vaccinated flocksMORTALITY— can be nearly 100 percent; gradually increasing for up to 10 weeks,higher in pullets than in cockerels

POSTMORTEM FINDINGS — in cases of sudden death, massive tumors, especiallyalong die spinal column; otherwise, enlarged nerves with nodules (usually onlyon one side — compare same nerve on opposite side o'f body); tumors in testesor ovary (ovary takes on a "cauliflower" appearance); solidified lungs; ex-tremely enlarged liver, spleen, or kidneys with grayish white, soft areas;sometimes coarse, granular liverRESEMBLES — primarily lymphoid leukosis (see page 128 for chart on how to tellthe two apart); respiratory disease when Marek's affects the lungs; transientparalytic Marek's (called "pseudo-botulism" or "false botulism") resemblesbotulism, except that in pseudo-botulism birds recover quickly; paralysis and/or internal changes may resemble blackhead, epidemic tremor, joint infectionor injury, Newcastle disease, slipped tendon, riboflavin deficiency, tuberculo-sis, or tick paralysis (see "Soft Ticks," page 73)DIAGNOSIS — flock history (birds not yet mature), symptoms (especially discolorediris and irregular pupil), postmortem findings (two or more organs

affected)CAUSE — six different herpes viruses concentrated in feather follicles, shed indander, survive for years in dust and litter; in pullets, often infect in combina-tion with coccidiosisTRANSMISSION — contagious; contact with carrier or infected birds or their

feathers;contact with contaminated litter; inhaled contaminated dust or

Chicken paralyzed with Marek's disease

Marek's Disease 287296 Malabsorption Syndrome

dander; spreadby darkling beetle or lesser mealworm (Alphitobius cliaperinus) found in litter;not transmitted through hatching eggs or on their shellsPREVENTION — breed for resistance (some chickens carry a resistance factor, "B21,"detected through blood testing); practice good sanitation; provide goodventilation; brood chicks away from adult birds until 5 months of age (bywhich time they develop resistance); keep turkeys with chickens (turkeys carrya related though harmless virus that keeps Marek's virus from causing tumors);inject vaccine under skin lifted at nape of neck of newly hatched chicks, one-time vaccination confers lifetime immunity; do not expose vaccinated chicksto infection until immunity develops within 7 days; not all vaccines areeffective against all six strains of Marek's virusTREATMENT — none, cull affected birds (unless you're breeding for resistance);some tumors, particularly those of the feather follicles, clear up and (he bird

298 Mesogenic Newcastle

recovers on its own, but survivors are carriersHUMAN HEALTH RISK— none known from the virus, but handling vaccine maymake your eyes itch for a few daysMesogenic Newcastle. See Newcastle DiseaseMoniliasis. SeeThnishMonocytosis. See BluecombMud Fever. See BluecombMuguet. See ThrushMuscular Dystrophy. See White Muscle DiseaseMushy Chick Disease. See OmphalitisMycoplasma gallisepticum. See Chronic Respiratory DiseaseMycoplasma synoviaeInfection. See Infectious SynovitisMycoplasmosis. See Air-Sac Disease, Chronic Respirator,'Disease, InfectiousSynovitisMycotic Pneumonia. See Aspergillosis (acute); Aspergillosis (chronic)Mycotoxicosis. SeeAflatoxicosis, Fusariotoxicosis, Ochratoxicosis

- N -Navel Ill/Infection. See OmphalitisNecrotic Dermatitis

ALSO CALLED — avian malignant edema, clostridial dermatomyositis, gangrenouscellulitis, gangrenous dermatitis, gangrenous dermatomyositis, gas edemadisease, wing rotINCIDENCE — worldwide but rareSYSTEM/ORGAN AFFECTED — skinINCUBATION PERIOD — 2 to 3 daysPROGRESSION — acuteSYMPTOMS — in birds 3 to 20 weeks old (commonly 4 to 8 weeks old):

suddendeaths (sometimes with small, moist sores between toes) or depression,lameness, incoordination, prostration, loose feathers or skin that easily nibsoff; skin that pops or crackles when rubbed (due to gas underneath); reddishblack patches of dead, featherless skin on wings, breast, abdomen, or legs;death within 24 hours, body decomposes rapidly, turning green within 1 or 2hours

Percentage Affected — LOWMortality — 60 TO 100 PERCENTPOSTMORTEM FINDINGS — bloody, gelatinous fluid beneath skin; gray or tan

breastand thigh muscles that look cooked; usually shriveled cloacal bursa; some-times enlarged liver and spleen, swollen kidneys, degenerated lungs

Nephrosis 299

RESEMBLES — blister burn or contact dermatitis caused by wet or improperlymanaged litter; nutritional deficiencies leaving skin unprotected due to slowfeathering

DIAGNOSIS — symptoms, postmortem findingsCAUSE — Clostridium septicum bacteria commonly found in

droppings, soil, dust,litter, feed; often occurs in combination with necrotic enteritis,

Nephrosis 300

staphylococcosis, and colibacillosis; usually follows an outbreak of infectiousbursal disease, sometimes follows infectious anemia or infectious stuntingsyndrome

TRANSMISSION — through wounds caused by caponizing, fighting, cannibalism,

injury on poorly designed equipmentPREVENTION — good sanitation and nutrition; good management to avoid wounds;ventilation to prevent excessive humidity in housing; breed for resistance toinfectious bursal diseaseTREATMENT—broad-spectrum antibiotic (penicillin, erythromycin, tetracyclines),proper selection requires laboratory identification of all organisms involved;vitamin-electrolyte supplement hastens recoveryHUMAN HEALTH RISK — none, if good sanitation is practiced after handling infectedchicksNecrotic Enteritis

ALSO CALLED — cauliflower gut, crud, enterotoxemia, NE, rot gutINCIDENCE — worldwide but rareSYSTEM/ORGAN AEEECTBD — intestinesINCUBATION PERIOD — 3 to 10 daysPROGRESSION — acute, appears suddenly, progresses rapidly, runs

through flock in5 to 10 days

SYMPTOMS — in intensively raised birds, 2 weeks to fi months old (commonly 2 to 5weeks old): depression, loss of appetite, ruffled feathers, reluctance to move,diarrhea, death within hours; or sudden death without symptomsPERCENTAGE AFFECTED— up to 15 percentMORTALITY — 2 to 50 percentPOSTMORTEM FINDINGS — cauliflower-like yellow or green membrane lining small

intestine filled with gas or foul-smelling brown fluidRESEMBLES — intestinal coccidiosis (Eimeria brunetti), except that cocci is usuallyless severe; ulcerative enteritis, except that necrotic enteritis rarely affects thececum or liver

DIAGNOSIS — postmortem findings, laboraiory identification of bacteriaCAUSE — Clostridium petfringens bacteria and their toxins, sometimes followingchange in feed; often found in conjunction with coccidiosis and occasionallysalmonellosis (both of which increase susceptibility)

Nephrosis 301

TRANSMISSION — droppings from infected birds and spores in built-up litter, dust,or feedPREVENTION — good sanitation management to prevent coccidiosis and other

intestinal infections; make feed changes graduallyTREATMENT— bacitracin in drinking water at the rate of V-> gram per gallon for 4days, combined with amprolium to control coccidia; vitamin supplementfollowing treatment hastens recoveryHUMAN HEALTH RISK — do not slaughter sick birds: toxins in meat contaminated byinfected droppings during butchering can cause mild to serious illness; see"Clostridium Poisoning," page 241Nephrosis. See Gout (visceral). Infectious Bursal Disease

302 Neuritis

Neuritis. See Marek's DiseaseNeurolymphomatosis. See Marek's DiseaseNeurotropic Velogenlc Newcastle Disease. See Newcastle Disease (exotic)Newcastle Disease

AI.so CALLED — avian distemper, domestic Newcastle, endemic Newcastle,parainfluenza, pneumoencephalitis, pseudofowl pest, mesogenic Newcastle,mild Newcastle, NDINCIDENCE — common worldwideSYSTEM/OKGAN AFFECTED — respiratory and nervous systemsINCUBATION PERIOD — 2 to 15 days (5 to 6 average)PROGRESSION — acute, starts suddenly, spreads rapidly, runs

through flock inabout a week

SYMPTOMS — in growing birds: wheezing, gasping, coughing, chirping, sometimesfollowed within 10 to 14 days by nervous disorders (drooping wing, draggy leg,nvisted neck), death due to being trampled by other chickens

— in mature birds: slight wheezing, temporary cessation of laying, eggs withsoft, rough, or deformed shells: sometimes nasal discharge, cloudy eyePERCENTAGE AFFECTED — high

MORTALITY — few or none but can be high when nervous symptoms appear

POSTMORTEM FINDINGS — none significant; sometimes mucus in throat andthickened air sacs containing yellowish matter

RESEMBLES — infectious bronchitis and other respiratory diseases, except thatNewcastle produces nervous symptoms; a disease known as "fowl plague" thatdoes not occur in North AmericaDIAGNOSIS — symptoms (chicks with both nervous and respiratory signs), labora-tory identification of virusCAUSE — paramyxovirus that affects many different birdsTRANSMISSION — contagious; spread by inhaling or ingesting the virus from body

excretions of infected birds or carriers in air, water, or feedPRI-VENTION — defies good management; breed for genetic resistance (tests forantibodies against the virus commonly find healthy reactors, suggesting a highdegree of resistance); vaccination not necessary unless virus is common inyour area, then vaccinaLe chicks at 1 day old (or between 7 and 10

days) andrepeat every 4 months or as required by risk of exposure; vaccinate all adultbirds when chicks are first vaccinatedTREATMENT — keep birds warm and well fed; watch for secondary bacterialinfections, particularly air-sac disease and chronic respiratory disease;survivors are immune but will be carriers for up to a monthHUMAN HEALTH RISK — temporary (3 to 7 days) eye infection may result fromhandling vaccine or infected birdsNewcastle Disease (exotic)

ALSO CALLED — Asiatic Newcastle disease, neurotropic velogenic Newcastledisease, NVND, the plague (in the Philippines), pseudo-poultry plague,velogenic Newcastle, viscerotropic velogenic Newcasde disease, WNDINCIDENCE—rare but worldwide, especially in young, concentrated, confined flocks

304 New England Disease

Newcastle Disease (exotic) 291

SYSTEM/ORGAN AFPECTED — respiratory and nervous systems, sometimes digestivesystem

INCUBATION PERIOD — 2 to 15 days (5 to 6 average)PROGRESSION— acuie, spreads rapidly, runs through Hock in 3 to 4 days,

lasts 3 to 4weeks

SYMPTOMS— in all ages: sudden, high rate of death without symptoms or— in chicks: gasping, sneezing, coughing, "chirping" sound, rattle in

tiiroat;followed by slow growth, drooping wings, dragging legs; sometimes twistedhead and neck, circling, somersaulting, walking backward, paralysis; birdsrecovering from respiratory symptoms but retaining nervous symptoms

— in mature birds: listlessness, rapid or difficult breathing, progressiveweakness, near total cessation of laying within 3 days (sometimes shells haveodd shapes or colors with flabby, blood-stained yolks and watery whites);followed by loss of coordination, loss of appetite, muscular tremors, twistedneck, wing and leg paralysis; sometimes watery, greenish (blood-stained)diarrhea, swollen, blackish eyes with straw-colored fluid draining from eyesand nose, bleeding through nose, death within 2 to 3 days

Percentage Affected — UP TO 100 PERCENTMORTALITY — usually 50 percent in adults, 90 percent in young birds,

can be 100percent in all ages

POSTMORTEM FINDINGS — yellow patches on roof of mouth; large and small reddishbrown spots or blotches (hemorrhages) in the upper and lower digestive tract,over abdominal fat, and on the ovary: wrinkled or discolored yolks; broken eggin abdominal cavity of hens

RESEMBLES — aflatoxicosis, blackhead, canker, coccidiosis, acute cholera, influ-enza, infectious laryngotracheitis, mild Newcastle, nutritional roup, thrush

DIAGNOSIS— (lock history (human handler's contact with infected chickens orsmuggled cage bird), symptoms, postmortem findings, confirmed by labora-tory identification of virus

CAUSE — several strains of paramyxovirus that survive for up to 30 days in brokeneggs, feathers, drinking water, and droppings in litter, but are sensitive tosunlight

TRANSMISSION — highly contagious; usually introduced by illegally imported cagebirds that have not gone through USDA quarantine; spread by contact withinfected birds and their body discharges; spreads in feed, water, air, and onequipment and the feet of rodents and humans; eggs laid by infected hensrarely hatch but may break in incubator and spread the virus

PREVENTION — avoid mixing birds of different ages or from different sources; avoidcontact with illegally imported birds; do not visit (locks or let people visit yourflock if an outbreak occurs in your area; vaccination does not offer 100 percentprotection and birds vaccinated with live vaccine become carriers

TREATMENT — none; this is a reportable disease, see "Reportable Diseases" page196; infected flocks are quarantined and destroyed; thoroughly clean up anddisinfect equipment and housing with lye, 2 percent quaternary ammoniumcompound, or 5 to 20 percent chlorine bleach


HUMAN HEALTH RISK — temporary (3 to 7 days) eye infection requiring medicaltreatment may resuli from handling vaccine or infected birdsNew England Disease. See Epidemic TremorNew Wheat Disease. See BluecombNutritional Myopathy. See White Muscle DiseaseNutritional Roup. See Roup (nutritional)

-O -Ochratoxicosis

INCIDENCE — sporadic in North America, Europe, and AsiaSYSTEM/ORGAN AFFECTED — kidneyPROGRESSION — gradual and cumulativeSYMPTOMS — in hens: yellow diarrhea, thin-shelled eggsPERCENTAGE AFFECTED — 5 to 50 percent, depending on age of birds and level oftoxicityMORTALI TY — usually low, depending on amount of toxin ingestedPOSTMORTEM FINDINGS — swollen, pale kidneys, sometimes swollen, spotted liver,

intesdne filled with mucusRESEMBLES — other mycotoxicosesDIAGNOSIS — symptoms, postmortem findings, feed analysis

CAUSE — ochratoxins produced by Aspergillus ochraceous and Penicillinniviridicatum fungi in barley, corn, sorghum, and wheat and in pelleted feedmade with contaminated grainTRANSMISSION— poisoning from contaminated rations; does not spread from birdto bird

PREVENTION — avoid moldy feedsTREATMENT — replace contaminated feedHUMAN HEALTH RISK — danger of ochratoxin residue in meat is low as

most of thetoxin is rapidly excreted in droppings; residue rarely appears in eggsOcular Lymphomatosis. See Marek's DiseaseOidica. See ThrushOidiomycosis. See ThrushOmphalitis

ALSO CALLED — mushy chick disease, navel ill. navel infection (one form ofcolibacillosis)

INCIDENCE — commonSYSTEM/ORGAN AFFECTED — navelINCUBATION PERIOD— 1 to 2 days (present at time of hatch)PROGRESSION — acuteSYMPTOMS — dead embryos late in incubation; newly hatched chicks feel

wet

— in chicks to 4 weeks of age: drooping head, puffed-up down, huddlingnear heat, lack of uniformity in size, lack of interest in food or water, distendedabdomen with unabsorbed yolk sac; unhealed, reddened, swollen, and wet,mushy or scabby navel; sometimes diarrhea; deathPERCENTAGE AFFECTED — usually low unless incubator sanitation is poor


Osteopetrosis 293

MORTALITY — up to 15 percent, starting just prior tohatch and continuing for up to 3 weeks; mayincrease as hatching season progressesPOSTMORTEM FINDINGS— incompletely healed navel,fluid under skin, bluish abdomen, unabsorbed yolkin abdomen (sometimes yellowish green and wateryor yellowish brown and cheese-like, often badsmelling)DIAGNOSIS — symptoms, postmortem findingsCAUSE — Escherichia coli combined with Staphylococcusaureus, Streptococcusfaecalis, and other bacteriaTRANSMISSION — contaminated droppings on hatchingeggs; high incubation humidity keeps navel fromclosing properly, infectious organisms in incubatoror brooder (or within egg, having penetrated shellbefore or during incubation) enter unhealed navel;feed, water, litter contaminated with droppings; nottransmitted between growing or mature birdsPREVENTION — hatch only clean, uncracked eggs; controlincubator humidity; clean and disinfect incubatorand brooder between hatchesTREATMENT— none effective, cull; if newly purchased chicks experience a high

death rate, notify seller and/or hatcheryHUMAN HEALTH RISK — none, if good sanitation is practiced after handling infectedchicks

Ornithosis. See ChlamydiosisOsteomalacia. See RicketsOsteopetrosis

ALSO CALLED — marble bone, thick leg disease (one disease in the lymphoid/sarcoma group)

INCIDENCE — commonSYSTEM/ORGAN AFFECTED—bonesINCUBATION PERIOD — 30 daysPROGRESSION — usually chronicSYMPTOMS — in young or mature birds (more often male than female): thickened(sometimes unusually warm) leg bones, puffy looking shanks, lameness orstilted gait, faulty body conformation, stuntingPERCENTAGE AFFECT ED — lowMORTALITY — up to 10 percentPOSTMORTEM FINDINGS — thickened, deformed bonesRESEMBLES — rickets, except that osteopetrosis does not cause bones to

becomeporous; cage fatigue, except that in cage fatigue the bones twist but do notthicken

DIAGNOSIS — flock history, symptoms, postmortem findings, laboratory testsCause — retrovirus; often occurs in combination with lymphoid leukosis

omphalitis

310 Osteoporosis

TRANSMISSION — contact with infected birds; spread by infected breeders throughhatching eggs or by infected chicks to non-infected chicks through droppings;mechanically by bloodsucking parasites or unhygienic vaccination methodPREVENTION — defies good management but can be controlled by: buying andbreeding resistant strains; identifying and eliminating breeders that produceinfected chicks (requires testing for reactors); not reusing chick boxes; raisingchicks on wire; not combining chickens of different ages or from differentsources; thoroughly cleaning facilities before introducing new birds; thor-oughly cleaning and disinfecting incubator and brooder between hatches;controlling bloodsucking parasites; avoiding flockwide injections or vaccina-tions using one needleTREATMENT— none, cull; clean up and disinfectHUMAN HEALTH RISK— none knownOsteoporosis. See Cage Fatigue

- P -Pale Bird Syndrome. See Infectious Stunting SyndromeParacolon. See ArizonosisParainfluenza. SeeNewcasde DiseaseParatyphoid

AI so CALLED — paratyphoid infection, PT (one kind of salmonellosis)INCIDENCE—very common worldwideSYSTEM/ORGAN AFFECTED — digestive or entire body (septicemic)Incubation Period — 5 DAYSPROGRESSION — acute or chronicSYMPTOMS — in embryos at time of hatch: numerous dead in shell,

pipped orunpipped

— in chicks up to 5 weeks old: death at time of hatch or depression,weakness, poor growth, droop :ng wings, decreased appetite, increased thirst,"chirping" or "peeping" sounds, huddling around heat with feathers ruffled,eyes closed, head down, wings drooping; sometimes swollen joints, swelling orblindness in one or both eyes, watery diarrhea with pasting, dehydration

— in adult carriers: no symptoms or reduced egg production; purplishhead, comb, and watdes (septicemic form)

Percentage Affected — HIGH

Pediculosis 311

MORTALITY—10 to 20 percent, sometimes 100 percent; peaks at 6 to 10 days of agePOSTMORTEM FINDINGS — in chicks: none recognizable, or unabsorbed yolk sac,dehydration, swollen liver with red streaks or white dots, creamy or yellowishcheesy cores in ceca

— in adult birds: none recognizable, or inflamed intestine, swollen liver,spleen, kidneys

RESEMBLES — arizonosis, typhoid, pullorum, septicemia due to colibacillosis (see

"Colibacillosis," page 112), infectious synovitis when joints are swollenDIAGNOSIS — flock history (birds' age), symptoms, postmortem Findings, labora-tory identification of bacteria

Pediculosis 312

CAUSE — over 150 different Salmonella bacteria (S. heidelberg and S. typhimuriummost commonly affect chickens, S. enteritidis also affects humans) that residein soil and litter and infect a variety of birds and mammalsTRANSMISSION — contaminated soil or litter (persists for up to 7 mondis); contami-nated droppings (persists for up to 28 months); contaminated feathers, dust,hatchery fluff (persists for up to 5 years); feed containing contaminated animalby-products (not including pellets and crumbles) or feed and water containingcontaminated droppings; spreads horn infected breeders to chicks throughhatching eggs (eggs can blow up during incubation, further spreading con-tamination); spread on dirty equipment, feet of rodents and humansPREVENTION — difficult, due to bacteria's wide range of animal hosts; collecthatching eggs often; hatch only eggs from paratyphoid-free breeders; replacenesting litter often; clean and disinfect incubator and brooder after each hatch;minimize chilling, overheating, parasitism, withholding of water or feed; keepdrinking water free of droppings; control rodents, reptiles, wild birds, cock-roaches, beetles, fleas, and Hies; avoid mixing chickens of various age groups;keep breeders on wire flooringTREATMENT — none effective, survivors may be carriers; Salmonella Enteritidisinfection is reportable, see "Reportable Diseases" page 190

HUMAN HEALTH RISK — mild to serious illness from eating raw or undercookedcontaminated meat or eggs, see "Salmonellosis," page 239Parrot Fever. See ChlamydiosisPasted Vent

ALSO CALLED — cloacitis, vent gleetINCIDENCE — common in chicks, less common in mature birdsSYSTEM/ORGAN AFFECTED — ventPROGRESSION — chronicSYMPTOMS — in chicks up to 10 days old: droopiness, droppings sticking to vent—in laving hens: offensive odor from droppings sticking to vent feathersPERCENTAGE AFFECTED — usually limitedMORTALITY — possible, if vent gets sealed shutPOSTMORTEM FINDINGS — distended rectum filled with droppingsRESEMBLES — in chicks: arizonosis and paratyphoid, except that pasted vent

Pediculosis 313

involves fewer chicks and ihey appear otherwise healthyDIAGNOSIS — symptomsCAUSE — in chicks: unknown, may be due to improper consistency of

droppingscaused by rations or chilling

— in hens: loss of muscle tone due to hereditary weaknessTRANSMISSION — does not spread from bird to birdPREVENTION— keep chicks warm; do not hatch eggs from affected hens to

avoidpassing on hereditary weakness

TREATMENT — carefully pick away adhering matter; cull chicks that don't recoverHUMAN HEALTH RISK — nonePasteurellosis. See Cholera (acute); Cholera (chronic)Pediculosis. See "Lice," page 63

314 Pendulous Crop

Pendulous Crop. See Crop ImpactionPerosis. See Slipped TendonPink Disease. See Fatty Liver SyndromeThe Plague. See Newcastle Disease (exotic)Plantar Pododermatitis. SeeBumblefootPlasmodium Infection. See MalariaPleuropneumonialike Organism (PPLO) Infection. See Chronic Respiratory DiseasePneumoencephalitis. See Newcastle DiseasePneumomycosis. See Aspergillosis (acute); Aspergillosis (chronic)Poisoning. Seepage 139Pox (dry)

ALSO CALLED — avian pox, chicken pox (has nothing to do with human chickenpox), cutaneous pox, fowl pox, sore head, (sometimes mistakenly called"canker")

INCIDENCE — common in some areas worldwide, especially in confined llocks in

COLD WEATHERSystem/Organ Affected — SKINIncubation Period — 4 TO 14 DAYSPROGRESSION — spreads slowly (except when spread by mosquitoes), lasts 3 to 5

weeks in individual birdsSYMPTOMS — in birds of all ages, except newly hatched chicks: raised clear orwhitish wart-like bumps on comb and wattles that grow larger, turn yellowish,and later become reddish brown, gray, or black bleeding scabs appearingsingly, in clusters, or clumping together; scabs fall off to form smooth scars;sometimes scabs spread to eyelids, unfeathered areas of head and neck, ventarea, feet, or legs; retarded growth or weight loss (sores around eyes inhibitfeeding), drop in egg productionPERCENTAGE AFFECTED — low to 100 percentMORTALITY —) to 2 percentRESEMBLES — comb wounds due to fighting, except that wounds do not spreadDIAGNOSIS — symptoms, confirmed by laboratory identification of virusCAUSE — pox virus that affects a wide variety of birds and survives for many

months on scabs and feathers of infected birdsTRANSMISSION — through skin wounds (due to insect biles, dubbing, fighting,cannibalism, or other injury); spreads by means of feathers and scabs from

Pox (wet) 315

infected birds; spread mechanically by mites, mosquitoes, and wild birds; mayspread from infected breeders to chicks through hatching eggs, causingdisease when infected birds come under stressPREVENTION — defies good management; control mites and mosquitoes; vaccinatewhere pox is prevalent (on day-old chicks, use only vaccine designated forchicks)\ if large number of vaccination sites do not swell and scab over within 7to 10 days, revaccinate with new batch of vaccine; since pox spreads slowly, itmay be checked by vaccinating while disease is in progressTREATMENT-— none; isolate infected birds in uncrowded housing; remove scabsaround mouth and eyes so birds can eat; prevent secondary infection with 300

316 Pseudo-Botulism

mg oxvtetracycline (Terramycin) per gallon of drinking water for 3 daysfollowed by vitamin supplement in water; infected birds naturally recover in 2to 4 weeks and are immune (but some remain carriers and may becomereinfected during molt and other times of stress); thoroughly clean housingafter outbreak to remove all infective scabsHUMAN HEALTH RISK — none known; "chicken pox" in humans is caused by adifferent virus that has nothing to do with chickens

Pox (wet)ALSO CALLED — diphtheritic pox, fowl diphtheriaINCIDENCE — worldwide, less common than dry poxSYSTEM/ORGAN AFFECTED — upper respiratoryINCUBATION PERIOD — 4 to 14 daysPROGRESSION — spreads slowly (except when spread by mosquitoes), lasts 3 to 5

weeks in individual birdsSYMPTOMS — in birds of all ages, except newly hatched chicks: transparent whitishwart-like or scabby bumps on face, eyes (can cause blindness), throat, andwindpipe (possibly becoming large enough to suffocate bird), growing largeruntil they join and turn yellow and cheesy; rales or wheezing, nasal or eyedischarge, death clue to suffocationPERCENTAGE AFFECTED — low to 100 percentMORTALITY — up to 50 percentPOSTMORTEM FINDINGS — yellowish or brownish cheesy masses in mouth, upper

throat, and windpipe, anchored by cheese-like rootsRESEMBLES— infectious laryngotracheitis, nutritional roup

— in chicks: biotin deficiency, cankerDIAGNOSIS — flock history, symptoms, confirmed by postmortem findings,

laboratory identification of virusCAUSE — same virus as dry pox invading the upper respiratory tractTRANSMISSION — same as for dry poxPREVENTION — same as for dry poxTREATMENT — if thick discharge interferes with breathing, clear airways with

Pox (wet) 317

Head of a chicken

with pox

318 Pseudo-Botulism

cotton swab coated with iodine; otherwise, treat as for dry poxHUMAN HEALTH RISK— none known, not related to diphtheria in humansPseudo-Botulism. See Marek's DiseaseProlapse. See "Prolapsed Oviduct," page 53Pseudofowl Pest. See Newcastle DiseasePseudomonasINCIDENCE — rare

System/Organ Affected — ENTIRE BODYIncubation Period — 3 DAYSProgression — ACUTE TO CHRONICSYMPTOMS — in embryos or newly hatched chicks: death

— in older birds: lameness, loss of coordination, swollen head and wattles,swollen hock joints and foot pads, diarrhea, death within 1 to 2 daysPERCENTAGE AFFECTED — up to 10 percentMORTALITY — usually no more than 10 percent but can be up to 90 percentPOSTMORTEM FINDINGS — swollen, spotty liver, spleen, kidneysRESEMBLES — septicemic colibacillosisDIAGNOSIS — characteristic fruity odor, laboratory identification of

bacteriaCAUSE — Pseudomonas aeruginosa bacteria commonly found in chicken drop-pings, soil, water, and humid environments: infects birds with reducedresistance due to some other causeTRANSMISSION — droppings of infected birds in feed, water, litter; infects chicksthrough shells of hatching eggs; spreads in vaccines and antibiotics handled inan unhygienic manner; infects chickens with reduced susceptibility due toother bacterial or viral diseasesPREVENTION — good incubator and brooder sanitation; hygienic handling ofvaccines and antibiotics; avoid mixing birds of different ages; avoid stressTREATMENT — bacteria are resistant to many antibiotics, but treatment may reducelosses //started early and a suitable antibiotic (such as gentamicin) is deter-mined through laboratory sensitivity testingHUMAN HEALTH RISK— rare but potentially serious infection due to bacteriaentering an open wound or deep puncturePseudo-Poultry Plague. See Newcastle DiseasePsittacosis. See ChlamydiosisPullet Disease. See BluecombPullorum

Aiso CALLED — bacillary white diarrhea, BWD, pullorum disease, PD. whitediarrhea (one kind of salmonellosis)

INCIDENCE — worldwide, rare in North

Pox (wet) 319

AmericaSYSTEM/ORGAN AFFECT ED — digestive or septicemicINCUBATION PERIOD — 7 to 10 daysPROGRESSION — acute or chronicSYMPTOMS — in chicks up to 4 weeks old: sudden death or loss of

appetite,sleepiness, weakness, huddling near heat, swollen hock joints, white (orgreenish-brown) pasty diarrhea; sometimes gasping, shrill peeping or chirpingwhile trying to expel droppings: uneven growth among survivors

Reovirus Infection 299

— in mature birds: no signs or loss of appetite, increased thirst; sometimespale, shriveled comb, green diarrhea, drop in egg production

PERCENTAGE AFFECTED — up to 100 percentMORTALITY— up to 90 percent in chicks, increasing on 4di or 5di day and

peakingat 2 to 3 weeks of age (100 percent if infected chicks are shipped, chilled, orkept in unsanitary conditions)POSTMORTEM FINDINGS — in chicks: none recognizable; or unabsorbed yolk; cheesymaterial in abdominal cavity or ceca; enlarged liver, heart, kidneys, and spleen;small white or gray nodules (pinpoint to pea-size) in liver, heart, gizzard,intestine, and lungs

— in adult birds: none recognizable; or enlarged liver, heart, spleen, andkidneys; swollen ceca or oviduct filled with firm, cheesy material

— in hens: brownish or greenish shriveled yolks, yolk material in abdominalcavity

— in cocks: shriveled testes (testicles)RESEMBLES — omphalitis, paratyphoid, typhoid; white diarrhea due to

simplechilling

DIAGNOSIS — history (birds' age), symptoms (pattern of deaths), laboratoryidentification of bacteria

CAUSE — Salmonella pullorum bacteria, survives for years in dry litter, but is easily

destroyed by cleaning and disinfectionTRANSMISSION — from infected breeders to chicks through hatching eggs; spreadfrom chick to chick in incubator or brooder; occasionally transmitted bycontaminated litter, shoes, equipmentPREVENTION — purchase certified pullorum-free stock; hatch eggs only frompullorum-free breeders; do not mix certified pullorum-free stock with otherbirds; control flies, rodents, and wild birds; breed for resistance (heavy breedssuch as Rocks and Reds are more susceptible than Leghorns and other lightbreeds); blood test birds (home kits are available) and eliminate carriers untiltwo tests, no less than 21 days apart, are negative (some states require bloodtesting of all exhibition birds)TREATMENT— cull, survivors are carriers; this is a reportable disease in most

states, see "Reportable Diseases" page 196HUMAN HEALTH RISK — eating highly contaminated meat can cause acute intesti-nal infection (characterized by explosive onset, high fever, and prostration);recovery is spontaneous and rapid

Pulmonary Aspergillosis. Sec Aspergillosis (acute), Aspergillosis (chronic)j

- Q -Quail Disease. See Ulcerative Enteritis

Rachitic Chicks. See RicketsRange Paralysis. See Marek's DiseaseRenal Failure/Gout See Gout (visceral)Reovirus Infection. See Viral Arthritis

300 Reticuloendotheliosis

Reticuloendotheliosis. See Runting SyndromeRickcts

Aiso CALLED — osteomalacia, rachitic chicksINCIDENCE— rare, yet the most common nutritional deficiency of growing

birds,especially those housed in confinement

SYSTEM/ORGAN AFFECTED — bonesPROGRESSION — depends on degree of deficiencySYMPTOMS — in young birds: depression, frequent squatting, stiff-

legged gait orinability to stand, slow growth, ruffled feathers, black feather parts in red orbuff breeds, easily bendable beak, bowed or twisted legs and wings, enlargedjoints, paralysis

— in mature birds: easily broken bones, bent keel dished ill near the middlePERCENTAGE AFEECTED — can be highMORTALITY — up to 20 percentPOSTMORTEM FINDINGS — soft, rubbery bones, string of round knobs caused bybeading of inner surfaces of rib heads where ribs join spine (called "ricketyrosary" or "rachitic rosary")RESEMBLES — cage fatigue, except that birds need not be in cages to get ricketsDIAGNOSIS — flock history (birds' age), symptoms (especially soft beak), postmor-tem findings (especially rib beading), ration evaluationCAUSE — deficiency of vitamin D3; deficiency or imbalance of calcium or phos-phorus (too much calcium ties up phosphorus); inability to absorb nutrientsdue to infectious stunting syndromeTRANSMISSION — nutritional, does not spread from bird to birdPREVENTION — feed oyster shell or coarse limestone free choice; use commerciallyprepared ration fortified with vitamin D3; let birds out into the sunshine; rangebirds on legume or legume-grass pastureTREATMENT — vitamin D3 supplement at three times the normal amount for 3iveeks, then reduce to normal amount (take care, excess vitamin D in feed can

Bent beak from rickets

324 Roup

Round Heart Disease 301

Beaded ribs from ricketsbe toxic); for chicks, one-time dose of 15,000 lU vitamin D3; in case of

paraly-sis, give a calcium phosphate supplementHUMAN HEALTH RISK — noneRotaviral Enteritis

ALSO CALLED — rotaviral infection, viral enteritisINCIDENCE — worldwide and increasingly more commonSYSTEM/ORGAN AFFECTED — digestiveINCUBATION PERIOD — 2 to 5 daysPROGRESSION — lasts 5 to 10 daysSYMPTOMS — in young birds: depression, profuse watery diarrhea,

inflamed vent,appetite loss, weight loss, dehydration,

deathPERCENTAGE AFFECTED — nearly 100 percentMORTALITY— up to 50 percentPOSTMORTEM FINDINGS — yellowish, watery, gas-filled matter in intestines and cecaRESEMBLES — any other (enteric) disease causing diarrheaDIAGNOSIS — laboratory identification of diarrhea's causeCAUSE — rotavirus common in the poultry environment, but doesn't always

causedisease

TRANSMISSION — contact with infected birds and their droppings; spreads oncontaminated equipment; maybe transmitted in or on hatching eggs

PREVENTION — clean and disinfect housing periodically; do not start new chickenson used litter

TREATMENT— none, cull; penicillin and supportive therapy (see page 192) help,but survivors do not grow well; thoroughly clean and disinfect before

introduc-ing new flockHUMAN HEALTH RISK — none knownRot Gut. See Necrotic EnteritisRound Heart Disease

INCIDENCE — extremely rare and only during winter in birds maintained on deeplitter

System/Organ Affected — HEART

326 Roup

Progression — ACUTESYMPTOMS — in birds 4 to 8 mouths old: sudden deathPERCENTAGE AFFECTED — no illness evidentMORTALITY — up to 50 percentPOSTMORTEM FINDINGS — enlarged, yellowish, soft heart, rounded at the

tipRESEMBLES — sudden death syndrome, except that in SDS birds go into convul-sions just prior to death and usually die on their backsDIAGNOSIS — symptoms, postmortem findingsCAUSE — unknown, possibly related to nutritional deficiencyTRANSMISSION — unknownPREVENTION — provide proper nutritionTREATMENT— noneHUMAN HEALTH RISK — none knownRoup. See Canker, Cholera (chronic), Infectious Coryza, Roup (nutritional)Roup (nutritional)

ALSO CALLED — A-avitaminosisINCIDENCE — rare except when homemade rations are fedSYSTEM/ORGAN AFFECTED — upper respiratory (eyes, nose, tliroat)PROGRESSION — chronicSYMPTOMS — in chicks 1 to 7 weeks old: droopiness, pale combs, and

failure togrow followed by sore, swollen eyelids, sticky or cheesy discharge from eyesand nostrils, swollen sinuses, difficulty breathing

— in hens: unthriftiness and decreased egg production followed by runnyeyes and nose, eyelids stuck together, ruffled feathers, whitish-yellow mouthsores in severe cases, weakness, emaciation, increased interval betweenclutches, increased blood spotsPERCENTAGE AFFECTED — highMORTALITY — up to 100 percentPOSTMORTEM FINDINGS — dry. dull respiratory lining; excess urates in cloaca! bursaRESEMBLES — cholera (chronic), chronic respiratory disease, infectious bronchitis,

infectious coryza, influenzaDIAGNOSIS — symptoms, postmortem findings, microscopic examination of body

tissue, ration evaluationCAUSE— vitamin A deficiency for 2 to 5 months; chicks hatched from deficient

breeders will be deficient unless fed fortified starter rationTRANSMISSION — does not spread from bird to bird

PREVENTION — use only fresh feed (buy small quantities so it won't go stale); allowbirds to free range or feed them good sources of vitamin A such as new yellow(not while) corn and alfalfa mealTREATMENT— water-soluble vitamin A supplement in drinking water; vitamin A

injections in severe casesHUMAN HEALTH RISK — noneRunting Syndrome

ALSO GULED — runting disease syndrome (a form of reticuloendotheliosis)INCIDENCE — rare, occurs in Australia, Israel, Japan, and southeastern United States

328 Roup

Slipped Tendon 303

System/Organ Affected—ENTIRE BODYSYMPTOMS — in birds 4 to 10 weeks, after receiving contaminated

vaccine as day-old chicks: poor growth, abnormal feathering (barbules compress against theshaft for a short distance); sometimes paralysis— in naturally infected birds of all ages: no symptoms

POSTMORTEM FINDINGS — sometimes enlarged nerves; atrophy of cloacal bursaRRSEMBI.ES — Marek's disease, except that runting syndrome involves nerves to alesser extent; infectious anemia, infectious bursal disease, infectious stuntingsyndrome (a different disease sometimes also called "broiler runting syn-drome")DIAGNOSIS — flock history (use of potentially contaminated vaccine),

symptoms,postmortem findings, laboratory identification of vims

CAUSE— retrovirus that affects a variety of birds accidentally introduced to

chickens through vaccines contaminated during manufactureTRANSMISSION — contact with infected birds, their body fluids, or droppings;occasionally spread from breeders (cocks as well as hens) through hatchingeggs; possibly spread by mosquitoes and other insectsPREVENTION — none known; insect control and good sanitation helpTREATMENT— none knownHUMAN HEALTH RISK — none knownRuptured Tendon. See Viral Arthritis

- S -Salmonella enteritidis. See ParatyphoidSalmonellosis. See Arizonosis Typhoid, Paratyphoid, PullorumSinusitis. See Chronic Respiratory DiseaseSlipped TendonAISO CALLED — chondrodystrophy, perosisINCIDENCE — common in heavy, fast-growing breedsSYSTEM/ORGAN AFFECTED — hockSYMPTOMS— in young birds, starting at 9 days of age: swollen, flat hock

joint;hopping on one leg, sometimes one or both legs twist or rotate to the side;death due to inability to obtain food andwater

Percentage Affected — 3 TO 5 PERCENT

MORTALITY— LOW ^FPostmortem Findings — sometimes .shortened,

thickened long bones of legs and wings 7\Resembles — twisted leg, except that in twisted U

leg the bones are not shortened jVi /Diagnosis — history (birds' age, size, breed), V

symptoms, postmortem findings, rationevaluation

CAUSE — deficiency in manganese or one of fiveB vitamins (biotin, choline, folic acid, Typical case of slipped tendon

330 Sod Disease

nicotinic acid, pyridoxine)TRANSMISSION — nutritional, does not spread from bird lo birdPREVENTION — breed for genetic resistance; feed at least 95 percent commercialration (no more than 5 percent com or odier treats); avoid crowding youngbirds; brood on litter rather than on slats, wire, or slick floorTREATMENT — manganese and B-vitamin supplement won't reverse permanent

damage but will minimize future damageHUMAN HEAI.TII RISK — noneSod Disease. Seel-.rgotismSore Head. See Pox (dry)Sour Crop. See ThrushSpirochetosis

Also CALLED— fowl spirochetosisINCIDENCE — common in free-ranged llocks in tropical and temperate climates,rare in North America (although the fowl tick that carries it is found in thesouthwestern United Stales)SYSTEM/ORGAN AITECIED — entire body (septicemic)INCUBATION PERIOD—3 to 12 daysPROGRESSION — acute or chronicSYMPTOMS — in birds of all ages: droopiness, ruffled feathers, huddling,

yellowgreen diarrhea with large amounts of white urates, increased thirst, loss ofappetite, weak legs, pale or purplish comb, incoordination, loss of interest inperching, lying with head on ground, convulsions, fever, paralysis, drop intemperature lo below normal just before deathPERCENTAGE AEEECIED — 1 to 2 percent in carrier flocks with immunity due toconstant exposure to ticks, up lo 100 percent in susceptible birds mingled withimmune birds

MORTALITY— usually no more than 75 percent, but can be up to 100 percentPOSTMORTEM FINDINGS — swollen, mottled spleen; sometimes greenish mucus inintestines, enlarged, spotted liver, swollen, pale kidneys and/or enlarged, paleheartRESEMBLES — influenza or Newcastle, except diat spirochetosis does not

causerespiratory symptoms and bloody intestines; Marek's disease, except thatspirochetosis does not produce tumors; cholera, typhoid, and

septicemiccolibacillosis, except that in spirochetosis Salmonella, Pasteurella, or E. colibacteria cannot be found by laboratoryDIAGNOSIS — flock history (presence of fowl ticks. Argus persicus), symptoms,postmortem findings, identification of spirochetes

CAUSE— liorrelia anserina bacteria that affect many birds but do not survive long

in the environmentTRANSMISSION — contact with moist droppings, blood, tissue, and mucus ofinfected birds; spread by eating or being bitten by an infective fowl tick,mosquito, or other bloodsucker; spread through cannibalism (includingpicking carcasses of dead infected birds), contaminated dropp ngs in feed orwater, using the same needle for flockwide inoculation, vaccination, or bloodtesting

332 Stomatitis

Sternal Bursitis 305

PREVENTION — control ticks and other bloodsucking insects; do not combine tick-infested and susceptible birds; do not house clean birds where outbreak hasoccurred within 3years; vaccine not available in the United StatesTREATMENT— none effective; inject individual birds with 20 mgoxytetracycline(intramuscular) once a day for 2 days or add 1 gram oxyletracvcline per gallonof drinking water for 3 days; survivors are immune and are not carriers; treatonly under supervision, this is a reportable disease, see "Reportable Diseases"page 196

HUMAN HEALTH RISK — none known (little is understood to date about the spreadof a related tick-borne spirochete, B. burgdorferi, which causes Lyme disease inboth birds and humans)Split-Wing Syndrome. See Infectious Stunting SyndromeSpondylolisthesis. See Kinky BackStaphylococcic Arthritis

ALSO CAI.IJ;D — arthritis/synovitis, staphylococcic septicemiaINCIDENCE — common worldwideSYSTEM/ORGAN AFFECTED — joints or entire body (septicemic)INCUBATION PERIOD — 2 to 3 days (septicemic form)PROGRESSION — acute (septicemic form) or chronic (arthritic form)SYMPTOMS — in all ages (most often growing birds): fever, reluctance to move,ruffled feathers, depression, swollen joints (hot to the touch), resting on hocksand keel, lameness (chronic), death (acute)PERCENTAGE AFFECTED — lowMORTALOY — lowPOSTMORTEM FINDINGS — joints (especially hock) and surrounding area

areinflamed and contain whitish, fleck-filled pus that appears cheesy in anadvanced infection; sometimes swollen, spotted liver and spleenRESEMBLES — in young birds: joint infections (synovitis) caused by other bacteria;viral arthritis, except diat in viral arthritis fluid surrounding joints is yellowishor pinkish

— in mature birds: acute cholera (septicemic form), except that cholerainvolves a greater number of deathsDIAGNOSIS — symptoms, laboratory identification of bacteria

CAUSE — Staphylococcus aureus bacteria common in the poultry environmentTRANSMISSION — bacteria entering body through woundsPREVENTION — prevent injuries by providing safe, uncrowded housingTREATMENT — staph bacteria are resistant to many antibiotics, but treatment mayhe successful if a suitable antibiotic is determined through laboratory sensitiv-ity testingHUMAN HEALTH RISK — unsanitary handling of meat during or following

butcher-ing can cause food poisoning in humans; see "Staphylococcal Food Poisoning"page 243

Staphylococcic Septicemia. See Staphylococcic ArthritisStaphylococcosis. See Bumblefoot, Omphalitis, Staphylococcic ArthritisStar-Gazing Syndrome. See Epidemic TremorSternal Bursitis. See Breast Blister

334 Stomatitis

Stomatitis. See ThrushStreptococcosis. (See also Omphalitis)INCIDENCE — worldwide but not commonSYSTEM/ORGAN AFFECTED — emire body (septicemic)INCUBATION PERIOD — 5 to 21 daysPROGRESSION — acute (septicemic) or chronicSYMPTOMS — in mature birds: depression, weight loss; sometimes

lameness, headtremors, yellow diarrhea, pale combs and wattles, fever (108-110"F, 42-43°C),eventual or sudden deathPERCENTAGE AFFECTED — up to 50 percentMORTALITY — up to 50 percent

POSTMORTEM FINDINGS — enlarged, pale heart; light-colored or dark red patchyareas on liver

RESEMBLES — septicemic forms of staphylococcosis, colibacillosis, pasteurellosis,erysipelas, other bacterial diseases

DIAGNOSIS — symptoms and laboratory identification of bacteriaCAUSE — Streptococcuszooepidemicusbacteria that normally live in a chicken'sintestines; infection is considered secondary, since it occurs only if resistanceis reduced by some other diseaseTRANSMISSION — inhalation, ingestion, skin wounds; bacteria are extremely

susceptible to drying and so cannot be spread on equipmentPREVENTION — practice good sanitation; avoid stressTREATMENT — bacteria are resistant to many antibiotics, but treatment

may reducelosses //started early and suitable antibiotic is determined through laboratorysensitivity testingHUMAN HEALTH RISK— none knownStress Disease. See Chronic Respiratory DiseaseStunting Syndrome. See Infectious Stunting SyndromeSudden Death Syndrome

ALSO CALLED — SDS, acute death syndrome, ADS, acute hean failure, fatalsyncope, flip-over disease, heart attack ("sudden death syndrome"

in maturingbroiler breeders in Australia is caused by an unrelated nutritional deficiency)INCIDENCE — common worldwide, especially in intensively managed broilersSYSTEM/ORGAN AFFECTED — heart and lungsINCUBATION PERIOD — days to weeksPROGRESSION — acute

SYMPTOMS—in apparently healthy broilers, 1 to 12 weeks of age, primarily cocks:extended neck, gasping or squawking, wing beating, leg pumping, Hippingonto back, death within 1 minute of first symptoms

— in laying hens: cloacal tissue protrudes through vent, deathPERCENTAGE AFFECTED — up to 5 percentMORTALITY—100 percentPOSTMORTEM FINDINGS — feed-filled intestine; bloated, bright red lungs;

pools offluid between ribs and lungs; empty gall bladder; sometimes mottled muscles,liver, and kidneys:

336 Stomatitis

Thick Leg Disease 307

— in hens: numerous blood vessels covering egg yolk cluster, sometimesinternal broken-shelled eggRESEMBLES — round heart disease, except in sudden death syndrome birds go into

convulsions before dyingDIAGNOSIS — symptoms, postmortem findingsCAUSE — unknown; may be caused by high carbohydrate feeds and rapid

weightgain relative to feed intake

TRANSMISSION — nutritional, does not spread from bird to bird; do not feed forrapid weight gainPREVENTION — low-intensity lighting; avoid noise and other

disturbancesTREATMENT — noneHUMAN HEALTH RISK — none knownSummer Disease. See BluecombSwollen Head Syndrome

ALSO CALLED — dikkop, facial cellulitis, SHS, thick headINCIDENCE— not found in North America; prevalent in Israel, South Africa,

andparts of Europe

SYSTEM/ORGAN AFFECTED — headINCUBATION PERIOD — 36 hoursPROGRESSION — spreads rapidlySYMPTOMS — in broilers and broiler breeders: sneezing, red swollen

eyes, progres-sive swelling of the head and wattles, scratching of face with feet, drop in eggproduction; sometimes nervous symptoms; deathPERCENTAGE AFFECTED—less than 4 percentMORTALITY—4 to 10 percent

POSTMORTEM FINDINGS— inflamed pus-filled tissue beneath the skin of headRESEMBLES — infectious bronchitis, infectious coryza, NewcastleDIAGNOSIS— tlock history (contact with infected turkeys), symptoms, laboratorytests

CAUSE — combination of Escherichia coli and possibly turkey coryza virus; often

follows debeaking or vaccination for NewcastleTRANSMISSION — contact with turkeys infected with turkey coryza (rhinotracheius)

or drinking water contaminated widi the virusPREVENTION — provide adequate ventilation; avoid crowding; practice goodsanitation and litter management; avoid mixing birds of different ages orspeciesTREATMENT— improve ventilation; keep birds warm and well fed with

high proteinrations and a vitamin E supplement; treat with broad-spectrum sulfonamidesHUMAN HEALTH RISK — none knownSynovitis. See Infectious Synovitis

-T-Tenosynovitis. See Viral ArthritisThick Head. SeeSwollen Head SyndromeThick Leg Disease. See Osteopetrosis

338 Thrush

ThrushALSO CALLED —candidiasis, crop mycosis, moniliasis, muguet, oidica,

oidiomycosis, sour crop, stomatitisINCIDENCE — commonSYSTEM/ORGAN AFFECTED— upper digestive tractINCUBATION PERIOD — 2 to 4 weeksPROGRESSION — chronicSYMPTOMS — in growing birds: depression, rough feathers, diarrhea,

distendedsour crop, slow growth or

weight lossPERCENTAGE AFFECTED — up to 20 percentMORTALITY — up to 5 percentPOSTMORTEM FINDINGS — grayish white, rough, circular, thickenings that

join tocreate a "Turkish towel" appearance in mouth, esophagus, and crop lining,sometimes in stomach, rarely in the intestineRESEMBLES — canker, capillary worms, pox (wet)

DIAGNOSIS — flock history (age of birds, outbreak of coccidiosis or use of antibiot-ics), symptoms (unthrifty birds), postmortem findingsCAUSE— Candida albicans yeast-like fungus commonly living in the bowels ofchickens that infect when normal flora are disrupted by coccidiosis or antibiot-ics, growth promoters, and other drugs; sometimes found in connection withanother disease (especially coccidiosis or chlamydiosis)TRANSMISSION — contaminated droppings in drinking waterPREVENTION — good nutrition and sanitation; avoid parasites; clean feeders andwaterers regularly; avoid crowding; avoid prolonged treatment with antibioticsand other dmgs

TREATMENT — isolate infected birds; clean and disinfect feeders and waterers; flushwith molasses or Epsom salts (see "Flushes," page 192), followed by '/a tea-spoon copper sulfate (powdered bluestone) per gallon drinking water everyother day for 5 days served ill a nonmetal waterer, repeat monthly; cleanmouth sores with an antiseptic such as hydrogen peroxide and treat withnystatin

HUMAN HEALTH RISK— C. albicans can cause mouth and genital infection inhumans, see "Candidiasis" page 232

Tibial Rotation. .SeeTwisted LegToxicoinfection. See BotulismToxoplasmosis

ALSO CALLED — toxoplasmaINCIDENCE — worldwide but sporadic and rareSYSTEM/ORGAN AFFECTED — central nervous system; sometimes reproductive

system, muscles, and organsINCUBATION PERIOD — 3 to 12 daysPROGRESSION — usually acute in young birds, chronic in older birds

SYMPTOMS — primarily in young, stressed birds: loss of appetite, emaciation, pale,shriveled comb, white droppings; sometimes diarrhea, incoordination,walking in circles with head twisted back, muscle spasms, paralysis, blindness;

340 Twisted Leg

Tuberculosis 309

lasts as long as 3 weeks, often ends in deathPERCENTAGE AFFECTED — highMORT ALITY— up to 50 percentPOSTMORTEM FINDINGS — enlarged, mottled liver; blood-Filled lungs

RESEMBLES — Marek's disease, Newcastle, or any other infection involving thenerves

DIAGNOSIS — laboratory identification of protozoaCAUSE— Toxoplasma gondii protozoan parasite

TRANSMISSION — picking in infected droppings of housecats or related animals,picking at infected meat (includinginfected chickens, dead or live), eatinginfected earthworms, eating flies or cockroaches carrying toxoplasma on theirbodies

PREVENTION — control Hies, cockroaches, dung beetles, rodentsTREATMENT— none knownHUMAN HEALTH RISK — eating undercooked meat contaminated with

infecteddroppings can (though rarely does) cause infection in humans, see"Toxoplasmosis" page 235Trichomoniasis. See CankerTrichothecene Mycotoxicosis. See FusariotoxicosisTuberculosis

ALSO CALLED— avian tuberculosis, AT, TBINCIDENCE — common worldwide, especially in backyard flocks in

temperatenorthern climates (northcentral United States)

SYSTEM/ORGAN AFFECTED — starts in intestinal tract and migrates to other internal

organsINCUBATION PERIOD — yearsPROGRESSION — usually chronic, rarely acute, spreads very slowly

SYMPTOMS — in birds 2 years old or older (especially living in contact with soil):dull, ruffled feathers, gradual weight loss despite good appetite, shrunkenbreast muscles, prominent (often deformed) keel; persistent diarrhea, pale(sometimes bluish) com bs and wattles, decrease in laying; sometimes lame-ness; death

PERCENTAGE AFFECTED— 10 to 50 percent, spread over many monthsMORTALITY — 100 percentPOSTMORTEM FINDINGS — hard, knobby grayish to yellowish nodules

(tubercles) in

liver, spleen, intestine, and bone marrow, increasing in size and number withthe length of time the bird is infectedRESEMBLES — blackhead, exeepi that in blackhead organ spots are dished ratherthan knobby; avian leukosis complex, except that leukosis usually affectsyounger birds; air-sac mites, which can be detected only by seeing tinytranslucent dots moving around in air sacs soon after bird dies (see page 71)DIAGNOSIS— flock history (bird's age, chronic disease conditions), symptoms(extreme emaciation, continuing deaths), postmortem findings, laboratoryidentification of bacteria, whole-blood test to identify live positive reactors; livebirds may be skin tested by using a 1 ml tuberculin syringe and '/2-inch (1.3

342 Twisted Leg

cm), 26 gauge needle to inject 0.05 ml avian tuberculin into wattle skin;swelling after 48 hours indicates test is positive, although infected birdsoccasionally react negativelyCAUSE — Mycobacterium avium bacteria that survive for 6 months or more in litter

and up to 4 years in soil, affect a wide variety of birdsTRANSMISSION — droppings of infected birds or picking at contaminated carcasses

of dead birds; spread on contaminated shoes and equipmentPREVENTION — do not keep chickens over 18 months old; do not mix birds fromdifferent age groups; design housing so birds can't pick in droppings; rotate'range; remove reactors to wattle testTREATMENT — none effective, cull; thoroughly clean and disinfect housing with acresylic compound, remove the top 4 inches of soil in dirt-floor housing andreplace it with uncontaminated soil; remove 2 inches of range topsoil or keepnew birds oft'contaminated range for at least 4 yearsHUMAN HEALTH RISK — M. avium is not the same bacterium that normally causeshuman TB; human infection is rare but possible in people who have beensensitized to human or bovine TB or who have acquired immune deficiencysyndromeTwisted Leg

Aiso CALLED — crooked legs, long-bone distortion, tibial rotation, valgus leg

deformity, valgus or varus deformation, WD, windsweptINCIDENCE—common in battery-raised broilersSYSTEM/ORGAN AFFECTED — long bones of legPROGRESSION — rapid onset (1 to 2 days)

SYMPTOMS — in broilers 1 week of age and older, primarily cockerels: one or both

legs bend outward at hock joints by as much as 90°, sometimes with a pointed

protrusion at the hock joint; sometimes birdswalk on bruised, swollen hocksPERCENTAGE AFFECTED — up to 2 percent in mixedflocks, up to 25 percent in all-cockerel flocks;highest in birds brooded on wireMORTALITY — nonePOSTMORTEM FINDINGS — outward or inward

angulation of upper or lower bonesRESEMBLES — slipped tendon, except that twisted

leg bones are not widened and shortenedDIAGNOSIS — symptomsCAUSE— unknown, may be genetic or nutri-tional; possibly related to slipped tendonTRANSMISSION — unknownPREVENTION — raise broilers on litter (rather than

on wire) and do not feed for rapid growthTREATMENT— none, condition is not reversibleHUMAN HEALTH RISK — none known

Twisted leg

344 Twisted Leg

Ulcerative Enteritis 3 1 1

TyphoidALSO CALLED— fowl typhoid, FT, infectious leukemia (one kind of salmonellosis)INCIDENCE — worldwide, rare in North AmericaSYSTEM/ORGAN AFFECTED — digestive or system wide (septicemic)INCUBATION PERIOD — 4 to 5 daysPROGRESSION — usually acute, running through flock in about 5 days,

sometimeschronic

SYMPTOMS — in chicks: sudden death soon after hatching or loss of appetite,sleepiness, weakness, droopy wings and head, labored breathing, increasedthirst

— in growing birds over 12 weeks old (mosl common group affected):sudden loss of appetite, droopiness, ruffled feathers, huddling near heat, paleheads, shrunken combs, temperature 1 lo 5 "F (I to 3"C) above normal,diarrhea

— in mature bird: depression, ruffled feathers; sometimes pale heads,increased thirst, dehydration, shrunken combs, greenish or yellowish diarrhea

PERCENTAGE AFFECTED — varies widelyMORTALITY — in chicks: up to 90 percent

—in growing and mature birds: 10 to 50 percentPOSTMORTEM FINDINCS — in young birds: swollen, red liver, spleen, and kidneys

— in older birds: dark, swollen green or bronze liver, sometimes with grayspots; enlarged, sometimes mottled spleen; swollen kidneys; slimy, inflamedintestines; brownish lungs; thin, watery blood

RESEMBI.ES — paratyphoid and pullorum, except that typhoid often continues formonths, usually affects older birds, and causes higher mortality

DIAGNOSIS— flock history, symptoms, postmortem findings, laboratory identifica-tion of bacteriaCAUSE — Salmonella gallinarum bacteria that affect turkeys as well as

chickensand survive for 6 months or more in litter and soil

TRANSMISSION — from infected breeders to chicks through hatching eggs; contami-nated litter, equipment, shoes, flies, feet of animals and wild birdsPREVENTION — purchase certified typhoid-free stock; blood test birds

and elimi-nate carriers; clean and disinfect regularly; control flies, rodents, animals, andwild birds; keep chickens away from contaminated ponds and other surfacewater; rotate range-fed flock; chickens raised in areas where typhoid isprevalent tend to develop resistanceTREATMENT— not recommended, survivors are carriers; this is a reportable

disease in most states, see "Reportable Diseases" page 196HUMAN HEALTH RISK — none known, not the same disease as typhoid fever inhumans

- u -Ulcerative Enteritis

Also CALLED — quail disease, UE

INCIDENCE— common worldwide

346 Urolithiasis

SYSTEM/ORGAN AFFECTED — digestive (lower intestine and ceca)INCUBATION PERIOD— 1 to 3 daysPROGRESSION — acute or chronic, runs its course in 2 to 3 weeksSYMPTOMS — in young birds, 4 to 12 weeks old (commonly 5 to 7 weeks): suddendeath with no symptoms; or listlessness, dull, ruffled feathers, hunched-upposture with head pulled in and eyes closed, diarrhea (sometimes bloody),extreme emaciation, death within 2 to 3 weeksPERCENTAGE AFFECTED — lowMORTALITY — less than 10 percent, peaking within a week

POSTMORTEM FINDINGS — yellowish button-like dots (ulcerations) throughoutintestinal tract, concentrating in lower intestine and cecum; patchy tan oryellow areas on liver: enlarged, mottled spleen; shriveled breast muscleRESEMBLES — blackhead, except that blackhead does not involve the spleen orlower intestine; coccidiosis, except that cocci often causes bloody droppings(UE rarely does not); necrotic enteritis, except that NE rarely involves the liveror ceca

DIAGNOSIS — symptoms, postmortem findings (buttons in intestine, colorfulpatchy liver)

G\USE— Clostridium colinum bacteria that affect game birds more often thanchickens, persist under varying conditions (hot, cold, dry, humid), and resistdisinfectants; often occurs in combination with coccidiosis, mycoplasmosis, orparasites (internal or external); often follows infectious anemia or infectiousbursal disease; outbreak results in permanent contamination of housingTRANSMISSION — contagious; spreads in droppings of infected or carrier birdspicked from litter, feed, or water; spread by flies

PREVENTION — in problem areas, remove and replace litter between flocks or raisebirds on wire; avoid crowding; manage flock to avoid coccidiosis, internal andexternal parasites, and viral diseases (all of which reduce resistance); do notcombine birds of different ages or from different sourcesTREATMENT — streptomycin in drinking water at the rate of 15 grams per gallon for

) 0 days, then 1 gram per gallon for 5 more days; remove old litter; naturalsurvivors are resistant, treated survivors remain susceptible, all survivors maybe carriersHUMAN HEALTH RISK — none knownUrolithiasis. See Gout (visceral)Uveitis. See Marek's Disease

- V -Valgus Leg Deformity. See Twisted LegValgus or Varus Deformation (WD). See Twisted LegVelogenic Newcastle. See Newcastle Disease (exotic)Vent Gleet. See Pasted VentVesicular Dermatitis. See ErgotismVibrionic Hepatitis. See Campylobacteriosis

348 Windpuff

White Muscle Disease 3 1 3

Viral ArthritisALSO CALLED — arthritis/tenosynovitis, reovirus infection, ruptured tendonINCIDENCE — worldwide but rareSystem/Organ Affected—JOINTS AND TENDONSIncubation Period— L TO 13 DAYSPROGRESSION — acute or chronicSYMPTOMS — in young birds (primarily heavy breeds) 4 to 16 weeks old: lameness,stunted growth, uneven gait, swollen hocks, foot, and other joints— in mature birds: bowed or spraddled legs (may go undetected)PERCENTAGE AFFECTED — nearly 100 percentMORTALITY — 2 to 10 percent, primarily in young birdsPOSTMORTEM FINDINGS — hocks and associated tendons sometimes surrounded by

yellowish or pinkish sticky fluidRESEMBLES — staphylococcic arthritis, except that in staph arthritis fluid surround-ing joints is whitish and contains flecks; simple leg injury, except that injuryinvolves only individual birdsDIAGNOSIS — flock history (age ol birds), symptoms (both shanks swollen),

confirmed by laboratory identification of virus

CAUSE — avian reovirus that infects only chickens

TRANSMISSION — contact with infected birds and their droppings or respiratory

discharges; spreads from breeders to chicks through hatching eggsPREVENTION — avoid crowding; do not hatch eggs from infected breeders; vacci-nate breeder flock to pass parental immunity to chicks; chicks start developingnatural immunity by 2 weeks of ageTREATMENT — none; mildly infected birds recover in 4 to 6 weeks; cull severelyaffected birds, as they rarely recover; following an outbreak, thoroughly cleanand disinfect housing with lye or 0.5 percent organic iodine solutionHUMAN HEALTH RISK — noneVisceral Lymphoma. See Lymphoid LeukosisVisceral Urate Deposition. See Gout (visceral)Viscerotropic Velogenic Newcastle Disease. See Newcastle Disease (exotic)Vitamin A Deficiency. See Roup (nutritional)Vitamin E Deficiency. See Encephalomalacia, Exudative Diathesis, White

MuscleDisease

- w -

Water Belly. See Broiler AscitesWestern Duck Sickness. See BotulismWet pox. See Pox (wet)White Comb, See FavusWhite Diarrhea. See PullorumWhite Muscle Disease

Also Called — muscular dystrophy, nutritional myopathyIncidence — not common

350 Windpuff

System/Organ Affected — MUSCLESSYMPTOMS — in chicks 4 weeks old: degeneration of breast and

sometimes legmuscles

PERCENTAGE AFFECTED—10 to 15 percent until diet is correctedMORTALITY—lowPOSTMORTEM FINDINGS — yellow to grayish white streaks (degenerated muscle

fibers) in leg or breast muscleDIAGNOSIS — symptoms, postmortem findings, ration evaluation, absence ofinfection

CAUSE— deficiency of vitamin E and seleniumTRANSMISSION — nutritional problem, does not spread from bird to bird

PREVENTION — use only fresh commercial rations fortified with Vitamin E andselenium; store feed in cool, dry place and use within 2 weeks of purchase

TREATMENT — vitamin E supplement by injection, in feed, or orally (300 IU per

bird); replace old feed; with proper treatment, condition is reversibleHUMAN HEALTH RISK — noneWindpuff. See EmphysemaWindswept. See Twisted LegWing Rot. See Necrotic Dermatitis

- X -X Disease. SeeAflatoxicosis, Bluecomb

- Y-YolkSac Infection. See Colibacillosis, Omphalitis

GlossaryThe following words are defined in the context of chicken health, In

anothercontext, some words may have other or broader meanings.

Abscess. Pocket filled with pus.Acariasis. Mite infestation.Acute. Having a severe and short development, often measured in

hours andending in death or recovery; opposite of chronic.

Anemia. Deficiency of the blood in quantity or quality due to blood loss ordisease, characterized by weakness and pale skin.

Andielmintic. Wormer.Antibiotic. A soluble chemical produced by a microorganism or fungus

andused to destroy or inhibit the growth of bacteria and other microorgan-isms.

Antibody. A natural substance in the blood that recognizes and destroysforeign invaders and that causes an immune response to vaccination orinfection.

Antigen. A foreign protein that differs from natural body proteins andtherefore stimulates the production of antibodies.

Antiseptic. Anything that destroys or inhibits microorganisms responsiblefor disease, decomposition, or fermentation.

Antitoxin. An antibody that neutralizes toxins produced by bacteria.Arthritis. Inflammation of the joint and surrounding tissue.Ascaridiasis. Roundworm infection.Ascites. Accumulation of fluid in the abdominal cavity.Atrophy. Shrinking or wasting away of a body part.Attenuated. Weakened so as not to produce disease but still induce

immu-nity when used as vaccine (said of viruses).

Avian. Pertaining to birds.

351


Bacteria. Microscopic, single-celled plants that may or may not producedisease (singular: bacterium).

Bactericide. A substance that kills bacteria.Bacterin. A vaccine produced from bacteria or their products.Bacteriostat. A substance that inhibits or retards bacterial growth.Ballooning. Distention of the intestine or ceca due to accumulated

blood,mucus, or other materials.

Benign. Not likely to recur or spread.Biosecurity. Disease-prevention management.

GLOSSARY 3 5 3

Blow-out. Vent damage due to laying an oversized egg.Booster. Vaccination other than the first in a series.Bursa of Fabricius. Cloacal bursa.Cannibalism. Eating one's own kind.Cancer. Malignant tumor diat tends to spread.Cankers. Whitish bumps diat erupt to form sores, usually on the face

or indie mouth.

Capillariasis. Capillary worm infection.Carrier. An apparently healthy individual that transmits disease-

causingorganisms to other individuals.

Cauterize. To use a hot iron to burn, sear, or destroy tissue.Cecum. A blind pouch at the juncture of the small and large intestine

thatresembles the human appendix (plural: ceca).

Cephalic. Pertaining to the head or skull.Cestode. Tapeworm.Cestodiasis. Tapeworm infection.Chondrodystrophy. Having short bones.Chromosome. Microscopic cell containing the genes that carry

hereditarydetermination.

Chronic. Having long duration measured in days, months, or even years andbeing somewhat resistani to treatment; opposite of acute.

Clinical. Having signs or symptoms that can be readily observed.Cloaca. The lower end of the digesdve tract where the digestive,

reproduc-tive, and excretory tracts come togelher.

Clubbed down. Down that fails lo emerge in an embryo or newly hatchedchick, most commonly around neck and vent.

Coccidiasis. Infection with coccidial protozoa without showing any signs.Coccidiosis. Infection with coccidial protozoa.Coccidiostat. A chemical added at low levels to feed or water to prevent

coccidiosis.Cockerel. A male chicken under 1 year of age.Coliform. Any bacteria resembling Escherichia coli bacteria.Congested. Filled with blood.Congenital. Existing at birth but not hereditary.Conjunctiva. Mucous membrane covering the eyeball and inner surface of

the eyelid.


Conjunctivitis. Inflammation of the conjunctiva.Contagious. Readily transmitted from one individual or (lock to another.Crop. To surgically remove wattles; also, the pouch at the base of a bird's

neck where feed is temporarily stored.Cull. To kill a diseased or otherwise unproductive bird.Culture. To incubate a sample from a diseased bird for several hours (or

GLOSSARY 3 5 5

days) and look for the presence of bacterial growth.Cyst. A sack-like structure containing fluid or semi-solid material.Debeak. To trim back the top beak to prevent cannibalism.Dehydration. Loss of body water (over 12 percent loss results in death).Depopulate. Get rid of an entire flock.Dermatitis. Inflammation of the skin.Diarrhea. Frequent, runny bowel movements.Diathesis. Susceptibility to certain diseases.Disease. Any departure from normal health or impairment of normal

bodyfunctions.

Disinfection. Killing infectious agents on facilities or equipment but not 011 abird's body.

Drench. To give liquid medication orally (by mouth); also die liquid medica-tion itself.

Dub. To surgically remove a bird's comb.Duodenal Loop. Upper small intestine (same as "duodenum").Ectoparasite. External parasite.Edema. Accumulation of excessive fluid in swollen or damaged tissues.Electrolyte. Natural chemical in the blood needed by body cells to maintain

balance; also, mineral solution used to treat dehydration.Emaciation. Wasting away of the body.Embryo. A developing chick within an egg.Embryonation. Development of an embryo into a larva inside an egg

without hatching.Encephalitis. Inflammation of the brain.Endoparasite. Internal parasite.Enteric. Affecting die intestines.Enteritis. Inflammation of the intestine.Enteropathogens. Microbes that cause enteritis.Enterotoxin. A substance that poisons cells lining the intestines.Enzootic. The continuing presence of a disease or infectious agent in a

specific area (equivalent to "endemic" human diseases).Epizootic. Epidemic among chickens or otiier animals (similar to the word

"epidemic" pertaining to humans).Esophagus. Channel that moves food from the throat to the stomach.


Etiology. The study of causes of diseases.Eversion. Turned inside out.Exudate. Fluid associated with inflammation or swelling.Exudative diatiiesis. Accumulation of fluid (exudate) under the skin or

around the heart.Fecal. Pertaining to feces.Feces. Droppings or body waste.

GLOSSARY 3 5 7

Flaccid. Limp.Fluke. Trematode flatworm parasite.Fomites. Inanimate objects such as shipping crates, feed sacks, clothing,

andshoe soles that may harbor disease-causing organisms and may be eithera vehicle or a reservoir of infection.

Fungus. A plant that does not contain chlorophyll and diat reproducesthrough spores (plural: fungi).

Genes. Parts of chromosomes that carry hereditary factors.Genetic. Pertaining to genes.Germs. Disease-causing microbes.Gangrene. Dead tissue that has no blood supply and no reaction to pain.Going light. Growing thin while eating ravenously; synonym for anemia.Gross. Can be seen with the naked eye.Gross lesions. Easily observable changes in tissues or organs.Helminth. A category of parasitic worms.Helminthiasis. Parasitic worm infestation.Hemorrhage. Heavy or uncontrolled bleeding.Hepatitis. Inflammation of the liver.Horizontal transmission. Transmitted from one bird to another.Host. A bird (or other animal) on or in which an infectious agent lives.Ileum. Lower small intestine.Immune. Resistant.Immunity. Resistance or ability to resist infection.Immunity, active. Resistance to a disease as a result of having had the

disease or having been vaccinated against it.Immunity, passive. Resistance to a disease as a result of injection with

antiserum.Immunoglobulin. Antigen.Impaction. Blockage of a body passage or cavity.Incidence. Number of cases of a particular disease diagnosed during a

particular time period.Incubation period. The time it takes from exposure to a disease-causing

agent until die first symptom appears; also, the time it takes for a bird'segg to hatch.

Infection. The entry of an organism into a body and causing of disease bydeveloping or multiplying therein.

Infectious. Capable of invading living tissue and multiplying dierein,causing disease.


Infertility. Inability to reproduce.Inflammation. Reaction of tissue to injur)' or irritation, whereby it

becomesred, hot, swollen, painful, and possibly loses its function.

Ingest. Eat.

GLOSSARY 3 5 9

Initial vaccination. First vaccination in a series.Inoculate. To give an injection.Inoculant. A substance that's injected.Intramuscular(IM). Placement of an injection into muscle tissue.Intraocular. In the eye.Intranasal. In die nose.Immunosuppressant. Anycause of reduced disease resistance.Intravenous (IV). Placement of an injection into a vein....itis. Suffix indicating inflammation (e.g. sinusitis means inflammation of

the sinus cavities).IU. International Unit, in which some drugs are measured,lejunum. Middle small intestine.Joint ill. Arthritis.Laceration. Jagged wound.Lesion. A change in size, shape, color, or structure of an internal organ.Leukosis. A disease of the blood-forming organs.Lymphatic system. Circulating system that contains the immune system's

white blood cells.Lymphoma. Cancer of the lymph system.Malabsorption. Excessive loss of nutrients through the feces.Malignant. Tending to worsen, recur, or spread; opposite of benign.Mechanical transmission. Carried on the surface.Metabolic disease. A disease involving a breakdown in the body's physical or

chemical processes.Metabolism. All the physical and chemical processes that produce and

maintain a living body.Metastasis. The transfer of disease from one organ to another diat it isn't

direcdy touching.Metastasize. Spread to other tissues or organs.Microscopic. Cannot be seen by the naked eye.Mite. A small to microscopic jointed-legged creature.Mold. A type of fungus.Molt. Natural shedding and renewal of feathers.Morbid. Having or causing a disease.Morbidity. Percentage affected by disease.Morbidity rate. The number of birds in a ilock that contract a disease within


a given time period.Moribund. Dying.Mortality. Deadi rate.Mortality rate. The number of birds in a flock that die from a disease within a

given time period.Mucous membrane. The lining of body cavities.

GLOSSARY 3 6 1

Mucus. Slimy substance produced by mucous membranes.Mycosis. Any disease caused by a fungus.Myopathy. Any disease of the muscles.Necropsy. A postmortem examination (equivalent to a human autopsy).Necrotic. Pertaining to dead tissue.Necrotic enteritis. Inflammation and decaying of intestinal tissue.Nematode. Roundworm.Neoplasm. A tumor or other abnormal growth.Nephritis. Inflammation of the kidneys.Neural. Pertaining to nerves.Noninfectious disease. A disease that is not caused by a biological organism.Noxious. Unpleasant.Ocular. Pertaining to die eye.Oocyst. The infective fertilized egg of certain one-celled animal parasites.Opportunistic. A microorganism that is non-infectious to healthy birds;

infectious only to birds with reduced resistance from some other cause.Organism. A living thing.Osteomyelitis. Inflammation of the bone marrow.Osteopetrosis. Increased size, density, and brittieness of the bone.Osteoporosis. Thinning and weakening of the bone.Oviduct. Channel through which an egg passes after it leaves a hen's ovary.Parasite. A living organism that survives on another living organism without

providing any benefit in return.Parental immunity. Resistance to disease passed from breeders to their

offspring through the egg.Parenteral. Located outside the intestines, used in referring to drugs intro-duced by injection rather than by mouth.Pasting. Loose droppings sticking to the vent area.Pathogen. Disease-producing organism or agent.Pathogenic. Capable of causing disease.Pathogenicity. Degree of ability to cause disease.Pathology. The study of damage caused by disease.Pathologist. A medical professional who looks for internal damage caused

by disease.Pediculosis. Louse infestation.Peracute. Having extremely severe and short duration, measured in

minutesor hours.


Perosis. Malformation of the hock joint.pH. A number that indicates acidity or alkalinity; 7 is neutral, above 7 is

alkaline, below 7 is acid.Pick-out. Vent damage due to cannibalism.Pneumonia. Any disease of the lungs.

GLOSSARY 3 6 3

Popeye. Emaciation of chicks (causing eyes to appear large in relation tobody).

Post. To conduct a postmortem examination.Postmortem. Pertaining to or occurring after death.Predispose. To cause susceptibility to disease.Prevalence. The number of cases of a disease in a flock during a given time.Priming vaccination. Vaccination that increases antibody levels

beforeanodier product is used to induce immunity.

Prolapse. Slipping of a body part from its normal position, often usedincorrecdy to describe an everted organ.

Progeny test. Evaluation of breeders based on the performance of theiroffspring.

Protective synergism. Phenomenon by which two vaccines confer greaterprotection than the sum of their individual effects.

Protozoan. A single-celled microscopic animal that may be either parasiticor beneficial (plural: protozoa).

Proventriculus. A chicken's stomach, lying between the crop and thegizzard.

Pullet. A female chicken under one year of age.Purulent. Full of pus.Pus. Liquid, produced by inflammation, containing dead while blood cells.Rales. Any abnormal sound coming from the airways.Rattling. Abnormal sound coming from the throat.Reactor. A bird that reacts positively to a lest for an infectious disease.Renal. Pertaining to ihe kidneys.Reportable. A disease that is so serious it must, by law, be reported to a

stateor federal veterinarian.

Reservoir of infection. Any animate or inanimate object on which aninfectious agent survives and multiplies and from which it can betransmitted to a susceptible host.

Resistance. Immunity or ability to resist infection.


Respiration rate. Number of cycles per minute by which air is moved intoand out of the lungs.

Rhinitis. Inflammation of the lining of the nasal passages.Rigor mortis. Stiffness following death.Roup. Any condition involving chronic infection ol skull membranes,

characterized by facial swelling.Salpingitis. Inflammation of the oviduct.Secondary infection. A disease that invades after a bird's immune

defenseshave been weakened by some other disease.

Secretion. Fluid coming from a body organ.Seleniferous. High in selenium.


Self-limiling. Any disease that runs its course in a specific amount of timethen stops without treatment.

Septicemia. Blood poisoning or invasion of the bloodstream by a micro-organism.

Serological. Pertaining to the testing of blood serum for antibodies againstspecific diseases.

Serum. The clear liquid portion of the blood left after clotting (plural: sera).Sign. Object ive evidence of disease consisting of symptoms and lesions.Sinus. A hollow space or cavity.Sinusitis. Inflammation of the sinus cavities.Spleen. Organ near the stomach that aids in the proper functioning of

blood.Spore. The seed of fungi or the inactive form of certain bacteria.spp. (as in Salmonella spp.). More bran one species.Starve-out. Failure of chicks to eat.Sterile. Entirely free of living organisms; also, permanently unable to

repro-duce.

Sternum. Breastbone or keel.Stress. Any physical or mental disruption that lowers resistance.Subclinical. An inapparent infection for which signs or symptoms can be

detected only di rough laboratory analysis.Subcutaneous. Directly beneath die skin.Symptom. Detectable evidence of disease.Syndrome. A group of symptoms that occur in combination in a

particulardisease, such as ninting syndrome.

Synergistic. Working in cooperation (same as "synergetic").Syringe. Tube with plunger that holds a drug to be injected.Systemic. Involving the entire body.Taeniasis. Obsolete word for cestodiasis (tapeworm infection).Tenosynovitis. Inflammation of the synovial shield of a tendon.Three-host tick. A tick that spends the diree stages of its life on three

differ-ent hosts.

Torticollis. Twisted or wry neck.Toxemia. Generalized poisoning resulting from circulation through die

bodyof toxins produced by bacteria.

Toxin. A poison produced by microorganisms.

Toxoid. An agent that confers immunity against toxins produced by bacteria.

Trachea. Windpipe.Transovarian transmission. Infection of a hen's egg before the shell is

formed.Trauma. Wound or injur)' that destroys tissue.Traumatic ventriculitis. Piercing of the gizzard from the inside by a

pointedobject.

366

GLOSSARY 3 6 7

Trematode. A fluke.Tubercle (as in tuberculosis). A tumor-like mass.Tumor. A mass of tissue that develops and grows without benefit to sur-

rounding tissue.Ulcer. A raw, red sore.Unthrifty. Unhealthy appearing and/or failing to grow at a normal rate.Urates. Uric acid (salts found in urine), appearing as white crystals or

paste.Uremia. Poisoning caused by accumulated wastes in the Body, usually

dueto kidney failure.

Urolith. Urinary stone.Vaccine. Product made from disease-causing organisms and used to

induceimunity.

Vascular. Pertaining to blood vessels.Vector. A living thing that carries disease organisms within its body

from onesource to another (examples: mosquitoes, ticks, flies).

Vehicle. Anything that mechanically carries disease from one place toanodier (examples: clodiing, equipment, dust).

Vent. The outside opening of the cloaca.Ventriculus. The gizzard.Venipuncture. Inserting a needle into the vein for the purpose of

withdraw-ing blood.

Vertebrae. Bones in the spinal column (singular: vertebra).Vertical transmission. Transmitted from parent to offspring through

hatching eggs.Veterinary ethology. The study of animal behavior as it relates to health.Viremic. Of or pertaining to a virus in the blood.Viscera. Internal body organs and glands.Viscous. Thick and sticky.Virulence. Pathogenicity or ability to cause disease.Virus. An ultra-microscopic organism that multiplies only in living cells.Warfarin. An anti-coagulant used to poison rodents.Zoonosis. A disease transmissible from a chicken (or other animal) to a

human (plural: zoonoses).

Suppliers

American Livestock and Pet Supply. Inc.Madison, Wisconsin800-356-0700www.americanlivestock.comCutler's Pheasant and Poultry Supply,Inc.Applegate, Michigan810-633-9450www.cutlersupply.comDouble R Discount Pet, Poultry, andAvian SupplyPalm Bay, Florida321-837-1625

www.dblrsupply.comFirst State Veterinary SupplySalisbury, Maryland410-546-6137www.firststateuet.supply.comG.Q.F. Manufacturing CompanySavannah, Georgia912-236-0651www.gcifmfg.coniElemental Scientific, LLC(formerly Hagenow Laboratories, Inc.)Appleton,

368

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GLOSSARY 3 6 9

Wisconsin920-882-1277www.hagenowlaboratories.comJeffers, Inc.Dothan, Alabama800-533-3377www.jefferslivestock.comMeyer HatcheryPolk, Ohio888-568-9755www.meyerhatchery.comMurray McMurray HatcheryWebster City, Iowa800-456-3280www.mcmurrayhatcheiy.comOmaha Vaccine CompanyCSR Company Inc.Omaha, Nebraska800-367-4444www.omahavaccine.coni

PBS Animal HealthMassillon, Ohio800-321-0235www.phsanimalhealth.comLohmann Animal Health InternationalLampasas, Texas800-639-1581www.iahinternational.com

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ALABAMA

Alabama Veterinary DiagnosticLaboratoriesDepartment of Agriculture & IndustriesAuburn, Boa/., Elba, and Hanceville. ALhttjr.lllabs.alahama.gov

ALASKAState VeterinarianDepartment of EnvironmentalConservationAnchorage, AK907-375-8200www.dec.state.ak.us/eh/vetARIZONAArizona Veterinary DiagnosticLaboratoryUniversity of ArizonaTucson, AZ520-621-2356http:llmicrovet.arizona.edu/A&/DLARKANSASArkansas Livestock & PoultryCommission Veterinary DiagnosticLaboratoryLittle Rock and Springdale, AR501-907-2430www.arlpc. org/lab. aspCALIFORNIACalifornia Animal Health and FoodSafety Laboratory SystemUniversity of California, DavisDavis, San Bernardino, Tulare, andTurlock, CA530-752-8700www.cahfs.ucdavis.eduCOLORADOVeterinary Diagnostic LaboratoriesColorado State UniversityFort Collins, Grand Junction, and RockyFord, CO970-297-1281www. dlab.colostate. edu

CONNECTICUT

Connecticut Veterinary MedicalDiagnostic LaboratoryUniversity of ConnecticutStorrs, CT860-486-3738http://cvmdl.uconn.edu

DELAWAREPoultry and Animal Health SectionDelaware Department of AgricultureDover, DE302-698-4561liitp://dda.delaware.gov/poultryahFLORIDABureau of Diagnostic LaboratoriesFlorida Department of Agriculture &Consumer ServicesKissimmee and Live Oak, FLwww.doacs.state.fl.us/ai/labs/labs_main.shtmlBureau of LaboratoriesFlorida Department of HealthJacksonville, Lantana, Tampa, Miami, andPensacola, FL850-245-4517www.doh.state.Jl. us/Lab

GEORGIAGeorgia Poultry Laboratory NetworkCamilla, C.arnesv:Ile, Dalton, Forsyth,Glennville, and Oakwood, GA770-535-5996www.gapoultrylab.org

370

State Poultry Pathology Laboratories

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http://www.doacs.state.fl.us/ai/labs/

http://www.doh.state.Jl/

http://www.gapoultrylab.org/

http://www.arlpc/

http://www.dec.state.ak.us/eh/vet

Georgia Veterinary DiagnosticLaboratoriesUniversity of GeorgiaAthens and Tifton, GA706-542-5568www. net. uga.edu/dlab

HAWAIIHawaii State Veterinary LaboratoryHawaii Department of Agriculturewww.liawaii.guv/lidoalailvlab

IDAHOAnimal Health LaboratoryIdaho State Department of AgricultureBoise ID208-332-8570www.idalioag.us/Categories/Laboratoiies/indexLabs.php

ILLINOISAnimal Disease LaboratoriesIllinois Department of AgricultureCentralia and Galesburg, ILwww. agr.state. il. us/An imalH W/labs

INDIANAIndiana Animal Disease DiagnosticLaboratoryPurdue UniversityWest Lafayette and Dubois, IN765-494-7440www.addl.puirlue.edu

IOWAVeterinary Diagnostic LaboratoryIowa State UniversityAines, IA515-294-1950http://vetmed.iastate.edu/diagnostic-

lab

KANSASKansas Slate Veterinary DiagnosticLaboratoryKansas Slate UniversityManhattan, KS866-512-5650www.uet.ksu.edu/depts/dtnp/service

KENTUCKYBreathitt Veterinary CenterMurray State UniversityI lopkinsville, KY270-886-3959http://breathitt.iniirraystate.eduVeterinary Diagnostic Laboratory(formerly the Livestock DiseaseDiagnostic Center)University of KentuckyLexington, KY859-257-8283www.tdclc.uky.edu

LOUISIANALouisiana Animal Disease DiagnosticLaboratoryLouisiana State UniversityBaton Rouge, LA225-578-9777http://laddl.Lsu.edu

MAINEMaine Veterinary Diagnostic LaboratoryUniversity of MaineOrono, ME207-581-2787www.umaine.edu/vetlab

MARYLANDAnimal Health Diagnostic LaboratoriesDepartment of AgricultureAnnapolis, Frederick, and Salisbury, MD410-841-5810www.mda.state.ind.us/animal_health/regional_animal_health_offices.phpMASSACHUSETTSDivision of Animal Health PoultryProgramMassachusetts Department ofAgricultural ResourcesBoston, MA617-626-1796www.inass.gov/agrlanimalhealihlpoultiyIDEXX Laboratories, Inc.North Grafton, MA888-433-9987www.idexx.com

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MICHIGANDiagnostic Center for Population andAnimal HealthMichigan State UniversityLansing, Ml517-353-1683www.aninialhealth.msit.edu

MINNESOTAVeterinary Diagnostic LaboratoryUniversity of MinnesotaSt. Paul, MN800-605-8787www.udl.urnn.edu

MISSISSIPPIDiagnostic Laboratory SystemMississippi State UniversityMississippi Slate and Pearl, MS601-420-4700www.cum.msstate.edu/diagnostieJabs/index.html

MISSOURIAnimal Health Diagnostic LaboratoriesMissouri Department of AgricultureJefferson Cilv and Springfield, MO573-751-3460http:llnida.mo.gov/animalslhealthldiagnosticlabs.phpResearch Animal Diagnostic LaboratoryUniversity of MissouriColumbia, MO800-669-0825www.mdil.missouri.edu

MONTANAMontana Veterinary DiagnosticLaboratoryMontana Department of LivestockBozeman, MT406-994-4885http://mt.gov/liv/lab/index.aspNEBRASKANebraska Veterinary DiagnosticLaboratoryUniversity of NebraskaLincoln, NE402-472-1434li ttp:Hn veils, iml.edu

NEVADAAnimal Disease and Food SafetyLaboratoryNevada Department of AgricultureElko and Reno, NV775-688-11802http://agri.nv.gov/Animal2_adl.htm

NEW HAMPSHIRENew Hampshire Veterinary DiagnosticLaboratoryUniversity of New HampshireDurham. NH603-862-2726www.unh.edu/nhvdl

NEW IERSEYAnimal Diagnostic LaboratoryNew lersey Department of AgricultureTrenton, NJ609-984-2293www.state.nj.us/agricidture/divisions/ah/progHab.html

NEW MEXICOVeterinary Diagnostic ServicesNew Mexico Department of AgricultureAlbuquerque, NM800-432-9110http://nmdaweb.nmsit.edu/laboratory-services

NEW YORKDepartment of Microbiology andImmunologyCornell UniversityIthaca, NY607-253-3400www. vet.coriiell.edu/microbiology

State Poultry Pathology Laboratories 327

http://www.udl.urnn.edu/

http://www.mdil.missouri.edu/

http://www.unh.edu/nhvdl

http://www.aninialhealth.msit.edu/

http://www.cum.msstate.edu/diagnostieJabs/

http://www.cum.msstate.edu/diagnostieJabs/

http://agri.nv.gov/Animal2_adl.htm

http://www.state.nj.us/agricidture/divisions/ah/

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http://nmdaweb.nmsit.edu/laboratory-

http://nmdaweb.nmsit.edu/laboratory-

http://mt.gov/liv/lab/index.asp

Duck Research LaboratoryCornell UniversityEastpori, NY631-325-0600i vivw.dtickhealrh.com/ditcklab.hrinl

NORTH CAROLINAVeterinary Diagnostic LaboratorySystemNorth Carolina Department of Agriculture& Const) mer ServicesArden, Elkin, Monroe, and Raleigh, NC919-733-3986www.ncagr.gov/vet/ncvdl

NORTH DAKOTANorth Dakota Veterinary DiagnosticLaboratoryNorth Dakota State UniversityFargo, ND701-231-8307www.vdl.ndsu.edu

OHIOAnimal Disease Diagnostic LaboratoryOhio Department of AgricultureReynoldsburg, OH614-728-6220www.ohioagriculture.gov/addl

OKLAHOMAOklahoma Animal Disease DiagnosticLaboratoryOklahoma State UniversityStillwater, OK405-744-6623www.cvm.okstate.edu/oaddl

OREGON

Animal Health LabOregon Department of AgricultureSalem, OR503-986-4686www.oregon.gov/ODA/AHlD/animal_heallh/labjnain.shtmlVeterinary Diagnostic LaboratoryOregon Slate UniversityCorvallis, OR541-737-3261

http://oregonstate.edu/vetmed/diagnosticPENNSYLVANIAAnimal Diagnostic LaboratoryPetin StateUniversity Park, PA814-863-0837h ttpj/vbs.psu. edu/J'acil i ties/ad IA member of PADLS

New Bollon CenterUniversity of PennsylvaniaKennett Square, PA610-444-5800www.vet.upenn.eduA member of PADLSPennsylvania Animal DiagnosticLaboratory SystemPennsylvania Department of AgricultureHarrisburg, PA717-787-8808www.padls.orgA member of PADLSPUERTO RICODepartment of AgricultureSan Juan, PR787-721-2120www.agriculiura.gobierno.pr

RHODE ISLANDDepartment of Fisheries, Animal, andVeterinary ScienceUniversity of Rhode IslandKingston, Rl401-874-2477www.uri.edu/cels/favs

SOUTH CAROLINAVeterinary Diagnostic CenterClemson UniversityColumbia, SC803-788-2260www.cletnson.edu/public/lph/lab

SOUTH DAKOTAAnimal Disease Research and DiagnosticLaboratorySouth Dakota State UniversityBrookings, SD

http://www.vdl.ndsu.edu/

http://www.vet.upenn.edu/

http://www.uri.edu/cels/favs

http://www.ohioagriculture.gov/addl

http://www.cvm.okstate.edu/oaddl

http://www.oregon.gov/ODA/AHlD/animal_

http://www.agriculiura.gobierno.pr/

http://www.cletnson.edu/public/lph/lab

http://www.padls.org/

http://oregonstate.edu/vetmed/diagnostic

http://oregonstate.edu/vetmed/diagnostic

http://www.ncagr.gov/vet/ncvdl


605-688-5171www.sdstate.edu/vs/adrdi

http://www.sdstate.edu/vs/adrdi

TENNESSEEC. E. Kord Animal Disease DiagnosticLaboratoryTennessee Department of AgricultureNashville, TN615-837-5125www.tn.gov/agriculture/regulatory/kord.html

TEXASDepartment ofVeterinary PathobiologyTexas A&M UniversityCollege Station, TX979-845-5941http://veimed.tainu.edu/vtpbTexas Veterinary Medical DiagnosticLaboratoryTexas A&M SystemAmarillo, Center, College Station, andGonzales, TX888-646-5623http://lvmdl. tamu.eduPoultry specific laboratories in Center andGonzales, TX

UTAHAnalytical/Chemistry LaboratoryUtah Department of Agriculture and FoodSalt Lake City, UT801- 538-7128http://ag.utah.gov/divisions/chemisiryUtah Veterinary Diagnostic LabUtah State UniversityLogan and Nephi, UT435-797-1895www. usu. edu/u veil

VERMONTAnimal Agriculture LaboratoriesVermont Division of Agricultural ResourceManagement and EnvironmentalStewardshipWaterburv, VT802- 244-4510

www.vermontagriculture.com/ARMESHabVIRGINIAOffice of Laboratory ServicesDepartment of Agriculture and ConsumerServicesHarrisonburg, Ivor, Lynchburg,Warrenton, and Wytheville, VA804-786-9202www.vdacs.virginia.gov/animals/labservices.shtmlVeterinary Teaching HospitalVirginia TechBlacksburg, VA540-231-4621www.vetnied.vt.edu/VTH

WASHINGTONWashington Animal Disease DiagnosticLaboratoryWashington State UniversityPullman and Puvallup, WA509-335-9696www. vetmed. wsu. edu/depts_ wadell1'he Avian Health and Food SafetyLaboratory is located within the PuyalluplaboratoryWEST VIRGINIAMeat & Poultry Inspection DivisionWest Virginia Department of AgricultureCharleston, WV304-558-2206www.wvagriculnire.org/Division_Webpciges/meat_poultiy.litmlWISCONSINWisconsin Veterinary DiagnosticLaboratoryUniversity ofWisconsinBarron and Madison, WI

http://www.vetnied.vt.edu/VTH



http://www.tn.gov/agriculture/regulatory/kord

http://www.tn.gov/agriculture/regulatory/kord

http://lvmdl/

http://www.vdacs.virginia.gov/animals/

http://www.wvagriculnire.org/

http://www.vermontagriculture.com/ARMESHab

http://www.vermontagriculture.com/ARMESHab

http://ag.utah.gov/divisions/chemisiry

http://ag.utah.gov/divisions/chemisiry

http://veimed.tainu.edu/vtpb


608-262-5432www. wvdl. wise, edit

WYOMINGWyoming State Veterinary LaboratoryUniversity of WyomingLaramie, WY307-766-9925http://wy o vet.uwyo.edu

State Poultry Pathology Laboratories 329

http://wyovet.uwyo.edu/

http://wyovet.uwyo.edu/

CanadaALBERTALivestock Pathology ConsultationProgramAgriculture and Rural DevelopmentAirdrie, AB403-912-3309iuivwl.agric.goii.ab.ca/ScleiJariment/deptdocs. nsf/all/afs 10898

BRITISH COLUMBIAAnimal Health CenterMinistry of AgricultureAbbotsford, BC800-661-9903www.agf.gov.bc.ca/ahc

MANITOBAVeterinary Diagnosis ServicesLaboratoryUniversity of ManitobaWinnipeg, MB204-945-8738www.gov.mb.ca/agriculture/programs/aaalls02.html

NEW BRUNSWICKVeterinary Laboratory and PathologyServicesDepartment of Agriculture, Aquacultureand FisheriesFredericton, NB

506-453-5412www.gnh.ca

NOVA SCOTIALaboratory ServicesNova Scotia Agricultural CollegeTruro, NS902-893-6540www.gov. ns. ca/agri/qe/labservPRINCE EDWARD ISLANDAtlantic Veterinary CollegeUniversity of Prince Edward IslandCharlottetown, PE902-566-0882www.upei.cci/avc

QUEBECDepartment of Pathology andMicrobiologyUniversity of MontrealSaint-Hyacinthe, QC450-773-8521www.mecluet.umontreal.ca/clepartements/PathologieMicrobiologie.html

SASKATCHEWANDepartment ofVeterinary PathologyUniversity of SaskatchewanSaskatoon, SK306-966-7280www.usask.ca/wcvm/ciepartments/pathology

ONTARIOAnimal Health LaboratoryUniversity of GuclphGuelph and Kemptville, ON519-824-4120www.guelphlabservices.com/AHl.

377

http://www.agf.gov.bc.ca/ahc

http://www.upei.cci/avc

http://www.gov.mb.ca/agriculture/programs/

http://www.gov.mb.ca/agriculture/programs/

http://www.gov/

http://www.mecluet.umontreal.ca/clepartements/

http://www.mecluet.umontreal.ca/clepartements/

http://www.usask.ca/wcvm/ciepartments/

http://www.guelphlabservices.com/AHl

http://www.gnh.ca/


Recommended ReadingSome ofihe following publications are regularly updated as new information andtreatments are made available. When requesting a copy, ask for the latest edition.Avian Disease Manual. The American Association of Avian Pathologists, 706-542-5645, wivw.aaap.info; easy-to-read handbook designed for avian pathologystudents.

Chicken Diseases, F. P. Jeffrey, American Bantam Association, 973-383-8633,www.ba n tamclub.co m.bo o Vl e l g eared toward the backyard enthusiast.

Code of Federal Regulations Title 9 (vaccines), Title 21 (drugs), Title 40 (pesticides),United States Government Printing Office, 866-512-1800, www.access.gpo.gov;U.S. government regulations, including drug use in poultry (available at manylibraries).

Poultry Diseases and Meat Hygiene: A Color Atlas, Drago I lerenda and Don Franco,Blackwell Publishing, 800-862-6657, www.blackwellpublishing.com; colorphotos illustrating internal organs with various disease conditions.Diseases of Poultry, Blackwell Publishing, 800-862-6657, www.blackwellpublisliing.com; comprehensive tome written in fairly technical language.

The Federal Register, United States Government Printing Office, 866-512-1800,www.access.gpo.gov; U.S. government regulations, including drug use in poultry(available at many libraries).

Feed Additives Compendium, Miller Publishing Company, 800-441-1410, www.feedstuffs.com; monthly report on current regulations governing livestock feeds(available at agricultural libraries).

http://www.bantamclub.com.booVlelgeared/

http://www.blackwellpublishing.com/

http://www.access.gpo.gov/

http://www.blackwellpublisliing/

http://www.access.gpo.gov/

Feedstuffs Reference Issue & Buyers Guide, The Miller Publishing Company,800-441-1410, www.feedstuffs.com; annual feed industry report on livestocknutrition and disease.

Poultry Disease Manual, Michael Davis, Texas Cooperative Extension, 888-900-2577, http:lltcebookstore.org; handbook for small-flock owners.

National Poullty Improvement Plan, http://www.aphis.usda.gov/vs/npip; onlinesearchable database of flock owners, dealers, and hatcheries of all fowl by state.

Nutrient Requirements of Poultry, National Research Council, National AcademyPress, 888-624-8373, www.nationalacademies.org; technical discussions andfeed charts for formulating rations.

379

http://www.feedstuffs.com/

http://www.aphis.usda.gov/vs/npip

http://www.nationalacademies.org/


Poultry Health Handbook, L. Dwight Schwartz, College of Agricultural SciencesPublications, 814-865-6713, http:llpubs.cas.psu.edu: guide to identifying andpreventing diseases of chickens and other fowl.

Veterinary Clinical Parasitology, Anne Zajac and Gary Conboy, BlackwellPublishing, 800-862-6657, wuiw.blackwellpublishing.com: laboratory manualdescribing how to conduct a fecal examination, with photos of some of theparasites that infect fowl

Index(Illustrations are indicated by page numbers in italics;charts and tables are indicated by pages numbers in bold.)

A-avitaminosis. Sec Roup (nutritional)Acanthucephalans, 77,79,88Acariasis. See MitesAconiatacarus. galli, 68, 72Acute death syndrome. See Sudden deathsyndromeAcute heart failure. See Sudden death syndromeAdenovirus, 120,120,121-122AE. See Epidemic tremorAetles spp. 63Aerosol vaccination, 203-204.204Aflatoxicosis. 140,141,156, 164,218, 245.275.291

and human health. 232,245Aggression, 25Al. See InfluenzaAirborne infections, 7Airsacculitis, 179. See also Air-sat diseaseAir-sac disease, H, 110,113-114,131,158,215,246.

175,176Air-sac mites. 68,71.309Air sacs, 48, 48-49,54, 179

Algae poisoning, 39,155,163,176, 246-247All-in all-out management, 9. 109Alpliatobiitsdiupernus. See Darkling beetleArnblyomniaspp, 68, 74, 74■Aminoglycosides, 189-190Ammonia blindness. SeeConjunctivitisAmmonia fumes, 15,16.112. 264Amoebotaenia cuneata, 90Anaphylactic shock. 164, 190Anemia, 55. See also Infectious anemiaAnthelmintics. 80-82,186Antibacterial drugs. See AntibioticsAntibiotic residues, 191-192Antibiotics. 116. 184-185,186-190.191and fungal infections, 129. 187and human health, 191-192,237

381


reactions to. 190. 194Antibodies, 44,45, 197. 198. 199. 199,200-201Antifreeze poisoning, 141, 153,155Anti-fungal drugs, 186. 187Antigens. 45, 103,199, 200Anti-infection vitamin, 28Antimicrobial. See AntibioticsAnti protozoal drugs. 186Antiseptic, 21Antitoxin. 186.197, 198Antiviral drugs, 186-187Aplastic anemia. See Infectious anemia/4rga.< spp. 68, 73, 73Argostemma gilhago, 142Arizonosis, 8, 110,

115, 152, 215,247-248, 294, 295and human health, 248symptoms of.

152, 154,163, 174,175, 176,247Arrow Universal Warning Symbol, 191, 191Arthritis, 121,179,281 .See also

Staphylococcic arthritis, Viral arthritisAscariilia galli. See RoundwormsAscaridiasis. See RoundwormsAscites. See Broiler ascitesAsclepias spp, 142

Aspergillosis. 129, 130, 130,248-249

and human health, 231,231-232,248,249resemblance to: chlamydiosis. 257:

dactylariosis, 265symptoms of, 158, 159, 161, 162, 176,218,248.249

Aspergillus flauus. 232. Sec also AflatoxicosisA. fitniigatus. See AspergillosisAspergillus infeci ion. See AspergillosisA. ochraceous. See OchratoxicosisA. parasiticus. .See AflatoxicosisAspergillus poisoning. See AflatoxicosisAttenuation, 201-202Autoinfection. 105Bacillary white diarrhea. See PullorumBacilli. 109. 109Bacitracin. 190Bacteria, 15, 109. 115, 199beneficial. 33. 107,107food-borne. 237-243, 238, 240opportunistic. 6. 107, 107, 116,118pathogenic, 107, 107. 108Bacterial diseases, 59,62,108-109, 110Bactericide, 21, 188, 189. 190

Bacterin, 200.202Bacteriostat, 21, 188. 189, 190Beak dip vaccination, 204Beak disorders, 34, 228Bedbug. 59.59-60Beetles. 59.60, 60.86,90. 90Behavior patterns, 23-25Big liver disease. See l ymphoid leukosisBiosecurity, 9,195Biotin deficiency, 35, 217,228,297. See alsoVitamin BBirnavirus, 120,120Blackhead, 8,39,84-85,97, 105, 198,250resemblance to: campylobacteriosis. 256;coccidiosis, 261; lymphoid leukosis, 285;Marek's disease, 287; Newcastle disease,

291;tuberculosis, 309; ulcerative enteritis, 312symptoms of. 152,159,163,174,176,250Blindness. 150. See also ConjunctivitisBlister burn, 288

383


Blood clotting. See Vitamin KBlood disorders, 56,106,179. Sec also SepticemiaBlood sampling, 149, 149Blood type. 55Bloom, 247Blowout. See Prolapsed oviductBluecomb, 8, 39. 123. 131. 251

postmortem results, 174, 175, 176, 251resemblance to: campylobacteriosis. 256:

cholera, 259symptoms of, 153, 159, 160, 161, 162,163, 164,

251Blue green algae, 247. See also Algae poisoningBluestone, 187Body temperature, 43,57.150. 162Bones. 34, 48-49, 50-51, 50. 56, 174, 228Booster shots, 199,206Horrelia auscrina. See SpirochetosisBotulism. 39,110.155, 163,164, 174, 111-112. 251-

252and human

health, 231, 240,243, 252resemblance to algae poisoning, 246: Marek'sdisease, 287: lick paralysis, 73Brain disorders, 34, 179Breast blister. 14.51, 117, 189,252-253,253

and human health. 243, 253Broiler ascites, 131, 163,164, 175, 176,253Broiler runting syndrome. See Infectious stunting

syndromeBronchitis. Set'Infectious bronchitisBrooder disorders, 135,138, 216.223-227,228, 229Brooder pneumonia. See AspergillosisBrooding instinct, 24-25Buffet germ, 241Bugs. 59. 59-60, 72. 73Built-up litter system, 15,30-31Bumblefoot, 14. 110, 117.155, 162, 188,189,254-255. 255and human health, 243, 254Bursa of Fabricius. See Cloacal bursaBursitis. 51. Seetilso Breast blisterCage confinement, 13,15and disease, 103, 105and nutrition, 28,31and worms, 81,83,89Cage fatigue. 33, 155, 157, 174, 255. 293. 300Cage osteoporosis. See Cage fatigueGige paralysis. See Cage fatigueCalcium, 29.31,34-35,

193, 189, 228Campylobacter fetus jejuni, 238, 238, 240. See also

CampylobacteriosisCampylobacteriosis, 8. 109, 110, 111.255-256, 271and human health, 109, 231,238, 238,240,241,256

symptoms of, 152, 156, 164, 175, 176,255Cancer. See TumorsCandida albicans. See ThrushCandidiasis. 231,232. See also ThrushCanker, 8,97, 106,256-257

resemblance to: Newcastle disease, 291: wet

pox, 297; thrush, 308symptoms of, 158, 160, 161, 162, 174, 256Cannibalism, 24,32, 113, 126, 135-138. 194Capillarui spp. 81.86-87Capillariasis. See Capillary wormsCapillary worms, 84, 80,86-87,256,308Caponizjng, 195. Stealso EmphysemaCarbohydrates, 32.35Carbolic acid. 19Carbon monoxide poisoning, 141, 163Carcass

disposal. 180Cardiovascular disorders, 56Carriers, 7-8, 8, 182Cassia ubrusefolia, 140Castor-bean poisoning, 142,251Cats, 106, 145Cauliflower gut. See Necrotic enteritisCeca, 47, 174Cecal droppings. 47. 151.153Cecal worms, 84-85,86-87,105Ceralapliyltus gallinae, 60C. Niger, 60-61Cestodes. See TapewormsCestodiasis. See TapewormsCheibspirura hamulosa, 86-87Chicken anemia agent. See Infectious anemiaChicken Little syndrome, 24Chicks

brooding of. 223-224disorders of, 224-275. 228, 229identification of, 221-223poisoning in, 141, 143vitamin supplement for. 28, 225Chiggers. 68, 72. 72.72Chlamydia psiliaci. See ChlamydiosisChlamydiosis, 59,66, 8, 18, 110,114.257

and human health, 168, 189, 190.196, 231,235-236,257

resemblance to: erysipelas, 270; influenza, 282

385


symptoms of. 153, 158, 176, 177,257Choanolaenia infundibulum, 90Cholera, 8, 18,39, 110,117.190, 191.204,205acute, 117, 153,158,159, 161, 162, 163,258-259.

282,291,305chronic, 117.154, 156, 158, 159, 161,162,259.

259-260, 302and human health, 117, 259resemblance to: campylobacteriosis. 256:chlamydiosis. 257; chronic respirator)'disease, 259; colibacillosis, 263; erysipelas,270: infectious coryza. 279; spirochetosis, 304symptoms of. 162,164, 174, 175, 176and ticks. 59,73Chloride. 193,228Chlorine-based disinfectants. 19.20,209Choking, 164Chondrodystrophy. See Slipped tendonChronic respiratory disease. 8, 110.113-114. 196,205,207,214 215, 260

resemblance to: air-sac disease. 246; infections

coryza, 279; influenza, 282symptoms of, 152, 156, 159, 161, 175, 176,260Cirnex spp. 59,59-60Circling disease. See ListeriosisCirculatory system, 55. 57,175Claviceps purpurea. See ErgotismClaw disorders, 34Cloacal bursa, 45. 45.45, 48. 174. See also

Cryptosporidiosis. Infectious bursal diseaseCloacitis. See Pasted ventClosed flock, 10-11Clostridial dermatomyositis. See Necrotic

dermatitisClostridial diseases, 110, 11 l-l 12, 188Clostridium botulinuin. 238, 240. See also BotulismC callnum. See Ulcerative enteritisC. petfringens, 238,240. See also Necrotic enteritisClostridium poisoning, 111-112,231. See also

BotulismC. septicttm. See Necrotic dermatitisClubbed down, 216.217Cocci, 109, 109Coccidiasis, .98Coccidiosis. 18, 18,97,98-9, 102-104,205, 188.225cecal. 102. 152, 163,250,261intestinal, 152, 156, 160, 163, 261-262, 289. 275.277

and nutrition, 28,32.33,228symptoms of, 100-101,102.174, 175See also CryptosporidiosisCoccidiostats. 29, 52.103,103-104. 143Cock-feathered hens, 54Coffee seed poisoning, 140. 153Colds. See Infectious coryza. Infectious bronchitis,

Respiratory disordersColibacillosis. 29.35, 110,112,215,218, 262-263and human health, 115,231,238,240postmortem findings, 175, 176, 177,262

resemblance to: chlamydiosis. 257; cholera, 258;erysipelas. 270symptoms of, 153,157, 161, 164,262treatment of. 188. 189, 190, 191Coliform, 112Colitis, 231,240,243Collyriclum f/tba, 92Comb. 148color, 159-160and fertility, 214.218frostbitten, 132-133removal, 133-134See also FavusCompetitive exclusion, 107, 19:1-194Compost, 15,21,180Confinement housing. 13, 15Congenital loco. See Congenital tremorCongenital tremor. 154,220, 263,268-269Conjunctivitis, 16,161,179,263-264

and human health, 231,236Constitutional vigor, 11,217Contagious catarrh. See Infectious coryzaCopper deficiency, 32, 35,228Copper sulfate. 187Corn cockle. 142Coronavirus. 120.120Coryza. See Infectious coryzaCrazy chick disease. See Encephalomalacia.

Congenital tremorCRD. See Chronic respiratory diseaseCreeper gene, 220Cresol, 19,20Cresylic acid, 19Crop binding. SeeCrop impactionCrop disorders. 160, 174Crop impaction, 46, 131. 160,264, 174,195Crop mycosis. See ThrushCropping, 116, 133-134. 195Crop worms, 84,86-87Crotalaria poisoning. 140.153Crowing, 24Crud. See Necrotic enteritisCryptococcocus neoformans, 231,232Cryptococcosis, 231,232Cryptosporidiosis. 97, 101-105, 154, 158, 159,163,

265,291,312Cryptosporidium baileyi. See CryptosporidiosisCttcloiogaster heterographus,


64,64,65,66Culex spp. 63Culicoides spp, 62Culling, 11-12, 181-182.220Curled-toe paralysis, 31.33.227. 268Cyanobacteria, 247Cytodites nudus, 68, 71

Dactylaria gallopava. See DactylariosisDactylariosis. 129, 130. 130, 154,248.265-266Darkling beetle, 59,60, 60.90Daubentonia longifolia, 142Davainea pmglottina. 89.90Dead birds, disposal of, 180Death

of chicks, 223, 225.226diseases causing, 79. 163-164of embryos. 211,216,217,218-219rate of. 165, 167See also SeplicemiaDeath camas, 142

Debeaking, 64, 116. 138-139, 139, 195Decrowing, 195Dehydration, 40-11.41, 48,54,156,180, 193,226Dermanyssus gallinae, 67,67.68Dermatitis, 288. See also Ergotism, Necrotic

dermatitisDermog)'lpluisspp. 68Detergent, 17, 19,21,209Diagnosis, 147, 148, 150, 165, 195,244Diarrhea. 151. 152-153and antibiotics, 190and dehydration, II, 193and drug absorption, 183

INDEX 335

INDE

X 389

Diarrhea (continued)and enteritis, 47,123.150and nutrition, 31,227and stress, 23treatment of, 190and worms. 79Digestive disorders, 56, 77Digestive system. 46-48, 46,172,172, 17.% 190Dikkop. See Swollen head syndromeDiphtheria. See Infectious laryngotracheitis. Pox

(wet)Direct contact, 6, 6Disease. 3Disease cycle, 211Disease history, 166Disinfectants. 19-21. 20,143.211-213Disinfection. 17-18Olspharynx nttsula, 86-87Displacement activity, 25Distemper. Sec Newcastle diseaseDonalc Duck syndrome, 220Drenching, 183.183-184Droppings. 148, 228cecal, 47,151.153and flies, 62-63and disease, 34,151. 152-153and parasites, 93See also DiarrheaDroppings boards, 14Dropsy. See Broiler ascitesDrugs. 13, 181. 182. 183-186. 195antibiotic, 186-190anticoccidial, 103, 103-104dilution of, 184and nutrition. 33and stress, 22

and water consumption, 23,40worming, 80-82Dubbing, 113. 116, 126,133-143. 195Dust baths, 24,75-76Ecbidn 'iphaga gallinacea, (i 1Ectoparasite. See Parasite (external)Egg binding, 33Egg drop syndrome, 120, 121-122, 131. 156,15",

215,266. 276Egg eating,

23. 29.137Eggs

double-yolked, 51and disease. 114-115.215, 215,216disorders of, 29.34-35, 52. .53, 156-157evaporation from. 209.210fertility of, 213-214formation of, 51-52, 52hatchability of, 215-217hatching-. 208-211,213, 218-219and human health, 237-241, 242Eimeria spp. See CoccidiosisElectrolytes, 193, 193Embryo death, 211. 216. 217.218-219Embryo dyeing. 221-222. 222F.inbryonariorj. 78.83Emphysema, 267Encephalitis, 179, 269Encephalomalacia. 33, 154, 156, 161.267,267-268.

263, 265. 269, 284Encephalomyelitis. See Epidemic tremorEndoparasites. See Parasites (external)Energy, 32Enlarged hock disease. See Infectious synovitisEnteric diseases. See EnteritisEnteric Newcastle disease, 125Enteritis. 39,47, 57, 123, 150, 152-153, 179,189,192,262. See also Bluecomb, Colibacillosis,Infectious stunting synd.-ome. Necroticenteritis. Rotaviral enteritis, UlcerativeenteritisEnlerohepatitis. See BlackheadEnterotoxemia. SeeNecrotic enteritisEpidemic tremor. 59, 73.120, 123.131,201. 205,215, 268-269, 269resemblance to: congenital tremor, 263;

listeriosis, 284: Marek's disease, 287symptoms of, 154, 156, 161. 163,268Epid&rmoptes bilobatus, 68, 70Epson salts. 192Ergotism, 140,141, 153,154, 160, 175, 269


Erysipelas, 8, 18, 110, 113, 204, 205, 258, 269-270and human health. 113.231.236.270postmortem findings, 174, 175,176,177,270symptoms of, 152, 156, 158, 163, 164,270Erysipeloid. 231, 236Brysipelotltrix rliusiopathiae. See ErysipelasErythroid leukosis, 128Erythromycin, 190Escherichia coli, 238, 238,240. See also Colitis,

ColibacillosisEthology, 23Ethylene-glycol, 141European fowl pesl. See InfluenzaExcretory system, 48Exhibition. See ShowingExudative diathesis, 33, 159,270 271Eye disorders. 28.35, 10S. 161, 179,228Eye vaccination. 2(14, 205Eye worms. 85.86-87,88, 161Facial Cellulitis. See Swollen head syndromeFalse botulism. SeeMarek's diseaseFalse layer, 53Fans, 16, 135Farmer's lung, 231,233Fatal sync ope. See Sudden death syndromePatty liver syndrome, 33, 131. 245.271-272postmortem Findings. 175,176,271symptoms of, 153, 154, 156,159, 164, 271EavUS, 129. 130. 130, 159, 160, 272

and human health. 272Feathers, 148

discoloration of. 159,228,229

INDE

X 391

disorders of, 27,35, 140and lice, 64,65,66loss of. 137and mites, 68,70-71and wounds, 194Fecal testing. 92-96. 102Feeders. 37,37,136Feeding schedule, 36Feedstuffs. .See RationsFertility. 23,213-214Fever, 43.57,150, 162Flatworms, 77. 79,89Fleas, 60-61, 61Flies, 59, 61-63, 62. 90Flip-over disease, .See Sudden death syndromeFlock history. 9, 147, 148,166Flooring, 14Floor space, 14,15Flukes, 77, 79, 89, 90-92, 92, 153Flushes, 192Fly trap, 63Fomites, 5, 7Food poisoning. See BotulismFormaldehyde, 178,212Fowl pest. See InfluenzaFowl plague, 290. .See also InfluenzaFree range, 13.26

and disease. 105. 103,113and worms. 79. 81. 83.88,89Frizzledness, 221.228Frostbite, 132-133Fumigation, 212-213Fungal diseases. 129, 130, 187

in humans. 231-232Fungal poisoning, 129,140-141. 141,

153.245.269,273,292

in humans, 232Fungicide. 21, 143. 190

Fltngistat, 21, 190Fusariotoxicosis, 140, 141,

156,157,162,163,272-273

and human health, 273l-'usarium spp. See Fusariotoxicosis

Gangrene, 133. See also Necrotic dermatitisGapes. .See Gape-wormsGapeworms, 80,86-87.88. 280Gas edema disease. See Necrotic dermatitisGeneralized disorders, 55,56. See also SepticemiaGenetic disorders, 156, 214. 218-219, 220-221, 226,227Genetic resistance. 11-13,198.207Gentamicin, 189Germicide, 21Gizzard worms, 86-87Cilottulium vesicarittm, 142Going light. See anemiaGongylonema ingluvicola, 84.86-87

Goniocotes gallinae, 65,66Gonioiles spp. 65,66Gossypolseed poisoning, 140. 160Gout, 27. 33, 39

articular. 48, 155,273visceral, 131,273-274postmortem findings, 174, 175, 176,177,274symptoms of. 157, 159,163, 164,273Gray eye. See Marek's diseaseGreens. See BluecombGrooming activities. 24Gross lesions, 173Growth promoters, 184-185,190.237Gumboro disease. .See Infectious bursal disease

Haenialosiplion modnra, 59Haemophilus paragaflinarum. See Infections

coryzaHatchability, 23, 215-217I latching eggs. 208-209I lead, swollen. See Swollen head syndromeHealth signs. 148Heart attack. See Sudcen death syndromeI lean rate. 43Heat

as disinfectant, 21and egg production, 52and nutrition. 32,33stress, 28. 134-135. 136. 140and water consumption, 40, 40, 41Helicopter syndrome. See Infectious stunting

syndromeHelminthiasis. SeeWcnnsHemophilus infection. .See Infectious coryzaHemorrhagic anemia syndrome. See InfectiousanemiaHemorrhagic septicemia. SeeCholeraHen worker's lung, 231, 232-233Hepatitis, 179. See also Blackhead,

Campylobacteriosis. Infectious anemiaHereditary disorders. 156, 214, 218-219,220-221,

226.227Herpes virus. 120. 120Heterakis gallinarum. See Cecal wormsHistomonad infection. See BlackheadHistomonas meleagridls. See BlackheadHistomoniasis. See BlackheadHistoplasma capsulatum. See I listoplasniosisHistoplasmosis, 129, 130, 130, 153,176, 177,274-275

and human health. 130,231,233-234.275Host, intermediate, 7tS, 78-79,81Housing, 13-14, 15, 17Human health, 230,231,244and antibiotics, 191-192,237and environment, 231-234and parasites, 234-235

and poultry products, 237-242. 238, 240, 242,243

and zoonoses, 235-237Humidity, 33,135


and incubation. 210-211.218-219,226

INDE

X 393

Hydrogen peroxide. 194Hymenolepis spp, 90Hypochlorites, 191BD. See Infectious bursa) diseaseImmunity, 197-199. 199and allaloxicosis. 140and blood type, 55boosters. 193-194breeding for, 11-13indicators of, 12.167natural, 12, 198,207,224and nutrition, 26.28,31and stress. 22, 23suppressed, 122,206,207and viruses, 119.121and wormers. 81-82to worms, 77, 79, 83 85Immune system. 44-45. 45Immunoglobulin. See AntibodiesImpetigo, 243, 254Imprinting. 25Inbreeding, 217,218,220-221Incidence, 244Inclusion body hepatitis. See Infectious anemiaIncubation. 210-211,218-219Incubation period, 244Incubator sanitation. 211-213Indicators, 12. 167Indirect contact, 6,6Infection. 4, 108Infectious anemia, 33, 45,55, 120,121, 131,215,200, 245, 275-276postmortem findings. 174, 176,177,275resemblance to: campylobacteriosis, 256:coccidiosis, 261: infectious stuntingsyndrome. 280; runting syndrome, 303and sulfa drugs, 190symptoms of, 152,159, 163, 164,275Infectious bronchitis, 8, 18,48, 120, 122,200, 214.276-277

postmortem findings. 174, 175,177,276resemblance to: Aspergillosis, 248, 249; chronicrespiratory disease, 259; egg drop syndrome,266: infectious coryza, 279: infectiouslaryngotracheitis, 279; influenza, 282;Newcastle disease, 290; swollen headsyndrome, 307

symptoms of. 156, 157, 158, 161,163,276vaccination against, 201,203,205, 207Infectious bursal disease. 18.18,39,45.45, 120,122-123. 277-278postmortem findings, 174, 175,177,277resemblance to: infectious anemia. 275; runting

syndrome. 303symptoms of, 152, 154, 162,163,277vaccination against. 201. 205, 207Infectious catarrh. Seelnfectious coryzaInfectious coryza, 8,18,39, 110,112-113,214, 278.278-279

resemblance to: cholera, 259; chronicrespiratory disease, 260; infectiousbronchitis, 276; swollen head syndrome, 307symptoms of, 156, 158, 160, 161,278vaccination against, 203-204. 205, 207Infectious diseases, 3-4, 4, 107Infectious encephalomyelitis. See Epidemic tremorInfectious enterohepatitis. See BlackheadInfectious hepatitis. .SeeCampylobacteriosisInfectious laryngotracheitis, 8. 11. 18, 120, 124.196, 279-280resemblance to: aspergillosis, 248, 249;

infectious bronchitis, 276: infectious coryza.279; influenza, 282; Newcastle disease, 291;wet pox, 297symptoms of, 156,157, 158, 161, 163, 279vaccination against, 201, 205, 206Infectious leukemia. See TyphoidInfectious sinusitis. See Chronic respiratory diseaseInfectious stunting syndrome. 121, 123.131.215,280-281,303symptoms of, 152,159,280,175, 177Infectious synovitis,


8,51,110,113-114,215,281,281

postmortem findings, 175, 176,281resemblance to: breast blister. 252: paratyphoid,

294, viral arthritis. 122symptoms of, 152, 154, 158, 159, 162, 262. 281vaccination against. 205Infertility, 133, 214, 218. Seealsn

Reproductive systemInflammation, 178,179Influenza, 8, 18, 120,123-124. 196, 200, 282and human health, 282resemblance to: chlamydiosis. 257; egg dropsyndrome. 266; infectious coryza, 279;Newcastle disease, 291; spirochetosis, 304symptoms of, 153, 156, 157, 158, 160, 161, 162,164,282Inhaled drugs, 183Injected drugs, 183Injected vaccines. 204, 205Injections, 183-184. 185-186Injury, 194Insecticides, 75-76.80, 143. 164,237,269Insects, 58.59Interferon, 187Intermediate hosts, 78, 78-79, 81Internal layer, 53Intestinal coccidiosis.Intestinal disorders. 56, 77, 175, 179

See also EnteritisIntraocular vaccination, 204Iodine deficiency, 217Iodine disinfectants. 19, 20,209Iritis. See Marek's diseaseIron deficiency, 228Ivermectin. 70.76.80,87Jittery chicks. See Congenital tremor

INDE

X 395

Joint disorders. 50-51. 56,179. See also Infectioussynovitis, Staphylococcic arthritis

Keel bursitis. See Breast blisterKeel cyst. See Breast blisterKeel deformity, 35Keratoconjunctivitis. See ConjunctivitisKidney disorders, 179Killing chickens, 168, 168-169, 182Kinky back. 154.163,283Knemidocoptes spp. 68.69-71lameness, 154-155, 173. .Seen/so l egsIjaminioptes cysticola, 68, 71Laryngotracheitis. See Infectious laryngotracheitisI.egs

color of, 154-155disorders of. 35,50, 228and mites. 68,69-70. 70thick. See OsteopetrosisLesions. 173-174,174-177,177,244.Seealso

Inflammation, TumorsLesser meal worm. See Darkling beetleLethal genes, 220-221Lencocytozoori spp. See LeucocytozoonosisLeucocytozootiosis. 8,39, 59,61-62,97,106,283-284,286

postmortem findings, 175,177,284symptoms of, 152,154, 158, 162, 163,283-284Leukosis complex, 126, 128,215,309Lice, 59,63-67, 6-1,65, 160Life span, 43Limberneck. .See BotulismLipeunis caponis, 65Listeria monocytogenes. See ListeriosisListeriosis. 8, 110, 118.284-285

and human health. 231,236-237,285symptoms of, 152,154, 164, 175, 176,284Litter, 14-15,62-63and coccidiosis, 99eating of, 24,225and scavenger mites, 72-73and worms. 89Liver disorders. 179Long-bone distortion. See Twisted legLymphatic system. 44

Lymphoid leukosis, 8,45.121,128, 215,285postmortem findings, 174, 175,176, 177,285resemblance to: fatty liver syndrome, 245;campylobacteriosis. 256; Marek's disease.128, 128, 287symptoms of, 152, 156, 159, 164,285Macrolides, 190Magnesium deficiency, 31.34-35.193,217Magnesium sulfate, 192Malabsorption, 33. See also Infectious stunting

syndromeMalaria, 59,63,97.106, 164,284,286Malignant edema. See Necrotic dermatitisManganese deficiency, 32.35, 138. 217,226.228Marble bone. .See OsteopetrosisMarek's disease, 8, 18, 45, 45. 59, 120,126-128. 127,214. 286-287, 287and human health, 127-128.288and natural resistance. 55. 198postmortem findings. 175,176, 177,287resemblance to: botulism, 251-252; cage fatigue,255; congenital tremor, 263; lymphoidleukosis, 128, 285; runting syndrome. 129,303; spirochetosis. 304; toxoplasmosis. 309symptoms of, 155,159, 161,163, 164,286vaccination against, 201, 202, 204, 205,207Mechanical vector, 6Medications. See DrugsMegninia spp, 68, 71Menacanthus spp, 64. (•'•/, 65,66Menopon gallinae, 65,66Mice. 143,143-146, 144Microflora, beneficial. 47, 108,

129, 187, 190, 193-194

Mycropolyspora faeni. 231,233Microsporum gallinae. See FavusMilkweed poisoning, 142Minerals, 31-32Mites

chigger, 68, 72, 72,72


external. 67-73, 67.68, 61). 72and human health, 231,234internal, 71-72resemblance to favus. 272scavenger, 72-73symptoms of. 160, 162See also TicksMolasses flush. 192

Moldy feed, 36,37. 129, 140-141, 141, 153,245, 269,

273. 292Moldy litter, 15Moiling, 27,54,137Moniliasis. See ThrushMonocytosis. See BluecombMortality. 244. See also DeathMosquitoes. 59,63. 106Mothballs. 139Mouth disorders. 35, 162, 228Musca domeslica, 62,62-63Mucous Membrane, 44Mud fevet. See BluecombMuguet. .SeeThrushMuscle disorders, 35, 150, 154-155,228Muscular dystrophy. .See White muscle diseaseMushy chick disease. See OmphalitisMus musculus. 143,144Mycoplasma gallisepticum. See Air-sac disease,

Chronic respiratory diseaseMycoplasmas. 109. 189Mycoplasma synoviae. See Air-sac disease,

Infectious synovitisMycoplasmosis. 18, 110, 113-114, 189.190,257Mycoses. See Fungal diseases

INDE

X 397

Mycotic diseases. See Fungal diseasesMycotic pneumonia. .See AspergillosisMycotoxicosis, 129, 140-141, 141,153,245.269.

273, 292Myeloid leukosis. 128National Poultry Improvement Plan. 10, 116Navel infection. See OmphalitisNecropsy. See Postmortem examinationNecrotic dermatitis, 110,111. 154,159,163,164,176, 288-289and human health, 289Necrotic enteritis. 110,261. 152,163,164, 175,289

and human health, 231, 240, 241.243, 289Nemalhelminthes, 77,79,82Nematodes. See RoundwormsNeomycin, 189-190, 194Neoplasm. See TumorsNeosckongasti a. americana. 68,72Nephritis, 179Nephrosis. See Gout (visceral), Infectious bursal

diseaseNeriium oleander, 142Nervous system, 54-55Nervous disorders, 55,56,57, 150, 154-155,228Neuritis. See Marek's diseaseNeurolymphomatosis. See Marek's diseaseNewcastle disease. 8, 18, 39,120. 124-125, 125,196,214,290 292and human health. 231, 236, 290.291resemblance to: Arizonosis, 247: Aspergillosis,248.249: cholera, 259: chronic respiratorydisease, 259. egg drop syndrome. 266;epidemic tremor, 269; erysipelas, 270;infectious bronchitis. 276; infectious coryza.279; infectious laryngotracheitis. 279;influenza, 282; listeriosis,

284; Marek'sdisease, 287; spirochetosis. 304: swollen headsyndrome. 307; toxoplasmosis, 309symptoms of, 153, 154, 155. 156,157, 158,159,

161, 162, 164, 290. 291vaccination against, 201, 205,207New England disease. Sec Epidemic tremorNew-house coccidiosis syndrome, 99New wheat disease. See BluecombNicotine sulfate, 76, 139Nightshade. 142Noninfectious diseases, 3NPIP, 10, 116Nutritional disorders. 26-27,33,33-34,34-35, 137,178-179,180,in breeder llocks. 214,216. 217in chicks. 225, 226.227, 228,229Nutritional myopathy. See White muscle diseaseNutritional roup. See Roup (nutritional)Nutritional supplements, 27, 28,31, 193,216. Seealso RationsObesity. 39,214,218Ochratoxicosis, 140.141.153. 157, 175,176,292

and human health, 292Ocular lymphomatosis. See Marek's diseaseOdor and disease, 160Oeciacus vicarius. 59Oidica. See ThrushOidiomycosis. SeeThrushOleander. 142Omphalitis, 39, 110, 111. 117.215,219,292-293,

293and human health,

293resemblance lo pullorum, 299symptoms of, 152, 160, 262. 292Oocysts, y& 98-99, 101, 104Open housing, 15Opportunistic infectious, 6,

107. 107, 116, 118. 121,129

Oral drugs, 183-185


Organic produciion, 237. See also Free rangeOrgans, internal. 46. 49.52, 169, 170membrane surrounding, 179tissue samples of, 178OmitlumyssiLS spp, 68,69. 69Ornithosis. See ChlamydiosisOrthomyxovirus, 120. 120Osteomalacia. See RicketsOsteopetrosis, 121, 128, 155, 162, 174,215, 293-

294Osteoporosis. See Cage fatigueOvaries, 51.52. 54, 126Oviduci disorders, 179Oviduct flukes, 91, 92,153Oxyspirura mansoni, 85,86-87,88Pale bird syndrome. See Infectious stunting

syndromePanting, 134-135Paracolon. See ArizonosisParainfluenza. See Newcastle diseaseParalysis, 154, 173,227Paramyxovirus, 120.120,290,291Parasites, 4, 58,136,214external. 58, 59,74-76and human health, 231, 234-235internal. 8,77,79-82,97-98.106and nutrition. 29.31. 33.35,79,228See also Bugs, Fleas, Flies, Lice, Mites, Ticks,WormsParatyphoid, 8, 110,

115,215,219,294-295and human health. 196,231,239-241. 241. 295postmortem findings, 175, 176,295resemblance lo: paratyphoid. 247; pullorum,

29.9: typhoid, 311symptoms of, 152, 156, 159,161,162,163, 294Parrot fever. See ChlamydiosisParvovirus. 275Pasted vent, 152, 160, 295-296Pasteurella multocida. See CholeraP septica, 259Pasteurellosis, 110.117,190,257Pathogenicity, 22,107

INDE

X 399

Pathogens, 18,107. 107, ISOPathologist, 165. 167Pathology laboratory, 165-167, 168, 178Peck order. 25,203,214Pediculosis. See LicePedigree. 12Pedigree baskets, 223Pendulous crop. SeeCrop impactionPenicillin. 188-189, 191, 192Penicillium puberulum. SeeAfiatoxicosisP. viridicaium. See OchratoxicosisPericarditis, 179Peristaltic action, 53Perosis. .See Slipped tendonPesticides, 75-76.80, 143. 164,237.269Phenol, 19,20Phihiphthalmus gralli. 92Phosphorus, 31.34,193.228Physiological zero. 209Phytolacca americana, 142Pickout, See Prolapsed oviductPicornavirus, 120,120Pink disease. See Fatly liver syndromePlague. See Newcastle diseasePlantar pododermalitis. See RnmblefootPlant toxins, 142Plasmodium spp. See MalariaPlalyhelminthes, 77,79,89Pleuropneumoniaiike organism infection. See

Chronic respiratory diseasePlumage. See FeathersPneumatic bones, 18-19. 50Pneumoencephalitis. See Newcastle diseasePneumomycosis. See AspergillosisPododermatitis. See BumblefootPoisoning, 139, 258.275algae, 39, 155, 163,246-247antifreeze, 141, 153, 155bacitracin, 190bacterialin chickens, 108. 111-112in humans. 231, 237-238, 238,239-242, 240,243coccidiostal. 143copper sulfate. 187fungal, 129, 140-141. 141naphthalene.

139nilrofurazone, 143pesticide, 143, 164,269plant, 142rodent, 145-146, 146rose chafer, 143seed,140selenium, 32sulfamethazine, 103treatment of, 192Pokeberry poisoning, 142Postmortem examination. 165, 169, 170, 171, 171173. 172, 173, 244documentation of, 177-178do-it-yourself, 167-168interpretation of, 173-174, 174-177, 177professional, 165-167specimen preparation for,

166.168-171, 171Potassium. 32.34-35,193Potassium permanganate, 212Potato poisoning, 142Poultry meat, 237-238.241. 242,243Pox. 8, 18,59,63. 120, 162, 126,297dry, 156, 160, 296-297wet. 28-29, 164, 256, 279, 297-298, 308vaccination against, 201,202. 205,206Poxvirus, 120,120PPl.O. See Chronic respirator)' diseasePreconditioning, 22,23Progeny testing, 12Prolapsed oviduct, 33, 52,53Prostliogoniinus spp, 92Protein. 27-28,32.34-35,228Protozoa, 15,97-98Protozoan diseases, 97Pseudo-botulism. See Marek's diseasePseudofowl pest. See Newcastle diseasePseudomonas. 110,118, 188,191,215,218,298and human health. 231,234,298symptoms of, 153, 155, 164, 175, 176, 177,298Pseudomonas aeruginosa. See PseudomonasPseudo-parasites, 93Pseudo poultry plague. See Newcastle diseasePsittacosis. See ChlamydiosisPierolichus obstuses, 68


Pullet disease. See BluecombPullorum. 8,110, 115. 196, 215, 298-299and human health. 299postmortem findings, 174, 175, 176, 177,299resemblance to: campylobacteriosis. 256;lymphoid leukosis. 285; paratyphoid, 294;typhoid. 311symptoms of. 152,153, 158,159,163,164,298-299Pycnoscelus surinumensis, 85, 88Pyrethrum, 75Pyridoxine deficiency, 268Quail disease. See Ulcerative enteritisQuaternary ammonium compounds. 19,20,209Quicklime. 19Rachitic chicks. See RicketsRaillietina spp, 90Range-fed chickens. See Free rangeRange paralysis. See Marek's diseaseRations. 25,31.36-37

and antibiotic resistance. 184. 191

and cannibalism, 136, 138consumption of, 37-38.38,

135,148, 192digestion of, 46—18drugs in.184-185and fungal toxins. 140-141,

141and hatchability, 216,217,

218

401 TI IE CI IICKEN HEALTI I HANDBOOK

Rations (continued)and pesticides, 237-related disorders, 3B, 226, 227and toxic seeds, 140Rats, 143, 143-144. 144. 144-146llallus spp, 143, 144Recessive genes, 220-221Reflex behavior, 23Renal failure. See Gout (visceral)Renal gout. See Gout (visceral)Reovirus. 83. 121.121Reportable diseases. 196, 196Reproduction, 23,29,30,55,213-214Reproductive system, 51-54, 52. 56, 156-157Reservoirs of infection. 4-5. 224Resistance. See ImmunityResistance factor. 55Respiration rale. 15-16, 43Respiratory disorders. 16,49-50,56,77,176, 188and cryptospoi idiosis, 105and Marek's disease, 287and salpingitis, 53-54symptoms of, 57,150, 158and vitamins. 28-29. 35Seealso Air-sac mitesRespiratory system, 48-19. 49, 172-173Restricted feeding, 38Reticuloendotheliosis. See Runting syndromeRetrovirus, 121,121Rhinitis. 179Rib disorders, 35Riboflavin deficiency.

180,216.217,227,228,269,287

Kicimu communis, 142Rickets, 33, 154, 155, 159, 174, 228. 300. 255, 269,

293. 300-301Hivoltasia bifurcata, 68,71Rodent bait station. 145Rodenlicides, 145-146,146Rodenls. 13,14, 143-146, 144. 143Roosts, 14Rotaviral enteritis. 121,123.152,163, 174, 175,

215,301Rotavirus, 121,121Rot gut. See Necrotic enteritisRound hearl disease, 131.164, 175,301-302,307

Roundworms, 14, 77, 78.78-79,79, 80,82-88. 86-

87, 173.228,261Roup, 49

nutritional, 28,33,158, 161, 161,276,279,291,297. 302Rumplessness, 221Hunting syndrome, 45, 121, 129, 131, 154, 174,215,

280,302-303Ruptured tendon. See Viral arthritisRye seed poisoning. 140. 153, 155Salmonella arizonae. See ArizonosisS. enleritldis, 238. See also ParatyphoidS. gallinarium. See TyphoidS. Iieidelberg. See ParatyphoidS. pullorum. See PullorumSalmonella spp, 238, 240. See also SalmonellosisS. typUinutrium. See ParatyphoidSalmonellosis. 18, 39,110,11^116, 174, 175,215,212,215. 224and human health, 231,238,239-241, 240resemblance to: blackhead. 250: coccidiosis,

261: erysipelas, 270and selenium, 32,35treatment of, 189. 190,191Salpingitis. 53-54. 179,262Salt, 31-32,35, 138deficiency, 156poisoning, 32.39,253,269Sanitation, 17,21.211-213, 238Sanitizers, 20,21, 209, 238-239Scaly-leg mites. <i8,69-70. 70.155Scalology, 151, 152-153Scoliosis, 221Secondary infection, 188. 193Selenium, 32.35,180,217,228Self-limiting infections. 182Septicemia, 55, 57, 108,117, 179,189,251.262. See

also Generalized disordersSex change, 54Sexual behavior,


24,54Shock, 164,190,194

electrical, 226Shots, 183-184, 185-186Showing

and debeaklng, 138and disease, 11,182

and dubbing, 134and stress, 23,214

Simtdiurnspp, 61-62. 62Sinusitis, 179, See also Chronic respiratory diseaseSkeletal system, 50,50-51Skin

disorders of. 35,56,228and immunity, 44miles, 68,69-71discoloration of, 159-160Slaked lime. 19Slipped tendon, 33,35, 155, 226, 228, 229, 287, 303.

303-304,310Sod disease. See ErgotismSodium, 193. See also SaltSolatium spp, 142Sore head. See PoxSorghum poisoning, 140, 155Sour crop, 160, 174Species specificity, 5Spirilla, 109, 109Spirochetosis, 39, 48. 59, 73. 110, 116, 196, 304-305and human health, 305postmortem findings. 175, 176, 177,304symptoms of. 153, 155, 160,162,164,304Split-wing syndrome. See Infectious stuntingsyndrome

INDE

X 403

Spondylolisthesis. .See Kinky backSpontaneous sex change. 54Spores, 108, 129Sporozoites, 98, 104Sporulation.98Staphylococci. 109, 109.188. 189.190Staphylococcic arthritis, 110,117, 155, 162,305,

313and human health, 231,305

Staphylococcic septicemia, 305Staphylococcosis. 110, 116-117, 188, 189,190, 191,199

and human health, 231,240, 243Staphylococcus aureus, 110,238,240Star-gazing, 227, 228. See also Epidemic tremorStarvation, 39,225Sterilizer, 2)Sternal bursitis. See Breast blisterSteroids, 194Stomach worms. 85,86-87Stomatitis. See ThrushStrep infection. See StreptococcosisStreptococci, 109,109. 110, 188, 189Streptococcosis, 110, 117. 199, 270,306postmortem findings. 175, 176,306symptoms of, 153, 155,162, 163,164,306treatment of. 188.189, 190Streptococcus equisimilis. 117S. faecalis. SeeOmphalitisS. zooepidemicus. See StreptococcosisStreptomycin. 190Stress, 3,22

behavior, 23-25and disease, 192,223heat-, 28, 134-135,136, 140and immunity, 199, 201and nutrition. 28,31,32,33, 193and shock. 194Stress disease. See Chronic respiratory diseaseSrrougyloides avium. 85.86-87Stunting syndrome. See Infectious stunting

syndromeSubulura spp, 86-87

Sudden death. 164Sudden death syndrome, 131,

154, 164, 175, 176,302, 306-307

Sulfa drugs, 188,189. 192Sulfonamides. 188. 189,192Summer disease. See BluecombSunlight

as disinfectant, 21and fertility, 214and nutrition. 26, 29Supportive therapy, 192-194Surgery, 195Susceptibility, 12,35,197Swollen head syndrome, 110, 131, 156,158, 161,307Symptoms, 148.150-

151,152-164.244. Seealsolesions

Syndrome, 131Synergism. 190Syngnrnus trachea, 86-87.88Synovitis, 50-51, 179. Seealso Infectious synovitisSyringe, 185. 185Syringopliilus hipectiuatus, 68, 71Systemic diseases, 55. See also SepticemiaSystemic inhibitors, 76Tanaisia bragai, 92Tapeworms. 62. 77, 78, 78-79. 79.89-90. 90, 155I'axus spp. 142Temperature. See Body temperature. Heat,

Incubation, Winter careTenosynovitis. See Viral arthritisTerritorialisin, 25Tetracyclines, 189,191Terra meres spp, 85, 86-87Thermoactinomyces vulgaris. 231.233Thirst, 24.32,39Thorny-headed worm. 86-87, 88Thrush. 8,39,129, 130, 130,308and human health, 130,231,308resemblance to: canker, 256; crop impaction,

264; Newcastle disease, 291

symptoms of. 152,


160, 162, 163,174,308

Tibial rotation. See Twisted leg

Tick paralysis. 73. 155, 251, 287

Ticks. 59, 68, 73. 73-74. 74. 116

and human health. 74,231,234Tissue sampling. 178Toe-punching. 222-223. 223Toes, crooked, 226-227Topical drugs, 183Torticollis. See Wry necktoxic fats. 39Toxicoinfection. See BotulismToxic plants, 142Toxins. See PoisoningToxoplasma gondii. See ToxoplasmosisToxoplasmosis. .97, 106, 188, 308-309and human health, 231, 235,309symptoms of. 152,154, 159, 161, 163, 176,308-309Transmission of disease,

6,6,114-115.215,216,244

Treatment or disease. 181-182.195Trematodes. See ElukesTriatoma spp, 59Trichomonas gallinae. See CankerTrichomoniasis. See CankerTrlchostrongulus tenuis. 86-87Trichothecene mycotoxicosis. See FusariotoxicosisTriple sulfa, 188Trombiculas spp, 68, 72.72Tuberculosis, 18, 18, 110,117-118,309-310and human health, 118.310postmortem findings. 174, 175, 176, 177,309resemblance to: lymphoid leukosis, 285: Marek'sdisease, 287

INDE

X 405

Tuberculosis (continued)symptoms of, 153,156,159,309I llinois, 52, 119, 126-129. 128, 178. See also LesionsTwisted leg, 131. 154,303,310, .110Typhoid. 8, 39, 110, 115, 196, 199,215,311postmortem findings. 175, 176,177,311resemblance to: campylobacteriosis, 256:cholera, 258: colibacillosis, 263: paratyphoid.294: pullorum. 299; spirochetosis. 304symptoms of, 152,158, 162, 163, 164,311Ulcerative enteritis, 8, 110,111, 115,311-312resemblance to: campylobacteriosis. 256;coccidiosis, 261: infectious anemia, 275;necrotic enteritis, 289symptoms of, 152,164, 174, 175,176. 177.312Urates. 48, 151. SeeflfaoGoutUrine salts, 48. 151. See also GoutUrolithiasis. SeeGout (visceral)Uveitis. See Marek's diseaseVaccination. 13.197, 199, 202-206,203

failure, 121, 122,200,206-207Vaccine, 200-202Valgus deformation. See Twisted legValg.is leg deformity. See Twisted legVarus deformation. See Twisted legVector, 6Vehicles, 5,6-7Vent brush vaccination. 204Vent gleet. See Pasted ventVentilation, 15-16,62-63. 192

and incubation. 210.218-219Vent pasting. 152, 160,295-296Vent picking, 53. 137Vesicular dermatitis. See ErgotismVetch poisoning. 142Veterinarians, 167Veterinary ethology, 23Vibrionic hepatitis. See CampylobacteriosisVicta spp, 142

Viral arthritis, 121,122,154,201.205,215,305,313Viral diseases, 119. 120-121, 122, 186-187Viral enteritis. 123Viricide, 21Virulence, 22, 107Viruses, 15. 119. 120-121, 120-121, 122, 186, 199.

See also VaccineVisceral lymphoma. See Lymphoid leukosisVisceral urate deposition. SeeGout (visceral)Vitamin A. 28-29, 30, 33, 34-35, 156, 180, 214, 217,

227, 228, 269, 264Vitamin B, 30,30-31. 35.217,227.228Vitamin C,30,31Vitamin D, 29. 30,31.34-35, 157, 180,217,223Vitamin E, 29.30,34-35, 180,214,217,227.228,229, 269Vitamin K, 29,30,34,180, ',88,190,217,228,229Vitamins, 28-31,30,31,33,216Vitamin therapy. 193WD. See Twisted LegWater

consumption. 39, 40,39-41, 135, 148deprivation. 40-41, 41.48, 54. 156, 180, 193,226and disease, 39,42, 192as disinfectants, 20and medications, 23. 184, 184and salt poisoning, 32, 39at shows, 23and vaccines. 203. 205Water belly. See Broiler ascitesWaterbloom, 247Waterers, 41,42Weather-related disorders. See Frostbite, Heat,

Winter careWeight disorders, 35Western duck sickness. See BotulismWhite comb. See FavusWhite diarrhea. See PullorumWhite muscle disease. 33,154, 174, 228, 313-314Wild birds. 11Windpuff. 267Windswept. See Twisted leg


Wing rot. See Necrotic dermatitisWing-web vaccination, 204. 205Winter care. 41.42,33,39, 132-133Withdrawal period, 82. 104, 191,237Wood floors, 14Wormers. 80,80-82,84Worms. 15.22, 77, 79, 79-82 87, 193detection of, 92-96and embryonation. 78,83and human health, 231,235symptoms of, 79,80. 87. 153, 160See also Capillary worms, Gapeworms,Roundworms, TapewormsWounds, 194Wryneck, 221Wry tail, 221Xanthomatosis, 39X disease. See Aflatoxicosis. BluecombYew poisoning, 142Yogurt, 193-194Yolk peritonitis, 53Yolk sac infection, 262. See also OmphalitisZinc deficiency. 217,228Zoonoses. 231,235-237/-YRadentts spp, 142

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