POULTRY DISEASES TEXAS m1 ‘umvmsnv uxns AGRICULTURAL zxrcusmu szawcc - - - mas AGRICULTURAL zxmumrnr smmm College Station, Taxas [Blank Page in Original Bulletin] A MANUAL o|= PCDULTRY DISEASES Written and edited by members of the Poultry Disease Bulletin Committee C. F. HALL, Chairman Professor, Veterinary Microbiology R. R. BELL Professor and Head, Veterinary Parasitology R. L. CLIFFORD, JR. Associate Poultry Pathologist, Poultry Disease Laboratory Center, Texas S. E. GLAss Associate Poultry Pathologist, Poultry Disease Laboratory Gonzales, Texas J. E. GRIMES Assistant Professor, Veterinary Microbiology L. C. GRUMBLES Professor and Head, Veterinary Microbiology E. E. KEAHEY Assistant Professor, Veterinary Microbiology B. C. WORMELI Extension Poultry Specialist Contents Page Page Section l— General Information ................................................ .. 5 Mycoplasma Meleagridis Infection ..................................... ..29 Poultry Disease Principles . 5 Infectious Corym 9Q Nature and Cause of Disease 5 Endemic (Localized) Fowl Cholera (Roup) ....................... .30 How Infectious Diseases Are Spread ............................... .. 6 Psittacosis and Ornithosis .... .31 Body Defenses Against Disease 6 Aspergillosis (Brooder pneumonia) ................................. .31 Manifestations of Disease ...................................................... .. 7 _ _ _ " "i Flock Health Management 7 secuon 4 _vlml Diseases - - (Exclusive of Respiratory Diseases) ..................... .33 Hatchery Management and Sanitation .............................. .. 8 Avian Pox 33 Principles of Reasonable Drug Administration ................... .. 9 Avian Leukmk ______________________________ "34 t Drug Administration 9 Lymphoid Leukom __ 345». _ Preventive Medication l0 Marekts Dkemf, __ 35* Treatment of Disease Outbreaks """"""""""""""""""""""""" "10 Epidemic Tremor 86 Vaccination to Prevent Poultry Diseases ............................... ..l0 Infectious Bursa] Disease (Gumbom) ___________________________________ "37 What Vaccines Are 10 Dangers of Vaccination ......................................................... _.lO Seeiioii 5 “ Diseases 9i Undetermined Cause ------------------------- ~38 vatcinatiothqqo Substitute for Sanitation _______________________ "11 Transmissible Enteritis of Turkeys (Bluecomb) ................ ..38 Diseases for Which Vaccines Are Available ...................... ..ll Heiiioiihagie Anemia sYiiiiieiiie --------------------------------------------- ~38 Administration of Vaccines .................................................. ..ll Aoiiie RiiPiiiie ---- -- a9 A Suggested Vaccination Program for Chickens .............. ..l2 Cage Faiigiie ----- ~~ i9 _ Use of Other Vaccines in Chickens and Turkeys _____________ __l2 FaiiY Liver sYiidioiiie ----------------------------------------------------------------- ~39 Using the Diagnostic Laboratory ............................................ ..l2 Uieeiaiive Enteritis (Qiiaii Disease) ------------------------------------- ~40 Q Laboratory Location‘ ____ __ 12 NCCTOtiC Enteritis 40 t. Using the Laboratories ........ ..l2 Section 6__Protozoan Diseases ___________________________________________________ "42 Wiiai i° EXPeei ----------------------------------------------------------------------- --i3 CQCCidiQQiQ 4g j; i Section 2 —Bacterial Diseases ............... ................................... ..l4 Biarkhead . 43 - s Salmonella and Paracolon Infections ..................................... ._l4 Trichomoniflsis . 44 f Pullorum Disease .................................................................... ..l4 Hexamitiflsis 44 ‘t Fowl Typhoid .... ..l5 ' Leucocytozoonosis .............................. ..45'7 Paratyphold Infécnons """""""""""""""""""""""""""""""""""""""""""""""" "l6 Sgefion 7 - Parasifig Diseases _ _ _ _ _ _ _ _ _ _ _ _ _ _ __ 4'] i Paracolon Infections ............................................................... ..l8 , 1 . . . . . Poultry Lice .. 47 . Coliform Infections, Colibacillosis ..... .. 19 ‘ Omphalim t 20 The Head Lolise ...... .. 47 Fowl Cholera 20 The Body LOW """" " 47 a EfYsiPelaq 22 The Shaft Lame . . """" " 47 Avian Vibrionic Hepatim 2g Qther Ktnds 0f Chlcksn Llse ----------------------------------------------- ..47 » Botultgrn Poultry Mltes": """"""" ‘Z """""""""""""""""""""""""""""""""" Arthritis/Synovih-Q _______ "24 Commeii (aiiiciieii Mite ---------------------------------------------------------- ~43 Staphylococcic Arthritis _________________________________________________________ "24 Feather Mite . 48 Infectious Synovitis ‘>4 scaly-Leg Mm? 48 i Hemorrha ic Enteritis 25 Deplumlng M"? 48 a g ' ' ' ‘ ' ' ' ' ' ' ' ' " Fowl Tick or Blue Bug . b 48 A. Section 3 — Respiratory Diseases ................................................ .26 Chiggers, Red Bugs or Harvest Mites ..................................... __49 Newcastle Disease 26 Large Roundworms .. 49 j Infectious Bronchitis ..... .. 27 Capillaria . 49 Laryngotrachteitis ------- -- 27 Cecal Worms .. 49 Quail Bronchitis s 98 Tapeworms ...... .. 50 i‘ Influenza/Parainflnenm 28 t: MYCOPIQQmOQiQ 9g Section 8 — Appendix I _____ u 61 Chronic Respiratory Disease-Air Sac Syndrome Glossary of Terms """""""""""""""""""""""""""""""""""""""""""""""" "51P. and Infectious Sinusitis 28 Tables of Weights and Measures ............................................ "52 A POULTRY INDUSTRY ranks fourth among agri- tural commodities as a source of gross income the United States and in Texas. The annual 1 as gross value to the farm is about 225 million ars. The production of poultry and eggs is Eqhly commercialized and intensified and operates “slarge units. Profit per bird is governed by fixed and variable ors. Variable factors usually determine the suc- or failure of an operation. A primary cost 'able in poultry production is the disease level the flock. Healthy birds are a prerequisite for ffit. ,. " Losses due t0 disease originate in many ways. I'd-H are obvious, such as death, medication costs j- condemnations. Others are sometimes less ob- , such as poor growth or rate of lay, poor i» conversion and downgrading. fThis manual attempts to provide the profession- "j exas poultryman with a basic understanding ow infectious disease processes are established, to prevent the introduction of diseases, char- o 'stics of more common infectious diseases of i try and specific treatment or control of diseases. POULTRY DISEASE PRINCIPLES > and Cause of Disease €isease is an alteration in the state of the body {any of the body organs which interrupts or '_ bs the body's proper functions. Such dis- nces often are recognized by detectable alter- of body functions. f-tiology is the study of disease causes. A disease often results from a combination of two or l causes: (1) the indirect or predisposing factors if» may lower the bird's resistance and (2) the l,» or determining factors which produce the disease state. disposing causes of disease are referred to fcntly as “stress” factors. Stress factors may _illing, poor ventilation, overcrowding, inade- n" feeding and watering space, overmedication, Disease itself may predispose another disease. iiexample, an outbreak of infectious bronchitis predispose “air sac” infection. ‘irect causes of disease are: _ 1. Bacteria 2. Viruses Section I. GENERAL INFORMATION Parasites Fungi Nutritional deficiencies Chemical poisons 7. Unknown causes 9914*.“ Infectious diseases are the greatest threat to poultry health. They are caused by bacteria, viruses, rickettsia and fungi. Some protozoan diseases, such as coccidiosis and blackhead, behave much as in- fectious diseases and often are considered as such. More correctly, they should be classed with the other parasitic illnesses. When living agents such as bacteria enter the body and multiply, they cause a disturbance of normal function and infection occurs. Disease is caused by the chemical toxins (poisons) produced by invading organisms. At one time some scientists believed that microorganisms caused disease by mechanical obstru.ction of vessels or tissue spaces. This theory has been disproved and it is now clear that damage is caused by chemical substances. But in some protozoan diseases, such as coccidiosis, mechanical damage to tissues is an important factor. All contagious diseases are infectious, but all infectious diseases are not contagious. A contagious disease is one that is transmitted readily from one individual or flock to another. An infectious dis- ease is one produced by living organisms. Most infectious diseases of poultry are contagious; how- ever, a few such as aspergillosis are not. The ability of an organism to cause disease in the particular hos-t is known as its virulence or pa-thogenicity. Many microorganisms that are un- able to cause disease under most conditions may cause disease under certain conditions and would, therefore, be considered pathogenic in that par- ticular host under the existing conditions. On the other hand, some organisms almost always are pathogenic and produce disease when they enter the body of a susceptible host. Some will invade the body of only one species of birds or animals and are said to be specific for that particular spe- cies. For example, infectious bronchitis virus will cause disease only in the chicken. Other organisms affect a‘ large number of species. For example, some of the Salmonella organisms affect a large" variety of species including reptiles, rodents, domestic ani- mals, poultry and man. The ability of an organism to cause disease is not a fixed characteristic. It depends upon many 5 factors, such as ability to invade tissues and pro- duce chemical toxin. Often pathogenicity can be altered intentionally. This characteristic has been used in developing some vaccines. Variation in pathogenicity of organisms also explains partially why the same disease may present different forms and degrees of severity. How Infectious Diseases Are Spread Some of the more common ways infectious dis- eases are introduced into and spread within the poultry flocks are: 1. Introduction of diseased birds. 2. Introduction of healthy birds that have recovered from disease but are still carriers. 3. Contact with inanimate objects (fomites) that are contaminated with disease organ- isms (poultry crates, feeders, waterers, etc.) 4. Carcasses of dead birds that have not been disposed of properly. 5. Impure water, such as surface drainage water. 6. Rodents and free-flying birds. Insects— fowl pox transmitted by mosqui- i068. 8. Shoes and clothing of men who move from flock to flock. 9. Feed or contaminated feed bags. l0. Contaminated premises through soil or old litter. ll. Airborne — organisms do not spread far through the air, but this source of infection can be very important in heavily populated poultry areas. l2. Egg transmission — a number of diseases such as pullorum and fowl typhoid are egg transmitted. Body Defenses Against Disease The body has a welldeveloped defense mechan- ism that must be understood and utilized in con- trolling infectious diseases. Immunity means the ability to resist infection; however, this ability can be overcome under certain conditions. Resistance is used interchange-ably with immunity. An animal has two types of protective mechan- isms: (1) those that hinder or prevent invasion of organisms and (2) those that combat agents which invade the body. Mechanisms which hinder or prevent invasion of organisms include the intact skin and mucous membranes which create a direct barrier, secretions 6 such as mucous which tend to dilute and wash out invading organisms and cilia (hair-like projections on some mucous membranes) which, with wavelike action, move foreign material out of such structures as the trachea (windpipe). Mechanisms which combat agents that invade the body include the white blood; cells and circulat- ing antibodies. Immunity or resistance is outlined as follows: l. Innate or inherited. a. Species b. Racial (strain or breed) c. Individual 2. Acquired a. Active (1.) Resulting from having the disease (2.) Stimulated by vaccination with dead or living disease agents b. Passive (1.) Injection of antiserum (2.) Transferred from dam to offspring Inherited resistance may be complete or partial; for example, turkeys are not susceptible to laryn- ; gotracheitis, and although chickens are more re- " sistant than turkeys to blackhead, they may become ; infected under certain conditions. Inherited resist- i. ance or susceptibility to lymphoid leukosis is well j established, but no completely resistant breed or f strain of chickens has been developed. Individual a resistance is apparent in practically every disease f outbreak in a poultry flock. Some birds, although exposed to the same chances for infection, fail to develop evidence of the disease. While inherited immunity is important, ac- ‘g quire-d immunity is a more controllable reaction that can be used intentionally by the poultryman. Q Acquired immunity is the reaction we hope to . stimulate by application of all vaccines. The pur- pose of vaccines is to stimulate an active production of antibodies by safe means. Active immunity de- j pends upon the production of antibodies within f, the body of each individual. Antibodies are pr0- ». teins associated with the globulin fraction of the blood serum. Antibody production is not under- v stood completely, but antibodies are apparently produced by various organs such as the liver, spleen i and bone marrow. In general, antibodies are spe- ' cific for the organism which stimulated their pro- duction; thus, immunity to one disease ordinarily g does not imply resistance to others. Passive immunity is the transfer of antibodies“ from the individual in which they are produced a if to another individual. This is done by the injection of serum from an immunized individual. Anti- bodies also are transferred from the dam to the y; offspring through the egg; thus, hens that have had Newcastle disease transfer antibodies through the yolk to their chicks. Such passive immunity is an - ;-; important consideration in vaccination programs. ~¥Passive immunity is of short duration and there .; is usually a marked decline in the antibody level f: within 21 to 30 days. Passive protection against infection usually lasts no longer than 4 to 6 weeks. yManifestatians of Disease Detectable signs of disease are known as symp- < toms. Visible changes in the size, color, shape or ifstructure of an organ are known as lesions. Loss fof body weight, decreased egg production, reduced Sliced consumption, droopiness and lameness are 1| e symptoms. An enlarged liver, tumor on the intestine, abscess in a lung or collection of exudate an air sac are examples of lesions. Many symptoms are general; they usually are Zpen in any diseased individual. Examples are iness, ruffled feathers, diarrhea and loss of petite. Other symptoms are specific; they are n only when certain diseases are present. Ex- in of such symptoms are the tremors associated "th avian encephalomyelitis (epidemic tremors) the flaccid paralysis associated with botulism. l; iLesions like-xvise may be of general or specific . yture. For example, enteritis is associated with , ny diseases, but the “gray eye" of ocular leukosis . '_ specific. ick Health Management Sanitation is a much used, but poorly defined . The usual implication is that sanitation is " universally understood practice that may be plied to prevent all diseases. This concept w leads to misunderstanding and disappoint- Good sanitation in relation to one disease 1-- ally may provide favorable conditions for the l lopment of other diseases. Although many in sanitation measures always should be applied, must be base-d on the nature of specific ises. The ambiguity surrounding the tenn ‘ itation" can be avoided by using the expression inagement and sanitation for disease preven- p. ." This phrase then would be defined as all , tices, specific and nonspecific, that the poultry- f. applies to pifevent disease or reduce severity E economic loss from diseases. v A standard disease prevention program that can ly on all poultry farms does not exist. But - - are some basic principles that always should observed. Some practices that aid in disease prevention HTC I l. l0. l1. 12. 13. l4. Select a well-known, reliable source from which to purchase chicks, poults or hatching eggs — one that can supply healthy stock, inherently vigorous and developed for a specific purpose. It is best to purchase only day-old chicks or hatching eggs. If it is necessary to purchase started birds, select the best possible source. Keep birds separate according to source and age groups- To mix birds is an invitation to trouble. ' Follow an “all in, all out” program. Change litter and thoroughly clean and disinfect the house and equipment between each group of birds. While litter selection and management is a large subject, applying this recommendation as a general practice will prevent many disease and parasite problems. Keep chickens and turkeys separate. Prefer- ably, only chickens or only turkeys should be kept on the same premises. Maintain hatchery supply flocks on separate premises from other birds. Select a reliable commercial feed, or, if farm mixing is done, mix carefully according to a dependable formula. Provide an adequate supply of wholesome water. Avoid watering from surface tanks, streams or ponds. Make and carry out a precise vaccination schedule for each flock. Work out the vaccination program with poultry disease authorities in each state or local area. Discourage persons other than the caretaker or essential personnel from visiting the poul- try house or yard. If a disease problem develops, obtain an early, reliable diagnosis and apply the best treatment, control and eradication measures for that specific disease. Dispose of all dead birds by burning, deep burying or by a disposal pit. This phase of management often is overlooked. Maintain good records relative to flock health. These should include vaccination history, disease problems and medication employed. Many facts of disease prevention are acquired only through experience and a well-rounded grasp of modern poultry husbandry. 7 Hatchery Management and Sanitation The information contained in this section has been adapted from recommended procedures of the National Poultry Improvement Plan and Na- tional Turkey Improvement Plan. Hatching egg sanitation. Collect hatching eggs from nests at frequent intervals and observe the following practices: l. Use cleaned and disinfected containers to collect the eggs and take precautions to prevent contamination from organisms that may be on hands or clothing. 2. Maintain the identity of all eggs as to the breeder flocks of origin. 3. Do not use dirty eggs for hatching purposes. Collect them in a separate container from hatching eggs. Slightly soiled eggs may be dry cleaned by hand or by a motor-driven buffer. 4. As soon as possible after collection, fumi- gate the visibly clean eggs as described under the subheading “fumigation.” 5. After fumigation, store eggs in a cool place. Store eggs for as short a period as possible before setting. Properly clean and disinfect racks used for storing eggs. 6. Use new or fumigated cases. to transport eggs to the hatchery. Discard soiled egg case fillers. Hatchery sanitation. An effective program for the prevention and control of Salmonella and other infections includes these practices: 1. Arrange the hatchery buildings so that sepa- rate rooms, with separate ventilation, are provided for each of the four operations; egg receiving, in- cubation and hatching, chick holding and disposal of offal and cleaning of trays. Place these rooms under isolation so that admission is granted only to specifically authorized personnel who have taken proper precautions to prevent introduction of diseases. 2. Thoroughly clean and disinfect frequently the hatchery rooms, tables, racks and other equip- ment in them. Burn all hatchery wastes and offal or otherwise properly dispose of them. Clean and sterilize containers use-d to remove such materials after each use. 3. Thoroughly clean and fumigate the hatch- ing compartment of incubators, including the hatching trays after each hatch. 4. Use only clean eggs for hatching purposes. Fumigate all eggs set prior to setting or within 12 hours after they are placed in the incubator. Also fumigate them after transfer to the hatching compartment. 5. Use only new or clean fumigated egg cases for transportation of hatching eggs. Destroy soiled egg case fillers. 6. Distribute day-old chicks, poults or other newly hatched poultry in clean, new boxes or in disinfected plastic cartons. Clean and disinfect all crates and vehicles used for transporting started or adult birds after each use. I, 7. Maintain the identity of all chicks and poults as to the breeder flock of origin. 8. Do not mix the progeny of different breede flocks if it can be avoided. Cleaning and disinfecting. l. In poultry houses and hatchery rooms, clean- ing and disinfecting should include these steps: a. Settle dust by spraying lightly with dis- infectant. b. Remove all litter and droppings to an isolated area where there is no opportun- ity for dissemination of any infectious disease organisms that may be present. c. Scrub the walls, floors and equipment with a ho-t soapy water solution. Rinse to remove soap. d. Spray with a cresylic disinfectant, such as liquor cresolis saponatus, 4 ounces to a gallon of water, or sodium orthophenyl- phenate, 1% ounces (1 heaping table- spoonful) to a gallon of hot Water. 2. In the hatchers, cleaning and disinfection include the following procedures: a. Remove trays and all controls and fans for separate cleaning. Thoroughly wet the ceiling, walls and floors with a stream of water; then scrub with a hard bristle brush. Rinse until there are no deposits on the walls, particularly near the fan opening. b. Replace cleaned fans and controls. Re- place trays, preferably still wet from cleaning, and bring the incubator up to the nonnal operating temperature. c. Before placing eggs in the hatcher, it should be fumigated. d. If eggs are hatched in the same machine as they are incubated, clean the entire machine after each hatch. Use a vacuum cleaner to remove chick down from the egg trays. F umigation. Fumigation of eggs and incubators is an essential part of a hatchery sanitation program. 1. Preincubation fumigation of eggs should be done as follows: a. Provide a room or cabinet proportionate to the number of eggs to be handled. The room should be relatively tight and equipped with a fan to circulate the gas during fumigation and to expel it after fumigation. b. Place the eggs in the room on wire racks which will not prohibit air circulation, . gas‘ c. Formaldehyde gas is provided by mixing . 0.6 grams of potassium permanganate with 1.2 cc of formalin (37 .5 percent) for each cubic foot of space in the room.. Mix ingredients in an earthenware or enamel- ware container having a capacity pf at least ten times the volume of the total g ingredients. I d. Circulate the gas within the room for 20 minutes; then expel. , e. Humidity for this type of fumigation is not critical but the temperature should be around 70 degrees F. Extra humidity may be provided in dry weather. Eggs which have not been fumigated prior 'ng should be fumigated as soon as possible 54o later than l2 hours after setting using the fng procedure: a. Determine the size of the incubator by multiplying the length times the width times the height. A b. After setting the eggs and allowing tern- perature and humidity to regain normal operating levels, release formaldehyde gas into the incubator. j c. For each cubic foot of space in the incu- I bator, use 0.4 grams of potass-ium per- manganate and 0.8 cc of formalin (37.5 percent). Use a container having a ca- pacity of at least ten times the volume of the total ingredients. d. Close vents and doors but keep circulat- ing fan operating and continue fumiga- tion for 20 minutes with normal operat- ing temperature and humidity. c. After 20 minutes of fumigation, open * vents to the normal operating positions i - to release the gas. Eggs not fumigated as described in para- Y or in, paragraph 2 of this section should "»'gated"after the ninety-sixth hour of incu- . Follow the procedure described in para- 7 2 of this section. Single or repeated fumi- “of eggs in the setter may be practiced, but the ‘on schedule should be such that no eggs and expose to circulating formaldehyde ' are fumigated during the period from the twenty- fourth to the ninety-sixth hour of incubation. ' 4. Refumigate all eggs after transfer to the hatcher, preferably as soon as the temperature and humidity regain normal operating levels. Follow the procedure described in paragraph 2 of this section. 5. Fumigate empty hatchers between each hatch. After the interior of the hatcher has been cleaned thoroughly and the cleaned trays returned, follow the procedure below: a. After temperature and humidity are brought to normal operating levels, use 0.6 grams of potassium permanganate and 1.2 cc of formalin (37.5 percent) per cubic foot of space in the hatcher. b. Close doors and vents and leave closed overnight. PRINCIPLES OF REASONABLE DRUG ADMINISTRATION Drugs and chemicals are used widely in poultry_ production. Arsenicals and antibiotics are added to the ration as growth stimulants. Various com- pounds known as coccidiostats are added to the ration to prevent coccidiosis. Often drugs are in- cluded in rations “just in case they might help prevent some potential disease.” _Antibiotics some- times are recommended at times of “stress” such as moving, vaccination or debeaking. While the use of any drug on a nonspecified basis may be of value, any real benefit is difficult to determine. A tremendous amount of money is spent by the poultry industry yearly for drugs that are of little or no value in preventing or reducing disease. The most valid use of drugs is in the application of known effective treatments for specific diseases. Such treatments must be based on a reliable diag- nosis. Recommendations for the treating of poultry diseases are changing constantly as new, more ef- fective drugs are developed, or as once effective compounds become ineffective because organisms have developed resistance or for other reasons. In using any drug, follow the recommendations of persons qualified to give such directions or fol- low the manufacturer's recommendations. Drug Administration Drugs may be administered to poultry in several ways. The choice of method depends upon a num- ber of factors including: (1) the disease in question; (2) the drug to be used; (3) available labor and ad- ministration equipment; (4) the condition of birds; and (5) the length of the medication period. The following outline shows commonly em- ployed methods of drug administration: 1. Mass methods a. Incorporation into feed b. Incorporation into drinking water c. Aerosol, or dusting the drug into the air over the birds 2. Individual bird treatment a. Parenteral (subcutaneous, intramuscular or intravenous injection) b. Drenching Mass methods of drug administration are popu- lar because they save labor; eliminate the necessity of handling each bird, a “stress” which may aggra- vate the disease state; and allow for continuous medication over a prolonged period. Disadvantages of mass methods include the inability to control individual bird doses. Conversely, individual bird treatment requires more labor, “stresses” the birds and does not lend itself to continuous medication. However, it does allow for accurate controlled dosage to each bird and offers a means of treating birds when an existing disease is not subject to mass methods of treatment. Drugs should always be used in accordance with the manufacturer's recommendations which take into consideration: (1) safe levels, (2) approved com- binations and (3) adequate withdrawal time to avoid residues, etc. Preventive Medication It is doubtful that there is a justification for the continuous use of drugs in the average poultry operation other than for growth stimulation and the prevention of coccidiosis and, on occasion, blackhead. There are several reasons why indiscriminate preventive medication should be discouraged. Among these are: 1. Expense 2. Indiscriminate use of drugs frequently al- lows drug-resistant strains of bacteria to develop. When this happens, previously-effective drugs lose their value for the treatment of actual disease out- breaks. 3. Preventive medication often allows the grower to develop a false sense of security about disease control. As a result, management and sani- tation practices are neglected. 4. Preventive medication often masks the true nature of a particular disease and may make diag- nosis extremely difficult. Frequently, it is impos- sible to isolate causative organisms by laboratory IO techniques when the birds have been on continuous medication. Treatment of Disease Outbreaks Initiate drug treatment of disease only after a reliable diagnosis has been established. To do otherwise is costly and often produces serious bird losses. For example, an outbreak of erysipelas in turkeys does not respond to the usual treatments employed for fowl typhoid or fowl cholera. Mis- diagnosis results in drug expense and a continued loss due to mortality. Hemorrhagic anemia syri- drome of chickens is confused easily with coccidi- osis. If a flock affected with the former condition is titrated for coccidiosis, the existing problem is aggravated and severe losses may occur. Once an accurate diagnosis has been established, follow the prescribed recommendations for treat- ment very closely. Many drugs produce toxic effects if used improperly. VACCINATION TO PREVENT POULTRY DISEASES What Vaccines Are Vaccines are suspensions of large amounts of the disease-causing organism or virus in a diluent. Most virus vaccines contain living organisms (except for the killed type of Newcastle disease vaccine). Virus vaccines are produced by growing laboratory V strains of virus in embryonated chicken eggs or in cell culture systems. Strains of virus differ just as do strains of chickens within a particular breed. Strains selected ‘for making vaccines usually are mild so they will not cause a serious infection but still stimulate immune body production. Bacterial vaccines (bacterins) are produced by growing selected strains of bacterial organisms in l artificial media. The organisms are killed after ' they are harvested for bacterin production. These products are incapable of producing infection but will stimulate antibody production. In general, living vaccines produce better im- I munity than dead ones; however, the dangers ass0- ciated with vaccination are greater. Dangers of Vaccination Most vaccines contain living viruses intended i to produce a mild infection. In other words, vac- l cines make the birds sick. The sickness will be mild if: 1. Birds are healthy at the time of vaccinationQ i 2. Chicken house or brooder house is clean and. I dry. 3. There are no sudden climate changes. Birds are at the proper age for vaccinations 5. There is ample heat available to the birds. (Raise the temperature about 5 degrees F. for a few days after vaccination.) 6. Instructions in the package of vaccine are followed. Since most vaccines contain living agents, vac- 'ne virus may spread to unprotected birds. on the u premise. This may cause adverse effects, par- “ larly in unprotected laying flocks. Seek expert istance when it appears desirable to initiate a ccination program on property where unpro- ted layers are present. The wing-web type of ewcastle vaccine, infectious bronchitis vaccine, l pox vaccine, infectious laryngotracheitis vac- e, infectious bursal agent (IBA) vaccine and idemic tremor vaccine may spread from flock flock on the same farm. accination—No Substitute for Sanitation w A sound vaccination program is part of a f. O 0 management and sanitation program and not substitute for it. A It is unnecessary to vaccinate against certain ieases in some parts of the country and in some w within a particular state. Vaccination should ~ tailored to meet the needs of a particular oper- u, 'on in a particular area. For example, Texas - ltrymen should not use laryngotracheitis vac- l’ e e or attempt to move laryngotracheitis vaccinated H’, a into the state. This disease is not a problem _- Texas and the Animal Health Commission has ued a restraining order against the introduction j this vaccine into the state. . fseases for Which Vaccines Are Available Of the products on the market for the control A virus infections, respiratory virus infections id the list but others are becoming increasingly portant. 1. Newcastle disease ' 2. Infectious bronchitis 3. Infectious laryngotracheitis (to be used only with the permission of the Animal Health g Commission) 4. Fowl pox (may cause symptoms and lesions ' of the respiratory system, but not primarily a respiratory disease) 5. Avian encephalomyelitis (epidemic tremors) f 6. Gumboro (infectious bursal disease)—to be used only under the direction of the state regulatory people or poultry pathologists 7. Marek’s disease vaccine (Turkey Herpes virus) — newest of vaccines and should be used under strict compliance with manufac- turer's directions Bacterins are available commercially for the control of: 1. Erysipelas 2. Fowl cholera 3. Mixed (not in wide acceptance) Coccidiosis control with the use of live oocysts administered early in the baby chicks’ life (Coc- civac*) has gained acceptance with poultrymen as one approach toward controlling coccidiosis outbreaks in both light and heavy breed layers. Administration of Vaccines Vaccines must be used properly if they are to be effective. For best results: 1. Store vaccines in the refrigerator according to manufacturer's recommendations. 2. Do not use outdated vaccines. 3. After a vial of vaccine has been opened, destroy by burning any remaining contents after use. Do not set back for use at a later date. 4. Administer in accordance with manufac- turer’s instructions. 5. Record serial numbers of all vaccines used. Vaccines, as drugs, may be applied in different ways, depending on the product used, age of birds and other factors. In general, Newcastle disease, infectious bronchitis, epidemic tremor, gumboro and coccidiosis vaccines are adapted to mass meth- ods of administration, whereas fowl pox, infec- tious laryngotracheitis, erysipelas, fowl cholera and Marek’s disease vaccines are adapted for individual bird administration. 1. Mass methods: a. Drinking water — Newcastle, infectious bronchitis, epidemic tremors, gumboro, cocci-vac 2. Individual methods: a. Intranasal; intraocular—Newcastle in- fectious bronchitis b. Wing-web stab — Newcastle, fowl pox c. Feather follicle — fowl pox (pigeon pox vaccine) d. Subcutaneous; intramuscular injection - Newcastle (killed), erysipelas, fowl pox, Marek’s and fowl cholera Vaccines frequently are combined to reduce labor and the number of immunization procedures required. Newcastle disease vaccine often is com- bined with that of infectious bronchitis. While the use of such combination products may have ‘Trade name of a product containing sporulated oocysts to be used in the immunization of chickens against coccidiosis. merit in some cases, their routine use is. not recom- mended. There are two good reasons why: l. Evidence exists that the host response to one virus. fraction may interfere with the develop- ment of adequate immunity to the other. 2. It is impossible to evaluate the vaccine re- action. (Is the reaction due to one or both fractions in the vaccine?) After live virus vaccination, birds must be ob- served for “takes” to the vaccination. A discussion of this is included in the individual disease sections. A Suggested Vaccination Program for Chickens Because of the fast changing size of poultry operations within the state, it must be pointed out that ea-ch operation should have its own “tailor- made” vaccination program. Seek advice from a poultry disease specialist and/or vaccine manufac- turer in developing a program. For those with smaller, isolated flocks the pro- grams as outlined should work. l. Replacement Chicks (Commercial egg or breeders) a. Vaccinate for Newcastle at 7 days and 4 weeks of age with intranasal Newcastle vaccine using the drinking water method. b. At 6 weeks of age, vaccinate for infec- tious- bronchitis using the drinking water method. c. When birds are 8 weeks old, vaccinate for fowl pox by the wing-web method. d. Revaccinate pullets against Newcastle disease when they are moved into the laying house if intranasal type of vaccine is used. If wing-web method is to be used, vaccinate 4 weeks before pullets start production. 2. Chicks for Broiler Production a. Vaccinate against Newcastle at 7 days of age using intranasal vaccine by the drink- ing water method. A second dose may be administered at 4 weeks. b. At 2 weeks of age, vaccinate against in- fectious bronchitis using the drinking water method. c. Vaccination of broilers against fowl pox is not recommended in areas except where experience shows it needs to be done, and then at a time experience indicates it will give the most satisfactory results. Use of Other Vaccines in Chickens and Turkeys Undertake vaccination of chickens for disease other than specifically outlined above only after getting expert advice. ‘l2 Vaccination of turkey flocks for Newcastle dis- ease, fowl pox, erysipelas and fowl cholera is dis- cussed under individual disease headings. Usually the decision to vaccinate, except for fowl pox, should be- made on the basis of area experience and expert advice. USING THE DIAGNOSTIC IjABORATORY The Texas Agricultural Experiment Station, under the direction of the College of Veterinary Medicine at Texas A8cM University, operates Poulf- try Disease Investigation Laboratories at College Station, Center and Gonzales. These laboratories serve several functions: l. To serve as diagnostic and information cen- ters where Texas poultrymen can obtain assistance with their poultry disease problems. 2. To accumulate information relative to the incidence and importance of the various. poultry diseases in the state. 3. To help formulate and carry out poultry disease research projects which reflect the needs of the Texas poultry industry. Laboratory Locations Locations of the Poultry Disease Investigation Laboratories are: 1. College Station. Room 101, Veterinary Med- ical Sciences. Building, Texas A8cM University, Telephone 713/845-5941. 2. Center. Corner of Childs Street and Malone Drive near Center High School. Telephone 713/ 598-4451. 3. Gonzales. One block South of U. S. High- way 90A on Water Street (1972). Telephone 512/ 437-2212. Laboratories are open from 8 a.m. to noon and l p.m. to 5 p.m. Monday through Friday, Univer- sity holidays excluded. Make prior arrangements to assure service at other times. In addition to the laboratories listed, there are some practicing veterinarians who are well quali- fied by training and interest to assist with poultry disease problems. Using the Laboratories Disease prevention is the best ap-proach to dis- 1 ease control. Utilize laboratory personnel to assist a in developing disease prevention programs and not solely as “firemen” to help when disease appears. When a disease problem develops, however, get help immediately rather than calling the labora- g tories as a last resort. If emergency treatment is essary, remove a sample of birds for diagnostic OSes before treatment is started. - The selection of a sample of birds for the labo- ‘gory should not be a culling ope-ration. Birds itted should be representative of the condition ght to be the flock p-roblem, and should be f» various stages of the disease. Submit three or birds, or more if young chicks or poults. When l» er ress p ber in flock Breed tchery source 1r of operation (Floor, cage, range, etc.) ing program 'nation history “ess first seen y bidity (No. affected) Mortality birds are dying rapidly with few preliminary symp- toms, bring in several dead birds with the sample. Dead birds should be placed in plastic bags and refrigerated. Diagnosis often is difficult if birds are submitted without adequate information. The following out- line includes information which should be routinely available. Phone No. I Age J ence of illness 'cation <=. rks (other flocks on farm, previous problems, etc.) f0 Expect i‘ When the pathologist is able] to diagnose " se of trouble without the necessity of time- _ ing tests, recommendations are made direct- fdie individual. submitting the birds. other instances, only a tentative diagnosis established when birds aresubmitted. In '§:ase, preliminary recommendations pending Jdiagnosis may be made depending upon the lar situation. Laboratory tests (culture, virus isolation, tissue pathology) are time consuming. When these tests are necessary for final diagnosis, a few days to a few weeks may be required to complete them. Then final diagnosis and recommendations are made to the owner by letter or phone. For the protection of the industry, it is the policy of the laboratories to dispose of all poultry submitted. l3 Section 2. BACTERIAL DISEASES Bacteria are microscopic living organisms. They are grouped into spherical forms, straight rods, curved or spiral rods and filamentous forms. Growth requirements of different species vary con- siderably, but most can be grown on artificial media. Bacteria, like other living organisms, have certain requirements as to environmental tempera- ture, moisture and nutrition for propagation. Not all bacteria are detrimental to animal health. In fact, most bacteria are necessary for such processes as food digestion. Classification of bac- teria into species so that disease-producing organ- isms may be separated from those that are harmless or beneficial is based on such laboratory techniques as staining of organisms for microscopic examina- tion, determination of fermentation reactions in various liquid media, serologic reactions and others. Successful control of bacterial diseases is based upon isolation and identification of the disease- producing species, if present, and prevention of multiplication or spread of the organism within the animal body or to other animals. This should be done with a minimum detrimental effect upon the beneficial organisms. SALMONELLA AND PARACOLON INFECTIONS There are more than 2,000 different species or serotypes of organisms belonging to the genus Salmonella, all of which are potential pathogens of poultry. Systemic effects usually are observed when infection occurs, but since the digestive sys- tem is affected primarily, they often are referred to as enteric organisms. The same is true of the group of organisms referred to as paracolons. Be- cause of similarities produced by infections by these groups of organisms, they are grouped un- der one heading. Both groups are worldwide in distribution. Pullorum Disease Pullorum disease is an infectious, acute or chronic, bacterial disease affecting primarily chick- ens and turkeys, but most domestic and wild fowl may be infected. Etiology: Salmonella pullorum — first isolated by Rettger in 1900 Transmission: primarily egg transmitted but transmission may occur by other means 1. Infected hen=egg=infected chickr-spread in incubatorr-in chicken boxes=in brooder house ‘l4 and on range I survivors become infected breeder birds " 2. Mechanical transmission -— carried about on ’ shoes, equipment 3. Carrier birds — apparently healthy birds which shed organisms . 4. Contaminated premises — from previous outbreaks 5 Portal of entry may be the respiratory (as in incubator) or digestive system. Most outbreaks. of acute pullorum disease in, chicks or poults result from infection while in the hatchery. Incubation period: 5 to 7 days Symptoms: Pullorum disease is highly fatal to young chicks or poults but mature birds are more’ resistant. Young birds may die so soon after hatch “p. ing that no symptoms are observed. Most acu outbreaks occur in birds under 3 weeks of agel Mortality in such outbreaks may approach 90 cent if untreated. Survivors usually are stunt or unthrifty. TYPICAL SYMPTOMS IN CHICKS OR POULTS: (not constant) o Droopiness o Ruffled feathers L‘ o Chilled appearance, huddled around sour of heat , o White diarrhea and pasted down around v v o Labored breathing SYMPTOMS IN ADULTS: (Usually no rec nizable symptoms) p) Lesions: Young birds dying during an . f! outbreak may present no recognizable gross lesi y Representative lesions in young birds include: o Necrotic foci in liver (varying from pinpoi», to pea size) i‘ o White nodular areas in muscle of heart a‘ gizzard; occasionally in wall of intestine i o Multiple small, firm, nodular areas in lu o Yellow or cream-colored cecal cores or plu Lesions in adults: if o Gross lesions may be lacking. o “Blighted” ova may be present. o Livers may contain areas of necrosis. o Oviducts may contain cheesy deposits. Diagnosis: o Blood testing may indicate presence of the disease. o May be suspected from history, symptoms and lesions. o Positive diagnosis depends upon isolation and identification of the organism by laboratory methods. Prevention: Complete eradication is the only sound way to prevent pullorum disease. Test all hatchery supply flocks and accept only pullorum- free flocks for the production of hatching eggs. The National Poultry Improvement Plan (NPIP) and the National Turkey Improvement Plan (NTIP) are national organizations fonned primarily for eradicating pullorum disease. These organizations began in 1935 and since then the disease virtually has been eliminated from areas where most hatcheries participate in the plan. These organizations are helped and coordinated by the Agricultural Research Service (ARS) and each state has a local organization with state super- visors to administer the plan. {Serologic tests: All tests for pu.llorum disease are agglutination tests; however, the three pro- cedures accepted as official testing methods are: l. Whole blood rapid plate test. This test employs stained antigen which is mixed with a drop of blood on a glass plate. The test ordinarily is conducted and read in the field. 2. Rapid serum plate test. This test is identical to the whole blood test except that serum is used ‘instead of whole blood. 3. Tube agglutination test. The test is con- ducted with an unstained antigen and serum, in- cubated at 37.5 degrees C. for 24 hours prior to reading and is performed in NPIP approved labo- ratories. The tube test is considered more reliable thin other tests and is the only official test for turkeys in Texas. Advantages of the tube test: 1. Conducted under controlled laboratory con- ditions. 2. A small number of designated well-trained individuals read and interpret the test. 3. The ratio of antigen to serum can be varied to help in interpreting the reaction. Advantages of whole blood rapid plate test: 1. Faster 2. Less expensive 3. Reactors can be removed from flock at the time of testing so that birds do not have to be handled a second time. Other procedures which must be followed in maintaining pullorum-free breeder flocks: l. If a flock is infected it is advisable to dispose of the flock rather than try to dispose of reactors and establish a negative flock. 2. After disposing of infected birds, thoroughly clean and disinfect the house and equipment. A 3 percent water solution of cresol (liquor cresolis saponatus) is excellent for such purposes. For incubator fumigation procedures follow procedures outlined in Section 1. Why “breaks” occur in a previously “clean” flock: l. Introduction of the infection since last test 2. Infection with a “variant” strain of the or- ganism not detected by the standard test Treatment: It is primarily a salvage operation and does not prevent birds from becoming carriers. Consequently, do not keep recovered flocks for egg production. The preferred drug for treating infected flocks is furazolidone, marketed under the trade names of NF-180 by Hess and Clark or Furox by Norwich Agriculture Products. The recommended level is 2 pounds NF-180 concentrate or Furox. 50 (100 grams furazolidone) per ton of feed for l0 days to 2 weeks or until mortality stops. In severe cases the drug level may be increased to 4 pounds (200 grams furazolidone) per ton of feed. Fowl Typhoid Fowl typhoid is an infectious, contagious bac- terial disease that is usually acute, but may be chronic. It affects most domestic and wild fowl including chickens, turkeys, ducks, pigeons and pheasants although in Texas, outbreaks most" often occur in turkeys. Do not confuse it with typhoid fever of humans which is caused by a separate and distinct organism. Etiology: Salmonella gallinarum, formerly known as Shigella gallinarum, discovered by Klein in England in 1889. Incubation period: Variablebut usually 4 to 5 days. ‘l5 Duration: Varies from 5 to 6 days in the acute form to weeks or months in the chronic form in which the daily mortality rate is often 10w. Transmission: Methods of transmission are the same as for pullorum disease, including egg trans- mission, but mechanical transmission is more im- portant than it is in pullorum disease. Age susceptibility: Any age bird may be af- fected, but the disease occurs primarily in young adults (usually those past 12 weeks of age). Mortality rates: Variable, ranging from less than 1 to 40 percent or higher, especially if treat- ment is not initiated promptly. Symptoms: Symptoms may be suggestive of fowl typhoid but they are not specific. Some typical symptoms include: o Sudden or sporadic mortality o Listlessness o Green or yellow diarrhea with pasting of the vent feathers o Loss of appetite o Increased thirst o Pale, anemic appearance of comb and Wattles Lesions: In addition to the symptoms men- tioned, certain lesions observed at necropsy will help substantiate a diagnosis of fowl typhoid. These include: o Enlargement of the spleen which may be mottled o Liver usually considerably enlarged and varying in color from. yellow to greenish brown, often with visible necrotic foci o Small pinpoint hemorrhages in the muscles and fat, particularly that surro-unding the organs o A slimy type inflammation of the anterior third of the small intestine In turkeys, the presence of small, white plaque- like areas visible through the walls of the intestine is very suggestive of fowl typhoid. Diagnosis: A tentative diagnosis usually may be made from consideration of the history, symp- toms and lesions. Final diagnosis must be based on isolation and identification of the causative organism since other diseases often will closely resemble fowl typhoid. Serology: Blood tests used for detection of pul- lorum reactors. also are used in control of fowl typhoid. Both organisms bear such close antigenic relationship that one test will suffice for both. But the test is suggestive rather than conclusive. ‘l6 Prevention and control: Vaccination — bacterins presently available are of little or no value and may cause the flock to react to the pullorum test for approximately 60 days after vaccination. Prevention and control depends upon: o Hatching from disease-free flocks as estab- lished by the pullorum test o Strict sanitation on the farm o A clean, safe water supply (Avoid watering from ponds or surface tanks) Q o Use of an incinerator or disposal pit for dis- posal of all dead birds (The causative organism may live for at least 6 months under certain conditions. Following an outbreak, thoroughly clean houses and equipment. When feasible, practice range rotation and other special precautions to prevent a carryover of in- fection to the next flock.) Drugs (e.g. furazolidone at the rate of 50 grams per ton of feed or even higher levels) cannot be depended upon as a means of prevention and are not recommended. Treatment: Furazolidone is the choice drug and levels of 100 grams per ton of feed for l0 to l4 days usually will stop mortality. However, since some strains of the fowl typhoid organisms are resistant to this drug, it may be necessary to use higher dosage levels (200 grams per ton of feed) for longer periods of time. After mortality is con- trolled the furazolidone level may be decreased to 50 grams per ton of feed. Give the lower level continuously until the flock can be marketed. In rare instances it may be possible to stop treatment after 3O days, but if mortality should recur, use the treatment level again for a few days. Sulfaquinoxaline is effective as a treatment and may be used for medication, except in laying chick- ens, through water while waiting for feed contain- ing the furazolidone. It also may be used for treating flocks which do not respond favorably to furazolidone. Commercial liquid preparations vary in con- centration so the manufacturer's recommendations should be followed to achieve the desired water concentration. For the first 2 days, the drug is mixed in the drinking water at a concentration of lz2500. Then reduce to a concentration of lz4000. Give the lower level until mortality is controlled. Parafyphoid Infections The term “paratyphoid” was used first to desig- nate a group of human, feverish conditions re- sembling typhoid fever. Related to poultry, para- is a term denoting the disease produced of the many Salmonella species other than um and S. gallinarum. Infection may re- f acute or chronic disease. Acute clinical dis- pcommon in young birds and rare in adult iOver 2000 species or serotypes of Salmonella Z-n‘ are recognized, and most birds, reptiles i}. u als can serve as host to one or more i‘ Economically, the disease is of greatest i? to the turkey industry. In 1895, Moore recorded the first au- ‘ case of paratyphoid when he isolated and _'ed a Salmonella from pigeons with an en- ‘ff The first report of paratyphoid infection ; in turkey poults- in the United States was Rettger et al. in 1933, although Pomeroy 7- stermacher observed the infection in tur- ‘*- Minnesota in 1932, according to a report pied in 1939. tlogy: The organisms of this group are sero- related and are Gram negative, nonspore _ , flagellated, motile rods. They can be ed from S. pullorum and S. gallinarum by ology and biochemical characteristics, but" typhoid organism cannot be differentiated i other member of the group except by sero- methods. ‘lhogenicity: Most acute paratyphoid infec- 'occur in birds less than 4 weeks old, except n; - ns and canaries in which acute disease and __ortality may occur in any age group. ,_ tality in young turkey poults usually varies than l percent to l0 or 20 percent, al- H rarely it may exceed 80 percent. Most death Fin young birds occur during the first 2 after hatching, the mortality curve closely ling that of pullorum disease. Outbreaks ks (“keel disease”) often result in severe erity of infection with each of the various " v s has been determined. There is a tendency i, ider S. typhimurium as a type species repre- of the whole group and as the mos-t im- n cause of paratyphoid in poultry. This commonly is isolated from birds involved typhoid outbreaks throughout the country. jults of research to date indicate that all ella species must be considered as potential 5;‘ in poultry. Outbreak severity depends 9 age and species of host, serotype or species I onella involved and certain environmental ‘ I agement factors. ost distribution: The host range of the Sal- species probably is as great as that of any jq" organism. It includes most domestic animals, birds, rodents, snakes, lizards and man. The greatest reservoir of Salmonella is probably poultry, and the organisms are encountered most frequently in turkeys, chickens and ducks. Transmission: The transmission of paratyphoid includes all factors involved in the transmission of pullorum and typhoid plus several other. Because of the multiplicity of hosts and wide distribution in nature, chances of clean flocks becoming in- fected are greater than for either of the other two diseases. Direct ovarian transmission may occur in both chickens and turkeys but is more common in ducks. Of greater importance in chickens and turkeys is contamination of the eggshell by fecal material during or after passage through the cloaca. The organism, being motile, rapidly penetrates the shell and shell membrane (rate of penetration depends upon such factors as temperature and humidity) and gains access to the interior where it may survive until hatching. Most instances of shell penetration occur during the first week of incubation. During incubation, “blow-up-” of infected eggs aids in spreading the organism. Many infected chicks or poults hatch which increases contamina- tion of the incubator. The incubator environment favors survival of the organisms to infect subsequent hatches unless fumigation procedures are practiced routinely. An additional source of infection may be indi- cated by reports of recovery of many serotypes from poultry feeds. Investigators in a number of states including Texas, have reported recovering one- or more species from 20 to 30 percent of the samples taken from certain materials such as animal by- products used as protein sources. The incidence is much lower in vegetable protein sources and there appears. to be no incidence in pelletized or crumbled feeds. Symptoms and” lesions: Symptoms are variable», depending mainly upon the species and age of the bird, pathogenicity of species of Salmonella involved and method of transmission, but in gen- eral, the symptoms resemble those associated with pullorum disease. Some characteristic symptoms include: o Huddling around the source of heat with lowered head, eyes closed and wings drooping 0 Increased thirst with decreased food consump- tion o Watery diarrhea and pasting of feathers around the vent 0 Increased “peeping" or “chirping" sounds Arthritis and swollen joints are observed com- monly in paratyphoid outbreaks in pigeons and sometimes occur in outbreaks in turkeys or chickens. l7 In acute outbreaks gross lesions may be absent in young birds. Characteristic lesions in young birds may include: o Emaciation and dehydration o Unabsorbed or coagulated yolks o Congested livers, sometimes with hemorrhagic streaks and/or pinpoint white foci of necrotic tissue o Inflammation of the intestine, especially the upper portion o Cores in the ceca having creamy or yellow color Acute infections in adult birds usually produce few if any lesions other than enteritis. Carriers and chronically infected adults usually have no specific lesions. Diagnosis: The disease may be suspected from flock history, symptoms and necropsy lesions, but a definite diagnosis depends upon isolation and identification of the organisms by qualified labora- tory personnel. Prevention and control: This is difficult be- cause of the wide range of hosts harboring organ- isms and because no single species or serotype of the organism is suitable as an antigen for de- tecting all other species in the testing program. S. typhimurium is used commonly as a represe-nta- tive for the group in attempting to standardize testing procedures. The pullorum-typhoid test of- rten will detect infected flocks even when the typhimurium antigen fails. Because of the many sources of infections, known clean flocks may be- come infected at any time subsequent to the last tffSt. An organized effort to control and eradicate paratyphoid exists in many states. Some hatcheries in other states reject eggs from flocks which have not been tested with the S. typhimurium antigen. Such control efforts are not the final answer to this problem, but they should be encouraged and additional information utilized as it becomes. avail- able. The possibility of contamination by organ- isms in feeds is now an important area in research and control programs. Pending additional information, hatchery and flock sanitation management practices are the most important factors in paratyphoid prevention and control. Some practices known to aid in paraty- phoid control include the following: o Do not use flocks known to be infected as a source of hatching eggs. o Follow hatchery and egg sanitation practices that reduce chances of introducing infection l8 into the incubator through fecal contamina- tion. o Early fumigation of eggs with formaldehyde gas (before incubation or within 24 hours afte-r the eggs are placed in the incubator). o Rodent control o Isolation from other sourceslof infection such as pigeons and ducks. o Serological testing of hatchery supply flocks and following outlined requirements of vol- _ untary programs. P“ g- . Treatment: Proper use of drugs may reduce mortality in acute outbreaks of paratyphoid. The drug of choice is furazolidone but some species or serotypes are more resistant to treatment than the pullorum or fowl typhoid organisms. Some para- typhoids have or will develop resistance to the . effects of furazolidone in time. The recommended level of furazolidone for _; treatment is 100 grams per ton of a complete ration = as the only source of feed. Continue treatment for L 2 weeks or until mortality is controlled. = Continuous use of furazolidone at a rate of 50 ' grams per ton of feed included frequently as a .= prophylactic measure. There is no assurance that such a practice will be effective in all cases. Fieldfi information indicates that in some instances such practices actually prevent the flock owner from, discovering a p-aratyphoid infection in the flocltr; Sulfonamides, such as sulfaquinoxaline and sul- famethazine, have some value in treating para?‘ typhoid outbreaks, but they are much less effective than furazolidone. r No treatment is known that will eliminate in 1 fection from the flock following an outbreak, and efforts to test and eliminate individuals harbori ;. the organisms. have been unsuccessful. Preventio is of primary importance. Regardless of treatmen never use infected birds to supply hatching eggs Puracolon Infections The paracolon bacteria comprise a large grou of related organisms that have certain character istics in common with the paratyphoids and a with the common coliforms. Most pathogenic pa u colon organisms are placed in the group known w Arizona paracolons. They can be differentia.t g from the paratyphoids by their biochemical _i actions, but the similarity between groups ca some delay and confusion in correct identificati 5 These organisms are distributed widely in natu I and have a host range which coincides with t. Salmonella. i‘ The role of the paracolons in causing poul disease is poorly established. Under certain r ditions, these organisms may cause disease in young turkey poults, and thus be of economic importance. Consider the disease produced, symptoms, le- sions, transmission, prevention and treatment as identical to the paratyphoid infections until re- search further clarifies the situation. Differentia- tion of paracolon from paratyphoid infections now depends on careful laboratory examination with isolation and identification of the causative organism. The importance of Arizona paracolon infection in chickens is not well defined. However, the Ari- zona organisms may produce severe losses in young turkey poults. The nature of the disease, including transmission, is similar to paratyphoid from which it cannot be differentiated except by laboratory means. Procedures employed to control Arizona in- fection are similar to those in use for paratyphoid infections. However, since infection is so wide- spread in many turkey breeder flocks, the disease in young poults is controlled largely by day old poult injection programs. COLIFORM INFECTIONS, COLIBACILLOSIS Coliform infections refer to the many and vari- ous diseases resulting from infection with bacteria referred to as Escherichia coli. In recent years these infections have become recognized as an important cause of morbidity, mortality and condemnations» in both chickens and turkeys. The incidence and severity of coliform infections have increased rap-id- ly, and current trends indicate they are likely to become an even bigger problem in the future. The problems attributed to coliform infections are often complex. There is a. marked variation in severity. They range from severe acute infections with sudden and high mortality to mild infections of a chronic nature with low morbidity and mor- tality. Infections may result in a respiratory dis- ease from air sac infection, a septicemic disease from generalized infections, an enteritis from in- testinal infection or a combination of any or all of these. Disease may result from coliform infec- tion alone as in primary infection or in combination with other disease agents as a complicating or secondary infection. Secondary infections common- i fly occur as a part of the classical air sac disease syndrome as a complication of Mycoplasma galli- 1 septicum infections. All ages may affected; however, it is more i common in young"; growing birds, especially the }__ acute septicemia in young turkeys and airsacculitis i in young chickens. High early mortality may occur 1 as the result of omphalitis or navel infections. Cause: The disease is caused by bacteria known as E. coli and from toxins it produces as it grows and multiplies. There are many different strains or serological types within the group of E. coli bac- teria. Many of these types are considered to be normal inhabitants of the intestinal tract of chick- ens and turkeys and consequently are common organisms in the birds’ environment. A marked variation exists between different strains in their ability to cause disease. On one extreme are the severely pathogenic strains which may alone cause disease. On the other extreme are the supposedly nonpathogenic strains which are considered to be innocuous. All degrees of pathogenicity exist between these two extremes. Certain types are recognized which normally live in harmony with the bird although they are cap- able of causing disease under certain conditions. The primary routes of entry by the infection are the respiratory system and the gastrointestinal tract. Omphalitis and infections in young birds may result from entry of the organism by way of the unhealed navel or penetration of the egg shell prior to or during incubation. Symptoms: The symptoms vary with the dif- ferent types of infections. In the acute septicemic form, mortality may begin suddenly and progress rapidly. Birds may die in good condition and mor- bidity may not be apparent. However, in most cases, morbid birds are evident as listless birds with ruffled feathers and indications of fever. In the chronic infection, debilitation and growth re- tardation are obvious. In the» event of respiratory infection, additional symptoms of labored breath- ing, occasional coughing and rales may be apparent. In the case of enteritis, diarrhea may be evident. Mortality may be high in recently hatched chicks or poults as a result of omphalitis due to coliform infections. Lesions: Extremely acute septicemic infection may result in sudden death with very few, if any, lesions apparent. The death resulted from the effects of the organisms’ toxins on the functions of the vital organs. However, lesions are usually present in various tissues depending on the location of therinfection. In acute infection, common lesions include dehydration, swelling and congestion of the liver, spleen and kidneys and pinpoint hemor- rhages in the viscera. The presence of caseous or fibrinous exudate in the air sacs, heart sac and on the surface of the heart, liver and lungs is a charac- teristic lesion. The intestines may be thickened and inflamed and may contain areas of hemor- rhage and excess amounts of mucous. In addition to these lesions, navel infections may be seen in young birds similar to those described for omphalitis. Diagnosis: Differential diagnosis by laboratory means is necessary since coliform infection in its ‘l9 various forms may resemble and be easily confused with many other diseases. Isolation and identifi- cation of the organism. by culture procedures can be readily accomplished; however, mere isolation is not sufficient to» make a diagnosis. One must take into consideration the organ from which the organism was isolated, the pathogenicity of the particular isolate and the presence of other disease agents. Prevention: Management and sanitation p-rac- tices designed to minimize the exposure level of these types of organisms in the birds’ environment are necessary in any preventive program. In addi- tion, these programs should include avoiding stress factors and other disease agents which may lower the resistance and predispose the birds to infection. Important points in these management and santitation practices include providing adequate ventilation, good litter and range conditions, properly cleaned and disinfected equipment and facilities and feed and water supply free of con- tamination. In addition, these programs should include avoiding overcrowding and environmental stressesisuch as chilling and overheating and avoid- ing vaccination and handling at critical times. Proper egg handling as well as a good hatchery management and sanitation program. is necessary to prevent early exposure. It should be emphasized that problems due to one of the more pathogenic strains may occur even under the most ideal conditions. Treatment: The response of coliform infections to various medications is erratic and often difficult to evaluate. Under practical conditions, treatment is disappointing and the results so variable that ...no one treatment can be recommended. Drug sensi- tivity varies with the strain, some of which may be partially or completely resistant to many if not all of the commonly used antibiotics. Tests performed in the laboratory to determine the sensitivity of the organism to the various drugs may prove useful in selecting the drugs which may be most bene- ficial. When practical, moving the birds to clean environment may be of more value than medica- tion. For example, when outbreaks occur in grow- ing turkeys in the brooder house, moving to range is often the best treatment. The management and sanitation practices listed under the heading “Pre- ventive Medication,” Section 1, also should be con- sidered as an integral part of any treatment. OMPHALITIS Omphalitis may be defined technically as an inflammation of the navel. As commonly used, the term refers. to improper closure o-f the navel with subsequent bacterial infection. (navel ill; mushy chick disease). 2O Cause: Considerable research as to the cause or causes of omphalitis has been undertaken during recent years. Apparently, most problems result from mixed bacterial infections including the com- mon coliforms and various species belonging to. the genera. Staphyllococcus, Streptococcus, Proteus - and others. Omphalitis usually can be traced to _ faulty incubation, poor hatchery ilsantitation or chilling or overheating soon after hatching (such as. in transit). The significance of isolating one of f the bacterial species mentioned above is compli- * cated in that many of the same species can be iso- . lated from the yolks of supposedly normal birds < immediately after hatching. l Transmission: Omphalitis occurs during the, first few days of life, so it cannot be considered, transmittable from bird to bird. It is transmitted‘ from unsanitary equipment in the hatchery to new-S ly hatched birds having unhealed navels. a Symptoms and lesions: Affected chicks usuall appear drowsy or droopy with the down bei ; “puffed up.” They also generally appear to u? of inferior quality and show a. lack of uniformit Many individuals stand near the heat source an are indifferent to feed or water. Diarrhea som‘ times is observed. Mortality usually begins withi 24 hours and peaks by 5 to 7 days. t. Characteristic lesions are poorly healed nave‘ subcutaneous edema, bluish colorof the abdomi muscles around the navel and unabsorbed y f material which often has a putrid odor. Often yo ' are ruptured and peritonitis is common. Diagnosis: A tentative diagnosis can be V on the basis of history and lesions. The pres of mixed bacterial infections and absence of specific disease-producing agent aids in confi if the diagnosis. - Treatment and prevention: Good manage and sanitation procedures in the hatchery o during the first few days following hatching l the only sure ways to prevent omphalitis. B spectrum antibiotics help- reduce mortality stunting in affected groups, but they do not rep sanitation. FOWL CHOLERA Fowl cholera was recognized as a separate, tinct disease by Pasteur in 1880. Salmon first ported its presence in the United States. in 188.‘ The disease occurs throughout the country __ ever poultry is produced and in recent years? become the most hazardous infectious dise‘ turkeys. Host range is extensive and includes chic turkeys, pheasants, pigeons, water fowl, spa _ and other free flying birds. * n iause: The causative organism of fowl cholera i)» teurella multocida (also called P. avicida), a ~ 'al organism in the form of a small oval rod, ' ctly bipolar when stains are made from (it or tissues. It is grown easily on artificial ’a provided its demanding nutritive require- are met. The organism is identified by stain- ftechniques which permit observation of the _‘“l morphology and by determination of bio- A 'cal reactions in artificial media. fansmission: Pasteurella multocida will sur- “ for (l) at least limonth in droppings, (2) 3 in decaying carcasses or (3) 2 to 3 months The organism may enter the body through gsdigestive tract or the respiratory system. The is not transmitted through the egg. liajor sources of infection are: to Body excreta of diseased birds which con- i: taminates soil, water, feed, etc.—this may be from visibly sick birds or apparently healthy carriers Carcasses of birds which have died of the I disease Contaminated water supply such as surface tanks, ponds, lakes or streams Mechanical transmission by contaminated shoes or equipment ' i’ ecent studies indicate that animals other than such as racoon, opossum, dog and pig may as reservoirs of infection and actively spread idisease. ‘iymptoms and lesions: The disease seldom is in chickens under 4 months of age, but is (only seen in turkeys under this age. The incubation period is from 4 to 9 days and aks may vary from. peracute to chronic in fre. In the peracute form, symptoms may be _ly absent; in the acute form some birds may without showing symptoms, but many others 'sibly ill before death. Characteristic symptoms A de: i‘ Stupor Complete loss of appetite Rapid weight loss Lameness resulting from joint infection Swollen wattles Difficult breathing Watery yellowish or green diarrhea Dull blue or purple color of head and wattles i due to cyanosis sions may be lacking in birds dying during V ute outbreaks. When present, lesions may resemble those associated with any acute septicemic bacterial infection, often those of fowl typ-hoid. Typical lesions include any or all of the following: Pinpoint hemorrhages in the mucous and serous membranes and/or abdominal fat Inflammation of the upper third of the small intestine Light, firm “parboiled” appearance of the liver Numerous small white necrotic foci through- out the liver Enlarged and congested s-pleen Creamy or solid collection of material in joints Cheesy material in the internal ear and air spaces of the cranium of birds having twisted necks Turkeys may have pneumonia with solidifi- cation of one or both lungs Diagnosis: A tentative diagnosis may be made on flock history, symptoms and postmortem lesions. Demonstration of bipolar staining rods in blood smears or impression smears of the lungs, liver or spleen helps to substantiate the diagnosis. A defi- nite diagnosis depends upon isolation and identifi- cation of the organism. Prevention and treatment: Bacterins properly applied are helpful in preventing fowl cholera, par- ticularly in turkeys. Their use must be combined with a rigid program of sanitation. In general, as it applies to the use of bacterins in turkeys, to expect 100 percent protection is unrealistic. Use commercial bacterin first and t auto- I 0 I I ry genous bacterin only 1n situations where com- mercial bacterins have failed. Follow manufacturer's recommendations as to age, time to vaccinate and dosage (this is usually two times, at 8 and 12 weeks of age). If breaks occur after 2 vaccinations, do not revaccinate; try to salvage on the market. Vaccination in conjunction with treatment is not recommended. Santitation practices which aid in preventing the disease are: - Complete depopulation each year between older birds and replacements A good rodent control program Proper disposal of dead birds A safe, sanitary water supply 21 o Adequate cleaning and disinfection of all houses and equipment on premises where outbreaks have occurred after disposal of affected flocks o Keeping birds of susceptible age confined to the house o Allowing contaminated ranges or yards to remain vacant for at least 3 months Sulfaquinoxaline is the preferred drug for the treatment of fowl cholera, except in laying hens, using the same level as recommended for fowl ty- phoid. It may be administered in feed or water, but treatment may be necessary for 3 to 4 weeks or longer. In outbreaks requiring prolonged treat- ment, give the medication in the ration to guard against danger of water starvation. Sulfaquinoxa- line at the rate of 0.033 percent (l pound of pure drug per 3,000 pounds of complete ration) can be used continuously without toxic effects. Since the sulfonamides are not cleared for use in laying chickens, the tetracyclines are commonly used for the treatment of fowl cholera in layers. ERYSIPELAS Erysipelas is a bacterial disease caused by Ery- sipelas insidiosa (formerly Erysipelas rhusiopathiae) and was once considered to be a serious disease only in swine and sheep. The disease in swine frequently is referred to as “diamondskin disease." It affects several species of birds including chickens, ducks and geese, but the only fowl in which it has been of importance is the turkey. Man is suscep- tible to infection and may contract the disease from turkeys. However, in man the disease known as erysipelas is caused by a bacteria of the genus Streptococcus, whereas infection of man with Ery- sipelas insidiosa is called erysipeloid. Since this or- ganism is pathogenic for man, care should be taken when handling infected birds or tissues. Cause: Erysipelas of fowl is caused by the bac- terium, Erysipelas insidiosa. In turkeys it occurs most often in the fall and winter months and usually affects birds which are 4 to 7 months old, although any age bird is susceptible. Incidence has often been reported to be higher in males than in females, possibly because in fighting, males receive numerous skin abrasions which may serve as portals of entry. However, in some instances the incidence may be higher in hens than toms and frequently follows artificial insemination which may be a means of transmission. The organism may survive for long periods in the soil and most outbreaks are thought to originate from contaminated soil or premises. Sheep, swine and rodents may be carriers. Recurrance of the dis- ease on a premise is common. 22 Predisposing or aggravating factors include over- crowding, damp or inclement weather and poor santitation and range management. Symptoms: The first indication of the disease may be the discovery of several dead birds. Usually several morbid birds can be found; however, most affected birds are visibly sick for only a short period before death. Symptoms are typical of a septicemic disease and include a general weakness, listlessness, inappetence and sometimes a yellowish or greenish diarrhea. Occasionally, the snood of toms may be turgid, swollen and purple in appearance. Some: birds may be found lame with swollen leg joints due to localization of the infection. In breeding flocks, it has occasionally been associated with de- creased fertility and hatchability. Daily morbidity and mortality are usually low; however, in untreated cases mortality may persist for some time and be- come excessive. Lesions: The most characteristic lesions are small or diffuse hemorrhages located in almost any tissue or organ. Such hemorrhages are commonly observed in the musculature, heart, liver, spleen, fat and other tissues of the body cavities. Hemor- rhagic conditions of the skin may result in purple blotches. The liver and spleen usually are enlarged, congested and occasionally contain necrotic foci. Enteritis or inflammation of the intestinal tract is commonly observed as in most septicemic diseases. Diagnosis: Symptoms and lesions may resemble other diseases so closely that a reliable diagnosis can be made only through isolation and identifi- cation of the causative organism. Prevention: Good management practices which aid in preventing erysipelas include avoiding the use of ranges previously occupied by swine, sheep ' or turkeys in areas where erysipelas is known to . exist, debeaking, removal of the snoods of toms and other measures which prevent injury from fighting, avoiding overcrowding and providing well- drained ranges. Bacterins are available and are useful on prem- ises where history indicates outbreaks may be ex~ _ pected. Three weeks are required to produce the maximum protection following an injection. If birds are vaccinated at l0 to l2 weeks of age, the * procedure should be repeated for birds held over ,l as breeders. The amount and duration of protec- I tion is relative to the amount of exposure and may not be sufficient for the laying period. Bacterins should be administered in accordance with the i manufacturer’s directions. Antiserum prepared in horses is available and ‘i effective under certain conditions. This product i is expensive and its use is very limited. Treatment: Sick birds should be removed from Qe flock to a hospital pen for individual treatment f,“ to prevent cannibalism. Moving unaffected fr to a clean range may aid in preventing the of the disease but will also contaminate fither range. In addition, bacterin may be used unaffected birds. Various antibiotics have shown efficacy in the tment of erysipelas; however, penicillin is the i g of choice. Injections of 150,000 to 200,000 'ts of penicillin into the leg or breast musculture visibly sick birds is very effective in decreasing _‘~ ality. One injection is usually sufficient, but ‘y be repeated if necessary. Water and. feed medi- = 'on may be of value under certain conditions. y AVIAN VIBRIONIC HEPATITIS ~Avian vibrionic hepatitis is a widespread trans- ible disease of chickens characterized primarily [swelling and necrosis of the liver. It may appear ‘an acute form resulting in death of affected _s, or it may occur in a chronic form and pro- economic loss by increasing flock cull rates. ; v of all ages may be affected, but the disease “u only occurs in semi-mature and mature birds. -._’Cause and transmission: The causative agent sfivibrionic hepatitis is a bacterial organism be- gfng to the vibrio group. fThe disease apparently spreads by contact, di- or indirect, between infected and susceptible iv . Ingestion of infectious material is the most _ly method of transmission. Some outbreaks an appearance that suggests possible egg i": ; l0 lSSlOIl. lSymptoms and lesions: Usual disease signs are ya ness, shrunken comb, loss of body weight , diarrhea. Acutely affected birds, however, may zwhile still in good flesh. Egg production may V» as much as 35 percent in severely affected . Mortality usually is low but may be as high ‘st to l5 percent. §The liver is the primary site of infection. Livers A ffected bir-ds usually are swollen and have i tic and hemorrhagic foci. The heart and kid- ’ may be swollen, and there may be excess fluids e abdominal cavity and the heart sac. iagnosis: Liver lesions are found in birds ted with many diseases. Because of this, vibri- ’ hepatitis may be confused with diseases such ullorum, typhoid, bluecomb, hemorrhagic dis- , blackhead and leukosis. Positive diagnosis i‘ tablished by laboratory means. iTreatment and prevention: Outbreaks are treat- iii-a by adding furazolidone to feed at a level of 200 grams per ton. Supply medicated feed for approximately l0 days. Furazolidone usually prevents outbreaks, but the use of the drug for preventive purposes is not recommended. Routine management and sanita- tion practices for disease prevention offer the most economical and reliable method of prevention. BOTULISM (Limberneck; Food Poisoning) Botulism is a disease caused by the ingestion of a toxin produced by the anerobic bacterium Clostridium botulinum. All domestic fowl and most wild birds are susceptible. An interesting excep- tion is the vulture which is apparently immune and feeds on decaying carcasses. Many human deaths have been attributed to eating food or drinking water containing the toxin. Cause: Botulism is not a bacterial infection but rather a condition produced by ingestion of a toxin produced by the bacterium Cl. botulinum. The organism is common in nature and is widely dispersed in soils. Ingestion of the organism is not harmful. It becomes dangerous only when con- ditions are favorable for the growth and multipli- cation of the bacteria and its subsequent toxin production. The organism grows best under con- ditions of high humidity and relatively high temperature and in an environment containing decaying organic material. Acid conditions are detrimental. Stagnant pools or damp areas con- taining decaying matter with an alkaline reaction are a danger area. Botulism may result from consumption of any decaying animal or vegetable material. Decaying carcasses are a frequent source of toxin and fly maggots feeding on such tissue may contain enough toxin to cause the disease when ingested. The toxin is water soluable; con- sequently, water sources may become contaminated. The toxin is one of the most potent known, being about 17 times as deadly for the guinea pig as is cobra venom. The toxin is relatively heat stable but may be destroyed by boiling. There are different types of the toxin. Types A and C usually are responsible for the disease in birds while type B most frequently affects man. Symptoms: First signs of illness generally are weakness, followed by progressive flaccid paralysis of the legs, wings and neck. When neck muscles are affected, the head hangs limp and this is often referred to as “limbemeck.” Affected birds may have a peculiar trembling, loose feathers in the follicle and dull and partly closed eyes. Because of the paralysis, birds are unable to swallow and mucous accumulates in the mouth. Fatally affected birds may lie in a profound coma appearing life- less for several hours before death. 23 Lesions: Usually there are no significant lesions evident in affected birds with the possible excep-tion of loose feathers and an excess amount of mucous and dirt in the mouth. Examining the contents of the crop and intestines may reveal maggots or other material to indicate that the birds may have consumed the toxin. Diagnosis: A tentative diagnosis may be made from the history and such factors as loose feathers, mucoid accumulations in the mouth and the ab- sence of other postmortem lesions. As an aid to diagnosis, sick birds may be given water into the crop, kept in a cool environment and treated with antitoxin intravenously. Recovery of a large per- centage of birds thus treated would substantiate the diagnosis. Additional supportive evidence for diagnosis may be obtained by production of the identical signs in other birds or laboratory animals by inoculating them with material from the di- gestive tract of affected birds or material from the suspected source of toxin. Prevention: Prevention should be aimed at elim- inating sources of toxin production and access to such material. These practices should include prompt removal of all dead animals from houses or pens, debeaking the birds, controlling fly popu- lations and avoiding access to decaying organic material and contaminated feed and water sources. Contaminated water supplies can be particularly dangerous. Treatment: Remove all visibly sick birds from the flock. Place in a cool shaded area and give water into the crop, twice daily. Mild laxatives may be used for birds which have been exposed but do not yet show the symptoms. Antitoxin may be useful in treating affected birds, but it is dif- ficult to obtain. In turkeys administer 2 to 4 cc of polyvalent antitoxin intravenously, interperi- toneally or intramuscularly. ARTHRlTlS/SYNOVITIS Inflammations of the joints and synovial mem- branes are a major cause of economic loss to the poultry industry. Inflammatory processes of this nature cause losses due to mortality, retarded growth, poor feed conversion, ‘condemnation and downgrading. There are many causes of arthritis/synovitis. Among them are injury, nutritional disturbances and infectious agents. Two of the most common infectious conditions are staphylococcic arthritis and infectious synovitis. Staphylococcic Arthritis Staphylococcic (staph) arthritis is an acute to chronic disease affecting chickens and turkeys, but 24 is of greater incidence among turkeys. The cause of this condition is Staphylococcus aureus. Transmission: The organism of staph arthritis is universally present wherever poults are raised. The manner by which the disease is established is not well understood, but injury may predispose the condition in some instancesll Symptoms and lesions: Morbidity is usually low. Acute cases of staph arthritis are commonly accompanied by a septicemia which may lead to , death in several days. Diarrhea, depression and;- * swollen joints are common signs. More chronic‘ l cases are characterized by lameness and loss of con- dition in addition to the above signs. Death due to cannibalism occurs commonly in affected turkeys. Lesions include synovitis and arthritis, particu- f larly of the hock joint and the surrounding region. » Affected joints and membranes contain large amounts of serous and caseous exudates. The livers and spleens of affected birds are commonly con- gested and swollen. a Diagnosis: A diagnosis of staph arthritis is based ;_ upon the presence of characteristic lesions and the I recovery of Staphylococcus aureus from tissues or ‘j exudates of affected birds. ‘ Treatment and prevention: Affected birds j should be segregated from the flock. In general, ' they will respond poorly to treatment. Of the 4 many drugs and antibiotics which have been used 5 in attempts to treat the disease, novobiocin at levels 1 of 200 to 350 grams per ton of feed has produced the best results. i Management practices which reduce the chances of injury are important in the prevention of the disease. ‘ Infectious Synovitis Infectious synovitis is a chronic disease of chick-i ens and turkeys and is characterized by inflammae tion of joints and synovi.al membrances. It is fou i» in all major poultry-producing areas of the coun and may cause severe losses due to mortality, tarded growth, poor feed conversion and d grading at processing plants. Although the di '- may appear in adults, it is primarily a disease growing birds, particularly in the 4-to-l2-week a groups. Cause: The cause of infectious synovitis _i Mycoplasma synoviae. * Transmission: As with other pathogenic avi_ mycoplasma, M. synoviae is egg transmitted, - f’ the infected breeder must be considered the priflf cipal reservoir of infection within an infected fl A Contact transmission readily occurs between L fected and susceptible pen mates. ' Symptoms and lesions: Morbidity of infectious itis may reach 20 percent or more before an leak has run its course. Mortality is low. is the first symptom observed. Swelling iated with the hocks, foot pads and shanks lly is seen in chickens; however, shank swelling _ infrequently in turkeys. Rap-id loss of con- in _, dehydration and diarrhea usually are seen. fratory signs may be present. utopsies of affected birds often reveal the fol- g lesions. Jointsand synovial membranes of fand wings usually are inflamed and contain 'ous mucoid exudates. In turkeys, such lesions except as associated with the hocks gfoot pads. Inflammation of the sternal bursa t blister) is also a common finding. Visceral ‘I * may include swollen livers with greenish Zloration, enlarged spleens and airsacculitis. ‘iagnosis: A presumptive diagnosis may be f» on flock history, symptoms and lesions. a atory tests may be necessary to differentiate ‘disease from staphylococcic arthritis and other 'tions producing leg weakness and sternal itis. ‘Treatment and prevention: Birds affected with Q 'ous synovitis. respond poorly to treatment. - ent, however, alters the course of an out- y’ , primarily by reducing disease spread. The 'otics of choice are chlortetracycline and ,_ cline. The drug is incorporated into the _ at a level of 200 grams per ton and fed for jl4 days, depending upon flock response. If _'cal, remove crippled birds from the flock they respond poorly to treatment and could "_ as a continued infection source. y relapses occur, it may be necessary to feed f levels of antibiotics continuously until time ket. i‘ L. present, the adoption of a sound sanitation u offers the best hope to prevent introduc- ,_.»0f infectious synovitis. Without question, an cation program, comparable to that for M. eptieum, will be developed in the foreseeable HEMORRHAGIC ENTERITIS cmorrhagic enteritis is an acute and fatal in- gal disorder of turkeys. Cause: Unknown. Numerous organisms have been isolated in laboratories from infected birds. However, experimental studies indicate that the disease is infectious and that the agent responsible for the disease is a filterable agent which can be serially passed with streptococci, suggesting that the cause of the disease may be a toxin elaborated by streptococci. Symptoms and lesions: Hemorrhagic enteritis has been observed in many strains of turkeys and on various feed programs. Greatest incidence ap- pears to be during hot, dry weather. It is seen most often in range birds 9 to l3 weeks of age. Fortunately, total mortality seldom exceeds l0 per- Cfiflt. Usually, the only sign is one or more dead birds on range. Mortality may continue for a few days and then stop. In some cases, daily loss of a few birds may last several weeks. Occasionally, a few birds may appear sick be- fore they die. Symptoms are not characteristic. Affected birds may appear drowsy and pale. Al- though there may be some bloody droppings, they usually are not observed in an infected flock. Lesions are confined primarily to the intestinal tract. The most characteristic finding is a severe hemorrhagic inflammation of the intestinal lining from the gizzard to- the ceca. The intestines are filled with blood and debris having a jam-like consistency. Free dark blood may extend into the ceca and gizzard. Occasionally, small hemorrhages may occur in the muscles of the breast and legs and on the heart, liver, kidneys and other internal organs. Diagnosis: Gross lesions are sufficiently charac- teristic to allow a diagnosis in most cases. Treatment and prevention: There has been no specific treatment. Changing the ration has ap- peared effective in some cases; however, spontane- ous recovery may have taken place irrespective of the change. Moving birds to new range may be beneficial. Provide affected flocks with an abun- dance of fresh, pure water; give them adequate shade from the sun if possible. Remove dead birds from the range promptly. Recent reports, however, indicate that the injection of serum collected from recovered birds effects a favorable response on a flock basis. 25 Section 3. RESPIRATORY DISEASES Diseases are often grouped according to the body system they affect. Those affecting mainly the air passages, windpipe, lungs and air sacs are classified as “respiratory diseases” and are among the major threats to poultry health. At first, all diseases of the respiratory system were known as “colds” and often were considered to be caused by environmental factors such as drafts or chilling. As more infonnation accumulated, it became apparent that “colds” were actually a group of separate infectious diseases having many common characteristics. Possibly all infectious agents causing respiratory symptoms have not been recognized, but many have been isolated and the diseases they produce well defined. Because the nature of the causative or- ganism tells much about a disease, the following outline according to cause is useful in understand- ing these diseases. Caused by viruses: o Newcastle disease o Infectious bronchitis o Laryngotracheitis o Quail bronchitis 0 Influenza / parainfluenza Caused by bacteria: 0 Mycoplasmosis o Infectious coryza o Endemic fowl cholera (roup) 0 Psitticosis/ornithosis Caused by molds: 0 Aspergillosis (Brooder pneumonia) NEWCASTLE DISEASE Newcastle disease is a contagious viral infection, causing a resp-iratory nervous disorder in several species of fowl including chickens and turkeys. It was first recognized in England in 1926 and was named after the town of Newcastle. It first ap- peared in the United States in 1944. Within the next few years, Newcastle disease was present throughout the country. Cause: Newcastle disease is caused by a virus. Different types or strains, varying in their ability t0 cause death and nervous disorders, have been 26 recognized. Some are highly fatal, but most Ameri- can strains are more fatal in young birds than in adult birds. Transmission: Newcastle disease is highly con- tagious. All birds in a flock usually become in- fected within 3 to 4 days. The virus can be trans. mitted through contaminated equipment, shoes; clothing and possibly free-flying birds. During the active respiratory stage, it can be transmitted through the air. Probably the virus does not travel any great distance by this method. Recovered birds are not considered carriers, and the virus usually does not live- longer than 30 days on the premises. Symptoms and lesions: Signs of Newcastle dis- ease are not greatly different from those of other respiratory diseases. The ones most frequently observed are: (1) nasal discharge, (2) excessive mucous in the trachea, cloudy air sacs, (4) casts or plugs in the air passages of the lungs and (5) cloudiness in the cornea of the eye. The disease in young chickens begins with dif- ficult breathing, gasping and sneezing. This phase continues for l0 to 14 days and may be followed by nervous symptoms. If nervous disorders develop, they may consist of paralysisiof one or both wings and legs or a twisting of the head and neck. The head is often drawn over the back or down between the legs. Mortality may vary from O to near 100 percent. In adult chickens, respiratory symptoms pre- dominate. Only rarely do nervous disorders de- velop. If the flock is laying, egg production usually drops rapidly. When this occurs, it takes from 4 to 6 weeks or longer for the flock to return to the former production rate. During the outbreak, . small, soft-shelled, off-colored and irregular-shaped i eggs are produced. Mortality in adult birds usually j is low but may be fairly high from some virus 3 strains. In turkeys, the symptoms usually are mild and y may be unnoticed unless nervous disorders develop. During an outbreak, turkeys will produce eggs with '- a chalky white shell. Reduced production in breed- i, er flocks is the main economic loss from this disease ‘ in turkeys. Diagnosis: The flock history, signs of_ a respira- . tory nervous disorder and other typical lesions often may be sufficient to allow a tentative diag- nosis. Usually, however, the disease cannot be dif- ferentiated from infectious bronchitis and some of the other respiratory infections except by lab- 1 y’ t methods. Laboratory procedures necessary y, blish a definite diagnosis sometimes are - and time consuming. They can be con- only in a well-equipped laboratory. 4" ention and treatment: There is no treat- Newcastle disease. The disease does not respect even the best management program, $1;- ctices outlined in other sections of this ' will help reduce the possibility of exposure ‘ stle disease virus. 1 l’ cination is practiced widely and is the recom- 4 method for prevention. Several types of are available but the most successful and ..used is the mild live virus vaccine known B1 type. This vaccine was used originally p i ping it into the nostril or eye. Now the a ' is usually added to the drinking water. A, 'lers usually are vaccinated when 7 to 10 e with this B1 type of vaccine. In some oper- _, two doses of vaccine are used. In such "the first dose is administered when birds are 'ately 7 days of age and a second dose is at about 4 weeks. “ckens to be kept for egg production should en three applications of the vaccine. The usually is given when the birds are approxi- 7 days, 4 weeks or 4 months of age. cination is not widely practiced in turkeys. 'times is used to protect egg production in V g flocks. Give one dose of the B1 type vaccine selecting the breeder birds. i. mrscnous BRONCHITIS tious bronchitis is an extremely contagious tory ‘disease of chickens characterized by .1 g, sneezing and rales (rattling). rise: Infectious bronchitis is caused by a virus _; affects chickens only. Other fowl or labora- imals cannot be infected with this virus. vnsmission: Infectious bronchitis is con- '- the most contagious disease known. When i , all susceptible birds on the premises be- jnfected regardless of sanitary or quarantine tions. The disease can spread through the Q- can “jump” unknown distances during an outbreak. It also can be spread by mechani- Hw such as clothing, poultry crates and lent. The disease is not egg transmitted _e virus will survive only for a short time, sly not more than l week in a poultry house. estroyed easily by heat or the ordinary dis- __I1l;S. .- ptoms and lesions: The infection is con- ‘I to the respiratory system. Symp-toms are difficult breathing, gasping, sneezing and rales. Some birds may have a slight watery nasal discharge. The disease never causes nervous symptoms. It prevails 10 to 14 days in a flock. Symptoms lasting longer than this usually are from some other cause. In chickens under 3 weeks of age, mortality may be as high as 30 to 40 percent. The disease does not cause a significant mortality in birds over 5 weeks old. Feed consumption decreases sharply and growth is retarded. When infectious bronchitis occurs in a laying flock, production usually drops to near zero in a few days. Four to 6 weeks or longer may be re- quired before the flock returns to production. Some flocks never regain an economical rate of lay. During an outbreak, small, soft-shelled, irregular- shaped eggs are produced. Diagnosis: Infectious bronchitis is difficult to differentiate from several of the other respiratory diseases. For this reason, a definite diagnosis usual- ly requires laboratory procedures. Treatment and prevention: Infectious bron- chitis is highly contagious and does not always respect sanitary barriers. Vaccinate chickens to be retained for egg production. Whether broilers should be vaccinated depends upon many factors and is an individual decision. Numerous vaccines are available commercially. Most of them repre- sent a modified or selected strain of infectious bronchitis virus. All vaccines contain live virus, and those that give good protection also are capable of producing symptoms and reducing egg produc- tion. The vaccine virus will spread to other sus- ceptibile birds. Vaccine is usually added to the drinking water, but may be administered by drop- ping it into the eye or nostril. There is no treatment for this disease. In young chickens it is helpful to increase the brooder tem- perature and to provide as nearly ideal environ- mental conditions as possible. LARYNGOTRACHEITIS Infectious laryngotracheitis is an acute, highly contagious disease of chickens and pheasants. It is characterized by respiratory distress, rapid spread and high mortality. Cause: This disease also is caused by a virus. Transmission: Recovered birds remain carriers for as long as 2 years. Carriers also develop follow- ing vaccination if the virus becomes established in the respiratory system. During an active out- break, the disease can spread by mechanical meth- ods such as clothing and equipment. The most important factor in spreading -the disease is the carrier bird. 27 * brane of the cloaca. Symptoms and lesions: The disease usually oc- curs in semi-mature or adult birds. It is acute and affected birds usually die or recover in 5 to 6 days. Some virus strains are more; mild and the course of the disease may be as long as 15 days or more. Coughing, sneezing and vigorous shaking of the head with a. gurgling or rattling sound is charac- teristic. The sound sometimes resembles a whistle and such birds have been known as “callers.” A blood-tinged exudate may be coughed up or shaken from the mouth. Mortality often is high. Effect on egg production is variable. The main signs usually are confined to the respiratory tract and vary from free_ blood in the windpipe to a cheesy or blood-tinged membrane formation. Diagnosis: This condition must be differen- tiated from Newcastle disease, infectious bronchitis and fowl pox. A tentative diagnosis sometimes can be made from the history and typical post- mortem lesions. Definite diagnosis can be made only by isolating the virus in chicken embryos or by inoculating susceptible and immunized birds with materials from suspected cases. Treatment and prevention: Occurrence of this disease varies in different geographic locations in the United States. While the disease is endemic and frequently occurs in some areas, it is rare in Texas and is not a pressing problem. for poultry- men of this state. In areas where the disease pre- vails, vaccination is necessary for prevention. In other areas where the disease does not occur often, vaccination is strongly discouraged. The standard vaccine should be used with care because it is a virulent virus. It is applied to the mucous mem- Newer vaccines are milder and may be applied by the intraocular route. Vac- cinated birds can become carriers of the infection. One vaccination gives good protection. There is no treatment for this disease. When an outbreak occurs, vaccinate the flock immediate- ly. This usually will stop the spread of infection among the group. Never use the vaccine for this purpose unless the diagnosis is definitely confirmed. Reference must be called to the list of vaccines available. The restriction for the use of laryngo- tracheitis vaccine is outlined and should be strictly complied with for the good of Texas poultrymen. QUAIL BRONCHITIS Quail bronchitis is a contagious, highly fatal disease in young quail. The virus causing this disease also infects chickens and turkeys. This agent also is known as CELO virus. It has been isolated from chicken eggs but does not produce a recognizable disease in chickens or turkeys. This 28 agent may play a part in respiratory diseases and in infertility problems, but its importance must be established by additional research. It is important because it is one of the agents that may be isolated from birds with respiratory symptoms and may be difficult to separate from other agents such as infectious bronchitis virus. -- INFLUENZA/PARAINFLUENZA This virus- disease or group of virus diseases q affecting turkeys, ducks and quail must have more ' research and study to fully determine their ec0- nomic importance to Texas poultrymen. To date, 1' on the basis of limited investigation, influenza is § not a problem in commercial turkey flocks in Texas. It must be pointed out, however, that this 1 group of viruses could become a problem in the I future. MYCOPLASMOSIS _ Organisms in the genus Mycoplasma are a sig-f nificant cause of respiratory disease in birds. Of the numerous species of Mycoplas-ma which hav been isolated from domestic poultry, three are ~l known significance: Mycoplasma gallisepticumi which is associated with chronic .respira o disease/air sac syndrome of chickens and infectio sinusitis of turkeys; Mycoplasma meleagridis, whi =‘~ is associated with an airsacculitis condition in keys; and Mycoplasma synoviae, the cause of i" fectious synovitis of chickens and turkeys (discuss i elsewhere in this text). » Chronic Respiratory Disease- Air Soc Syndrome and Infectious Sinusitis Chronic repiratory disease (CRD),-air sac s drome and infectious sinusitis of turkeys have _q common cause. CRD was recognized first as ing a chronic but mild disease in adult chick, It reduced egg production but caused little or r mortality. After CRD had been recognized, a u” dition known as “air sac disease" became a p p, lem in young birds. It caused high mortality , some flocks. Many birds became stunted; th was poor feed efficiency and many were rej i; as unfit for human consumption when proc' The third condition, infectious sinusitis of =5 keys, was recognized as early as 1905. It ca I a sinus swelling under the eye as well as an infi mation of other respiratory organs. It is a c ~ l_ disease adversely affecting growth and feed ~ version. In young poults it may cause signifil mortality. y; Cause: A peculiar bacterial organism kn, as Mycoplasma galliseptieum (Mg) is common all three conditions. CRD, in a strict interp I tion, is caused by a pure Mg infection. On~ y and, the air sac syndrome has a complicated d is a result of infection with several or- . This condition is caused by Mg in com- i with another common bacterial organism, and is triggered by an acute respiratory infection such as Newcastle disease or infec- u o chitis. cause of infectious sinusitis of turkeys is f- ~ plicated Mg infection. fcoplasma gallisepticum is widespread and jmany speciesiof birds. Until recently most, g all, chicken flocks and about 40 percent of gflocks were infected. Eradication programs reduced the incidence in recent years. Qnsmission: The primary method by which spread is through the egg. Infected hens vit organisms and the chick or poult is in- when it hatches. Organisms also may be itted by direct contact with infected or car- v and possibly by other unknown methods. ptoms and lesions: The true CRD produces ‘respiratory symptoms such as coughing, sneez- _ i a nasal discharge. In the air sac syndrome 7 is an extensive involvement of the entire ”< ory system. The air sacs often are cloudy tntain large amounts of exudate. There is ga film of exudate covering the liver as well heart muscle and heart sac. Affected birds A droopy, feed consumption decreases and is a rapid loss of body weight. “ectious sinusitis of turkeys occurs in two When the “upper” form is present, there y a swelling of the sinus under the eye. In _ ower” form, the lungs and air sacs are in- W The air sacs become cloudy and may con- ‘ e amounts of exudate. Both forms of the usually are present in the flock and fre- y are present in the same bird. Agnosis: Diagnosis of either of these condi- Ymust be based on flock history, symptoms ions. Blood tests are useful in determining a flock is infected. atment and prevention: The treatment of , air sac syndrome and the lower form of in- f‘ s sinusitis usually is not satisfactory. Many otics have been used with varying success. fer to give treatment is a decision that must ide on each flock based on economic factors. f‘ tment is‘. attempted, give high levels of one k broad ‘spectrum antibiotics either in the ‘drinking water or by injection. The “upper” _ of infectious sinusitis can be treated with L»; by injecting antibiotics into the swollen The answer to the Mg problem in both chickens and turkeys is eradication of the diseases. This goal has been achieved essentially in turkeys through voluntary programs conducted under The National and State Turkey Improvement Plans. Because all commercial chickens were infected un- til recently, obtaining Mg-free chicken flocks was more difficult. However, most foundation broiler breeder stock is now free of Mg, and many foun- dation breeders of commercial egg stock have Mg- free birds available. Mycoplasmu Meleagridis Infection Mycoplasma meleagridis (Mm) infection is a cause of airsacculitis in young turkey poults. As in the case of other avian Mycoplasma infections, the agent is egg transmitted, and the infected breed- er must be considered the prime perpetuator of infection. The true significance of Mm infection is not known. The air sac lesions associated with the egg transmitted disease are usually transitory in nature and disappear early in life, usually by the sixth org, eighth week; and the performance of most infected birds does not appear to be impaired significantly. In recent years, however, Mm has been incriminated in an assortment of conditions including osteo- dystrophy and other skeletal deformities. There is no solid evidence to substantiate these claims. The dipping of turkey hatching eggs in anti- biotic solutions is being widely practiced. The practice is said to reduce the incidence of air sac lesions and to increase the livability and perform- ance of poults produced by Mm-infected breeders. Breeders and hatcheries contemplating such proce- dures should seek ex-pert advice before proceeding. INFECTIOUS CORYZA Infectious coryza is a specific respiratory disease of chickens which occurs more often in semi-mature or adult birds. It is often confused with endemic fowl cholera. Infection may result in a slow spread- ing, chronic disease which affects only a small number of birds at one time or in a rapid spreading disease with a higher percentage of the birds af- fected. This variation in the spread of the infec- tion apparently depends upon the virulence of the organism, certain management practices and other factors. The occurrence of infectious coryza is not widespread and the incidence is relatively low in Texas. However, the incidence appears to have increased in recent years in certain areas, where the infection has been introduced and has become endemic. Cause: The disease is caused ‘by a bacterium known as Hemophilus gallinarum. Outbreaks usually result from the introduction of infected 29 or carrier birds into a flock or onto a farm. Trans- mission of the infection within tl1e flock occurs by direct contact, airborne infective dust or drop- lets or drinking water contaminated with infective nasal exudate. Incubation period following experi- mental inoculation may be as short as 18 to 36 hours; however, susceptible b-irds exposed ‘by contact to infected birds usually develop symptoms in l to 3 days. Individuals which have recovered from the disease may appear normal, yet remain carriers of the organism for long periods. Once a flock has been infected, each individual bird must be considered a carrier. Symptoms and lesions: The most characteristic symptoms of infectious coryza include: edema.tous swelling of the face around the eyes and Wattles, nasal discharge and swollen sinuses. Watery dis- charge from the eyes frequently results in the lids adhering together. Vision may be affected because of the swelling around the eyes. The disease results in a decrease in feed and water consumption and an increase in the number of cull birds. An ad- verse effect on egg production usually occurs in proportion to the number of affected birds. Diagnosis: Diagnosis can be confirmed only by isolation and identification of the causative organism. The organism, Hemophilus gallinarum, is extremely fastidious and often difficult to isolate. Birds should be submitted to a diagnostic labora- tory early in the course of the infection, before complications of secondary bacterial infections oc- cur and make recovery of the organism even more difficult. Prevention: Prevention is the only sound ap- proach in controlling infectious coryza. It usually can be p-revented by management programs that prevent contact between susceptible and infected birds. It requires only separating affected or car- rier birds from the susceptible population. In order to prevent the introduction of the infection, intro- duce started or adult birds only from sources known to be free of the infection. If infection does occur, complete depopulation is necessary for elimination of the disease and should be followed by thor- ough cleaning and disinfection of facilities and equipment. l Bacterins do not provide complete protection but may be useful in certain instances on infected farms where depopulation is not feasible. Treatment: There are a number of drugs which have efficacy in treating this infection. Various antibiotics and sulfonamides are used. In the event sulfonamides are used, caution should be exercised in the administration since lengthy treatments or high drug levels can result in toxicity, a drop in egg production and mortality. One should consult 30 with diagnostic personnel concerning a recom- mended treatment regimen. Treatment does not eliminate the infection in carrier birds; therefore, dispose of affected flocks as soon as practical to eliminate them as a source of infection. ENDEMIC (LOCALIZED) FOWI CHOLERA This disease is very similar to “infectious coryza. The two diseases are often confused even in text- books on poultry disease and pictures of this dis- ease are often mislabeled as infectious coryza. The disease is a specific respiratory infection caused? by an organism similar to the one causing acute fowl cholera. This condition, however, is- not as- sociated with acute fowl cholera. It never reverts to the acute form of the disease but chronic cases following an outbreak of acute fowl cholera may show symptoms and lesions closely resembling this condition. The disease affects chickens primarily, although turkeys can be infected by inoculation. Twenty years ago, it was estimated that 80 per- cent of the chicken flocks in Texas were infected. Today the disease occurs only rarely in commercial operations, having been largely eliminated by man- agement programs. Cause: The disease is caused by a bacterium belonging to the Pasteurella genus, and the organ- ism cannot be differentiated by ordinary methods from Pasteurella multocida which causes acute fowl cholera. The disease is transmitted only by direct con- tact between susceptible and infected birds. Re- covered birds may“ remain carriers indefinitely. Separation between susceptible and carrier birds to prevent such contact will prevent the spread of the disease. Symptoms and lesions: This is a chronic disease which affects only a small percent of the birds at one time. It causes nasal discharge, inflammation of the eye and swelling of the sinus under the eye. The sinus becomes filled with hard caseous-type exudate that has a characteristic odor. Sometimes the lungs and air sacs are affected. The disease causes little direct mortality but does result in poor performance, reduced egg production and an in- crease in cull birds. Diagnosis: A trained diagnostician can recog- nize this infection by the history, symptoms and lesions. A confirmed diagnosis can be made only t_. by the isolation and identification of the causative organism. This is sometimes difficult because 0f the chronic nature of the infection and the presence of secondary and complicating bacterial organisms. Prevention: As with infectious coryza, this dis- ,1 ease can be readily prevented by certain manage- ' ..¢.2x{..s¢~ ...._. u . -. . t practices. It requires only separating affected Ycarrier birds from the susceptible population. {Jorder to prevent the introduction of the infec- l» , introduce started 0r adult birds only from es known to be free of the infection. In the nt of infection, complete depopulation is a ne- ity and should be followed by thorough clean- and disinfection of facilities and equipment. Treatment: In general, treatment is unsatis- 1 ory. Various sulfonamides and antibiotics are f-~ and lengthy treatments are usually necessary. . tment only serves to prevent other birds from I loping the disease and is not a cure for those - dy affected. If sulfonamides are used, caution should be 1 'sed in its administration since lengthy treat- g- on high drug levels can result in toxicity, p in egg production and mortality. PSITTACOSIS AND ORNITHOSIS jPsittacosis is an acute 0r chronic bacterial in- 'on of psittacine birds (parrots, parakeets, love- f»- etc.). The term psitticosis also is used in nce to the generalized infection of man when l‘!- infection is contracted from birds. The term "thosis is reserved for infections of similar eti- in nonpsittacine birds (ducks, pigeons, tur- , chickens, etc.). In domestic poultry produc- __ , the disease has been a problem only in turkeys. A {importance is magnified because it is trans- _;'ble to man. Workers in poultry processing p; ts have become infected as a consequence of T: ~ ing the infected turkeys. ause: The disease is caused by agents now ‘dered to be bacteria with the scientific name Chlamydia psittaci. They are very special- Qfbacteria in that they need living cells in which ultiply. The pathogenicity of different isolates i’ vary with some producing a mild disease in ~ s and others causing significant mortality. ransmission: It is not known how turkey become infected. The disease is not egg pitted and recovered birds do not appear to in carriers. It is suspected, but not proved, imigratory shore and wading birds may intro- lithe infection. Many turkey flocks having the v w have been in contact with surface water nted by such birds. f mptoms and lesions: Infected turkeys become iy, go off feed and usually have a greenish- ‘ diarrhea. Symptoms can be confused with _ other diseases. When a turkey that died i this infection is examined, the main findings inflammation of the heart sac resulting » accumulation of exudate in this organ, cloudy air sacs which may contain exudate and a film of clear exudate over the liver. Diagnosis." Omithosis in turkeys must be dif- ferentiated from infectious sinusitis, fowl cholera and some other diseases. Postmortem lesions are suggestive but a definite diagnosis can. be ma.de only by isolating the agent in chicken embryos or mice. Blood tests also may be useful in establish- ing a diagnosis. Prevention and treatment: No specific methods of prevention can be given until more is known about transmission of the disease, Do not let turkeys have access to ponds, lakes or other bodies of surface water. When ornithosis is suspected, obtain a definite laboratory diagnosis because of the public health aspect of the disease. Once the disease is diagnosed, quarantine the flock and give a 3-week supervised treatment with aueromycin at a rate of 200 gm/ ton of ration. This treatment usually will stop flock losses and allow birds to be processed without dan- ger of human infection. ASPERGILLOSIS (Brooder pneumonia) Aspergillosis has been observed in almost all birds and animals including man. The disease is encountered in poultry in two main forms: (1) acute outbreaks with high morbidity and high mortality in young birds and (2) in adults as a chronic con- dition affecting individual birds. It is more of a problem in turkeys but also may affect chickens. Cause: This condition is caused by Aspergillus fumigatus, a mold or fungus-type organism. Oc- casionally, other types of molds are involved. These organisms are present in the environment of all poultry. They grow readily on many substances such as litter, feed, rotted wood and other similar materials. Transmission: The bird comes in contact with the organisms through contaminated feed, litter or premises. The disease is not contagious and does not spread from one bird to another. Host healthy birds can withstand repeated exposure to these organisms. Inhalation of large numbers of the infectious stage of the mold or reduced resistance apparently results in infection. In adult turkeys, the disease more often affects the male. Symptoms and lesions: In the acute form in young birds, main symptoms are gasping, sleepiness, loss of appetite and sometimes convulsions and death. Occasionally the organism invades the brain, causing paralysis or other forms of nervous symp- toms. The more chronic form in older birds usually 31 results in the loss of appetite, gasping or coughing and a rapid loss of body weight. Mortality is usual- ly low and only a few individual birds are affected at one time. The disease produces hard nodular areas in the lungs and an infection of the air sacs. Some- times the air sac lesions are similar to those pro- duced by infectious sinusitis or CRD. In some birds, colonies of mold growth can be seen on the air sac membranes. 32 Diagnosis: Diagnosis usually can be made from history, symptoms and lesions. Sometimes it is ne- cessary to base diagnosis on microscopic lesions. Treatment and prevention: There is no trea.t- ment for the flock or the affected bird. The disease usually can be prevented by avoiding moldy litter, feed or premises. A careful examination of the environment usually reveals the trouble source which should be eliminated. Often this means replacing the litter. 1k n v number of viral diseases of poultry produce "toms and lesions primarily exclusive of the tory system. Among them are some of the i devastating diseases of chickens and turkeys. f’ 'dered in this group are avian pox, leukosis, 7| encephalomyelitis (epidemic tremor) and “V-w b disease. AVIAN POX (Fowl pox, Canker, Avian diphtheria) A vian pox is a relatively slow spre-ading viral j~ 'on of birds, characterized by wart-like nodules lithe skin and diphtheritic necrotic membranes ; the oral cavity and upper. respiratory system. ». been present in birds since the earliest avail- _ history, is universal in distribution and may severe economic loss in chickens and turkeys {to poor growth, feed efficiency, reduced pro- j'0n, increased cull rates and downgrading. ” lity usually is not significant unless the res- tory involvement is marked. The disease may A in any age bird at any time during the warm iths, particularly when mosquito populations high. ause: Avian pox is. caused by a viral agent. are at least three different strains or types vian pox virus: fowl pox virus, pigeon pox and canary pox virus. Although some work- include turkey pox virus as another distinct f?" many feel that it is identical to fowl pox virus strain is infective for a number of ies of birds in addition to its primary host. f example, among others, fowl pox virus may _.~ chickens, turkeys, pheasants, quail and ducks; l» pox virus may infect pigeons, chickens and s; and canary pox virus may infect canaries, ens, pigeons and sparrows. atural occurring pox in chickens, turkeys and f4 domestic fowl is considered to be caused by pox virus. ransmission: Fowl pox can be transmitted by .- or indirect contact. The virus is highly re- u in dried scabs, and under certain conditions survive for months on contaminated premises. 7 disease may be transmitted by a number of , -- of mosquitoes, this being the usual manner = ich the infection is introduced to a premise. uitoes may harbor infective virus for a month vi re after feeding on affected birds. After the i 'on is introduced, it spreads within the flock Section 4. VIRAL DISEASES (EXCLUSIVE OF RESPIRATORY DISEASES) by mosquitoes as well as by direct and indirect contact. Recovered birds do not remain carriers. Symptoms and lesions: Since fowl pox usually spreads slowly, a flock may be affected for several months. The course of the disease in the individual bird is 3 to 5 weeks. Affected young birds are retarded in growth. Adult birds drop in produc- tion. Birds of all ages which have oral or respi- ratory system involvement have difficulty in eating and breathing. The disease manifests itself in one or two ways. Cutaneous or dry pox: Lesions start as small whitish foci which develop into wart-like nodules. The nodules eventually are sloughed and scab for- mation precedes final healing. Lesions are seen most commonly around the featherless facial parts (comb, wattles, ear lobes and eyes) but may be found on the body. Diphtheritic or wet pox: Lesions are associated with the oral cavity and the upper respiratory tract, particularly the larynx and trachea. The lesions are diphtheritic in character and involve the mucous membranes to such a degree that when removed, an ulcerated or eroded area is left. Diagnosis: Fowl pox is readily diagnosed on the basis of flock history and presence of typical lesions. In some instances, laboratory diagnosis by tissue or transmission studies is necessary. Treatment and prevention: There is no treat- ment for fowl pox. Disease control is accomplished best by preventive vaccination since ordinary man- agement or santitation practices will not prevent it. Several kinds of vaccines are available: pigeon pox, pigeon pox-like and fowl pox vaccine. The pigeon pox vaccine is of questionable value and its use is not usually recommended. The pigeon pox- like vaccines are newer and have wider acceptance. Fowl pox vaccine is an efficient product and is the vaccine in common use in Texas. Its use varies according to the type of operation, but generally the following recommendations apply: Broilers: Vaccination usually is not required; but in some areas where the mosquito population is high, as in parts of Texas, it may be necessary to prevent the disease. In such instances, the vac- cine is applied to chicks (as young as l day) using the wing-web method but using only one app-li- cator needle. Replacement birds: Vaccinate all replacement chickens against fowl pox. One application of fowl 33 pox vaccine results in permanent immunity. Birds can be vaccinated at any convenient time during the growing period, usually between 6 and l0‘ weeks of age. Turkeys: Fowl pox vaccine does not produce lasting immunity in turkeys. Vaccinate turkeys when they are between 4 and l0 weeks of age. Turkeys to be retained as breeders should be re- vaccinated as adults. This usually is done as the breeding flock is selected. Birds not selected and vaccinated should be marketed within a day or two. Examine vaccinated birds for “takes” about 7 to l0 days following vaccination. A high per- centage showing a reaction indicates a satisfactory vaccination. AVIAN LEUKOSIS The diseases which make up the avian leukosis complex are transmissible virus diseases of birds characterized by tumor formations. The diseases are widespread and have been the most devastating of those affecting mature laying chickens, and in recent years have become increasingly significant as a cause of losses~ in broilers and growing birds. Of the separate and distinct diseases which form the complex, lymphoid leukosis and Marek’s disease produce the most losses. Lymphoid Leukosis (L.L.) Characteristically, lymphoid leukosis is a disease of adult chickens; however, the disease ap-pears to be 0f increasing importance in turkeys and other species, e.g. the pheasant. Although the virus of lymphoid leukosis may produce various responses (e.g. blood forms-erythroblastosis and myeloblas- tosis; bone fonns-osteopetrosis), the lymphoid tu- mor response is the most common. Cause and transmission: Lymphoid leukosis is cause-d by a group of enveloped RNA viruses which closely resemble those of the myxovirus group. The disease is transmitted in a number of ways. The agent is eliminated naturally from the body of the infected bird via eggs and feces. The virus may be transmitted mechanically from infected birds to susceptibles by blood-sucking parasites or by man in such procedures as fowl pox vaccination. Most infections are acquired during the first few weeks of life. This suggests that most flocks acquire the disease by egg transmission or by direct or indirect contact with older infected birds during the early brooding period. Manifestations of disease: Lymphoid leukosis is characterized by the formation of lymphoid tu- mors, particularly in the liver and spleen. Affected 34 ‘particular, may be greatly enlarged. birds may die without preliminary symptoms, but the disease is usually chronic in nature with affected birds showing loss of appetite, progressive emacia- tion and diarrhea. Clinically affected birds in- variably die. Although losses due to the disease may be most severe shortly after the onset of pro- duction, losses in the affected flocks will continue as long as it is retained and may}; total 20 percent or more during the productive life of the flock. Autopsies of affected birds. reveal tumors. Al- though the liver and the spleen are commonly involved, other visceral organs may be affected. I“ The neoplastic process may be diffused involving 100 percent of the affected organ, or it may be a nodular type. Affected structures, the liver in Osteopetrosis is the bone form of the disease. Until recently it was thought to be a disease pri- marily of older birds, particularly males; however, it is now known to be quite: common in young chickens and is one of the more serious causes of broiler condemnations. The disease is character- ized by a thickening and deformation of bone, the long bones in particular. This frequently re- sults in lameness and faulty body conformation. Blood forms of L.L. are diagnosed infrequently. Diagnosis: The clinical diagnosis of L.L. is based upon flock history and disease manifesta- tions. The lymphoid disease cannot be readily distinguished from the visceral response to Marek's disease (M.D.); however, there are some features which aid in differential diagnosis. Some of these = features are outlined in the following table. DIFFERENTIAL DIAGNOSIS OF L.L. AND M.D. Lymphoid Leukosis Marek's Disease Prolonged Short Over 6 months Most commonly liver and spleen Generalized Feature Incubation period Usual age incidence Visceral lesions Skin lesions No Yes Ocular lesions No Yes Neural lesions No Yes 1t should be kept in mind that the clinical f: differentiation of L.L. and M.D. is often presump- tive at best. Histopathological differentiation is ; more accurate, but even it is not completely so. Treatment and prevention: There is no treat- ment for lymphoid leukosis. Although the disease i cannot be prevented completely, there are certain steps which can be taken to help- control the level i of infection in a flock. Some of these are listed below. Buy resistant strains of birds. Most reputable breeders have invested a great deal of time and money breeding for L.L. resistance. Under 6 months _ Brood in isolation. Most L.L. is acquired early ’der 6 weeks of age). If replacement birds are "3." '0 in strict isolation, contact transmission 4- and indirect) from adult carriers will be himal. Keep incubator sanitary. "Control blood-sucking parasites. Do not use gimmicks in disease control (e.g. {losive outbreaks of L.L. have occurred following l indiscriminate use of turkey blood in M.D. ; g tro " programs). ~ ek’s Disease (M.D.) Marek’s disease is characteristically a disease fyoung chickens; however, the disease is com- ‘y ly seen in adult birds. In contrast to L.L., i tumor response of M.D. is limited to that of lymphoid type. However, the response may finuch more diverse in location than that usually i. in lymphoid leukosis. . Cause and transmission: Marek’s disease is by a virus belonging to the Herpesvirus "p. Much is- unknown about the transmission ‘the virus; however, it appears that virus is con- v ted in the feather follicles of affected birds R is shed in dander. The virus apparently has $1 g survival time in dander and viable virus be demonstrated in depopulated houses months p‘ infected birds have been removed. The usual ,e of transmission is by aerosols containing iri- 1 dander and dust. As is the case with L.L., L g birds are most susceptible to infection with Tl .; however, since the incubation period of M.D. ‘ iihort, clinical disease can appear much earlier A is the case with lymphoid leukosis. éManifestations of disease: Marek’s disease may _ ‘uce a variety of clinical responses, all lymph- in character. These are acute visceral, neural, i and skin; or, as is commonly the case, a gibination of the responses may be seen. ;Marek's disease of the visceral type may be cterized by widespread involvement. The le- i. s are most commonly associated with the gonads tes or ovaries), liver, spleen and kidney; however, 1r organs such as the lungs, heart and muscula- are commonly involved. The disease is often ’_ - in nature, with apparently healthy birds I g very rapidly and having massive internal ors. The disease may appear in broiler-age ‘f-w and be a significant cause of death loss and iemnations. More ‘commonly the disease pro- r -.. the most severe losses in replacement pullets or at the onset of production. At this time, L-sdisorder is seen frequently in birds with acute 'diosis leading some to suspect that there is a gtionship between the two diseases. Presently, the only relationship is considered to be that of a bird with coccidiosis or M.D., whichever the case, being more susceptible to the other disease. Marek’s disease of the neural type is the classi- cal type of the disease. Neural leukosis was the first disease known as M.D. before the etiologic relationships of the various diseases in the leukosis complex were established. Neural leukosis is char- acterized by a progressive paralysis of the wings, legs and neck. Loss of body weight, anemia, labored respiration and diarrhea are common symptoms. When affected birds are autopsied, lesions, if ob- served in uncomplicated cases, are confined to the nerve trunks and plexuses innervating the paralyzed extremities. Affected nerve tissue is swollen as a result of an accumulation of lymphocytes and tissue fluids. Frequently no gross lesions are observed. Ocular leukosis (gray eye) is responsible for much of the blindness in chickens. This type of M.D. usually is seen in early maturity. Morbidity and subsequent mortality are usually low but in some instances approach 15 to 25 percent. Ocular leukosis is characterized by spotty depigmentation or diffuse graying of the iris of the eye caused from lymphocytic infiltrations. The pupil develops an irregular shape and fails to accommodate light. Emaciatio-n, diarrhea and death usually follow be- cause of partial to complete blindness. Skin leukosis is the form of M.D. that produces the most severe losses in broilers. Losses are more commonly due to condemnation at processing time. The disorder is characterized by enlargement of the feather follicles due to accumulations of lymph- ocytes. As has been stated, most infective virus is produced in the regions of the feather follicle and is shed with skin dander. Course of disease: Acute M.D. can be extremely rapid in its course producing mortality in appar- ently healthy birds. However, it has been demon- strated that the lesions of M.D., particularly of skin leukosis, may regress and clinically affected birds may make complete recoveries. Diagnosis: The clinical diagnosis of M.D. is based upon flock history and disease manifestations (refer to table under the diagnosis of lymphoid leukosis). Accurate diagnosis may depend on the employment of sophisticated laboratory procedures. Treatment and prevention: As is the case with L.L., there is no treatment for Marek’s disease and until recently, there have been no effective pre- ventive measures. A vaccine is now available which appears to be extremely effective (90 percent) in the preven- tion of M.D. The vaccine is made with a Herpes- 35 virus of turkeys (H.V.T.) that prevents the virus of M.D. from transforming cells to p-roduce tumors. The vaccine is quite expensive and therefore is used principally in replacement layers and breeders. The vaccine should be applied in strict accordance with the manufacturer's recommendations. Prevention of the disease in market broilers by vaccination is not economically feasible at this time. Different empiric approaches to control have been attempted, but results have been erratic. A program, still in experimental stages, that may have merit in the future is the use of filtered air positive pressure (F.A.P.P.) housing to start broiler chicks. Chicks started in such a controlled environ- ment can be maintained free of exposure to M.D. virus during the first few weeks of life. When transferred to conventional housing at an age of several weeks, the chickens may be exposed to M.D. virus; but disease does not have sufficient time to develop before marketing. Other approaches to control include the genetic and management/sanitation. EPIDEMIC TREMOR (Avian Encephulomyelitis) Avian encephalomyelitis is a viral infection which affects chickens of all ages, but usually pro- duces clinical manifestations only in young birds. In recent years, the disease also has been observed in turkeys. Signs of infection include incoordina- tion, nervousness, a jerky or irregular gait, falling over on the side with outstretched wing and muscu- lar tremors that are especially noticeable in the head and neck. The commonly used tenn epidemic tremor is misleading because muscular tremors are not evident in many otherwise typical outbreaks. This disease, reported first in New England in 1932, now exists in all poultry-producing areas of the United States and has been reported in several other countries. The custom of hatcheries to adjust for losses due to epidemic tremor has led other segments of the poultry industry to regard the disease as of minor importance and significant primarily to hatcherymen. Such losses are costly, troublesome and reduce efficiency in all operations, especially the breeder and broiler flocks. Thus, epidemic tremor poses a major problem for the entire poultry industry. Cause: Epidemic tremor is caused by a rela- tively small virus which produces microscopic le- sions in the bird's nervous system. Transmission: The virus is transmitted through eggs of infected parent flocks. Such outbreaks in parent flocks often are unnoticed and usually last 36 21 to 30 days. It appears that affected flocks do not remain carriers and are not susceptible to the dis- ease again for a reasonable time; consequently, such flocks are desirable as hatchery supply flocks. Apparently, other modes of transmission are responsible for outbreaks in production flocks. The disease can be transmitted by direct or indirect contact, but this is not of major “significance. Symptoms and lesions: In a. small percentage of outbreaks, the disease may be suspected because of poor hatchability or morbidity in birds at hatch-.. ing time. The incubation period varies from 5E to 40 days with an average of 9 to 21 days. The typical outbreak becomes noticeable when birds are 17 to 21 days old. Some individuals in flocks exposed during hatching may develop clinical evi- dence of infection up to 7 weeks later. Morbidity rates vary from only a few individuals to 30 per- cent but average 5 to l0 percent. Outbreaks in young chicks are characterized by an inability to walk normally or they become paralyzed and lie propped on one wing. Visible trembling of the head and neck may be present, but is not apparent in many outbreaks. Affected birds usually do not recover, but they will survive for long periods if food and water are provided. New cases developing after the fifth or sixth week are rare. Mortality usually is negligible but vis- ibly affected individuals should be removed and destroyed. No lesion is visible with the naked eye. Micro- scopic lesions are widespread and are a diagnostic aid. In adult flocks, there may be no evidence of infection other than. a 5 to l0 percent drop in egg production, with a decrease in hatchability. Most outbreaks in adult flocks are not suspected unless the caretaker is a keen observer and keeps good records. Diagnosis: The disease usually is diagnosed on the basis of case history and typical signs. Atypical -cases present diagnostic problems and every reliable aid must be used to make an accurate diagnosis. v Prevention and treatment: There is no treat- l ment. Remove and kill all birds showing clinical - evidence of the disease, since they do not develop ‘ into profitable birds. The disease is readily prevented by vaccinating L breeder replacements prior to the onset of produc- _ tion. Vaccine is applied. in the drinking water when the birds are approximately l0 to l4 weeks j old. The vaccination of breeder stock in this way L: prevents subsequent infection and egg transmission i of the virus. INFECTIOUS BURSAL DISEASE (Gumboro) ectious bursal disease (I.B.D.), commonly T» to as Gumboro disease, is an acute, highly “ous viral disease of young chickens. It "R1 most often in the highly concentrated producing areas of the state. It causes f-morbidity and mortality in affected flocks l1.» ly disappears after l to 2 weeks. e: A virus or virus-like agent referred to ‘infectious bursal agent causes this disease. insmission: The transmission or spread of Vase can occur by direct contact (bird to Intaminated litter and feces, caretaker, con- (‘ted air, equipment, feed, servicemen and ‘y insects and wild birds. It is extremely Q H S. lptoms and lesions: Birds have ruffle-d ‘l; , a slight tremo-r at onset of the» disease, ,1: defecation, loss. of appetite and are de- f- Affected birds have a tendency to sit, en made to move have an unsteady gait. ‘icking is common. Early in the disease, a rise in body temperature but it soon subnormal. This is often followed by . If ion and death. The litter of contaminated becomes sticky during the course of the 1‘ Postmortem lesions- include dehydration and changes in bursa, skeletal muscle, liver and kidney. All affected birds have some bursal changes com- monly characterized by swelling, change in shape (oblong), color (pink, yellow, red, black) and the formation of a gelatinous film around the bursa. Diagnosis: The diagnosis of I.B.D. is usually based on flock history and postmortem lesions. Laboratory procedures may be used to substantiate the diagnosis. Treatment and prevention: There is no specific treatment for I.B.D. In fact, indiscriminate medi- cation with certain drugs (e.g. the sulfon.amides) may severely aggravate mortality. Supportive meas- ures, such as increasing heat and ventilation and increasing water consumption, are beneficial. Management and sanitation practices alone can- not be relied upon to prevent the occurrence of the disease. Early exposure (before l4 days of age) to the agent of I.B.D. ap-parently acts as an immuniza- tion procedure, and many flocks that are exposed and infected do not develop noticeable disease symptoms. Vaccines are available but must be given under the supervision of a poultry pathologist or regula- tory official. If given correctly, good control can be obtained. 37 Section 5. DISEASES OF UNDETERMINED CAUSE The causes of some disease conditions have not been established. Some of the diseases in this group have the characteristics of infectious diseases, but many of them appear to be associated with disturb- ances in nutrition or metabolism. TRANSMISSIBLE ENTERITIS OF TURKEYS (Bluecomb) Transmissible enteritis is an acute t0 chronic disease of turkeys characterized by sudden. onsets, marked depression and severe diarrhea. Death losses may be high, particularly in young poults; but heaviest losses in adults are due to loss of con- dition. The disease at one time was considered to be the same as so-called “bluecomb” of chickens. Now it is recognized as a distinct entity. Cause: The etiologic agent of turkey bluecomb is considered to be a virus. Substantial evidence exists; however, the disease as seen in the field is the result of an interaction of several agents, among which the virus is considered to be primary. Transmission: The disease spreads by contact with infected birds or premises or droppings of infected birds being especially rich in virus. No specific environmental factors appear to influence the occurrence. Symptoms and lesions: When the disease strikes young poults under 3 or 4 weeks of age, onset is sudden. Affected poults appear cold and seek heat. Feed and water consumption drops markedly and poults lose weight rapidly. Morbidity and mortal- ity may approach 100 percent in uncontrolled outbreaks. Young poults show few lesions other than those associated with the intestinal tract. Intestines usual- ly are distended and lack muscle tone. Intestinal contents are fluid and gaseous (foamy). Morbidity is variable in older flocks of turkeys. It may be extremely low in some flocks but ex- tremely high in others. Feed intake drops markedly and birds may lose up to 4 to 5 pounds of body weight in just a few days. Birds usually have profuse diarrhea. Cyanosis of the head parts is common. When older birds are autopsied, the following lesions may be seen. The body musculature is dehydrated. Minute hemorrhages may be seen on the viscera and necrotic foci on the liver. Kidneys are commonly swollen and contain an excess of 38 urates. Severe catarrhal enteritis is seen often and mucous casts may be present. The pancreas usually presents multiple chalky white iliareas. The crop frequently is distended and contains sour smelling contents. Diagnosis: Transmissible enteritis mus-t be dif-__ ferentiated from common bacterial infections such ‘ as paratyphoid, fowl cholera, fowl’ typhoid and erysipelas. Diagnosis usually is based on history, symptoms, lesions and negative bacteriological find- ings for the common bacterial infections. Treatment and prevention: Older turkeys can be flushed with molasses at the rate of 1 pint mo- lasses to 5 gallons of drinking water for l day. Then give antibiotics in feed or drinking water at the rate o-f at least 200 grams/ ton of feed or 200 t0 400 milligrams/gallon of water. Continue treatment for at least 5 to 7 days. Do not flush young turkey poults. Give anti- biotics at the rate of up to 400 grams/ton of feed g or 1 gram/gallo-n of drinking water. Give this high level for 2 to 3 days, after which time antibiotics may be reduced, depending on flock response. Total v treatment period should be at least 5 to 7 days. Until more is known about the spread of blue comb, no specific recommendations for prevention * can be made. However, consider recovered birds ' as potential carriers. Clean and disinfect houses _ in which outbreaks have occurred. Leave vacant _ for at least 30 days. Apply routine management . and sanitation practices for disease prevention. HEMORRHAGIC ANEMIA SYNDROME (Hemorrhagic Disease: Aplastic Anemia) Hemorrhagic anemia syndrome is a disease characterized by hemorrhage and anemia. It is con- .y sidered to be a disease of chickens only, although Q poorly substantiated reports indicate the occurrence of a similar disease of turkeys. The condition may affect birds of all ages, but usually affects those between the ages of 4 and l2 weeks. Economic loss A. results from mortality and retarded growth. Cause: The cause of hemorrhagic anemia syn- drome has not been determined, but it is not j considered infectious. Symptoms and lesions: Usual signs are ruffled feathers, weakness, loss of body weight, diarrhea a Morbidity usually is high, but mortality is extremely variable, depending upon and anemia. ‘l. ther the disease is acute or chronic. Acutely ected birds may die with few preliminary sym.p- if u . Flock mortality may approach 20 to 30 per- i t although it usually is lower. e; Lesions vary from anemia to frank hemorrhages. jorrhages may be found anywhere on or in the y. Usually they are found in the musculature, J icularly of the thighs and breast. Hemorrhages i commonly petechia (pinpoint in size), but they igl- be diffuse involving large areas. Hemorrhages f en are seen in the wall of the intestines, the entriculus, the musculature of the gizzard and ,heart musculature. Less often there may be it.“ into the anterior chamber of the eye _~~ into the wattles. Anemia is characterized by A eness of the comb, mucous membranes and other F ues. Commonly, the bone marrow appears pale , ow and fatty (ap-lastic anemia). Diagnosis: Diagnosis is based on history, symp- “v and lesions. When intestinal lesions are t, care must be taken to differentiate from a 'diosis. ‘I Treatment: There is no specific treatment for orrhagic anemia syndrome, but good response uently is obtained by adding liver solubles to ‘ at a level of 8 gallons per ton of feed for 5 s, followed by a level of 5 gallons per ton for additional 5 to 7 days. - Avoid sulfa drugs and high levels of antibiotics p" they may aggravate the condition. AORTIC RUPTURE i ‘Aortic rupture is a disease of turkeys character- by rapid onset and immediate death due to 1 . hemorrhage. It seldom is observed in other _§ s, but may occasionally affect chickens. Male eys, usually the most rapidly growing birds in iflock, are affected most frequently. The disease ally appears in growing birds between the ages and 20 weeks, although older birds may be ; ed. Q ause: The cause has not been determined. :_ energy intake during rapid growth appears »- related to occurrence. Deposition of fa-tty ces in the blood vessel walls weaken the i ls, making them more subject to rupture. uent increases in blood pressure, common ledolescent male turkeys, produce the actual . re. .. ransmission: QAortic rupture is not infectious not transmitted from one bird to another. ii mptoms and lesions: Seldom are preliminary ms observed. Affected birds usually are »~ dead. Occasionally, an apparently healthy bird drops to the ground in terminal convulsions and dies within minutes. Daily losses are low, but total losses may approach l0 percent or more in serious outbreaks. Autopsies on affected birds reveal massive amounts of free blood in the body cavities. The site of aorta rupture usually is in the kidney region but may be anywhere posterior to the aorta origin at the heart. Diagnosis: Diagnosis is based on lesions. Treatment and prevention: Losses can be re- duced by limiting energy intake. Tranquilizers, such as reserpine, are also of value. Prevention is accomplished best by limiting energy intake or by continuous low level feeding of tranquilizers during the critical 12- to 20-week- old period. CAGE FATIGUE (Cage Layer Fatigue, Cage Layer Paralysis) Cage fatigue is a paralytic condition observed in birds held in cages. The disease is most common among high-producing young pullets during sum- mer. It was prevalent during the late 1950's, but it is now seen infrequently. The decrease probably is due to dietary changes in the last few years. Cause: The exact cause is not understood; how- ever, the disorder is considered to be a disturbance in mineral metabolism. Symptoms and lesions: Affected birds are para- lyzed but they will continue to eat and drink if feed and water are within reach. Many birds lay on the day paralysis develops and some may con- tinue to lay for a day or two after becoming para- lyzed. Shell quality remains good. Morbidity usually is low but may approach 20 percent. Bones of affected birds are extremely fragile and are broken easily when the birds are handled routinely. The walls of the long bone are thin due to erosion of bone from the interior. Diagnosis: Diagnosis is based on history, symp- toms and lesions. Other causes of paralysis such as neural leukosis should be ruled out. Treatment: Although impractical in most op- erations, affected birds usually make a spontaneous recovery if placed on the floor or on a cage bottom covered with newspaper or other material. Proper ration fortification usually prevents the disorder. FATTY LIVER SYNDROME Fatty liver sydrome is characterized by deranged fat metabolism resulting in the deposition of excess fat in the liver and body cavities. It is seen most 39 commonly in caged birds, but on occasion may strike floor birds, particularly in heavy breeds. Cause: The cause is unknown. Factors which predispose the condition, however, include reduced activity as in cage operations and use of high-energy feeds. Symptoms and lesions: Affected birds usually experience a drop in egg production. They may be anemic and occasionally may be found dead without preliminary symptoms. Diarrhea, though common in caged birds, especially is pronounced in birds with fatty liver syndrome. Postmortem findings are characteristic, but vary with severity. Livers of affected birds are pale, yellow and extremely friable. The livers may have subcapsular hemorrhages varying in size from pin- point to massive. Deaths associated with fatty liver syndrome usually are due to hemorrhage from spon- taneously ruptured livers. Fat content of the liver may be 55 to 70 percent. on a dry-weight basis, as compared to 5 to 10 percent for normal birds. Deposition of excess. abdominal fat is also a com- mon finding; such fat usually is extremely liquid 1n nature. Diagnosis: Diagnosis is based on history, symp- toms and lesions. Treatment: The treatment most likely to effect a favorable response is to add 500 grams of choline, 12 milligrams. of vitamin B12, 5,000 to 10,000 units of vitamin E and 500 mg of Inositol per ton of feed. The reduction of energy by 50 calories per pound of feed and adjustment of protein level to at least 19 percent is effective in treatment as well as pre- vention. These modified rations must be fed for an indefinite period. ULCERATIVE ENTERITIS (Quail Disease) Ulcerative enteritis is an acute or chronic in- fection of game birds, chickens, turkeys and other domestic fowl. Death losses may be high in young quail or in pullets being raised for egg production. Cause: The cause of the disease is not definitely known, but it is probably caused by a bacterial organism. Transmission: Infection spreads by the drop- pings of sick or carrier birds. The disease organism is very resistant to disinfectants and will persist under varying environmental conditions» (e.g. hot, cold, moist or dry). Symptoms and lesions: Birds with the acute form may die suddenly while in good flesh, whereas the mos-t chronically affected birds will become list- 4O less, have ruffled feathers and develop- a humped- up attitude. Such birds will die in an extremely emaciated state. The droppings may be confused with those of birds with coccidiosis. These two diseases often are seen in the same bird. The droppings of birds with only ulcerative enteritis will never contain blood. The postmortem. lesions are characteristic. The entire intestinal tract often has button-like ulcers but the lower portion is» most often affected. These ulcers often perforate, resulting in local or general? ized peritonitis. “i Diagnosis: Although the disease is character- istic in nature, anyone suspecting the infection . should seek professional confirmation before treat- ment is started. if Treatment and prevention: Streptomycin and j bacitracin are effective drugs in the treatment and . prevention of this disease. If streptomycin is used, i it should be incorporated into the drinking water * at a level of 5 grams per gallon for 5 to l0 days, i followed by 1 gram per gallon for an additional I 5 days. If bacitracin is used, it should be incorpor- ‘ ated into the feed at a. level of 200 grams per ton ~- and fed over a period of 2 weeks. ' _ Raising birds on wire is an effective preventive"; measure. Bacitracin, fed at a rate of 20 grams per; ton of feed, is an effective prevention in probl_ operations where the use of wire is impractical. NECROTIC ENTERITIS Necrotic enteritis is an acute disease, parti y. larly of broiler type chickens, that is characteriz i’: by marked destruction of the intestinal lini 3f Common field names applied to the conditi! are quite descriptive, (e.g. rot gut, crud and ca i flower gut). Cause: The cause of the disease is not wp defined. Evidence indicates that bacterial o ’ isms and their toxins are primary but that cocci osis is a contributing factor. Most of the d if to the intestinal lining is apparently due to to produced by the bacterial organisms. i ' Transmission: Little is known about the sp J of necrotic enteritis, but in all likelihood, trans sion takes place by oral contact with the droppik o-f infected birds. Nature of the disease: Necrotic enteritis ap if very suddenly in the affected flock. Birds W are apparently healthy may become acutely“ pressed and die within hours. Mortality in af - { flocks is usually between 2 and l0 percent, bu if». be as high as 30 percent in severe outbreaks. .~ - due to retarded growth and poor feed con- y ion may be more costly than mortality in many breaks. The lesions of the disease usually involve the i‘ er half of the small intestine, but in some in- ces the entire length of the tract is involved. presence of a diphtheri-tic cauliflower-like brane is characteristic. I Diagnosis: Diagnosis is based upon history, ptoms and the findings of characteristic lesions. {iTreatment and prevention: Bacitracin is an ef- “ve treatment and is given for 72 to 96 hours a level of 100 grams per ton of feed or at a y. é’ < level of l0 to 25 grams per 50 gallons of drinking water. Strep-tomycin is also effective if applied for 72 hours at a level of 5 to 15 grams per 50 gallons of drinking water. Supportive vitamin treatment may increase response. Preventive medication may be of value on some premises where prior experience with the disease dictates the need. Bacitracin (25 grams/ton of feed) may bemused during the first 6 weeks for this purpose. Since coccidiosis may be a contributing factor, attention should be give-n to the coccidiosis control program. 41 Section 6. PROTOZOAN DISEASES Protozoa are the smallest members. of the ani- mal kingdom. Although many microscopic proto- zoan organisms are harmless, others can produce severe disease. This section includes five of the more common and serious poultry diseases caused by these organisms. COCCIDIOSIS Coccidiosis is a protozoan disease of fowl charac- terized by diarrhea, unthriftiness and variable mor-~ tality. It is a problem in all poultry-producing areas. Despite recent advances in control and treat- ment, the disease remains one of the principal causes of economic loss to the poultry industry. Cause: Coccidiosis is caused by minute, micro- scopic animal forms called coccidia. There are a number of species of coccidia, each of which pro- duces a distinct disease process. Following an out- break of coccidiosis, a flock will be protected against subsequent exposure to the species which produced the outbreak, but it will remain susceptible to other species. This means a given flock may have several outbreaks of coccidiosis, depending on the number of coccidia species in an are-a and exposure to them. The species of coccidia affecting chickens and turkeys are: Chickens Eimeria tenella"‘ Eimeria ne'catrix* Eimeria aceruulinzfl Eimeria brune-tti* Eimeria maxima* Eimeria mivati* Eimeria mitis Eimeria hagani Eimeria praecox Turkeys Eimeria adenoeidefl‘ Eimeria meleagrimitis‘ Eimeria gallopavonis‘ Eimeria meleagridis Eimeria dispersa Eimeria innocua Eimeria subrotunda ‘Considered the major causes of clinical outbreaks. Transmission: Coccidiosis is transmitted by di- rect or indirect contact with droppings of infected birds. When a bird ingests coccidia oocysts, the organisms invade the intestinal tract lining where they produce tissue damage while undergoing re- production. Within a week after ingesting coccidia oocysts, an infected bird will shed descendant coc- cidia in its droppings. So great is the reproductive potential that a single organism may produce about a million descendants. This means that contami- nation can build up rapidly, even in a new house. 42 Coccidia shed in droppings. are incapable of infecting other birds until certain maturation changes (sporulation) take p-lace. These changes occur in 24 to 72 hours if the litter is warm and damp. The number of infective coccidia that a bird“ eats detennines whether-an infection will be mild enough to go unnoticed or severe enough to cause visible illness. Coccidia are extremely hardy and may survive for long periods outside of the bird’s body. They are transmitted easily from one house or premise to another by such things as dirty boots, free-flying birds, feed sacks and equipment. Symptoms and lesions: Coccidiosis usually oc- curs in growing birds and young adults. It seldom is seen in birds under 3 weeks of age unless they are brooded on contaminated litter. Old birds usually are immune because exposure during early life is difficult to avoid. Signs of a coccidiosis outbreak are usually gen- eral. Affected birds become pale and droopy, tend to huddle, consume less feed and water, have diar- rhea and may become emaciated and dehydrated. Laying birds will experience a drop in production. Cecal coccidiosis of chickens, caused by E. - tenella, is often acute and characterized by bloody Y droppings, severe anemia and high mortality. In turkeys, cecal coccidiosis, caused by E. adenoeides, 5 also is often acute, producing high mortality but seldom bloody droppings. l Intestinal coccidiosis may be acute, but more f frequently is chronic in nature. Droppings of " affected birds are usually tan and watery, although a acute E. necatrix infection may produce consider- able hemorrhage. Since there is a slower buildup ; of infection of intestinal coccidia, intestinal coccidi- .- osis usually occurs in birds in the latter part of the _ - growing period or in early production. Mortality usually is not significant unless acute E. necatrix, ‘ E. brunetti or E. maxima infection is present. _ Autopsies of birds with coccidiosis reveal lesions T: that vary, depending upon type of coccidiosis pres- I ent and severity and stage of the disease. 1 Chickens in the acute phase of cecal coccidiosis V‘ will have ballooned cecal pouches full of free blood. In the recovery stage, cheesy cores tinged ‘ with variable amounts of blood will be present in the cecal pouches. Free blood usually is not found » oeca of turkeys with cecal coccidios-is, but _--< contains a white-to-gray, semi-gelatinous , resembling cottage cheese in consistency. ' ~ of intestinal coccidiosis vary from a mild enteritis to a severe necrotic/hemor- f type of enteritis. l; osis: Cecal coccidiosis may be confused ackhead and salmonellosis, both of which Q uce similar cecal lesions. Intestinal coc- may be confused with hemorrhagic anemia tie and other diseases characterized by en- y Establish definite diagnosis by labora.tory _j so that medication can be specific. Do this id- ». o ic examination of intestinal or cecal gs to demonstrate the presence or absence W 'dial organisms. Since most healthy birds i a few organisms, it is necessary to cor- microscopic findings with flock history ‘ topsy lesions before making diagnosis and j; endations. i tment and prevention: There are a num- p’ drugs which are quite effective in the treat- of coccidiosis. Drug selection is dependent many factors including withdrawal regula- ‘M (if approved for layers), toxicity problems, i~ involved and other disease conditions. _u expert advice in setting up a treatment . ll . g is difficult, if not impossible, to prevent coc- ,is by sanitation practices alone. Coccidiosis , ented best by feeding a coccidiostat. A coc- V’ ‘tat is a drug added to feed at low levels and ‘ntinuously to prevent coccidiosis. A good l» '0stat should: i‘ Prevent clinical outbreaks of coccidiosis- liiHave no undesirable side effects (e.g. de- pressed weight gain) Allow a natural immunity to coccidiosis to develop in the flock if exposure is present if Be inexpensive broilers a ration containing a coccidiostat 1 uously until the last week before marketing. replacement birds a ration containing a coc- l tat continuously until they are about 16 weeks ; Give turkeys a coccidiostat during the grow- i a 'od while confined and for an added week days after moving them to range. any coccidios-tats are available on the market. 'on should based on several factors includ- i t, type of operation and past experience. "f coccidiosis vaccine is available commercially. i‘ product is useful in certain types of operations, i it should not be used indiscriminately. Seek f. advice before using the product. BLACKHEAD (Histomoniasis, Infectious Enierohepafifis) Blackhead is an acute or chronic, infectious protozoan disease of fowl, primarily affecting the ceca and liver. The disease is- present wherever poultry is raised. Blackhead is one of the critical diseases of growing turkeys. It may cause stunted growth, poor feed utilization and death loss. It is of lesser economic importance in chickens since chickens are more resistant. Cause: Blackhead is caused by a protozoan parasite called Histo-monas meleagridis. Transmission: The blackhead organism, His- tomonas meleagridis, is passed in the fecal material of infected birds. In many instances, the organism is shed within the eggs of Heterakis gallinae, the cecal worm of chickens and turkeys. Free-living forms do not survive long in nature, but organisms contained within cecal wonn eggs may survive for months or years. Because of this, most blackhead transmission is considered due to ingestion (eating) of cecal worm eggs infected with the blackhead organisms. Chickens frequently are infected with black- head without showing signs of the disease. These chickens may shed enormous numbers of blackhead organisms, many of which are protected by cecal worm eggs since cecal worms are so common in chickens. Because of this, outbreaks in turkeys often can be traced to direct or indirect contact with ranges, houses or equipment previously used by chickens. Free-flying birds also may introduce an infection. Symptoms and lesions: Most blackhead losses occur in birds 6 to 16 weeks old. Among the symp- toms are: loss of appetite, increased thirst, droopi- ness and drowsiness, darkening of the facial regions (“blackhead”) and diarrhea (sulfur-colored drop- pings). Morbidity and mortality are variable, but mortality is seldom above l0 to 15 percent; however, it may approach 8O to 90 percent in uncontrolled turkey outbreaks. In chickens, losses usually are low. Lesions of uncomplicated blackhead are con- fined to the ceca and liver, thus the reason for the synonymous term, enterohepatitis. The ceca are ballooned and walls may be thickened, necrotic and ulcerated. Gaseous (cheesy) cores which may be blood tinged usually are present. Peritonitis may be present if ulcers have perforated the ceca walls. Livers are swollen and display circular de- pressed areas of necrosis about V; inch in diameter. Lesions are yellowish to yellow green and extend deeply into the underlying liver tissue. Healing lesions may resemble those seen in visceral leukos-is. 43 Lesions observed in chickens frequently are atypical as the liver lesions may be absent or less pronounced. Diagnosis: Blackhead presenting typical lesions is diagnosed readily on the basis of the lesions. Atypical forms, particularly in chickens, must be differentiated from cecal coccidiosis and Salmon- ella infection in particular. Laboratory tests may be required for positive diagnosis in such cases. Treatment and prevention: A number of drugs on the market can be added to drinking wate=r to bring blackhead outbreaks under control. Use these compounds in accordance with the manufacturer's recommendations. Palatability may be a problem with certain compounds, thus making it difficult to get proper drug intake. Good management practices can do much to control the blackhead problem. Do not maintain turkeys and chickens on the sam.e premises. Do not range turkeys on ground previously used by chickens unless several years have elapsed. Rotate ranges at periodic intervals if possible. Cecal worm control may help reduce blackhead incidence. Wire or slatted floors around feeders and waterers will reduce exposure. Despite good management practice, there are certain premises which are so contaminated that it is necessary to feed drugs continuously at a low level to prevent blackhead. Such drugs are used in the same manner as coccidiostats are used to prevent coccidiosis. TRICHOMONIASIS Trichomoniasis is an infectious protozoan dis- ease of fowl, primarily affecting the upper digestive tract. It is universal in distribution. It is a. par- ticularly hazardous disease of turkeys, pigeons and quail, and is of lesser importance in chickens. Cause: A protozoan parasite called Trichomonas gallinae is the cause in turkeys and chickens. Other species affect pigeons and quail. Transmission: Birds. most frequently acquire trichomoniasis by ingestion of contaminated feed and water. Stagnant water ponds and ditches fre- quently are contaminated. Free-flying birds may introduce an infection to a premise. Once in.tro- duced, the disease spreads as birds eat or drink materials contaminated by droppings or oral dis- charges of infected birds. Recovered birds may become carriers indefinitely. Symptoms and lesions: Most turkey losses due to trichomoniasis occur in young and growing birds. Among the symptoms are loss of appetite, droopiness, loss of weight and darkened heads. The chest may be depressed as the crop usually is 44 empty, although occasionally the crop is distended and filled with foul smelling fluid contents. Mor- bidity in a flock may be high, but mortality usually is low except in severe outbreaks. The course of the disease is prolonged in turkeys unless affected birds are cannibalized. Lesions of uncomplicated trichomoniasis usually are confined to the upper digestive tract, affecting the crop in particular. Occasionally oral lesions are observed. Lesions consist of necrotic ulcer- f ations with accumulations of caseous material?‘ which build up over the affected areas. i’ Early reports described les-ions of trichomoni- asis involving the ceca and liver which resembled j those of blackhead. Although trichomonads fre- A quently are found in the lower intestinal tract, _' it is now recognized that blackhead-type lesions j are not associated with the organisms. Diagnosis: Trichomoniasis is diagnosed on the a basis of lesions and demonstration of the causative if organism viewed on slides through the microscope. r Since other diseases, such as crop capillaria infection . and fungus infections of the crop, may produce! similar lesions, do n.ot make a diagnosis without: a microscopic examination. ' Treatment and prevention: Move birds to sani- tary surroundings, if possible. Birds may be treated with copper sulfate (“bluestone”) in the drinkin water at a l:2000 dilution for 4 to 7 days. Mak the copper sulfate solution as follows: i‘ Stock solution: Add l pound of copper sulfa to a gallon of water containing 1 cup of vin Mix thoroughly to get into solution. (Never undiluted stock solutions to birds.) l Drinking water solution: Add l tablespoon ounce) of stock solution to each gallon of drinki p water. ' Trichomoniasis is not a problem if birds _ supplied with sanitary surroundings, includi‘ well-drained ranges and clean drinking water -~ feed. 5 HEXAMITIASIS (Infectious Cuturrhal Enteritis) Hexamitiasis is an acute infectious disease, turkeys, quail, ducks, chukar partridges and H») Heavy losses have been reported in one out among ringnecked pheasants. Chickens appar i", are not affected. It was reported first in ducks pigeons in 1923 and in turkeys in 1938. Befori tablishing the true nature of the disease in tur l_ the condition was thought to be trichomonias Hexamitiasis is recognized as a disease prof in every commercial turkey-producing area. It _ be a major problem in localized areas during a particular year followed by one or more years in which incidence is very low. Cause: Hexamitiasis is caused by albilate-rially symmetrical, flagellated, one-celled parasite of the genus Hexamita. H exami ta meleagridis is the cause in turkeys; in pigeons it is Hexamita columbae. Experimentally, the Hexamita of turkeys can be transmitted to young quail, chicks and ducklings, and that of quail and partridges can be transmitted a to poults. However, poults cannot be infected with the organism isolated from p-igeons. Transmission: Hexarnitiasis is primarily a dis- . ease of young birds and outbreaks seldom occur , in poults past l0 or ll weeks of age. Losses are f} most severe in birds 3 to 5 weeks. old. Apparently, resistance develops rapidly with increasing age, if regardless of previous exposure. The primary infection source- is droppings from _ carrier birds. About a third of recovered birds be- ‘ come carriers. Most outbreaks result from a build- up of organisms through several broods of poults- in such manner that exposure of the following ibrood is overwhelming. Indirect transmission may result from fecal material carried from one location to another on shoes or equipment. Free-flying birds such as quail also may be carriers. Symptoms and lesions: Symptoms primarily are ' eight loss due to the dehydrating effect. Birds 1 will huddle together near the heat source d cry or “chirp” constantly as though in pain. jnvulsions due to lowered blood sugar levels ortly precede death. Affected birds suffer losses» a weight and survivors remain stunted for long ~ ods. g Dehydration and emaciatlion are the principle . a o s lesions. The intestine usually appears to have p. tone with loca.l bulbous areas of congestio-ns. testinal contents usually are thin and watery. Diagnosis: Diagnosis depends upon history, ptoms and microscopic examination of intes- FR al contents. A definite diagnosis cannot be made ess typical flagellates can be demonstrated in __tinal contents taken from the duodenum f-w Most flagellates observed in the ceca are npathogens. a Treatment and prevention: Prevention depends i}: sanitation with: particular emphasis upon arating age groups. If an individual must care p. several age groups, the younger group should l. cared for first. y, Hepzide, fed continuously at levels of 0.025 and v35 percent, will aid in preventing losses. i ' tlessness and foamy or watery diarrhea with rapid i Hepzide at a level of 0.02 percent in water now appears to offer the most promise as a therapeutic measure. The disease does not respond well to treatment but l:2000 solutions of copper sulfate with dried whey (3 to 4 ounces per gallon of the dilute solu- tion) is an old stock remedy. This solution should serve as the only source of drinking water for 5 to 7 days, repeating after a 3-day rest if necessary. Aureomycin at a level of 200 grams per ton of ration is of some benefit. LEUCOCYTOZOONOSIS Leu-cocytozoonosis is an acute, sometimes highly fatal disease of young turkeys and ducklings. The causative protozoan parasites invade the: circulatory system where they destroy great numbers of leuco- cytes (monocytes and macrophages). In certain re- spects, the disease resembles true malaria, but birds are the sole hosts of the genus Leucocytozoon. The disease occurs in many areas of the country, but is found more frequently in the South and Southeast. Mortality may reach 100 percent in ducklings up to 8 weeks of age, and losses may be severe in turkeys up to 12 weeks of age. Clinical symptoms usually are not apparent in older birds, but they may remain carriers for months. Cause: A protozoan parasite similar to the true malaria parasite is the cause. The organism re- sponsible for the disease in turkeys is designated as Leucoeytozoon smithi; in ducks it is called Leu- coeytozoon simondi. Transmission: The disease is transmitted by several species of the black fly, Simulium sp., which breeds in running streams. After feeding on in- fected birds, the flies can transmit the disease at the end of 4 days and remain infective for about l8 days. Direct transmission from bird to bird does not occur. Recovered birds remain carriers and serve as reservoirs of infection in subsequent years. Symptoms and lesions: Younger affected birds may lack appetite and exhibit droopiness, weak- ness, increased thirst and rapid labored breathing. If drowsy birds are made to move they may become greatly excited. The course of infection usually is rapid with visible symp-toms seldom lasting more than 2 or 3 days, terminating in death or beginning recovery. Recovered birds may appear stunted with the flock as a whole appearing to lack uniformity. In adult birds, clinical symptoms are seldom detectable. The most consistent pronounced gross lesion is spleen enlargement and congestion. Anemia 45 and emaciation usually are evident in clinically ill birds. The flesh of affected birds often is flabby and yellowish. Mild congestion. of the upper in- testinal tract is common. Diagnosis." A positive diagnosis may be rendered only after demonstration of the causative organism in stained blood smears (Giemsa or Wright's stain may be used). Treatment and prevention: Prevention. depends upon control of black fly populations and turkeys being reared away from running streams. Segre- gate breeding and brooding operations since adults A may be carriers. Brooding in screened houses will l prevent infection in young birds. Drugs effective against malaria appear to have little if any value in the treatment of leucocytozo- Q onosis. Sulfaquinoxaline is considered valuable in a reducing losses. Administer flit in the drinking 1 water at a level of 0.025 percent for 5 to 7 days, P. and following by adding it in feed at a level of 5 0.0175 to 0.025 pe-rcent until losses are controlled. = .4 POULTRY LICE The chief effects of lice on their host are due the irritation they cause. The birds become less and do not feed or sleep well and may f ‘ure themselves or damage their feathers by peck- .“ ; or scratching the parts irritated by lice. Weight 'ns and egg production may drop. is All lice infecting poultry and birds are of the ‘ping and chewing type. Mites may be confused I I t lice. The mites suck blood. In general, each species of lice is confined to l articular kind of poultry, although some may w from one kind of poultry to another when 1 are closely associated. Chickens usually are ‘f, ested with one or more of seven different spe- d; turkeys have three common species. .All species of poultry lice have certain common ‘its. All live continuously on feathered hosts W soon die if removed from them. The eggs attached to the feathers. Young lice resemble , ts except in color and size. They differ in ‘_ erred locations on the host, and these prefer- f. have given rise to the common names applied :various species. l‘ to 7 days, and development of the lice from A ing to the adult stage requires 17 to 21 days. ting takes pla-ce on the fowl, and egg laying g 2 or 3 days after lice mature. The number eggs probably ranges from 50 to 300 per female f Head Louse As the name suggests, this species (Cuclotogaster rographus) is found mainly on the head, al- p gh it occurs occasionally on the neck and here. It usually is located near the skin. in I down or at the base of the feathers on the top I back of the head and beneath the bill. In fact, _' head of the louse often is found so close to ' skin that poultrymen may think it is attached e skin or is sucking blood. Altllough it does f suck blood, the louse is very irritating and I first among lice as a pest to young chickens turkeys. Heavily infested chicks soon become py and weak and may die before they are a th old. When the chickens become fairly well u ered, head lice decrease but they may increase when the fowls reach maturity. This louse is oblong, grayish and about 1/10 f». long. The pearly-white eggs are attached In general, the incubation period of lice eggs I Section 7. PARASITIC DISEASES singly to the down or at the base of the small feathers on the head. They hatch in 4 or 5 days into minute, pale, translucent lice resembling adults in shape. The Body louse The body louse (Menacanthus stramineus) of chickens prefers to stay on the skin rather than on the feathers, and it chooses parts of the body that are not densely feathered, such as the are-a below the vent. In heavy infestations, it may be found on. the breast, under the wings and on other parts of the body, including the head. When the feathers are parted, straw-colored body lice may be seen running rapidly on the skin in search of cover. Eggs are deposited in clusters near the base of small feathers, particularly below the vent, or in young fowls, frequently on the head or along the throat. Eggs hatch in about a week and lice reac.h maturity in 17 to 20 days. This is the most common louse infesting grown chickens. When present in large numbers, the skin is irritated greatly and scabs may result, especially below the vent. The Shaft louse The shaft louse, or small body louse (Menopon gallinae) is similar in appearance to the body louse, but smaller. It has a habit of resting on the body feather shafts of chickens where it may be seen running rapidly toward the body when feathers are parted suddenly. Sometimes as many as a dozen lice may be seen scurrying downward along a feather shaft. Since the shaft louse apparently feeds. on parts of the feathers, it is found in limited numbers on turkeys, guinea fowl and ducks kept in close asso- ciation with chickens. It does not infest young birds until they become well feathered. Other Kinds of Chicken Lice Four other kinds of lice usually are found on chickens, but they are less abundant and more important than the ones previously discussed. The wing louse (Lipeurus caponis), a slender gray spe- cies resembling the head louse, is the most widely distributed and is found in the greatest numbers. It is sluggish and usually is seen resting between the barbules of the wing and tail feathers or oc- casionally on the neck hackles and back feathers. The fluff louse (Goniocotes gallinae), which is found (as the common name implies) on the fluff 47 of the body feathers, is small, rather broad, yellow and inactive. As it stays mostly in the fluff, it causes little irritation or other injury. The large chicken louse (Goniodes gigas) is a robust, dark, smoky-gray species of striking appear- ance. It is seldom found in poultry flocks. The brown chicken louse (Goniodes dissimilis), occurring mainly in the southern states, is large and reddish brown. It seldom occurs in large enough numbers to cause serious damage. Poultry Mites All classes of poultry are susceptible to mites, some of which are blood-suckers, while others bur- row in the skin or live on or in the feathers. Still others occur in the air passages and in the lungs, liver and other internal organs. Poultry mites cause retarded growth, reduced egg production, lowered vitality, damaged plum- age and even death. Much of the injury, consisting of constant irritation and loss of blood, is not ap- parent without careful examination. Common Chicken Mite This mite (Dermanyssus gallinae) is probably the m.ost common mite found in all types of poultry. It is a blood-sucker, and when present in large numbers, loss of blood and irritation is sufficient to cause anemia. Egg production is re- duced seriously. This mite feeds at night, and usually remains hidden in cracks and crevices during the day and attacks birds at night while on the roosts. In very heavy infestations, some mites may remain on the birds during the day. About a day after feeding, the female lays eggs in cracks and crevices. The eggs hatch and the mites develop into adults in about 1 week. During cold weather, the cycle is slower. A poultry house remains infested 4 to 5 months after it is vacated. Since the mite will feed on wild birds, they may be responsible for some infestations, but spread more likely is caused by using contaminated coops. Human carriers are important. Since these mites do not stay on the birds during the day, apply treatment only to the houses and equipment and not on the birds. Feather Mite This mite (Ornithonyssus sylviairum) is an oc- casional but serious pest of chickens. Heavy infes- tations result in lowered condition of thebirds and egg production, as well as a scabby skin con- dition. This mite remains on the bird and does more damage than the common chicken mite. It 48 resembles the common chicken mite, but can be differentiated in that it is present on birds in large numbers during the day. It prefers the feathers below the vent and around the tail, but can be found on all parts of the body. Females lay eggs on feathers where the young mites complete their development without leaving the host. Since they remain on the fowl most of the time, treatment of birds is necessary to destroy the mites. Scoly-Leg Mite t This mite (Cnemidocoptes mutans) is one of the itch mites and lives under the scales on feet and ~ legs. It also may attach to the comb and wattles. This mite causes a thickening of scales on the feet and legs. It spends its entire life cycle on the 1 birds and spreads from bird to bird, mainly by 7 direct contact. I Depluming Mite This mite (Cnemidocoptes gallinae) causes severe irritation by burrowing into the skin near é the base of feathers, and frequently causes feathers I to be pulled out or broken. The mite is barely . visible to the naked eye and can be found in follicles 7 at the base of the feathers. The mites crawl around -. the birds at times, thus enabling them to spread from bird to bird. Fowl Tick or Blue Bug This pest (Argus persicus) is one of the most ‘ serious parasites of poultry when it becomes nu- 7 merous in poultry houses or on a poultry range. i The tick is a blood-sucker, and when present in §. large numbers it results in weakened birds, re- duced egg production, emaciation and even death. * The fowl tick is found throughout most of the ~ South and is extremely hardy. Ticks have been i. kept alive without food for more than 3 yearsf Ticks will feed on all fowl types. * The ticks spend m.0st of their life in cracks 1 and hiding places, emerging at night to take a»; blood meal. Mating takes place in the hiding areas. -_. A few days after feeding, the female lays a batchj of eggs. She may lay several batches with a blood ‘ meal between each. In warm weather, the eggs; hatch in 10 to l4 days. In cold weather, they may take up to 3 months. Larvae that hatch from the f. eggs crawl around until they find a host fowl. TheyQ remain attached to the birds for 3 to l0 days. Then? they leave the birds and find a hiding place. After. a few days, they m.olt and then seek another bloodj meal. This is followed by another molt and blood: meal. ~ Ticks are difficult to eradicate, and methods employed must be performed very carefully. It is not necessary to treat the birds, but houses and .g surrounding areas must be treated thoroughly. Chiggers, Red Bugs or Harvest Mites These pests (Eutrombicula alfreddugesi) attack chickens and turkeys, as well as human beings. Normally these small mites feed on wild animals, birds, snakes and lizards. Only the larvae of chig- ~ attack poultry or animals; adult mites feed plants. Larvae usually attach to the wings, breasts and ks of poultry. They inject a poisonous substance f: t sets up local irritation and itching. After a i w days, it becomes engorged and drops off. Injury '3 grown fowl may not be apparent or noticed til the bird is dressed; then the lesion shows up ‘N greatly reduces carcass value. Young chickens l turkeys may become droopy, refuse to eat and _. Due to methods of raising poultry, turkeys affected more frequently than chickens. p, e Roundworms One of the most common parasitic roundworms gpoultry (Ascaridia galli) occurs in chickens and g keys. Adult worms are about 11/; to 3 inches i‘; and approximately the size of a.n ordinary med eye. i1_ Birds heavily infected may show droopiness, ciation and diarrhea. Death may occur in heavy infections, but the primary damage is ced efficiency. i? hickens 3 to 4 months old show resistance i ection. pecimens of this parasite are found occasion- ‘ in eggs. The worm apparently wanders from iintestine up the cloaca and is incorporated in as it is formed. e life history of this p-arasite is simple and 1~ Females lay thick heavy-shelled eggs in the ine and these pass in the feces. A small g o develops in the egg. They do not hatch. 11 larvae in the egg reaches infective stage in 2 weeks. These embryonated eggs are very hardy giunder laboratory conditions may remain alive years. Under ordinary conditions, probably any live more ithan l year. Disinfectants and i cleaning agents do not kill eggs under farm 'tions. Birds become infected by eating eggs _,. they have reached the infective stage. ivailable drugs will remove only the adult '_'te. The immature fonn probably produces T lead. Thus, they can be seen easily with th.e , the most severe damage. The treatment of choice is piperazine. Many forms of piperazine are pro- duced and all are effective if administered properly. Follow the manufacturer's instructions carefully. The parasite can be controlled by strict sani- tation. If the birds are confined, clean the house thoroughly and completely before a new group is brought in. Segregate birds by age groups, with particular care applied to sanitation of young birds. If birds are on range, use a clean range for each group of birds. Cupilluria , There are several species of Capillaria that occur in poultry. Capillaria annulata and C. contorta occur in the crop and esophagus. These may cause thickening and inflammation of the mucosa, and occasionally severe losses are sustained in turkeys and game birds. However, the parasites are not usually present in large enough numbers to pro- duce economic loss. In the lower intestinal tract there may be- several different species but usually C. obsignata is. the most prevalent. The life cycle of this parasite is dire-ct. The adult worms may be embedded in the lining of the intestine. The eggs are laid and passed in the droppings. Following embryonation which takes 6 to 8 days, the eggs are infective to other poultry which may eat them. The most severe damage occurs within 2 weeks of infection. The parasites produce a catarrhal inflammation and sometimes cause hemorrhage. Erosion of the- in- testinal lining may be extensive and result in death. These parasites may become a severe problem in deep litter houses. Reduced growth, egg produc- tion and fertility may result from heavy infections. If present in large numbers, these parasites are usually easy to find at necropsy. Eggs may be dif- ficult to find in droppings, due to the small size and time of infection. Since there is no good treatment for capillaria infection, control is best achieved by preventive measures (refer to the paragraphs on flock health management in Section 1). Some drugs, fed at low levels, may be of value in reducing the level of infection on problem farms. Game birds should be raised on wire to remove the threat of infection. As some species of capillaria have an indirect life cycle, control measures may have to be directed toward the intermediate host. Cecul Worms This parasite (Hetemkis gallinae) is found in the ceca of chickens, turkeys and other birds. The worms are small, white and measure % to 1/2 inches in length. 49 This parasite, probably the most common worm parasite of poultry in the United States, apparently does not seriously affect the health of the bird. At least no marked symptoms or pathology may be blamed on its presence. The main importance is that is has been incriminated as a vector of H istomonas meleagridis, the agent that causes black- head or infectious enterohepatitis. This protozoan parasite is apparently carried in the cecal worm egg and is transmitted from bird t0 bird through the egg. The life history of this parasite is similar to that of the common roundworm. The eggs are produced in the ceca and pass in the feces. They reach the infective form in about 2 weeks. In cooler weather, this may take longer. The eggs are very resistant to environmental conditions and will re- main for long periods. The cecal worm can be removed by treatment with piperazine compounds. Since the worm itself produces no observable damage and the eggs live for long periods, it is advisable and necessary to keep chickens and turkeys separated to prevent spread of infectious enterohepatitis. Tapeworms Tapeworms or cestodes are flattened, ribbon- shaped worms composed of numero-us segments or 5O divisions. Tapeworms vary in size from very small to several inches in length. The head or anterior end is much smaller than the rest of the body. Since the tapeworm may be very small, careful examination often is necessary to- find them. A portion of the intestine may be opened and placed in water to assist in finding the tapeworms. The pathology or damage wtapewonns produce in poultry is controversial. In young birds, heavy infections result in reduced efficiency and slower growth. Young birds are more severely affected than older birds. " Q All poultry tapeworms apparently spend part of their life in an intermediate host, and birds become infected by eating the intermediate hosts. These hosts include snails, slugs, beetles, ants, grasshoppers, earthworms, houseflies and others. The intermediate host becomes infected by eating p the eggs of tapeworms that are passed in the feces. Although several drugs are in use to remove tapeworms from poultry, mos-t are of doubtful ef- ficacy. In general, tapeworms are most readily controlled by preventing the birds. from eating the . infected intermediate hosts. Trade names are used occasionally for better understanding of information presented. No en- ‘. dorsement of name products is intended nor is ‘g criticism implied of similar products not mentioned. a GLOSSARY OF TERMS give immunity — immunity or resistance to that has been acquired by host response to w: agent. It can be acquired by having a and recovering or by vaccination. I te — as applied to disease, one which has a and relatively severe course. ia — a condition in which the blood is t in quantity or quality. If deficient in . there is a reduction in the hemoglobin 4 t of the blood or in the number of circulating 00d cells, or both. Anemia is characterized l eness of skin and mucous membranes and energy. tibody — an immune substance found in the produced in response to stimulation by an i- tigen — a suspension of microorganisms. A ‘ice which, when taken or injected into the 3 will stimulate antibody production. ,1 gnostic Antigen — used to detect the presence f ific antibodies in the blood of an animal; fin serological tests. p‘ ~ treat a specific disease. gtitoxin - a specific kind of antibody that _ tralize toxin. teria — microscopic, single-celled plant forms t; distributed in nature. Those capable of "ng disease are referred to as pathogenic i, terin — killed suspension of bacterial organ- w as an immunizing agent. olar — as applied to a bacterial cell, one I will stain deeply at the cell ends and takes I in centrally. lent — as applied to antigens or bacte-rins, I ich is made up of two strains of organisms. i 'er — an apparently healthy animal that . disease organisms and is capable of trans- ; them to other susceptible animals. rrhal — describes an inflammatory process " g the mucous membranes characterized by w ed flow of mucous. onie — as applied to disease, one of long in ei — bacterial forms which, when fully de- ‘t and free, are spherical. eidiostat — drug incorporated into the feed l tiserum — serum containing specific antibody Section 8. APPENDIX at low levels and fed continuously to prevent coc- cidiosis. Congestion — excessive accumulation of blood in a part. Contagious-as “contagious” disease, refers to an infectious disease that may be transmitted readily from one individual to another. Culture — used as a verb, to attempt to isolate a causative organism from a diseased bird. Used as a noun, a population of microorganisms propa- gated in artificial media. Cyanosis -- bluish discoloration of the skin, particularly the comb and wattles in birds. Diffuse — as applied to hemorrhage, one which is spread over considerable area. Disease — any departure from a normal state of health. Ecchymotic — as applied to hemorrhage, a rather large hemorrhagic spot. Edema — presence of abnormal amounts of fluid 1n tissues. Etiology — study of the causes of disease. Exudate — fluid associated with an inflamma- tory reaction. Flagellated — an organism, bacterial or proto- zoan, possessing slender whip-like processes. Fomite — inanimate object that may harbor disease organisms. Friable — easily pulverized or crumbled. Fungi — low order of vegetable organisms; some are capable of producing disease. Gross — as applied to tissue changes which can be seen with the naked eye. Hemorrhage — escape of blood from the vessels, bleeding. Immune — resistant to a particular disease. Immunity — condition of being immune. Infection — invasion of the tissues by pathogenic organisms resulting in a disease state. Infectious — as applied to disease, one produced by living organisms. As applied to living organisms, those which are capable of producing disease. Inflammation —— response of tissues to an injury or other irritant. “Itis” — suffix denoting an inflammatory state, such as enteritis — inflammation of the intestines, airsacculitis — inflammation of the air sacs. Lesion — visible change in size, shape, color or structure of an organ. 5'l Listless -— indifferent to surroundings. Microscopic — invisible to the naked eye, visible only by the aid of a microscope. Morbidity — incidence of disease in a flock, the percentage of diseased individuals in a population; percentage affected. Mortality — death rate. Necrosis — death of a circumscribed portion of tissue. Neoplasm — abnormal growth such as a tumor. Parasite — as used in this publication, an animal form that lives on or within a bird to the detriment of the bird. Parboiled — having a boiled or cooked appear- ance. Parenteral — as applied to drug or vaccine ad- ministration, to inject as subcutaneously, intramus- cularly. Pathogen — as app-lied to organisms, one capable of producing disease. Pathogenicity — disease-producing capability of a disease organism. Pathognomonic — as applied to symptoms and lesions, one which is specific or characteristic for a particular disease. Peracute — excessively acute, as. applied t0 dis- ease that has extremely sudden onset and a short, severe course. Petechial — as applied to hemorrhage, character- ized by small hemorrhagic spots. Polyvalent — as ap-plied to antigens and bac- terins; one made up of several strains of organisms. Predispose-to confer a tendency toward dis- ease. Protozoa — unicellular animal forms, some of which are parasitic. Rales — abnormal respiratory sound; rattling, wheezing. Rickettsial — a group of microorganisms inter- mediate between the bacteria and the viruses, som.e of which are pathogenic to man and animals. Rod — as applied to bacteria, a cylindrical shaped organism. Scrological test — test performed on the serum of an animal to determine if specific disease anti- bodies are present. Serotype — as applied to microbial organisms, a strain of microorganisms as determined by sero- logical methods. Sign — any objective or discernible evidence of disease; symptoms and lesions. Sporadic — as applied to disease outbreak, those occurring here and there; not widely diffused. Spore — as applied to bacteria and fungi, a re- 52 productive element capable of resisting unfavorable environmental conditions. Stress — factor tending to lower resistance of an animal to disease, such as chilling, moving, etc. Symptom — detectable signs of disease. Toxin — poison produced by microorganism. Tumor — neoplasm; a mass __‘Of new tissue which persists and grows independently of its surrounding structures, and which has no physiologic use. Vaccine — suspension of large amounts of disease organisms used to produce immunity in the animals I to which it is administered. , Virulence — as applied to a pathogenic micro- _. scopic organism, its ability to overcome the body ‘ defenses of the host. Virus — ultramicroscopic microorganisms; some capable of producing disease. TABLES OF WEIGHTS AND MEASURES Weights 1 gram (g) I 1000 milligrams (mg) 1 kilogram (kg) I 1000 grams 1 ounce (oz) I 28.35 grams 1 pound (lb) I 16 ounces I 0.4536 kilograms ‘a I 453.6 grams Liquid Measure 1 Liter (L) I 1000 milliliters (ml) I 33.81 ounces 1 gallon I 4 quarts I 8 pints I 231 cubic inches I 3.785 liters gallon of water I 8.34 pounds. teaspoon I 4.93 milliliters fluid ounce I 2 tablespoons cup I 8 fluid ounces I 16 tablespoons I 236.6 milliliters 1 pint I 2 cups I 16 fluid ounces I 473.2 milliliters )-4)_||—|p_4|_| Working Tables of Weights and Measures (Approximate Values) Parts per million (p.p.m.) l gram in 1 ton (2000 lb.) I 1 p.p.m. 1 pound in 500 tons I 1 p.p.m. 4 milligrams in 1 gallon of water I 1,p.p.m.i If feed is to be medicated at a level of 200 p.p.m., add the. medicant at the rate of 200 grams _ PCT [OIL - If water is to be medicated at a level equivalent ~ to a feed level of 200 p.p.m., add the medicant at, the rate of 400 milligrams per gallon. (Based on c water intake being 2 times that of feed.) Dilutions To make a 1-2000 dilution of a drug in drink- ing water, add 1 ounce of drug to 16 gallons of ‘ water. tablespoon I 3 teaspoons I 14.79 milliliters [Blank Page in Original Bulletin] [Blank Page in Original Bulletin] [Blank Page in Original Bulletin] Cooperative Extension ’Work in Agriculture a of Agriculture cooperating; Distributed in furth 10 M—12-71, Revised i ., n’ v‘ nd Home i Economics‘,- Texas A8cM University and the United’ States Depai‘ i P erance ‘of theActsof Congress ofwMayln 8, 1914, as amended, and June” 30, '