8-1031 rexnsnxmucaavznsnv W rsxns AGRICULTURAL? cxrzusmu sumo: - - mas AGRICULTURAL EXPERlMENIjflATwNj v College Station, Texas? [Blank Page in Original Bulletin] 1. 2. 3. 4. 5. 6. 7. A MANUAL OF POULTRY DISEASES (Errata Sheet) Page 6 - Paragraph 2, 2.b. (1.). Change !infection" to "injection". Page ll - Footnote. Insert "not" in the last phrase so as to read “......, but it is not primarily a respiratory disease". Page 35 - Paragraph 2. Insert "not" in sentence 3 so as to read "......, and not primary causative agents". Page 39 —- Paragraph 4, Sentence 3. Change "flood tinged" to "blood tinged". Page Ll - Paragraph 2, Sentence 2. Change "dimondi" to "simondi". Page 45 - Under Anti en, sentence 2. Change "antigen" to "antibody" so as to read "......, will stimulate antibody production". Page 46 - Under Rickettsial. Change "bacterin" to "bacteria" so as between bacteria and the viruses, .-~..." to read "...... ritten and Edited . i1? a Poultry Disease Bulletin Committee imprised of f‘ . R. BELL, Associate Professor of . i" eterinary Parasitology . I. FLOWERS, Professor of eterinary Microbiology . C. GRUMBLEs, Professor and Head, A epartment of Microbiology . F. MEINECKE, Assistant Professor {of Veterinary Microbiology M. PATTERSON, Extension Veterinarian C. WQRMELI, Extension Poultry Husbandman SC. F. HALL, Associate Professor of jsVeterinary Microbiology, Chairman ifTexas A8cM University R. R. BELL. D.V.M., Univ. of Georgia, 1952; M.S., Texas A8cM Univ., 1955. veterinary parasitology. Research and teaching A MANUAL OF POULTRY DISEASES A. I. FLOWERS. D.V.M., Texas A8¢M Univ., 1950; B.S., 1942; M.S., 1959. Research and teaching in poultry diseases; special interest, Salmonellosis, respiratory dis- eases and avian encephalamyelitis. L. C. GRUMBLES. D.V.M., Texas A8¢M Univ., 1945; M.S., 1957. Eighteen years of experience in poultry disease research and teaching. C. F. MEINECKE. D.V.M., Kansas. State Univ., 1952; M.S., Oklahoma State Univ., 1960. In charge of diag- nostic and pullorum testing laboratories. C. M. PATTERSON. D.V.M., Texas A8¢M Univ., 1947. Special field of interest, preventative veterinary medicine. B. C. WORMELI. M.S., Univ. of Wisconsin, 1933; B.S., 1929. Twenty-three years of experience in commercial poultry industry. Current major emphasis, poultry production. C. F. HALL. D.V.M., Kansas State Univ., 1951; M.S., Michigan State Univ., 1959; B.S., Kansas State Univ., 1949. Eleven years of experience in poultry disease research and teaching. Contents Section l — General Information Page Poultry Disease Principles... . . . . . . . . . . . . .. 5 Nature and Cause of Disease .............................................. .. 5 How Infectious Diseases Are Spread ................................ .. 6 Body Defense Against Disease ............................................ .. 6 Manifestations of Disease .................................................... .. 7 Hatchery and Breeder Flock Health Management ...... .. 7 Hatchery Management and Sanitation ............................ .. 8 Principles of Reasonable Drug Administration ................ .. 9 Drug Administration .. ......l0 Preventive Medication . . . . . . . . . . . . . . . . . . ..10 Treatment of Disease Outbreaks ....................................... ..10 Vaccination to Prevent Poultry Diseases ............................. ..10 What Vaccines Are .... .. .. l0 Dangers of Vaccination ......................................................... ..10 Vaccination N0 Substitute for Sanitation .................... .. ll Diseases for Which Vaccines Are Available .................. .. ll Administration of Vaccines ................................................ ..ll A Suggested Vaccination Program for Chickens .......... ..l2 Use of Other Vaccines in Chickens and Turkeys .......... ..l2 Using the Diagnostic Laboratory .......................................... ..l2 Laboratory Locations ............................................................. ..l2 Using the Laboratories. .... ..l2 What to Expect .. l3 Section 2 —Bacterial Diseases ....l4 Salmonella and Paracolon Infections ..................................... ..l4 Pullorum Disease l4 Fowl Typhoid ...... .. 16 Paratyphoid Infections... 17 Paracolon Infections ______ __ l9 Omphalitis .... .. l9 Fowl Cholera ....20 Erysipelas 21 Botulism 22 Section 3 —Respiratory Diseases ............................................... .23 Newcastle Disease 2% Infectious Bronchitis . 24 Laryngotracheitis 24 Ornithnsis 25 Quail Bronchitis , . 2s Chronic Respiratory Disease —Air-Sac Syndrome and Infectious Sinusitis .... .. 26 Infectious Coryza . . . . . . . . . . . . . . . . . . . . . . . .. 26 Section 4 — Viral Diseases Section 5 — Diseases of Undetermined Cause ......................... .. _ Infectious Hepatitis ................................................................... .. Hemorrhagic Anemia Syndrome ............................................. .. Section 6 — Protozoan Diseases ................................................... .. Trichomoniasis ....... .. g Hexamitiasis ................................................................................. .. p’ Leucocytozoonosis ........................................................................ .. I Section 7 — Parasitic Diseases ................................................. Poultry Lice ............................................................................. I The Head Louse .. The Body Louse ................................................................... y. The Shaft Lonse Section 8 — Appendix ........ .. Endemic (Localized) Fowl Cholera ..................................... Aspergillosis .................................................................................. .2 (Exclusive of Respiratory Diseases). .................. ..‘ Avian Pox .................................... .................................... .. Avian Lymphomatosis ............................................................... .. Infectious Synovitis .................................................................... .. I Epidemic Tremor .................................................................... .. y Bluecomb Disease ..................................................................... j Hemorrhagic Enteritis ............................................................... .. Aortic Rupture . . . . . . . . . . . . . . . .. Cage Fatigue .......................................... .. Fatty Liver Syndrome ............................................................... .. Coccidiosis ..................................................................................... .. Blackhead ...................................................................................... .. I Other Kinds of Chicken I ice Poultry Mites Common Chicken Mite ....... .. Feather Mite Scaly-Leg Mite Depluming Mite Fowl Tick or Blue Bug Chiggers, Red Bugs or Harvest Mites ................................... .. Large Roundworms Cecal Worms Tapeworm s Glossary of Terms A Tables of Weights and Measures SECTION 'l. p, POULTRY INDUSTRY is the third largest farm l‘ rise in the United States. In Texas poultry eggs rank fourth as a source of farm income. * annual Texas gross value to the farm is about j million dollars. The production of poultry F eggs is highly commercialized, intensified and y tes as large units. Profit per bird is governed by fixed and variable gors. Variable factors usually determine the ess or failure of an operation. A primary cost 'able in poultry production is the disease level ithe flock. Healthy birds are a requisite for . it. Losses due to disease originate in many ways. w are obvious, such as death, medication costs _ condemnations. Others are sometimes less 'ous, such as poor growth or rate of lay, poor W conversion and down grading. This manual attempts to provide the profes- 1 l Texas poultryman with a basic understand- Yof how infectious disease processes are estab- , ways to prevent the introduction of diseases, = cteristics of more common infectious diseases Sign and specific treatment or control of 8S. _ POULTRY D|$EA$E PR|NC|PLE$ re and Cause of Disease isease is an alteration in the state of the body y of the body organs which interrupts or rbs the body's proper functions. Such dis- nces often are recognized by detectable altera- . of body functions. tiology is the study of disease causes. A disease often results from a combination of two or causes: (1) the indirect or predisposing grs which may lower the bird's resistance and the direct or determining factors which pro- ‘ the actual disease state. V‘ edisposing causes of disease are referred to ently as “stress” factors. Stress factors may illing, poor ventilation, overcrowding, inade- '__' feeder and waterer space, over medication others. Disease itself may predispose another For example, an outbreak of infectious . itis may predispose “air sac” infection. irect causes of disease are: 1. Bacteria 2. Viruses 3. Parasites GENERAL INFORMATION Fungi Nutritional deficiencies 9”?!‘ Chemical poisons 7. Unknown causes Infectious diseases are the most important poultry diseases. They are caused by bacteria, viruses, rickettsia and fungi. Some protozoan dis- eases, such as coccidiosis and blackhead, behave much as infectious diseases and they are considered here with infectious disease. More correctly, they should be classed with the other parasitic illnesses. When living agents, such as bacteria, enter the body, multiply and cause a disturbance of normal function, infection has occurred. Disease is caused by the chemical toxins (poisons) produced by in- vading organisms. At one time some scientists believed that microorganisms caused disease by mechanical obstruction 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 host is known as its virulence or pathogenicity. 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 species. For example, infectious bronchitis virus will cause disease only in the chicken, but not turkeys. Other organisms affect a large number of species. For example, some of the Salmonella organisms affect a large variety of species ranging from and including reptiles, rodents, domestic animals, 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 frequent ways infectious diseases are introduced into poultry flocks are: 1. Contact with a diseased individual. 2. Contact with a healthy bird that has re- covered, but still is a carrier. 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 mosquitoes. Shoes and clothing of man, who moves from flock to flock. 9. Feed or contaminated feed bags. l0. Contaminated premises through soil, old litter. ll. Airborne — organisms do not spread far through the air. This source of infection is probably not as important as was once believed. 12. Egg transmissiom-a number of diseases such as pullorum and fowl typhoid are egg trans- mitted. Body Defenses Against Disease The body has a well-developed defense mecha- nism 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 interchangeably with immunity. An animal has two types of protective mecha- nisms: (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 p. on some mucous membranes) which, with wave-like _ action, move foreign material out of such structures ‘ as the trachea (wind pipe). Mechanisms which combat agents that invade the body include the white blood cells and circu- e lating antibodies. Immunity or resistance is outlined as follows: 1. Innate or inherited Z» a. Species I b. Racial (strain or breed) c. Individual 2. Acquired a. Active ( (1.) Resulting from having the disease (2.) Stimulated by vaccination with ‘I dead or living disease agents b. Passive (1.) Infection of antiserum _ a (2.) Transferred from dam to offspring Inherited resistance may be complete or partial; T» for example, turkeys are not susceptible to laryngo- 1; tracheitis. And while chickens are more resistant g than turkeys to blackhe-ad, they may become in- fected under certain conditions. Inherited resist- ance or susceptibility to the fowl leucosis complex is well established, but no completely resistant breed or strain of chickens has been developed. 1 Individual resistance is apparent in practically .1 every disease outbreak in a poultry flock. Some birds, although exposed to the same chances for ‘a infection, fail to develop evidence of the disease. j While inherited immunity is important, ac- f quired immunity is a more controllable reaction i’, that can be used intentionally by the poultrymanfi Acquired immunity is the reaction we hope to stimulate by application of all vaccines. The purpose of vaccines is to stimulate an active pro- duction of antibodies by safe means. Active im- munity depends upon the production of antibodies 5 within the body of each individual. Antibodies . are proteins associated with the globulin fraction’, of the blood serum. Antibody production is not . understood completely, but it is apparently pr0- \ duced by various organs such as the liver, spleen and bone marrow. In general, antibodies are- specific for the organism which stimulated their f production; thus, immunity to one disease ordi- * narily does not imply resistance to others. A I Passive immunity is the transfer of antibodies f from the individual in which they are produced - to another individual. This is done by the injec- a tion of serum from an immunized individual. 1 Antibodies also are transferred from the dam to it offspring through the egg; thus, he-ns that have i’ had Newcastle disease transfer antibodies through “I the yolk to their chicks. Such passive immunity § is an important consideration in vaccination pro- ; grams. Passive immunity is of short duration and i there is usually a marked decline in the antibody level within 21 to 30 days. Passive protection against infection usually lasts no longer than 4 to A~ 6 weeks. l’ Manifestations of Disease The detectable signs of disease are known as » symptoms. Visible changes in the size, color, shape ‘ or structure of an organ are known as lesions. Loss i of body weight, decreased egg production, reduced ' feed consumption, droopiness and lameness are k some symptoms. An enlarged liver, tumor on the , intestine, abscess in a lung or collection of exudate 1 in an air sac are examples of lesions. p Many symptoms are general; they usually are ‘l seen in any diseased individual. Examples are i droopiness, ruffled feathers, diarrhea and loss of appetite. Other symptoms are specific; they are f seen only when certain diseases are present. f Examples of such symptoms are the tremors associ- . ated with avian encephalomyelitis (epidemic ‘ tremors) and the flaccid paralysis associated with botulism. a Lesions like-wise may be of general or specific ' . l nature. For example, enteritis is associated with many diseases, but the “grey eye" of ocular leucosis » . is specific. f‘ Hatchery and Breeder Flock Health Management v Sanitation is a much used, but poorly defined T word. The usual implication is that sanitation is i a universally understood practice that may be _ applied to prevent all diseases. This concept often " leads to misunderstanding and disappointment. . Good sanitation in relation to one disease actually may provide favorable conditions for developing . other diseases. Although many good sanitation . measures always should be applied, others must be _ based on the nature of specific diseases. The [jimbiguity surrounding the term “sanitation” can ;be avoided by using a term “management and ‘sanitation for disease prevention.” This phrase ; then would be defined as all practices, specific and nonspecific, that the poultryman applies to prevent disease or reduce severity and economic loss from diseases. q A standard disease prevention program that can apply on all poultry farms does not exist. But there are some basic principles that always should be observed. Some practices that aid in disease prevention are: 1. Select a well-known, reliable source from which to purchase chicks, poults or hatching eggs- one that can supply healthy stock, inherently vigor- ous and developed for a specific purpose. 2. Purchase only day-old chicks or hatching eggs. Some require frequent access to replacement birds, thus making it difficult for each individual to grow all of hisreplacements. If it is necessary to purchase started birds, select the best possible source. 3. Keep birds separate according to source and age groups. To mix birds is an invitation to trouble. 4. Change litter and thoroughly clean and dis- infect the house and equipment between each group of birds. While litter selection and manage- ment is a large subject, applying this recommenda- tion as a general practice will prevent many disease and parasite problems. 5. Keep chickens and turkeys separate. Prefer- ably, only chickens or only turkeys should be kept on the same premises. 6. Maintain hatchery supply flocks on separate premises from other birds. 7. Select a reliable commercial feed, or, if farm mixing is done, mix carefully according to a de- pendable formula. 8. Provide an adequate supply of safe water. Avoid watering from surface tanks, streams or ponds. 9. 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. For example, in some areas it is necessary to vaccinate against laryngotracheitis, while in other areas such vaccination actually leads to a disease problem. l0. Discourage persons other than the care- taker or essential personnel from visiting the poultry house or yard. ll. If a disease problem develops, obtain an early, reliable diagnosis and apply the best treat- ment, control and eradication measures for that specific disease. l2. Dispose of all dead birds by burning, deep burying or preferable by a disposal pit. This phase of management often is overlooked. l3. 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. Hatchery Management and Sanitation The information contained in this section has been adapted from recommended procedures of the National Poultry Improvement Plan and National Turkey Improvement Plan. Hatching egg sanitation. Collect hatching eggs from nests at frequent intervals and observe the following practices: 1. Use cleaned and disinfected containers in collecting the eggs and take precautions t0 prevent contamination from organisms that may be on hands or clothing of the person making the col- lections. 2. 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. 3. As soon as possible after collection, fumi- gate the visibly clean eggs as described under the subheading on fumigation. 4. 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. 5. 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 separate rooms, with separate ventilation, are pro- vided for each of the four operations; egg receiving, incubation and hatching, chick holding and dis- posal of offal and cleaning of trays. Place these rooms under isolation so that admission is granted only 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 used 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. j ' Fumigate all eggs set prior to setting or within ;A 12 hours after they are placed in the incubator. I Also fumigate them after transfer to the hatching ‘j compartment. 5. Use only new or clean fumigated egg cases _ for transportation of hatching eggs. Destroy soiled Y; egg case fillers. 6. Distribute day-old chicks, poults or other newly hatched poultry in clean, new boxes. Clean 5 and disinfect all crates and vehicles used for trans-a porting started or adult birds after each use. {'1 Cleaning and disinfecting. l. In poultry houses and hatchery rooms, clean- * ing and disinfecting include these steps: a. Settle dust by spraying lightly with the . disinfectant to be used. b. Remove all litter and droppings to an » isolated area where there is no oppor- . tunity for dissemination of any infec- tious disease organisms that may be PFCSCIIII. c. Scrub the walls, floors and equipment with a hot soapy water solution. Rinse * [O TBIIIOVC 8021p. d. Spray with a cresylic disinfectant, such ‘ as liquor cresolis saponatus, 4 ounces to - a gallon of water, or sodium ortho- 1 phenylphenate, 11/5 ounces (1 heaping _ tablespoonful) to a gallon of hot water. ~- 2. In the hatchers, cleaning and disinfecting "r includes the following procedures: a. Remove trays and all controls and fans 1 for separate cleaning. Thoroughly wet g the ceiling, walls and floors with a I stream of water, then scrub with a hard bristle brush. Rinse until there are no g deposits on the walls, particularly near ‘; the fan opening. b. Replace cleaned fans and controls. Re- i; place trays, preferably still wet from cleaning, and bring the incubator up to I normal operating temperature. c. Before placing eggs in the hatcher, it _ should be fumigated. d. If eggs are hatched in the same machine j ‘ as they are incubated, clean the entire I machine after each hatch. Use a vacuum Y . cleaner to remove chick down from the Y egg trays. F umigation. Fumigation of eggs and incubators is an essential part of a hatchery sanitation pro- g gram. fl. Preincubation fumigation of eggs should be vie 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, and expose to circulating formaldehyde gas. ‘A c. Formaldehyde gas is provided by mixing 0.6 grams of potassium permanganate with 1.2 cc of formalin (37.5%) for each cubic foot of space in the room. Mix ingredients in an earthenware or enamelware container having a capacity of at least ten times the volume of the total ingredients. 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 tting should be fumigated as soon as possible , qwing procedure: a. Determine the size of the incubator by multiplying the length times the width times the height. b. After setting the eggs and allowing temperature and humidity to regain normal operating levels, release forrnal- dehyde gas into the incubator. c. For each cubic foot of space in the incu- bator use 0.4 grams of potassium per- manganate and 0.8 cc of formalin (37.5%). Use a container having a capacity of at least ten times the volume of the total ingredients. d. Close vents and doors but keep circu- lating fan operating and continue fumi- gation for 20 minutes with normal operating temperature and humidity. e. After 20 minutes of fumigation open vents to the normal operating positions to release," the gas. .3. Eggs not fumigated as described in para- ‘h l or in paragraph 2 of this section should fumigated after the 96th hour of incubation. ow the procedure described in paragraph 2 of , no later than 12 hours after setting using the a this section. Single or repeated fumigation of eggs in the setter may be practiced, but the fumigation schedule should be such that no eggs are fumigated during the period from the 24th to the 96th 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 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. Other drugs, such as the antibiotics and NF 180* are included in many rations “just in case they might help prevent some potential disease.” Antibiotics sometimes are recommended at times of “stress” such as moving, vaccination or debeaking. WVhile the use of any drug on such a nonspecific 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 appli- cation of known effective treatments for specific diseases. Such treatments must be based on a reliable diagnosis. Recommendations for the treat- ing of poultry diseases are changing constantly as new, more effective 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 follow the manufacturer’s recommendations. ‘Trade name of a product which contains 50 grams of furazolidone per pound. 9 Drug Administration Drugs may be administered to poultry in several ways. The choice of method depends upon a number of factors including: (1) the disease in question; (2) the drug to be used; (3) available labor and administration equipment; (4) the con- dition of birds; and (5) the length of medication period. The following tableshows commonly employed methods of drug administration: l. 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. Preventive Medication It is doubtful that there is 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 allows drug resistant strains of bacteria to develop. “(hen 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 10 diagnosis extremely difficult. Frequently, it is im-. possible to isolate causative organisms by laboratory- 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 birdf losses. For example, an outbreak of erysipelas in‘ turkeys does not respond to the usual treatments: employed for fowl typhoid or fowl cholera. Mi diagnosis results in drug expense and a continue ; loss due to mortality. Hemorrhagic anemia syn-i drome of chickens is confused easily with coccidi-i osis. If a flock affected with the former condition, is treated for coccidiosis, the existing problem is; aggravated and severe losses may occur. i Once an accurate diagnosis has been established, j follow strictly the prescribed recommendations for treatment. Many drugs produce toxic effects if used improperly. * VACCINATION TO PREVENT POULTRY DISEASES What Vaccines Are i Vaccines are suspensions of large amounts of‘ _ the disease 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 the virus in: embryonated chicken eggs. Fluids and tissues from»? the infected embryos contain large amounts of virus and are collected to make the commercially avail-i able vaccines. 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 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- munity than dead ones; however, the dangers‘ associated with vaccination are greater. " Dangers of Vaccination . Most vaccines contain living virus intended to produce a mild infection. In other words, vaccines. make the birds sick. The sickness will be mild if: 1. Birds are healthy at the time of vaccination i, 2. Chicken house or brooder house is cle 4 and dry. 3. There are no sudden climate changes. _ i L. l 4. Birds are at the proper age for vaccination. 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, vaccine virus may spread to unprotected birds on the same premise. This will cause adverse effects, particularly in unprotected laying flocks. Seek expert assistance when it appears desirable to initiate a vaccination program on property where unprotected layers are present. The wing-web type of Newcastle vaccine, infectious bronchitis vaccine, fowl pox vaccine and infectious laryngotracheitis vaccines may spread from flock to flock on the same farm. Vaccination No Substitute for Sanitation A sound vaccination program is part of a good management and sanitation program and not a substitute for it. It is unnecessary to vaccinate against certain diseases in some parts of the country and in some areas within a particular state. Tailor vaccination programs to meet the needs of a particular opera- tion in a particular area. For example, it is not recommended that Texas poultrymen use laryngo- tra.cheitis vaccine since the disease is not a current problem. Individual premise or area experience also governs the efficient use of such products as erysipelas or fowl cholera bacterin. Diseases for Which Vaccines Are Available Most products now on the market are for the control of virus infections, particularly the virus respiratory infection. These diseases are: l. Newcastle disease 2. Infectious bronchitis 3. Infectious laryngotracheitis 4. Fowl poxi" In addition, experimental vaccines are under- going extensive testing for the control of avian envfiephalomyelitis (epidemic tremors). Bacterins are; available commercially for the control of: 1. Erysipelas g 2. Fowl cholera-I. ' A “so-called” vaccine to control coccidiosis has received much publicity in recent years. The use ‘Fowl pox may cause symptoms and lesions of the respiratory system, but it is primarily a respiratory disfiéiql of the product presently is not encouraged in" Texas. Administration of Vaccines Vaccines must be used properly if they are to be effective. For best results: ' I. Store vaccines in the refrigerator according to manufacturer’s recommendations. 2. Do not use out-dated vaccines. 3. After a vial of vaccine has been opened, destroy by burning any remaining contents after use. D0 not set back for use at a later date. 4. Administer in accordance with manufac- turer’s instructions. Vaccines, as drugs, may be applied in different ways, depending on the pro-duct used, age of the birds and other factors. In general, Newcastle and infectious bronchitis vaccines are adapted to mass methods of administration, whereas fowl pox, infectious laryngotracheitis, erysipelas and fowl cholera vaccines are adapted for individual bird administration. l. Mass. methods: a. Drinking water-Newcastle, infectious bronchitis. b. Dust —- Newcastle, infectious bronchitis. c. Spray — Newcastle, infectious bronchitis. 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 and fowl pox. Vaccines frequently are combined to reduce labor and number of immunization procedures re- quired. Newcastle disease vaccine often is com- bined with that of infectious bronchitis. While the use of such combination products may have merit in some cases, their routine use is not recom- mended. There are two good reasons why: 1. Evidence exists thatthe host response to one virus fraction may interfere with the develop- ment of adequate immunityqto the other. 2. It is impossible to evaluate the vaccine reaction. (Is the reaction due to one or both fractions in the vaccine?) After live virus vaccination, birds must be observed for "takes" to the vaccination. A discus- 1.1 sion of this is included in the individual disease sections. A Suggested Vaccination Program for Chickens Following is an outline of one vaccination pro- gram that will produce good results in Texas. As previously suggested, individual farm situations will call for varied procedures to meet individual needs. l. Chicks for Market Eggs or Hatching Egg Flock Replacement. a. Vaccinate for Newcastle at 7 days and 4 weeks of age with intranasal New- castle 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 begin production. 2. Chicks for Broiler Production a. Vaccinate against Newcastle at 4 days and 4 weeks of age using intranasal vaccine by the drinking water method. b. At 2 weeks of age, vaccinate against infectious 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 satis- factory 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. A Vaccination of turkey flocks for Newcastle disease, fowl pox», erysipelas and fowl cholera is discussed under individual disease headings. Usually the decision to vaccinate, except for pox, should be made on the basis of area experience and expert advice. USING THE DIAGNOSTIC LABORATORY The Texas Agricultural Experiment Station, under the direction of the School of Veterinary 12 Medicine of Texas A8cM University, operates Poultry Disease Investigation Laboratories at Col- 7 lege Station, Center, Gonzales and Stephenville. These laboratories serve several functions: l. To serve as diagnostic and information centers where Texas Poultrymen can obtain assist- if ance with their poultry disease problems. 2. To accumulate information relative to the p incidence and importance of the various poultry ‘ diseases in the state. 3. To help formulate and carry out poultryfi disease research projects which reflect the needs i of the Texas poultry industry. Laboratory Locations Locations of the Poultry Disease Investigation Laboratories are: 1. College Station, Room 101, Veterinary Medi- v cine Building, Texas A8cM University, Telephone i 846-5781. 2. Center. Fairgrounds. Telephone LY 8-4451. 3. Gonzales. Texas Agricultural Experiment i Station, Substation 21, 9 miles southwest of Gon- Y ‘ zales, off State Highway 97. Telephone 437-3621. 4. Stephenville. On the corner of the College I Poultry Farm across the street from the Tarleton State Campus. Telephone WO 5-5749. Laboratories are open from 8 a.m. to noon and l p.m. to 5 p.m. Monday through Friday, college“ holidays excluded. Make prior arrangements t0 _ assure service at other times. In addition to the laboratories listed, there "are some practicing veterinarians who are well quali- 2 fied by training and interest to assist with poultry ‘ disease problems. Using the Laboratories Disease prevention is the best approach to Utilize laboratory personnel to y assist in developing disease prevention programs 5- and not solely as “firemen” to help when disease; disease control. appears. When a disease problem develops, howevenget; help immediately rather than calling the laboraQ tories as a last resort. If emergency treatment y. necessary, remove a sample of birds for diagnostic purposes before treatment begins. e The selection of a sample of birds for the? laboratory should not be a culling operation. Birds submitted should be representative of their condition thought to be the flock problem. Submit; Adjacent to the Shelby County three or four birds, or more if young chicks or poults. When birds are dying rapidly with a few preliminary symptoms, bring in several dead birds with the sample. Diagnosis often is difficult if birds are submitted without adequate information. The following out- line includes information which should be routinely available: Owner Address Phone No. _ Number in flock Breed Age Hatchery source Type of operation (Floor, cage, range, etc.) Feeding program Vaccination history Illness first seen Morbidity (No. affected) Evidence of illness Mortality Medication Remarks (other flocks on farm, previous problems, etc.) Wfnat to Expect i When the pathologist is able to diagnose the cause of trouble without the necessity of time- consuming tests, recommendations will be made directly to the individual submitting the birds. In other instances, only a tentative diagnosis can be established when birds are submitted. In this case, preliminary recommendations, pending final diagnosis, may be made, depending upon the particular 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. Bacteria are microscopic living organisms gen- erally considered as belonging to the plant king- dom, although they may possess certain character- istics such as motility, common to members of the animal kingdom. Usually they are grouped accord- ing to spherical forms, straight rods, curved or spiral rods and filamentous fonns. Growth require- ments of different species vary considerably, but most can be grown on artificial media. Bacteria, like other living organisms, have certain require- ments as to environmental temperature, moisture and nutrition for propagation. Nutritive require- ments are satisfied by absorption through a thin permeable cell membrane, but moisture is necessary before such processes can occur. The growth re- quirements of the species dictate the environment in which it may be encountered; soil, water or animal tissues. Not all bacteria are detrimental to animal health. In fact, most bacteria are necessary for such processes as food digestion. Classification of bacteria into species so that disease-producing organisms may be separated from those that are harmless or beneficial is. based on such laboratory techniques as staining of organisms for microscopic examination, determination of fermentation re- actions in various liquid media, serological 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. Antibiotics in disease control create an environ- ment unfavorable to multiplication of the species being attacked. Most antibiotics are selective in action, effective only against certain species or possibly types of organisms, and then only while present in the blood and tissues at sufficient levels. In the latter respect, antibiotics are very different from vaccines. Control of disease by vaccination is completely different than control through anti- biotics and consequently, using antibiotics for pre- vention of disease is unsound basically. '_ iSiALMONELLAiAND PlAkAClOlON nurecrlous “More than 800 different species or serotypes of organisms belong to the genus Salmonella, all of which are potential pathogens of poultry. Systemic effects usually are observed when infection occurs, but since the digestive system is affected primarily, they often are- referred to as e-nteric organisms. 14 BACTERIAL DISEASES The same is true of the group of organisms referred’ to as Paracolons. Because of similarities produced by infections by these groups of organisms, th - are grouped under one heading. Both groups are-I world-wide 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 f0 ' i; may be infected. Etiology: Salmonella pullorum-first isolated"? by Rettger in 1900. 1 Transmission: Primarily egg-transmitted but; transmission may occur by other means. i 1. Infected hen —- egg — infected chick — spread in incubator — in chick boxes — in brooder: house and on range — survivors become infectedf breeder birds. I 2. Mechanical transmission (carried about on. shoes, equipment). ; 3. Carrier birds (apparently healthy bi ~ y’ which shed organisms). 4. Contaminated premises (from previous out-f breaks). i Portal of entry may be the respiratory (as i incubator) or digestive system. ~ Most outbreaks of acute pullorum disease e2 chicks or poults result from infection while in hatchery. i Incubation period: 5 to 7 days. Symptoms: Pullorum disease is highly fatal y young chicks or poults but mature birds are mo resistant. Young birds may die so soon after hat ing that no symptoms are observed. Most acu if outbreaks occur in birds under 3 weeks of where mortality may approach 90 percent if ti. treated. Survivors usually are stunted or u‘ thrifty. ~ ‘TSO P" E40 "' 3 3O '- E E 2O - 310 —' cu O- 0 I l l l I 2 3 4 5 Ageinweeks Figure 1. i Typical mortality curve in young biri A Typical symptoms in chicks 0r poults: (not constant) Droopiness. Ruffled feathers. A‘ Chilled appearance, huddled around source of y jheat. i White diarrhea and pasted down around vent. Labored breathing. a Symptoms in adults: usually no recognizable isymptoms. I Lesions: Young birds dying during an acute outbreak may present no recognizable gross lesions. i_Representative lesions in young birds include: _ Necrotic foci in liver—varying from pin point _’ to pea size. White nodular areas in muscle of heart and lpgizzard; occasionally in wall of intestine. Multiple small, firm, nodular areas in lungs. Yellow or cream-colored cecal cores or plugs. Lesions in adults: Gross lesions may be lacking. “Blighted” ova may be present. Livers may contain areas of necrosis. Oviducts may contain cheesy deposits. Diagnosis: p. Blood testing may indicate presence of the _f disease. I May be suspected from history, symptoms and _ lCSlOIlS. \ 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 hatching purposes. . The National Poultry Im.provement Plan 1 (IQIPIP) and the National Turkey Improvement ;”Blan (NTIP) are national organizations formed i primarily for eradicating pullorum disease. These _ organizations began in 1935 and since then the i disease virtually has been eliminated from areas ‘wherein most hatcheries participate in the plan. i. In other areas, the‘ disease appears to be gaining ground. These organizations are helped and co- j ordinated by the Agricultural Research Service (ARS) and each state has a local organization with i‘ state supervisors to administer the plan. Serologic tests: All tests for pullorum disease are agglutination tests; however, the three pro- cedures accepted as official testing methods are: 1. 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 iden- tical 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, incubated at 37.5 degrees C. for 24 hours prior to reading and is performed in NPIP approved laboratories. The tube test is considered more reliable than 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 rapid plate whole blood 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 there is a high percentage (over l0 per- cent) of reactors, it generally is advisable to dispose of the flock rather than try to dispose of reactors and establish a negative test. 2. If an isolation and identification of the organism has been made from a flock, consider the whole flock infected and do not keep it as a breeder flock. It may be held as a commercial egg flock if circumstances warrant and no breeder flocks are maintained on the premises, but it will serve as a potential source of infection to the other breeder flocks in the area. " ‘ ‘ 3. After disposing of infected birds, thoroughly clean and disinfect the house and equipment. A 3 percent water solution of cresol (Liquor Cresolis Compositus) is excellent for such purposes. Incubator fumigation procedures: Follow procedures outlined in Section l. 15 Why “breaks” occur in a previously “clean” flock: l. Introduction 0f the infection since last test. 2. Infection with a “variant” strain of the organisms. Antigenic structure is the only differ- ence between variant and standard strains of the organism. Differences are shown by the following illustration of antigenic composition: Standard 1X, X11 (1) 2 Variant 1X, X11 1 (2) 3 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 best drug in treating infected flocks is furazolidone, marketed under the trade name of NF-180 by Hess and Clark (Furoxone by Eaton Laboratories). The recommended level is 2 pounds NF-180 (100 grams furazolidone) per ton of feed for 10 days to 2 weeks or until mortality stops. In severe cases the drug level may be increased to 4 pounds 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 m.ost domestic and wild fowl including chickens, turkeys, ducks, pigeons and pheasants, but 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: Variable but usually 4 to 5 days. 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 low. 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 l2 weeks of age). Mortality rates: Variable, ranging from less than 1 to 40 percent or higher, especially if treat- ment is not instituted promptly. Symptoms: Symptoms may be suggestive of fowl typhoid but they are not specific. 16 ‘Some typical symptoms include: Sudden or sporadic mortality. Listlessness. Green or yellow diarrhea with pasting of th vent feathers. l Loss of appetite. Increased thirst. Pale, anemic appearance of comb and wattl Lesions: In addition to the symptoms t; tioned, certain lesions observed at necropsy ', help substantiate a diagnosis of fowl typho' These include: _ Enlargement of the spleen which may r1 mottled. l’ Liver usually considerably enlarged and varyi if in color from yellow to greenish brown, often wi - visible necrotic foci. " Small pin-point hemorrhages in the muscles a fat, particularly that surro-unding the organs. A slimy type inflammation of the anterior of the small intestine. In turkeys, the presence of small, white plaqul like areas visible through the walls of the intesti l is very suggestive of fowl typhoid. 3 Diagnosis: A tentative diagnosis usually n ~ be made from consideration of the history, s u a toms and lesions. Final diagnosis must be on isolation and identification of the causati. organism since other diseases often will clos resemble fowl typhoid. l Serology: Blood tests used for detection f pullorum reactors also are used in control of ff typhoid. Both organisms bear such close anti - t» relationship that one test will suffice for both. the test is suggestive rather than conclusive. A Prevention and control: Vaccination- bacterins presently available ~ of little or no value and may cause the flock react to the pullorum test for approximately days after vaccination. " Prevention and control depends upon: Hatching from disease-free flocks as establis by the pullorum test. a Strict sanitation on the farm. A clean, safe water supply. (Avoid wat from ponds or surface tanks.) Use of an incinerator or disposal pit for disp ‘ of all dead birds. (The causative organism may live for at "-1 6 months under certain conditions. Following)‘ 7 I sembling typhoid. outbreak, thoroughly clean houses and equipment, practice range rotation and other special precau- tions to prevent a carry over of infection to the next flock.) 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 is not recom- mended. Treatment: Furazolidone (NF-180, Hess and Clark) is the choice drug and levels of 100 grams per ton of feed for l0 to l4 days usually will stop mortality. In view of recent experimental results indicating that some strains of fowl typhoid organ- isms 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 controlled the furazolidone level may be de- creased 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 30 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 through water while waiting for feed containing the furazolidone. It also may be used for treating flocks which do not respond favorably to furazolidone. The commercial liquid preparation contains 3.44 percent sulfaquinoxaline. For the first 2 days, mix the drug in the drinking water at the rate of 3 tablespoonsful (or 11/2 ounces) per gallon, giving a concentration of l:2500. Then reduce to 2 table- spoonsful (1 ounce) per gallon, making a concen- tration of lz4000. Give the lower level until mortality is controlled. Purutyphoid Infections The term “paratyphoid” was used first to desig- nate a group of human, feverish conditions re- Literally, the term means resembling typhoid fever of the typhoid bacterium. Related to poultry, paratyphoid is a term denoting- the disease produced by any of the many Salmo- nella species except S. pullorum and S. gallinarum. Infection may result in acute or chronic disease. Acute clinical disease occurs more often in young bfrds and rarely in adults. Over 600 species or serotypes of Salmonella organisms are recognized with most birds, reptiles and mammals serving as host to one or more species. Economically the disease is of greatestffconcern to the turkey industry. History: Moore, in 1895, recorded the first authentic case of paratyphoid when he isolated and identfied a Salmonella from pigeons with an enter- itis. Moore referred to this organism as a member of the hog-cholera group. The first report of para- typhoid infections occurring in turkey poults in the United States was that of Rettger et al. in 1933, although Pomeroy and Fenstermacher observed the infection in turkeys in Minnesota in 1932 according to a report published in 1939. Paratyphoid infec- tion in disease outbreaks in man, many species of fowls and various species of domestic animals has been well substantiated. Etiology: The organisms of this group are sero- logically related and are Gramnegative, nonspore forming, flagellated, motile rods. They can be separated from S. pullorum and S. gallinarum by morphology and biochemical characteristics, but one paratyphoid organism cannot be differentiated from another member of the group except by serologic methods. Pathogenicity: Most acute paratyphoid infec- tions occur in birds less than 4 weeks old, except in pigeons and canaries in which acute disease and high mortality may occur in any age group. Mortality in young turkey poults usually varies from less than 1 percent to l0 or 20 percent, although rarely it may exceed 8O percent. Most death losses in young birds occur during the first 2 weeks after hatching, the mortality curve closely resembling that of pullorum disease. Outbreaks in ducks (“keel disease”) often result in staggering losses. Severity of infection with each of the various serotypes has not been determined. There is a tendency to consider S. typhimurium as a type species representative of the whole group and as the most important cause of paratyphoid in poultry. This species commonly is isolated from birds in- volved in paratyphoid outbreaks in the Midwest and North Central area, but until recently it rarely has been a problem in the Southwest. Results of research to date indicate that all Salmonella species must be considered as potential pathogens in poultry with outbreak severity de- pending upon age and species of host, serotype or species of Salmonella involved and certain environ- mental or management factors. Host distribution: The host range of the Salmonella species probably is as great as that of any pathogenic organism. It includes most do- mestic animals, birds, rodents, snakes, lizards and man. The greatest reservoir of Salmonella is prob- ably poultry and these 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 others. Because of the multiplicity of hosts and wide distribution 17 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 egg shell 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 subse- quent 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 New York, Minnesota, Iowa, Texas and others have reported recovering one or more species from 20 to 30 per- cent of the samples from certain materials such as animal byproducts 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 in- volved and method of transmission, but in general, the symptoms resemble those associated with pul- lorum disease. Some characteristic symptoms in- clude: Huddling around the source of heat with low- ered head, eyes closed and wings drooping. Increased thirst with decreased food consump- tion. Watery diarrhea and pasting of feathers around the vent. Increase-d “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. In acute outbreaks gross lesions may be absent in young birds. Characteristic lesions in young birds may in- clude: 18 Emaciation and dehydration. Unabsorbed or coagulated yolks. Con.gested livers, sometimes with hemorrhagic. streaks and/or pin-point white foci of necrotic tissue. ‘ Inflammation of the intestine, especially the; upper portion. i f » Cores in the ceca having creamy or yellow color. Acute infections in adult birds usually produce‘ few if any lesions other than an enteritis. Carriers and chronically infected adults usually have n0 specific lesions. Diagnosis: The disease may be suspected from flock history, symptoms and necropsy lesions, bu é» a definite diagnosis depends upon successful isola‘ tion and identification of the organisms by qual"f fied laboratory personnel. 7 Prevention and control: This is difficult be- cause of the wide range of hosts harboring orgaf isms and because no single species or serotype the organism is suitable as an antigen for detectin all other species in the testing program. S. typh murium is used commonly as a representative f» the group in attempting to standardize testi pi procedures. The pullorum-typhoid test often ' detect infected flocks even when the typhimuri - i antigen fails. Because of the many sources of 5 fection, known clean flocks may become infec at any time subsequent to the last test. i‘ An organized effort to control and eradi w paratyphoid exists in many states. Some hatcheri in other states reject eggs from flocks which ha not been tested with the S. typhimurium antif Although no control program is included in p National Poultry or National Turkey Impro ment Plans, Texas now has a voluntary test? program which may be used by producers shippi’ eggs to such hatcheries. Such control efforts J not the final answer to this problem, but t should be encouraged and additional informati utilized as it becomes available. The possib' g of contamination by organisms in feeds is now l important area in research and control pr Pending additional information, hatchery 4f flock sanitation management practices are the m, important factors in paratyphoid prevention . control. Some known to aid in paratyphoid trol include: : Do not use flocks known to be infected source of hatching eggs. Follow hatchery and egg sanitation pra ' that reduce chances of introducing infection the incubator through fecal contamination. i ' Early fumigation of eggs with formaldehyde gas v fore incubation or within 24 to 48 hours after eggs ‘are placed in the incubator). "Rodent control. 4 Isolation from other sources of infection such pigeons, ducks and others. I Serological testing of hatchery supply flocks and u lowing outlined requirements of voluntary state rograms. ' Treatment: Proper use of drugs may reduce ‘qortality in acute outbreaks of paratyphoid. The oice drug is furazolidone (NF-180), but some is» cies or serotypes are more resistant to treatment an the pullorum or fowl typhoid organisms. it paratyphoids have or will develop resistance the effects of furazolidone in time. i_ The recommended level of furazolidone for , u atment is 2 pounds NF-l80 (100 grams fura- g_ lidone) per ton of a complete ration as the only itrce of feed. Continue treatment for 2 weeks "until mortality is controlled. y Continuous use of furazolidone at a rate of 5O “hams per ton of feed is included frequently as a j- ophylactic measure. There is no assurance that i ch a practice will be effective in all cases. Field ormation indicates that in some instances, such ractices actually prevent the flock owne-r from ' covering a paratyphoid infection in the flock.» ,_ Sulfonamides, such as sulfaquinoxaline and lfamethazine, have some value in treating para- ’ phoid outbreaks, but they are much less effective an furazolidone. - » No treatment is known that will eliminate in- I cation from the flock following an outbreak, and i ‘orts to test and eliminate individuals harboring the organism have been unsuccessful. Prevention ' ‘of primary importance. Regardless of treatment, ever use infected birds to supply hatching eggs. L urqcolon Infections . The paracolon bacteria comprise a large group flrelated organisms that have certain character- istics in common with the paratyphoids and also "th the common coliforms. Most pathogenic fr» acolon organisms are placed in the group known f. Arizona paracolons. They can be differentiated fifom, the paratyphoids by their biochemical re- actions, but the similarity between groups causes if me delay and confusion. incorrect identification. Edwards et al. have pointed out the close relation- ship of this group of the Salmonellas and have ‘suggested that they should be called “parasalmo- ginellas" rather than “paracolons.” These organisms are distributed widely in nature and have a host range which coincides with the Salmonella. The role of the paracolons in causing poultry disease is poorly established. Under certain con- ditions, these organisms may cause disease in young turkey poults, and thus be of economic importance. For unknown reasons, Texas poultry producers" have had fewer disease outbreaks from paracolon infections than are reported for some other sections of the country. Consider the disease produced, symptoms, lesions, transmission, prevention and treatment as identical to the paratyphoid infections until re- search futher clarifies the situation. Differentia- tion of paracolon from paratyphoid infection now depends on careful laboratory examination with isolation and identification of the causative organism. OMPHALITIS Omphalitis is technically an inflammation of the navel. As commonly used, it refers to improper closure of the navel with subsequent bacterial in- fection. (Navel Ill; Mushy Chick Disease.) Cause: Considerable research as to the cause or causes of omphalitis has taken place during the past 3 years. Apparently, most problems result from mixed bacterial infections including the com- m.on coliforms and various species belonging to the genera Staphylococcus, Streptococcus, Proteus and others. Omphalitis usually can be traced to faulty incubation, poor hatchery sanitation or chill- ing or over-heating soon after hatching (such as in transit). The significance of isolating one of the bacterial species mentioned above is complicated in that many of the same species can be isolated from the yolks of supposedly normal birds immedi- ately after hatching. Transmission: Omphalitis occurs during the first few days of life, so it cannot be considered as being transmitted from bird to bird. It is trans- mitted from unsanitary equipment in the hatchery to newly hatched birds having unhealed navels. Symptoms and lesions: Affected chicks usually appear drowsy or droopy with the down being “puffed-up” and in general appear to be of inferior quality and show lack of uniformity. Many indi- viduals stand “near the heat source and are indif- ferent to feed or water. Diarrhea sometimes is observed. Mortality usuallybegins within 72 hours but may not occur before the tenth day. Characteristic lesions are poorly healed navels, bluish color of the abdominal muscles around the navel and unabsorbed yolk material which often 19 has a putrid odor. Often yolks are ruptured and peritonitis is common. Diagnosis: A tentative diagnosis can be made on the basis of history and lesions. The presence of mixed bacterial infections and absence of any specific disease producing agent aids in confirming the diagnosis. Treatment and prevention: Good management and sanitation procedures in the hatchery and during the first few days following are the only sure way to prevent omphalitis. Broad spectrum antibiotics help reduce mortality and stunting in affected groups, but they do not replace sanitation. FOWL CHOLERA Fowl cholera was recognized as a separate, dis- tinct disease by Pasteur in 1880. Salmon first re- ported its presence in the United States in 1880-83. The disease occurs throughout the country wher- ever poultry is produced. Host range is extensive and includes chickens, turkeys, pheasants, pigeons, water fowl, sparrows and other free-flying birds. Cause: The causative organism of fowl cholera is Pasteurella multocida (also called P. avicida), a bacterial organism in the form of a small oval rod, distinctly bipolar when stains are made from blood or tissues. It is grown easily on artificial media provided its demanding nutritive requirements are met. The organism is identified by staining tech- niques which permit observation of the typical morphology and by determination of biochemical reactions in artificial media. Transmission: Pasteurella multocida will sur- vive for (l) at least 1 month in droppings, (2) 3 months in decaying carcasses or (3) 2 to 3 months in soil. The organism may enter the body through the digestive tract or the respiratory system. The disease is not egg transmitted. Major sources of infection are: Body excreta of diseased birds which contami- nates soil, water, feed, etc.—this may be from visibly sick birds oriapparently healthy carriers. Carcasses of birds which have died of the disease. Contaminated water supply such as surface tanks, ponds, lakes or streams. Mechanical transmission as on shoes or equip- ment. Symptoms and lesions: The disease seldom is seen in birds under 4 months of age. Usual incubation period is from 4 to 9 days and outbreaks 20 may vary from peracute to chronic in nature. In i the peracute form, symptoms may be entirely absent; in the acute form, some birds may die _ without showing symptoms, but many others are 1 visibly ill before death. Characteristic symptoms include: Stupor. i 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. Lesions may be lacking in birds dying during . peracute: outbreaks. When present, lesions may resemble those associated with any acute septicemic i-i bacterial infection, often resembling those of fowl typhoid or possible bluecomb. Typical lesions in- f clude any or all of the following: Pin-point 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 throughout the liver. Spleen enlarged and congested. Creamy or solid collection of material in joints. Cheesy material in the internal ear of birds having twisted necks. Turkeys may have pneumonia with solidifica- tion of one or both lungs. Diagnosis: A tentative diagnosis may be made based on flock history, symptoms and post mortem i lesions. Demonstration of bipolar staining rods in . blood smears or impression smears of the lungs, liver or spleen helps to substantiate the diagnosis. A definite diagnosis depends upon isolation and i identification of the organism. Prevention and treatment: larly the old typhoid-cholera bacterin. affected flocks. ‘It. Until recently, i vaccines for fowl cholera have been useless, particu- e Recent i research programs have developed a fowl cholera iii i bacterin that appears to produce good results. l Field reports indicate that it may be valuable in a halting the spread of chronic fowl cholera within i‘ Management practices that aid in preventing a1 cholera are: Complete depopulation each year between older w and replacements. { Proper disposal of dead birds. A safe, sanitary water supply. ’ Adequate cleaning and disinfection of all houses id equipment on premises where outbreaks have rred after disposal of affected flocks. . Keeping birds of susceptible age confined to house. i Allowing contaminated ranges or yards to re- f vacant for at least 3 months. Y7 Sulfaquinoxaline is the drug of choice, using ‘e same levels as recommended for fowl typhoid. 'may be administered in feed or water, but treat- nt may be necessary for 3 to 4 weeks or longer. ,1 outbreaks requiring prolonged treatment, give e medication in the ration to guard against nger of water starvation. Sulfaquinoxaline at rate of 0.033 percent (1 pound of pure drug ‘r 3,000 pounds of complete ration) can be used fntinuously without toxic effects. Sulfamerazine d sulfamethazine also may be used, but they are effective than sulfaquinoxaline. In all in- I ces, follow the manufacturer’s directions care- . 1y. ERYSIPELAS (Swine Erysipelas) Erysipelas is a bacterial disease caused by ib-rysipelothrix insidiosa (formerly E. rhusiopathiae) '1 hich was once considered to be an important 'ease only in swine and sheep. The disease in I; ine frequently was referred to as “diamondskin" ' ase. It affects several species of birds including ickens, ducks and geese, but the only fowl in lhich it has been of importance is the turkey. 3» an is susceptible to infection and may contract It disease from turkeys. However, in man the ' ease known as erysipelas is caused by bacteria f» the genus Streptococcus, whereas infection of R with Erysipelothrix insidiosa is called erysipe- ‘oid. v Cause: Erysipelas of fowl is caused by a bac- ia, Erysipelothrix insidiosa (E. rhusiopathiae). in turkeys, it occurs most often in the fall or winter ‘onths and usually affects birds 4 to 7 months old, though any age birds are susceptible. Incidence ' higher in males than in females, possibly because gi fighting, males receive numerous skin abrasions hich may serve as entry portals. Transmission: Apparently, the primary route 5 infection is via wounds or skin abrasions which become contaminated with soil. The organism survives for long periods in the soil and most out- breaks are thought to originate from contaminated soil or premises. Sheep and swine may be carriers, but many outbreaks occur on premises that have not been occupied by sheep or swine for many years. Symptoms and lesions: The first indication of trouble may be the discovery of several dead birds. Usually several sick birds can be found. Symptoms include: Birds may appear listless with drooping wings and tail. ' Many birds may have a yellowish-green diarrhea but the vent feathers usually are not soiled. Infrequently some birds may be found lame with swollen leg joints. The snood or carnucle of the toms may present a turgid, swollen, purple appearance. In breeding flocks there is usually decrease in fertility and hatchability. Difficult breathing may be evident in advanced cases. Mortality rates vary from 2 to 25 percent. Typical gross lesions are: Purple-colored blotches on the skin. Inflammation of the intestinal tract. Small or diffuse hemorrhages in almost any tissues or organs. Enlarged, congested livers and /or spleens. Thickened o-r vegetative type growths on heart valves. 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 and treatment: Antiserum prepared in horses is available and effective under certain conditions, but it is expensive. Use of this product is very limited. Bacterins now available are useful on premises where history indicates that outbreaks may be ex- pected. Three weeks are required to produce a high level of immunity. If vaccinated at l0 or 12 weeks of age, repeat the procedure for birds held over as breeders. The vaccine is relatively expensive. Use according to manufacturer's direc- tions. - _ Good management practices for preventing erysipelas include: Avoiding use of ranges previously occupied by swine or sheep. 21 Debeaking and other measures which prevent injuries from fighting. ' Removal of the snoods of the toms. Removal of sick birds to a hospital pen for treatment and to prevent other birds from killing them, plus moving unaffected birds to clean range may aid in stopping the spread of the disease. In addition to using bacterin for unaffected birds, 150,000 to 200,000 units of penicillin injected into the leg or breast muscle of visibly sick birds is very effective in decreasing mortality. One in- jection usually is sufficient, but treatment may be repeated in 3 to 4 days if necessary. Penicillin has no value as a prophylactic measure because of its short period of activity. BOTULISM (Limberneck; Food Poisoning) Botulism is a disease caused by the ingestion of a toxin produced by the bacterial organism, Clostridium botulinum. All domestic animals and fowls are susceptible. To some degree, swine are resistant and vultures apparently are immune. 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 toxin of the bacteria Clostridium botulinum, an organism common in nature. This organism grows best under conditions of high humidity, relatively high temperature andin an environment contain- ing decaying vegetable or animal matter. Acid conditions are detrimental. Stagnant pools or damp areas containing decaying matter with an alkaline reaction are a danger area. 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 water soluble and relatively heat stable, but may be destroyed by boiling. Fly maggots feeding on decayed tissue may contain enough toxin to cause the disease when ingested by poultry. 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 and lesions: Ingestion of small amounts of toxin may produce a mild form with recovery in 24 to 48 hours. First signs of illness generally are weakness with flaccid paralysis of the 22 legs, neck and wings, followed by prostration t “the toxin source. For this reason: death. Affected birds may have ‘a peculiar tr‘, bling of the feathers which are loose in the follicl and generally shed freely during examination 5 birds. Because of the paralysis, birds are unabv to swallow and mucus accumulates in the mou r Usually there are no significant lesions evide. on dead birds with the possibler exception of 1 t, feathers and an excessive amount of mucus and d' in the mouth. Examining the contents of the cr and intestine may reveal maggots or other mate to indicate that the birds have consumed the to ' Diagnosis: A tentative diagnosis may be ma from the history and such factors as loose feathe mucoid accumulations in the mouth and thy absence of other post mortem lesions. 1 As an aid to diagnosis, give sick birds watl keep in a cool environment and treat with an toxin intravenously. Recovery of a large percen, age of birds treated this way would substantia a the diagnosis. Additional supportive evidence for diagnosl may be obtained by producing the identical illn signs in other birds or laboratory animals rj inoculating them with material from the digesti j tract of affected birds. = Prevention and treatment: Aim at eliminating Do not feed spoiled canned foods. Promptly removeall dead animals from hou =2 or pens. A Control fly populations. Debeak birds to prevent cannabalism. i Do not allow wet feed to accumulate aroun feeders. ?- To treat this disease: Remove all visibly sick birds from the floc i place them in a cool shady area and fill the croi with water twice daily. a Use mild laxatives such as molasses at a rate o i; 1 pint per 5 gallons of water for birds which hav been exposed but do not yet show symptoms. Antitoxins may be useful in treating affect birds, but are expensive. In turkeys use 2 to 4 j of polyvalent antitoxin, administered intraven‘? ously, intraperitoneally or intramuscularly. ' * Diseases are often grouped according to the y system they affect. Those affecting mainly e air passages, windpipe, lungs and air sacs are ;sified as “respiratory diseases.” From the be- g ing, this group of diseases has been important. g At first all diseases of the respiratory system e known as “colds" and often were considered be caused by environmental factors such as drafts __ chilling. As more information accumulated, it j me apparent that “colds" were actually a group ' separate infectious diseases having many common ~ - acteristics. Possibly all infectious agents causing respiratory lptoms have not been recognized, but many have ‘on isolated and the disease they produce well _,- ined. Because the nature of the causative “nism tells much about a disease, the following f-tline according to cause is useful in understand- these diseases. Caused by viruses: Newcastle disease. Infectious bronchitis. a Laryngotracheitis. Omithosis. Quail bronchitis. Caused by bacteria: i i“ Chronic respiratory disease-air sac syndrome of chickens and infectious sinusitis of turkeys. * Infectious coryza. Endemic fowl cholera (roup) . Caused by molds: Aspergillosis (brooder pneumonia). NEWCASTLE DISEASE Newcastle disease is a contagious viral infection, l“ using a respiratory nervous disorder in several ‘ cies of fowl including chickens and turkeys. It 1 first recognized in England in 1926 and was w u after the town of Newcastle. It first ap- “ared in the United States in 1944. Within the t.» t few years, Newcastle disease had been reported s at least 30 states. This indicates that within very few years the disease became widespread. Cause: Newcastle disease is caused by a virus. iifferent types off-strains, varying in their ability ‘- cause death and nervous disorders, have been ' ~ ognized. Some are highly fatal, but most Ameri- Zn strains are more fatal in young birds than in ults. SECTION 3. RESPIRATORY DISEASES Transmission: Newcastle disease is highly con- tagious. All birds in the group usually become infected within 3 to 4 days. The virus can be transmitted through contaminated equipment, shoes and clothing of man 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 disease are not greatly different from those of other respiratory diseases. The ones mo-st frequently observed are: (l) nasal discharge, (2) excessive mucus in the trachea, cloudy air sacs, (4) cast or plugs in the air passages of the lungs and (5) cloudiness of the cornea of the eye. The disease in young chickens begins with difficult breathing, gasping and sneezing. This phase continues for l0 to 14 days and may be followed by nervous symptoms. If nervous dis- orders develop, they may consist of paralysis of 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 zero t0 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. l/Vhen 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 shell, off-color and irregular-shaped eggs are produced. Mortality in adult birds usually is low but may be fairly high from some virus strains. In turkeys, the symptoms usually are mild and may be unnoticed unless nervous disorders develop. During an outbreak, turkeys will produce eggs with a chalky white shell. Reduced production in breeder 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, this disease cannot be differentiated from infectious bronchitis and some of the other respiratory infections except by labora- tory methods. Laboratory procedures necessary to establish a definite diagnosis sometimes are complex and time consuming. They can be conducted only in a well-equipped laboratory. Prevention and treatment: There is no treat- ment for Newcastle disease. This disease does not 23 always respect even the best management program, but practices outlined in other sections of this bulletin will help reduce possibility of exposure to Newcastle disease virus. Vaccination is practiced widely and is the recommended method for prevention. Several types of vaccine are available but the one most successful and widely used is the mild live virus vaccine known as the B1 type. This vaccine was used originally by dropping it into the nostril or eye. Now, however, the vaccine is applied also in the drinking water, as a dust or as a spray. In broiler production use two doses of the B1 type vaccine. The first vaccination usually takes place when birds are between l and 5 days of age and is followed by a second dose at about 3 to 4 weeks. Give chickens to be kept for egg production three applications of the vaccine. The vaccine usually is given when the birds are 1 to 5 days, 3 to 4 weeks and 4 to 5 months of age. Vaccination is not widely practiced in turkeys. It sometimes is used to protect egg production in breeder flocks. Give one dose of the B1 type vaccine after selecting the breeder birds. INFECTIOUS BRONCHITIS Infectious bronchitis is an extremely contagious respiratory disease of chickens characterized by coughing, sneezing and rales. Cause: Infectious bronchitis is caused by a virus which affects chickens only. Other fowl or laboratory animals cannot be infected with this virus. Transmission: Infectious bronchitis is con- sidered the most contagious disease known. When it occurs, all susceptible birds on the premises become infected regardless of sanitary or quaran- tine precautions. The disease can spread through the air and can “jump" unknown distances during an active outbreak. It also can be spread by mechanical means such as clothing, poultry crates and equipment. The disease is not egg-transmitted and the virus will survive only for a short time- probably not more than 1 week in a poultry house. It is destroyed easily by heat or the ordinary dis- infectants. Symptoms and lesions: This infection is con- fined to the respiratory system. Symptoms are difficult breathing, gasping, sneezing and rales (rattling). 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. 24 In chickens under 3 weeks of age, mortality I may be as high as 30 to 40 percent. The disease AI does not cause a significant mortality in birds over ' 5 weeks old. Feed consumption decreases sharply I and growth is retarded. i 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 f. required before the flock returns to production. i Some flocks never regain an economical rate of lay. During an outbreak, soft shell, small, irreguk; lar-shaped eggs are produced. 5‘ _ Diagnosis." Infectiousbronchitis is difficultto * differentiate from several of the other respiratory ‘ diseases. usually requires laboratory procedures. Treatment and prevention: retained for egg production. Whether broilers 5 should be vaccinated depends upon many factors 1 and is an individual decision. Numerous vaccines‘. are available commercially. Most of them repre- i: sent a modified or selected strain of infectious 1 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 otherf susceptible birds. Vaccine may be applied through i drinking water, as a dust, spray or by dropping it into the eye or nostril. i There is no treatment for this disease. In ' young chickens it is helpful to increase the brooder I temperature and to provide as nearly ideal environ- mental conditions as possible. 7 LARYNGOTRACHEITIS Infectious laryngotracheitis is an acute, highly ‘ contagious disease of chickens and pheasant. It l is characterized “by respiratory distress, rapid spread ; and often, 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 ini the respiratory system. During an active outbreak? the disease can spread by mechanical methods such‘. as clothing and equipment. The mostimportant‘ factor in spreading the disease is the carrier bird.~. Symptoms and lesions: The disease usually. occurs in semi-mature or adult birds. It is acutei and affected birds usually die or recover in 5 tof 6 days. Some virus strains are more mild and the course of the disease may be as long as 15 days? For this reason, a definite diagnosis Infectious bron- y: chitis is highly contagious and does not always res ect sanitar barriers. Vaccinate chickens to be ; P Y . .91.‘ 2; or more. Coughing, sneezing and vigorous shaking of the head with a gurgling or rattling sound is characteristic. 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 differenti- ated 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 inocu- lating susceptible and immunized birds with ma- terial 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 prevails, vaccination is necessary for prevention. In other areas where the disease does not occur often, vaccination is strongly discouraged. Use the vaccine with care because it is a virulent virus and vaccinated birds can become carriers of the infec- tion. When vaccine is indicated, it is applied to the mucous membrane of the clo-aca. One vacci- nation gives good protection. There is no treatment for this disease. When an outbreak occurs, vaccinate the flock immedi- ately. This usually will stop the spread of infec- tion among the group. Never use the vaccine for this purpose unless the diagnosis is confirmed completely. ORNITHOSIS Ornithosis, also known as psittacosis, is an acute or chronic virus infection of a number of fowl and other animals, including man. When the disease is in birds of the parrot family, it is known as psittacosis. Ornithosis is the name used when the disease occurs in other species of wild or domestic birds. In domestic poultry production, the disease has been a problem only in turkeys. Its importance is magnified because it is transmissable to man, and in the past, workers in poultry processing plants have become infected from handling turkeys. Cause: The disease is caused by an agent usually considered to be a large particle virus. Numerous virus types have been recognized. Some roduce onl a mild disease in turke s while others P Y . . . Y may cause significant mortality. Transmission: How turkey flocks become in- fected is not known. The disease is not egg- transmitted and recovered birds do not appear to remain carriers. It is suspected, but not proved, that migratory shore and wading birds may intro- duce the infection. Many turkey flocks having the disease have been in contact with surface water frequented by such birds. Symptoms and lesions: Infected turkeys become droopy, go off feed and usually have. a greenish- yellow diarrhea. Symptoms can be confused with many other diseases. When a turkey having died from this infection is examined, the main findings are an inflammation of the heart sac resulting in an accumulation of exudate in this organ, cloudy air sacs which may contain exudate and a film of clear exudate over the liver. Diagnosis: Ornithosis in turkeys must be differentiated from infectious sinusitis, fowl cholera and some other diseases. Post mortem lesions are suggestive but a definite diagnosis can be made only by isolating the virus 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 aureomycin at a rate of 200 gm / ton of ration. This treatment usually will stop flock losses and allow birds to be processed without danger of human infection. 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 the CELO virus. It has been isolated from chicken eggs but does not pro- duce a recognizable disease in chickens or turkeys. This 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. 25 CHRONIC RESPIRATORY DISEASE-—AIR-SAC SYNDROME AND INFECTIOUS SINUSITIS Chronic respiratory disease (CRD), air sac syn- drome and infectious sinusitis of turkeys have a common cause. CRD was recognized first as caus- ing a chronic but mild disease in adult chickens. It reduced egg production but caused little or no mortality. After CRD had been recognized, a con- dition known as “air-sac disease" became a prob- lem in young birds. It caused high mortality in some flocks. Many birds became stunted; there was poor feed efficiency and many were rejected as unfit for human consumption when processed. The third condition, infectious sinusitis of turkeys, was recognized as early as 1905. It causes a sinus swelling under the eye as well as an inflam- mation of other respiratory organs. It is a chronic disease adversely affecting growth and feed con- version. In young poults it may cause significant mortality. Cause: A peculiar bacterial organism known as PPLO or Mycoplasma is common to all three conditions. CRD, in a strict interpretation, is caused by a pure PPLO infection. On the other hand, the air-sac syndrome has a complicated cause and is a result of infection with several organisms. This condition is caused by PPLO in combination with another common bacterial organism, E. coli, and is triggered by an acute respiratory virus in- fection such as Newcastle disease or infectious bronchitis. The cause of infectious sinusitis of turkeys is an uncomplicated PPLO infection. PPLO are widely spread and affect many species of birds. They exist in most, if not all, chicken flocks. They also are widely spread among turkeys, but only about 40 percent of turkey flocks are infected. Transmission: The primary method by which PPLO are spread is through the egg. Infected hens transmit organisms and the chick or poult is in- fected when it hatches. Organisms also may be transmitted by direct contact with infected or carrier birds and possibly by other unknown methods. Symptoms and lesions: The true CRD produces slight respiratory symptoms such as coughing, sneez- ing and a nasal discharge. In the air-sac syndrome there is an extensive involvement of the entire respiratory system. The air sacs often are cloudy and contain large amounts of exudate. There is often a film of exudate covering the liver as well as the heart muscle and heart sac. Affected birds become droopy, feed consumption decreases and there is a rapid loss of body weight. 26 Infectious sinusitis of turkeys occurs in two forms. When the “upper” form is present, there’ is only a swelling of the sinus under the eye. In v the “lower” form, the lungs and air sacs are in-2 volved. The air sacs become cloudy and may con- " tain large amounts of exudate. Both forms of the 1 disease usually are present in the flock and fre- quently are present in the samelbird. ‘ Diagnosis: Diagnosis of either of these condi-i- tions must be based on flock history, symptoms and‘ lesions. Blood tests are useful in determinin whether a flock is infected. Treatment and prevention: The treatment of’. CRD, air-sac syndrome and the lower form of in- fectious sinusitis usually is not satisfactory. Many a antibiotics have been used with varying success. i; Whether to give treatment is a decision that must 5 be made on each flock based on economic factors. ~ If treatment is attempted, give high levels of one of the broad spectrum antibiotics either in the feed, ; drinking water or by injection. The “upper” form of infectio-us sinusitis can be treated with success ~ by injecting antibiotics into the swollen sinus. I The ultimate answer to this problem in both chickens and turkeys must be eradication. To, accomplish this, it is necessary to develop PPLO; free breeder flocks. This goal can now be reached‘ in turkeys because satisfactory blood tests are avail-l able to detect infected flocks. Testing and hatch-i ing from noninfected flocks provides a good chance for eradicating infectious sinusitis in turkeys. A voluntary eradication program is available to Texas; ‘ turkey producers operating under the Texas Turkey Improvement Plan. e Because all chicken flocks are infected, obtain- ing PPLO free flocks is more difficult. An eradi- cation program has not been well formulated for use in chickens. Such a program should become‘ available as additional information develops. INFECTIOUS CORYZA Infectious coryza is a bacterial infection 09 chickens. It is a slow-spreading, chronic dise * that does not affect all birds at one time. It occu more often in semi-mature or adult birds. I Cause: The cause is a bacterial organis known as Hemophilus gallinarium. The organis remains endemic in some areas but is only rarel l; found in Texas. Transmission: Transmission is by contact wi affected or carrier birds. Individuals which ha recovered from the disease may appear normal, w‘ carry the organism for long periods. Once the i fection has been in a flock, each individual m ? be considered a carrier. Preventing contact een susceptible and affected or carrier birds ually will prevent spreading. Symptoms and lesions: Main disease signs are .;;puffy” or “doughy” swellings around the face and ' t the wattles. There is a discharge from the ' ' w tril, and the sinus under the eye may be swollen. _ ause of a watery discharge from the eyes, the 'ds may be stuck together. Vision may be affected ause of the swelling around the eye. g Diagnosis: Because the disease is rare in this V‘ te, can be confused with other respiratory dis- es and is difficult to diagnose, submit suspected V es to a trained diagnostician who has laboratory cilities. Diagnosis can be made only by isolating Y d identifying the organism. This frequently is f: fused with endemic or localized fowl cholera which is a much more common disease in Texas. b Treatment and prevention: Infectious coryza ually can be prevented by management programs lat prevent contact between susceptible and in- ted birds. Introduce started pullets or mature irds with extreme care to prevent introduction f the infection onto the premises. _ There are effective drugs for treating this con- jition. The first requirement prior to treatment 7K a correct diagnosis. The disease can be treated fectively with sulfa drugs such as sulfathiazole, lfamethazine and sulfaquinoxaline. , Prevention is the only sound approach to con- -_- l. Dispose of affected flocks as soon as practical 7E1 eliminate them as a source of infection. ENDEMIC (LOCALIZED) FOWL CHOLERA This disease is very similar to infectious coryza. , e two often are confused even in textbooks on ultry diseases, and pictures of this disease often f‘ e mislabeled as infectious coryza. The disease, it occurs in Texas, is a specific respiratory in- ection caused by an organism similar to the one using acute fowl cholera. This condition, how- er, is not associated with acute fowl cholera. It ever reverts to the acute form of the disease, but § a onic cases following an outbreak of fowl cholera _ay show symptoms and lesions closely resembling is condition. The disease affects chickens pri- “rily, although turkeys can be infected by inocu- (i011. Cause: The bacterial organism causing this isease is a Pasteurella that cannot be differentiated ordinary methdfds- from Pasteurella multocida, i’ e bacteria causing acute fowl cholera. g Transmission: This disease is transmitted only ‘H direct contact between susceptible and infected irds. Recovered birds remain carriers indefinitely. They will spread it, however, only by direct contact. Separation between susceptible and carrier birds, even by a short distance, will prevent spread. Symptoms and lesions: This is a chronic disease affecting only a small percentage of birds at one time. It causes a nasal discharge, an inflammation of the eye and a swelling of the sinus under the eye. The sinus becomes filled with hard, “cheesy" type exudate that has a putrid odor. Sometimes the lungs and air sacs are affected. The disease causes little direct mortality, but it does cause reduced egg production, and increased cull birds and in general poor performance. Diagnosis: A trained diagnostician usually can identify this infection by the history, symptoms and lesions. A confirmed diagnosis can be made only by the isolation and identification of the causative organism. This sometimes is difficult and requires a long time. Because of this, diagnosis usually is based on other characteristics of the disease. Treatment and prevention: As with infectious coryza, this disease can be prevented readily by management. It requires only separating infected or carrier birds from the susceptible population. Fifteen years ago, it was estimated that 8O percent of the chicken flocks in Texas were infected. By management programs, infection has been almost eliminated from commercial operations. Introduce started or adult birds with extreme caution to prevent introducing the infection. In general, treatment is unsatisfactory. Prob- ably the most effective drug is sulfaquinoxaline. This must be given in the ration at a rate of .033 percent. It has to be given a long time and simply serves to prevent other birds from developing the disease. It does not cure those already affected. This drug level is near the toxic range and must be used with care to prevent causing a drop in egg production. Injection with some antibiotics ap- pears to be useful in treating the affected bird. ASPERGILLOSIS (Broader 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 condition 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. Occa- sionally, other types of molds are involved. These organisms are present in the environment of all 27 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 isn't contagious and does not spread from one bird to another. Most 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 a paralysis or other forms of nervous symptoms. The more chronic fonn in older birds usually results in the losses of appetite, gasping or 28 coughing, and a rapid loss of body weight. Mortal- . ity is usually 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. Sometimes N the air-sac lesions are similar to those produced by infectious sinusitis or In some birds, 1 colonies of mold growth can beseen on the air-sac = membranes. Diagnosis: Diagnosis usually can be made from‘ history, symptoms and lesions. Sometimes it ' necessary to base diagnosis on microscopic lesionfl Treatment and prevention: There is no treat-T ment for the flock or the affected bird. The disease usually can be prevented by avoiding moldy litter, s. feed or premises. A careful examination of the. environment usually reveals the trouble source: which should be eliminated. Often this means . changing litter and replacing with new litter. EA number of viral diseases of poultry produce ptoms and lesions primarily exclusive of the iratory system. Among them are some of the It devastating diseases of chickens and turkeys. idered in this group are avian pox, avian phomatosis (leucosis), avian encephalomyelitis idemic tremor), avian infectious synovitis and yecomb disease. AVIAN POX ~ (Fowl pox, Canker, Avian diphtheria, contagious epithelioma, Sore head) l Avian pox is a relatively slow-spreading viral ection of birds, characterized by wart-like ules on the skin and diphtheritic necrotic mem- es lining the oral cavity and upper respiratory item. It has been present in birds since the ‘I liest available history, is universal in distribu- g and may cause severe economic loss in chickens f: turkeys due to poor growth, feed efficiency, Luced production, increased cull rates and down- / ding. Mortality usually is not significant. The may occur in any age bird at any time ' 'ng the year; but the greatest seasonal incidence ‘ during the warm months, particularly when quito populations are high. . Cause: Avian pox is caused by a viral agent. ere are at least three different strains or types e avian pox virus: fowl pox virus, pigeon pox I s and canary pox virus. Although some work- '. include turkey pox virus as another distinct I in, most feel that it is identical to fowl pox i Each virus strain is infective for a number of _- ies of birds in addition to its primary host. r example, among others, fowl pox virus infects ickens, turkeys, pheasants, quail and ducks; )4‘ pox virus infects pigeons, chickens and ‘i keys; and canary pox virus infects canaries, A“ 'ckens, pigeons and sparrows. H?’ Natural occurring pox in chickens, turkeys and er domestic fowl is considered to be caused by i I pox virus. , Transmission: Fowl pox can be transmitted p, direct or indirect contact. The virus is highly istant in dried scabs, and under certain condi- i} may survive for months on contaminated l ises. The disease may be transmitted by a Q ber of species of mosquitoes, which is the usual v ner this infection is introduced to a premise. osquitoes may harbor infective virus for a month I more after feeding on affected birds. After the ection 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 indi- vidual bird is 3 to 5 weeks. Affected young birds are retarded in growth. Adult birds drop in pro- duction. Birds of all ages which have oral or respiratory system involvement experience diffi- culty in eating and breathing. The disease manifests itself in one of, or a combination of, 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 formation precedes final healing. Lesions are seen most commonly around the featherless facial parts (comb, wattles, ear lobes and eyes) but may be found elsewhere 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 usually is readily diag- nosed 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 sanitation practices will not prevent it. Two kinds of vaccines are available: pigeon pox and fowl pox vaccines. The pigeon pox vaccine is of questionable value, and its use nonnally is not recommended. Fowl pox vaccine is an efficient product. Its use varies according to type of opera- tion, but generally the following recommendations apply: Broilers: Vaccination usually is not required; but in some sections where mosquito population is high, as in parts of Texas, it may be necessary to prevent’ the disease. In such instances, the vaccine is applied to chicks (as young as 1 day) using the wing-web method but using only one applicator needle. Replacement birds: Vaccinate all replacement chickens against fowl pox. One application of fowl pox vaccine results in permanent immunity. Birds can be vaccinated at any convenient time during 29 the growing period, usually between 6 and 10 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. Market birds not selected and vaccinated within a day or two. Examine vaccinated birds for “take" about 7 to l0 days following vaccination. A high per- centage showing a reaction indicates a satisfactory vaccination. AVIAN LYMPHOMATOSIS (Avian Leucosis Complex) Avian lymphomatosis is a widespread, trans- missible virus disease complex of chickens, turkeys and other fowl characterized by tumor formations which may involve any body structure. The dis- ease is the most devastating condition affecting mature laying chickens and is becoming increas~ ingly important as a cause of losses in broilers, growing birds and turkeys. Cause and transmission: Avian lymphomatosis is caused by a virus or group of viruses. Some researchers believe that variable host response to a single agent explains its different manifestations; others feel that disease variability is explained best by assuming that several agents or strains of virus are involved. The disease may be transmitted in a number of ways. The agent(s) of lymphomatosis is eliminated naturally from the body of infected birds via eggs or feces. The virus may be transmitted mechan- ically from infected birds to susceptibles by blood- sucking parasites (mites, ticks and others) or by man in such procedures as fowl pox vaccination or blood testing. Most infections are acquired during the first few weeks of life. This would suggest that most flocks acquire this disease by egg transmission or by direct or indirect contact with older infected birds during the early brooding period. Manifestations of avian lymphomatosis: Five distinct types are recognized: visceral, neural, ocular, osteopetrosis and blood type. Visceral lymphomatosis (big liver disease) is the most common form and the one (which produces the most economic loss. Although visceral lym- phomatosis may cause losses in birds as young as 3 to 4 weeks, it is seen most commonly in adults, particularly in the first production year. Severe losses frequently are associated with the onset of 30 production; however, in such flocks, occasional = losses will continue as long as the flock is retained. ' Visceral lymphomatosis is characterized by the = formation of lymphoid tumors, particularly of the 1 visceral organs. Affected birds may die without = preliminary symptoms; but the disease usually is 5 chronic in nature with affected birds showing loss i of appetite, progressive emaciation and diarrhea. if Clinically affected birds invariably die. ’ Autopsies of affected birds reveal characteristic f tumors. Although the liver, spleen, kidneys and ii ovary most commonly are involved, any organ in-g: .1 cluding muscle and skin may be affected. The ;_ neoplastic process may be diffuse involving 100 percent of the affected organ, or it may be a Affected structures, the liver in . nodular type. particular, may be greatly enlarged. Neural lymphomatosis (range paralysis, fowl __ paralysis) attacks primarily young birds between l 2 and 5 months of age; however, it has been seen as early as 3 weeks and as late as 3 years. Losses may run as high as 25 percent but usually are much- lower. A flock which has had a neural lymphoma- f tosis problem frequently will become- a visceral‘ V’ p lymphomatosis problem flock. Neural lymphomatosis is characterized by a: f " progressive paralysis of the wings, legs and neck. I Loss of body weight, anemia, labored respiration f and diarrhea are other common symptoms. ‘i When affected birds are autopsied, lesions, if observed in uncomplicated cases are confined to j the nerve trunks and nerve plexuses innervating " the paralyzed extremities. Affected nerve tissue is_ l swollen due to accumulation of lymphocytes and i“ tissue fluids. Frequently no gross lesions are i? observed. ‘ Ocular lymphomatosis (grey eye, pearl eye)_i_s l responsible for most blindness in chickens. ‘This "1 type usually is seen in early maturity. Morbidity ‘ and subsequent mortality usually are low but in j.; some instances approach 15 to 25 percent. l The disorder is characterized by a spotty de- i, pigmentation or diffuse greying of the iris of the ; eye due to lymphocytic infiltrations. The pupil i develops an irregular shape and fails to accommo- date light. Emaciation, diarrhea and death usually follow because of partial to complete blindness. Osteopetrosis is the bone form of the disease.»_5i A Until recently it was thought to be a diseasef primarly of older birds, particularly males; how-i ever, it is now known as an extremely common‘ disease in young chickens and is one of the more s important causes of broiler condemnation. ‘ '1; The disease is characterized by a thickening and formation of bone, the long bones in particular. is frequently results in lameness and faulty body ormation. ' Blood forms of lymphomatosis are diagnosed AJ- equently. Treatment and prevention: There is no treat- , nt for lymphomatosis. Although the disease Inot be prevented completely, certain steps can we taken to control infection in a flock. Among e are: a ;, Buy resistant strains of birds. Most reputable A ders have invested a great deal of time and w ey developing strains which have increased istance to lymphomatosis. f Brood in isolation. Most lymphomatosis in- g tions are acquired early (under 6 weeks of age). § replacement birds are brooded in strict isolation, ntact transmission (direct and indirect) from jult carriers will be minimal. l‘ Incubator sanitation. Control of blood-sucking parasites. INFECTIOUS SYNOVITIS (Infectious Arthritis) _ Infectious synovitis is a chronic disease of Wickens and turkeys characterized by inflammation joints and synovial membranes. It is found in I major poultry-producing areas of the country ‘il- may cause severe losses due to mortality, tarded growth, poor feed conversion and down ‘ding at processing plants. Although the disease _ " y appear in adults, it is primarily a disease of wing birds, particularly in the 4 to 12-week groups. l Cause: The agent producing infectious syno- _'tis has been characterized as a large-particle virus, ltrecent research indicates that the primary cause 3- be a PPLO, known as Mycoplasma synoviae. l s p) Transmission: Mode of transmission is not fell understood. Contact transmission does occur, t the natural route of invasion is not known. Wxperimentally, the disease can be reproduced by ny routes. Egg transmission studies are incon- sive, but some field and experimental evidence s egg transmission does exist. Symptoms and lesions: Morbidity of infectious ' ovitis may reach-,.2_(_) percent or more before an tbreak has run its course. Mortality is low. eness is the first symptom observed. Swelling ociated with the hocks, foot pads and shanks ually are seen in chickens; however, shank swell- w; is seen infrequently in turkeys. Rapid loss of condition, dehydration and diarrhea usually are seen. Autopsies of affected birds often reveal the following lesions. Joints and synovial membranes of legs and wings usually are inflamed and con- tain tenacious mucoid exudates. In turkeys, such lesions are rare except as associated with the hocks and foot pads. Inflammation of the sternal bursa (breast blister) is also a common finding. Visceral lesions may include swollen livers with greenish discoloration and enlarged spleens. Diagnosis: A presumptive diagnosis may be based on flock history, symptoms and lesions. Laboratory tests may be necessary to differentiate the disease from staphylococcic arthritis and other conditions producing leg weakness and sternal bursitis. Treatment and prevention: Birds affected with infectious synovitis respond poorly to treatment. Treatment, however, alters the course of an out- break, primarily by reducing disease spread. The antibiotic of choice is aureomycin. The drug is incorporated into the feed at a level of 200 grams per ton and fed for 7 to l4 days depending upon flock response. If practical, remove crippled birds from the flock since they respond poorly to treat- ment and serve as a continued infection source. If relapses occur, it may be necessary to feed lower levels of antibiotics continuously to market time. The adoption of a sound sanitation program offers the best hope to prevent introduction of infectious synovitis. EPIDEMIC TREMOR (Avian Encephalomyelitis) Avian encephalomyelitis is a viral infection primarily affecting susceptible chickens of all ages, but usually producing clinical manifestations only in young birds. Signs of infection include inco- ordination, nervousness, a jerky or irregular gait, falling over on the side with outstretched wing and muscular tremors especially noticeable in the head and neck. The commonly used term 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 from several other countries. The custom of hatcheries to adjust chick losses has led other segments of the poultry industry to regard this disease as of minor importance and significant only to hatcherymen. Such losses are 31 costly and troublesome, and as they reduce effi- ciency 0f all operations including breeder and broiler flocks, the disease poses a major problem for the entire poultry industry. Cause: Epidemic tremor is caused by a rela- tively small virus which produces microscopic lesions 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 21 to 30 days. It appears that affected flocks do not remain carriers and are not susceptible to the disease 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 it is doubtful that this is of major significance. Additional work is needed before effective controls can be formulated. Symptoms and lesions: In a small percentage of outbreaks, the disease may be suspected by poor hatchability or morbidity in birds at hatching time. The incubation period varies from 5 to 40 days with an average of 9 to 21 days. The typical out- break becomes noticeable when birds are l7 to 21 days old. Some individuals in flocks exposed dur- ing hatching may develop clinical evidence of infection up to 7 weeks later. Morbidity rates vary from only a few individuals to 30 percent but averages 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 is provided nearby. New cases developing after the fifth or sixth week are rare. Mortality usually is negligible but always remove visibly affected individuals and destroy them. 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, together with a decrease in hatch- ability. 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 avail- able aid must be used to give an accurate diagnosis. 32 Prevention and treatment: There is no treat-g ment. Remove and kill all birds showing clinical" evidence of the disease, since they do not develop into profitable birds. ' Prevention depends upon hatching from flocks ' which have recovered from thexdisease. Vaccines are used widely but are still the experimental ~ stage. Eventual control and eradication depend: upon continued research. Methods for detennin-le ing whether flocks are susceptible or immune need to be perfected and simplified. All transmissio methods must be determined. Better immunizin. methods are needed also and better diagnostic’. methods would be a great aid. I BLUECOMB DISEASE (Pullet Disease, Avian Monocystosis of Chickens; . Non-specific Enteritis, Trunsmissible Enteritis and Mud Fever of Turkeys) Bluecomb is an acute, subacute to chronic,‘ contagious disease of chickens and turkeys char- acterized by sudden onset, marked depression and severe diarrhea. Death losses may be high, par-l ticularly in young turkey poults; but heaviest losses in adults are due to loss of condition or . production. i Cause: Bluecomb is presumably caused by large-particle virus. The agent has not been well‘ characterized. Some evidence exists that the turkey agent and chicken agent are not identical. e Transmission: Method of natural transmission} in chickens is not known. In turkeys, the disease spreads by contact with affected birds or infected; premises. » The agent from chickens will reproduce the‘ disease in chickens and turkeys, but the turkey’- agent will not reproduce the disease in chickens. The disease in chickens occurs most frequently in hot weather, particularly in heavy breeds, re-T, cently housed and in a good rate of production. ‘ No specific environmental factors influence occurrence in turkeys. r Symptoms and lesions: Bluecomb disease pro- duces different symptoms and lesions in chickens‘ than in turkeys. a Chickens: The disease appears most often if young adults and is characterized by sudden onset with 25 percent or more of the flock becoming sick i within a day’s time. Affected birds usually exhibi marked depression, decreased feed consumption‘ decreased egg production, profuse whitish or wate diarrhea and cyanosis of the head (bluecomb); ‘ Early mortality may be high, but flock mortali seldom exceeds 5 percent. The disease usually ru its course in about 2 weeks, followed by rapid clinical recovery in most instances. When affected birds are autopsied, the following lesions may appear. The body musculature is t. dehydrated and may display a degenerative fish- L flesh like appearance. Minute hemorrhages may A be seen on the viscera and necrotic foci on the liver. The ovary usually undergoes rapid degenera- tive changes, and many misshapen and ruptured ova may be seen. Kidneys commonly are swollen f and contain an excess of urates. Severe catarrhal enteritis is seen often and mucous casts may be j. present. The pancreas usually presents multiple chalky white areas. The crop frequently is dis- tended and contains sour smelling contents. Turkeys: 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 drop markedly and poults lose weight rapidly. Morbidity and mortality may approach 100 percent in uncontrolled outbreaks. ._ Young poults show few lesions other than those asociated with the intestinal tract. Intestines i usually are distended and lack muscle tone. Intes- tinal 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 g and birds may lose up to 4 to 5 pounds of body i weight in just a few days. profuse diarrhea. Cyanosis of the head parts is ' common. i’ ‘w Birds usually have l Lesions observed in older turkeys are essentially the same as those for chickens. Diagnosis: Bluecomb must be differentiated from common bacterial infections such as para- typhoid, fowl cholera, fowl typhoid and erysipelas. Diagnosis of bluecomb usually is based on history, symptoms and lesions and negative bacteriological findings for the common bacterial infections. Treatment and prevention: Flush chickens and older turkeys with molasses at the rate of l pint molasses to 5 gallons of drinking water for 1 day. Then give antibiotics in feed or drinking water at the rate of at least 200 grams / ton of feed or 200- 400 milligrams/gallon of water. Continue treat- ment 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 or 1 gram/gallon of drinking water. Then give this high level for 2 to 3 days, after which time antibiotics may be reduced, depending on flock response. Total 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. Other than these, apply routine management and sanitation practices for disease prevention. 33 SECTION 5. The cause 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. INFECTIOUS HEPATITIS Infectious hepatitis is a widespread transmissible disease of chickens characterized primarily by swell- ing and necrosis of the liver. It may appear in an acute form, resulting in death of affected birds, or it may occur in a chronic form and produce economic loss by increasing flock cull rate. Birds of all ages may be affected, but the disease com- monly occurs in semi-mature and mature birds. Cause and transmission: The causative agent of infectious hepatitis has not been definitely characterized. Some workers feel the agent is a bacterial organism belonging to the vibrio group, while others feel it may be a large-particle virus. The disease apparently spreads by contact, direct or indirect, between infected and susceptible birds. Ingestion of infectious material is the most likely method of transmission. Some outbreaks present an appearance suggestive of possible egg transmission. Symptoms and lesions: Usual disease signs are listlessness, shrunken comb, loss of body weight and diarrhea. Acutely affected birds, however, may die while still in good flesh. Egg production may drop as much as 35 percent in severely affected flocks. Mortality usually is low but may be as high as 10 to l5 percent. The liver is the primary site of infection. Livers of affected birds usually are swollen and have necrotic and hemorrhagic foci. The heart and kidneys may be swollen, and there may be excess fluids in the abdominal cavity and the heart sac. Diagnosis: Liver lesions are found in birds affected with many diseases. Be-cause of this, in- fectious hepatitis may be confuse-d with diseases such as pullorum, typhoid, bluecomb, hemorrhagic disease, blackhead and lymphomatosis. Positive diagnosis is established by laboratory means. Treatment and prevention: Outbreaks are treated best by adding furazolidone to feed at a level of 200 grams (4 pounds of NF-180) per ton. Supply medicated feed for approximately l0 days. Until more is known about the causative agent of infectious hepatitis, specific prevention recom- mendations are not possible. Furazolidone as a preventive medicant usually prevents outbreaks, 34 DISEASES OF uuosrsnmiueo CAUSE but the use of the drug for this purpose is =. recommended. Routine management and sani tion practices for disease prevention offer the H‘ economical and reliable method of control. i HEMORRHAGIC ANEMIII “SYNDROME (Hemorrhagic Disease: Aplasfic Anemia) Hemorrhagic anemia syndrome is a dis. characterized by hemorrhage and anemia. It 1. considered to be a disease of chickens only, if though poorly substantiated reports indicate 0c "I rence of a similar disease of turkeys. The conditi‘ may affect birds of all ages, but usually aff those between the ages of 4 and l2 weeks. , nomic loss results from mortality and re o‘ growth. 1' Cause: The cause of hemorrhagic w‘ syndrome has not been determined, but it is _ considered infectious. * Symptoms and lesions: Usual signs are ruf feathers, weakness, loss of body weight, dia and anemia. Morbidity usually is high, but mo s ity is extremely variable, depending upon whe I the disease is acute or chronic. Acutely affec birds may die with few preliminary sympt Flock mortality may approach 20 to 30 per’ although it usually is lower. Lesions vary from anemia to frank hemorrh I Hemorrhages may be found anywhere on or in f body. Usually they are found in the musculat“ particularly of the thighs and breast. Hemorrh are commonly petechial (pin point in size), I they may be diffuse involving large areas. H i; rhages are often seen in the wall of the intest' the proventriculus, the musculature of the giz and the heart musculature. Less often there y be hemorrhage into the anterior chamber of I eye and into the wattles. Anemia is charact by paleness of the comb, mucous membranes i, other tissues. Commonly, the bone marrow ap ‘ pale yellow and fatty (aplastic anemia). ‘ Diagnosis: Diagnosis is based on history, s ' toms and lesions. When intestinal lesions ; present, care must be taken to differentiate I coccidiosis. ' Treatment: There is no specific treatment hemorrhagic anemia syndrome, but good res’ frequently is obtained by adding liver solubl feed at a level of 8 gallons per ton of feed 5 days, followed by a level of 5 gallons per for an additional 5 to 7 days. 2 Avoid sulfa drugs and high levels of antib since they may aggravate the condition. I HEMORRHAGIC ENTERITIS _ Hemorrhagic enteritis is an acute and fatal tinal disorder of turkeys. ; Cause: Unknown. Numerous organisms have v_ isloated in laboratories from affected birds. ' iong these have been E. coli, paratyphoid species , yeasts; in a few instances, coccidia have been g d in the intestinal contents. However, it is A ieved generally that these organisms are coinci- tal or secondary invaders, and primary causa- agents. Experimental transmission studies have proved that this is a contagious disease. fxins, such as might be produced by poisonous g1». nts, have been suspected, but not proved. I. Symptoms and lesions: Hemorrhagic enteritis -.~ been observed in many strains of turkeys and Z» various feed programs. Greatest incidence pears to be during hot, dry weather. It is seen i. often on range or drylot in birds 9 to l3 weeks ; age. Fortunately, total mortality seldom ex- ?» l0 percent. Usually, the only sign is one or more dead f o on range. Mortality may continue for a few __ ys, then stop. In some cases, daily loss of a few " u may last several weeks. Occasionally, a few birds may appear sick before l‘ die. Symptoms are not characteristic-the i s may appear drowsy and pale. Although there i. observed in an infected flock. Lesions are confined primarily to the intestinal i t. The most characteristic finding is a severe orrhagic inflammation of the intestinal lining j. n gizzard t0 ceca; the intestines are filled with f..." and debris having a jam-like consistency. -.- dark blood may extend into the ceca and d- Occasionally, small hemorrhages may occur in muscles of the breast and legs and on the heart, er, kidneys and other internal organs. 7;, Diagnosis: Gross lesions are sufficiently char- ristic to allow a diagnosis in most cases. i; Treatment and prevention: There is no specific :4». tment. Changing the ration has appeared gective in some cases; however, spontaneous re- i ery may have taken place irrespective of the nge. Moving birds to new range may be bene- 'al. Provide affected flocks with an abundance j fresh, pure water; also give them adequate shade ‘g- u the sun if possible. Remove dead birds from l range promptly; ' AORTIC RUPTURE r Aortic rupture is a. disease of turkeys char- “erized by rapid onset and immediate death due be some bloody droppings, they usually are to internal hemorrhage. It seldom is observed in other birds, but may occasionally affect chickens. Male turkeys, usually the most rapidly growing birds in the flock, are affected most frequently. The disease usually appears in growing birds be- tween the ages of 8 and 20 weeks, although older birds may be affected. Cause: The cause has not been determined. High energy intake during rapid growth appears to be related to occurrence. Deposition of fatty substances in the blood vessel walls weaken the vessels, making the birds more subject to rupture. Subsequent increases in blood pressure, common in adolescent male turkeys, produce the ‘actual rup- ture. Transmission: Aortic rupture is not infectious and is not transmitted from one bird to another. Symptoms and lesions: Seldom are preliminary symptoms observed. Affected birds usually are found 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 10 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 rather 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; however, the disorder is considered to be a disturb- ance in mineral metabolism. Symptoms and lesions: Affected birds are para- lyzed but they will continue t0 eat and drink if feed and water is within reach. Many birds lay on the day paralysis develops and some may con- tinue to lay for a day or two after becoming 35 paralyzed. Shell quality remains good. Morbidity usually is 10w 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 leucosis should be ruled out. Treatment: Affected birds usually make a spontaneous recovery if placed on the floor or if the cage bottom is covered with newspaper or other such material. FATTY LIVER SYNDROME Fatty liver syndrome is characterized by de- ranged fat metabolism resulting in the deposition of excess fat in the liver and body cavities. It is seen most 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. 36 Symptoms and lesions: Affected birds usuall experience a drop in egg production, may r-i» anemic and occasionally may be found dead with out preliminary symptoms. Diarrhea, though comf mon in caged birds, especially is pronounced t; birds with fatty liver syndrome. a Post mortem findings are characteristic, but v with severity. Livers of affected birds are pale yellow and extremely friable. The livers may hav subcapsular hemorrhages varying in size from pin point to massive. Deaths associated with fatty liv syndrome usually are due to hemorrhage fr’, spontaneously ruptured livers. Fat content of that liver may be 55 to 70 percent on a dry-weight. basis, as compared to 5 to l0 percent for normal birds. Deposition of excess abdonimal fat is alsg a common finding; such fat usually is extremely liquid in nature. a Diagnosis: Diagnosis is based on history, sympi toms and lesions. j Treatment: The treatment most likely to effect a favorable response is to add 500 grams of choline, 12 milligrams of vitamin B12 and 5,000 to 10,0, units of vitamin E per ton of feed. Hold protein level at l7 percent. Feed the modified diet for an; indefinite period. i: SECTION 6. i’ otozoa are the smallest members of the animal iom. Although many microscopic protozoan a isms are harmless, others can produce severe e. This section includes five of the more in and important poultry diseases caused by organisms. V COCCIDIOSIS g occidiosis is a highly contagious, protozoan - e of fowl characterized by diarrhea, unthrifti- l and variable mortality. It is a problem in all f‘ try producing areas. Despite recent advances ‘ ntrol and treatment, the disease remains one e principal causes of economic loss to the ' try industry. l ause: Coccidiosis is caused by minute, micro- “ic, animal forms called coccidia. There are a hber of species of coccidia, each of which pro- a distinct disease process. Following an out- of coccidiosis, a flock will be protected j t subsequent exposure to the species which ’uced the outbreak, but it will remain suscep- to other species. This means a given flock have several outbreaks of coccidiosis, depend- ’ on the species of coccidia in an area and . ure to them. The species of coccidiosis affecting chickens and up keys are: Chickens ‘ 1 Eimeria tenella* Eimeria necatrix* Eimeria acervulina* ‘ Eimeria brunetti* i Eimeria maxima* Eimeria mitis Eimeria hagani i Eimeria praecox Turkeys Eimeria aden0eides* Eimeria meleagrimitifi Eimeria meleagridis Eimeria dispersa Eimeria gallopavonis Eimeria innocua Eimeria subrotunda lidered the major causes of clinical outbreaks. ‘ Transmission: Coccidiosis is transmitted by ect or indirect contact with droppings of infected s. When a bird eats coccidia, the organisms l. ade the intestinal tract lining where they pro- l e tissue damage while undergoing reproduction. 'thin a week after eating coccidia, an infected é- will shed descendant coccidia in its droppings. g great is the reproductive potential that a single nism may produce about 1 million descendants. 's means infectiolnman build up rapidly, even l a new house. A Coccidia shed in droppings are incapable of ecting other birds until certain maturation a nges (sporulation) take place. These changes PROTOZOAN DISEASES occur in 24 to 72 hours if the litter is warm and damp. The number of infective coccidia that a bird eats determines whether an infection will be mild enough to go unnoticed or severe enough to cause visible illness. Coccidia are extremely resistant to environment and may survive for long periods. They are trans- mitted easily from one house or premise to another by dirty boots, free-flying birds, feed sacks, equip- ment and others. ' 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 diarrhea and may become emaciated and de- hydrated. Laying birds will experience a drop in production. Cecal coccidiosis of chickens, caused by E. tenella, is often acute and characterized by bloody droppings, severe anemia and high mortality. In turkeys, cecal coccidiosis, caused by E. adenoeides also is often acute, producing high mortality, but seldom bloody droppings. Intestinal coccidiosis may be acute, but more frequently is chronic in nature. Droppings of affected birds are usually tan and watery, although acute E. necatrix infection may produce consider- able hemorrhage. Since there is a slower build up of infection. of intestinal coccidia, intestinal coccidi- osis usually occurs in birds in the latter part of the growing period or in early production. Mortal- ity usually is not significant unless acute E. necatrix or E. maxima infection is present. Autopsies of birds with coccidiosis reveal lesions that vary depending upon type of coccidiosis present and severity and stage of the disease. Chickens in the acute phase of cecal coccidiosis will have ballooned cecal pouches full of free blood. In the recovery stage, cheesy cores, tinge-d with variable amounts of blood, will be present in the cecal pouches. Free blood usually is not found in the ceca of turkeys with cecal coccidiosis, but the ceca contain a white to gray semi-gelatinous ma- terial resembling cottage cheese in consistency. Lesions of intestinal coccidiosis vary from a rather mild enteritis to a severe necrotic /hemor- rhagic type of enteritis. 37 Diagnosis: Cecal coccidiosis may be confused with blackhead and Salmonellosis, both of which may produce similar cecal lesions. Intestinal coccidiosis may be confused with hemorrhagic anemia syndrome and other disease characterized by enteritis. Establish definite diagnosis by labora- tory means so that medicatio-n can be specific. Do this by microscopic examination of intestinal or cecal scrapings to demonstrate the presence or absence of coccidial organisms. Since most healthy birds possess a few organisms, it is necessary to correlate microscopic findings with flock history and autopsy lesions before making diagnosis and recommendations. Treatment and prevention: An outbreak of coccidiosis usually can be controlled by medication with certain sulfonamides. Sodium sulfaquinoxa- line or sodium sulfamethazine (Sulmet) may be used. Use drugs according to directions on the label. In general, they are used as follows: Chickens: Sulfaquinoxaline The commercial liquid preparation contains 3.44 percent sulfaquinoxaline. For the first 2 or 3 days, mix the drug in drinking water at the rate of 3 tablespoons (or 11/2 ounces) per gallon, giving a concentration of l:2500 (0.04 percent). Supply non-medicated water for 3 days and follow with sulfaquinoxaline for 3 days at the rate of 2 tablespoons (or l ounce) per gallon, giving a concentration of l:4000 (0.025 percent). If neces- sary to continue treatment, supply nonmedicated water for 3 days, after which the 114000 (0.025 percent) concentration can be given an additional 2 days. Sulfamethazine (Sulmet). The commercial liquid preparation contains 12.5 percent sulfa- methazine. Mix the drug in drinking water at the rate of 2 tablespoons (or l ounce) per gallon, giving a concentration of 1:l000 (0.1 percent). Supply medicated water for 3 days followed by 3 days on nonmedicated water. Repeat treatment for 3 days and follow with nonmedicated water another 3 days. Continue treatment for an addi- tional 1 or 2 days if necessary. Turkeys: Sulfaquinoxaline Mix the drug in drink- ing water at the rate of 2 tablespoons (1 ounce) per gallon, giving a concentration of 124000 (0.025 percent). The medication schedule is: Medicated water for 3 days; nonmedicated water for 3 days; medicated water for 3 days; nonmedi- cated water for 3 days; medicated water for an additional 1 or 2 days if necessary. Sulfamethazine (Sulmet). Administer the drug as outlined for chickens. 38 lment chickens and at a level of 0.0175 percent, for When sulfonamides are used in drinking wat _ to treat coccidiosis, do not use feed containin sulfonamides since toxicity problems- may result. l It is difficult, if not impossible, to preven coccidiosis by sanitation practices alone. Coccid'f osis is prevented best by feeding a coccidiostat. Al coccidiostat is a drug addedtd feed at low leve and fed continuously to prevent coccidiosis. good coccidiostat should: Prevent clinical outbreaks of coccidiosis. F’ Have no undesirable side effects (depress weight gain, production and others). ‘ Allow a natural immunity to coccidiosis to d velop in the flock if exposure is present. i“ Be cheap. p) Feed broilers a ration containing a coccidiostat.-f continuously until the last week prior to marketing, Feed replacement birds a ration containing coccidiostat continuously until about l6 weeks oldfi Give turkeys a coccidiostat during the growi ;v period while confined and for an added week or; l0 days after moving to range. y: Many coccidiostats are available on the market} Most are suitable for broilers. However, sulfaf quinoxaline, fed at a level of 0.015 percent, considered the coccidiostat of choice for replace-f‘ turkeys. A “so-called” vaccine to control coccidiosis available commercially. Use of the product not encouraged in Texas now. BLACKHEAD (Histomonicsis, Infectious Enteroheputitis) Blackhead is an acute or chronic, infectio protozoan disease of fowl, primarily affecting the? ceca and liver. The disease is present wherever poultry are raised. Blackhead is one of the mosti important diseases of growing turkeys, causing. stunted growth, poor feed utilization and death? loss. It is of lesser economic importance in chickensj since chickens are more resistant. Cause: Blackhead is caused by a protozoan parasite called H istomonas meleagridis. . Transmission: The blackhead organism, Histoé ‘ monas meleagridis, is passed in the fecal materi of infected birds. In many instances, the organis - is shed within the eggs of Heterakis gallinae, th, , cecal worm of chickens and turkeys. Free livi forms do not survive long in nature, but organis l»; contained within cecal worm eggs may survive f0 months or years. Because of this, most blackhea transmission is considered due to ingestion (eatin v worm eggs infected with the blackhead 'sm. A hickens frequently are infected with blackhead v out showing signs of the disease. These chick- fimay shed enormous numbers of blackhead or- 1 ms, many of which are protected by cecal _,~»| eggs since cecal worms are so common in ens. Because of this, outbreaks in turkeys oft- iw be traced to direct or indirect contact with , houses or equipment previously used by ens. l; tee-flying birds also may introduce an infec- fymptoms and lesions: Most blackhead losses L‘ in birds 6 to 16 weeks old. Among the symp- y)»: are: loss of appetite, increased thirst, droopi- a and drowsiness, darkening of the facial regions ackhead”) and diarrhea (sulfur-colored drop- Morbidity and mortality are variable, but if lity is seldom above l0 to l5 percent; how- , it may approach 80 to 90 percent in uncon- ed turkey outbreaks. In chickens, losses usually 510W. A sions of uncomplicated blackhead are con- ’ v to the ceca and liver; thus the reason for the F ymous term, enterohepatitis. The ceca are bal- ed and walls may be thickened, necrotic and a ted. Gaseous (cheesy) cores, which may be resent if ulcers have perforated the ceca walls. l, are swollen and display circular depressed of necrosis about 1/2 inch in diameter. Lesions “yellowish to yellow green and extend deeply in- _ e underlying liver tissue. Healing lesions may ible those seen in visceral lymphomatosis. _ - ions observed in chickens frequently are 'cal as the liver lesions may be absent or less i; unced. 5 iagnosis: Blackhead presenting typical lesions iagnosed readily on the basis of the lesions. ical forms, particularly in chickens, must be ‘rentiated from cecal coccidiosis and salmonel- ection in particular. Laboratory tests, micro- ic and cultural, may be required. Treatment and prevention: A number of drugs , e market can be added to drinking water to F; blackhead outbreaks under control. Use these f. pounds in accordance with the manufacturer’s f." endations. Palatability may be a problem A certain compounds, thus making it difficult to proper drug intake. management practices can do much to I: ol the blackhead problem. Do not maintain l‘ eys and chickens on the same premise. Do not turkeys on ground previously used by chick- 5e tinged, usually are present. Peritonitis may» ens unless several years have elapsed. Rotate ranges at periodic intervals if possible. Cecal worm control may help reduce blackhead incidence. Wire or slat- ted 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 pre- vent 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 particu- larly important disease of turkeys, pigeons and quail, and is of lesser importance in chickens. Cause: A protozoan parasite called Trichomon- as 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 in- troduce an infection to a premise. Once intro- duced, the disease spreads as birds eat or drink ma- terials contaminated by droppings or oral dis- charges of infected birds. Recovered birds may be- come indefinite carriers. Symptoms and lesions: Most turkey losses due to trichomoniasis occur in young and growing birds. Among the symptoms are loss of ap-petite, droopi- ness, loss of weight and darkened heads. The chest may be depressed as the crop usually is empty, although occasionally the crop is distended and filled with foul smelling fluid contents. Morbidity in a flock may be high, but mortality usually is low except in severe outbreaks. The course of the disease usually is prolonged in turkeys unless affected birds are cannibalized. Lesions of uncomplicated trichomoniasis usual- ly are confined to the upper digestive tract, affect- ing the crop in particular. Occasionally oral lesions are observed. Lesions consist of necrotic ulcerations with accumulations of caseous material which build up over the affected areas. Some research workers have described lesions of trichomoniasis involving the ceca and liver which resemble those of blackhead. Although trichomon- ads frequently are found in the lower intestinal tract, workers have not found that blackhead-type lesions are associated with the organisms. Diagnosis: Trichomoniasis is diagnosed on the basis of lesions and demonstration of the causative 39 organism on slide preparations viewed through the microscope. Other diseases, such as crop capillaria infection or fungus infections of the crop, may pro- duce similar lesions; do not make a diagnosis with- out microscopic examination. Treatment and prevention: Move birds to sani- tary surroundings, if possible. Birds may be treated with copper sulfate (“bluestone”) in the drinking water at a lz2000 dilution for 4 to 7 days. Make the copper sulfate solution as follows: Stock solution — Add l pound of copper sulfate to a gallon of water containing l cup vinegar. Mix thoroughly to get into solution. (Never give undiluted stock solu- tion to birds.) Drinking water solution — Add 1 tablespoon (1/2 ounce) of stock solution to each gallon of drinking water. Trichomoniasis is not a problem if birds are supplied with sanitary surroundings, including well-drained ranges, clean drinking water and feed. HEXAMITIASIS (Infectious Cutarrhul Enteritis) Hexamitiasis is an acute infectious disease of turkeys, quail, ducks, chukar partridges and pig- eons. Heavy losses have been reported in one out- break among ringnecked pheasants. Chickens ap- parently are not affected. It was reported first in ducks and pigeons in 1923 and in turkeys in 1938. Before establishing the true nature of the disease in turkeys, the condition was thought to be tricho- nomiasis. Hexamitiasis is recognized as a disease problem in every commercial turkey-producing area. It may be a major problem in localized areas during a par- ticular year, followed by one or more- years in which incidence is very low. Cause: Hexamitiasis is caused by a bilaterally symmetrical, flagellated, one-celled parasite of the genus Hexamita. Hexamita meleagridis is the cause in turkeys; 'in pigeons it is Hexamita columbae. Experimentally, the H examita of turkeys was trans- mitted to young quail, chicks and ducklings, and that of quail and partridges was transmissable to poults. However, poults could not be infected with the organism isolated from pigeons. Transmission: Hexamitiasis is primarily a dis- ease of young birds and outbreaks seldom occur in poults past 10 to ll weeks of age. Losses are most severe in birds 3 to 5 weeks old. Apparently resist- ance develops rapidly with increasing age, regard- less of previous exposure. 40 The primary infection source is droppings n1 carrier birds. About a third of recovered birds r? come carriers. Most outbreaks result from a build? up of organisms through several broods of poul J in such a manner that exposure of the followin brood is overwhelming. Indirect transmission ma result from fecal material carried from one locati t} to another on shoes or equipmierit. Free-flying birds such as quail also may be carriers. Symptoms and lesions: Symptoms primarily a f listlessness and foamy or watery diarrhea with ran" id weight loss due to the dehydrating effect. Bir often will huddle together near the heat source 1L cry or “chirp” constantly as though in pain. Con vulsions due to lowered blood sugar levels shortly- precede death. Survivors suffer great losses ini weight and remain stunted for long periods. i‘ Dehydration and emaciation are the principle gross lesions. The intestine usually appears to have," lost tone with local bulbous areas of congestionsi Intestinal contents usually are thin and watery. A Diagnosis: Diagnosis depends upon historyj; symptoms and microscopic examination of intestin- al contents. A definitive diagnosis cannot be made unless typical flagellates can be demonstrated in in- testinal contents taken from the duodenum area; ' Most flagellates observed in the ceca area are non-{ pathogens. Treatment and prevention: Prevention depend upon sanitation with particular emphasis upon; separating age groups. If an individual must care)‘ for several age groups, care for the younger group? first. Hepzide fed continuously at levels of 0.025 and 0.035 percent will aid in preventing losses. > Hepzide at a level of 0.02 in water now appe to offer the most promise as a therapeutic measure; The disease does not respond well to treatment: but 112000 solutions of copper sulfate with dried whey (3 to 4 ounces dried whey per gallon of the. dilute solution) is an old stock remedy. This solui tion 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 ration is of some benefit. 1 LEUCOCYTOZOONOSIS Leucocytozoonosis is an acute, sometimes highl. fatal disease of young turkeys and ducklings. A causative protozoan parasites invade the victi circulatory system where they destroy great "i i bers of leucocytes (monocytes and macrophages)- In certain respects the disease resembles true n a t birds are the sole hosts of the genus Leu- 0n. A; disease occurs in many areas of the country, i“ frequently in the South and Southeast. 'ty may reach 100 percent in ducklings up f a ks of age and losses may be severe in tur- _» to 12 weeks of age. Clinical symptoms us- ‘3- are not apparent in older birds, but they f7:- ain carriers for months. e: A protozoan parasite similar to the true . parasite is the cause. The organism respon- for the disease in turkeys is designated as g tozoon smithi; in ducks it is called Leuco- gn dimondi. “transmission: The disease is transmitted by l? species of the black fly, Simulium s12. which -_in running streams. After feeding on infect- ~ , the flies can transmit the disease at the if 4 days and remain infective for about l8 ‘Direct transmission from bird to bird does not Recovered birds remain carriers and serve rvoirs of infection in subsequent years. mptoms and lesions: Younger affected birds ‘flack appetite and exhibit droopiness, weak- increased thirst and rapid labored breathing. wsy birds are made to move they may become y excited. The course of infection usually is f with visible symptoms seldom lasting more 2 or 3 days, terminating in death or begin- irecovery. Recovered birds may appear stunted with the flock as a whole appearing to lack uni- formity. In adult birds clinical symptoms seldom are detectable. The most consistant pronounced gross lesion is spleen enlargement and congestion. Anemia and emaciation usually are evident in clinically ill birds. The flesh of affected birds often is flabby and yellowish. Mild congestion of the upper intes- tinal 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 not rear- ing turkeys near running streams. Segregate breed- ing and brooding operations since adults may be carriers. Brooding in screened houses will prevent infection of young birds. Drugs effective against malaria appear to have little if any value in Leucocytozoonosis. Sulfaquin- oxaline is considered valuable in reducing losses. Administer it in the drinking water at a level of 0.025 percent for 5 to 7 days, and follow by adding it in feed at a level of 0.0175 to 0.025 percent until losses are controlled. Refer to Texas Agricultural Extension Service publication MP-69l, Texas Guide for Controlling External Parasites of Livestock and Poultry, for rec- ommended insecticides and methods of use. 41 SECTION 7. POULTRY LICE The chief effects of lice on their host are due to the irritation they cause. The birds become restless and do not feed or sleep well and may injure them- selves 0r damage their feathers by pecking or scratching the parts irritated by lice. Weight gains and egg production may drop. All lice infecting poultry and birds are of the sucking.and chewing type. Mites may be confused with lice. The mites suck blood. In general, each species of lice is confined to a particular kind of poultry, although, some may pass from one kind of poultry to another when birds are closely associated. Chickens usually are infested with one or more of seven different species; turkeys have three common species. All species of poultry lice have certain common habits. All live continuously on feathered hosts and soon die if removed from them. The eggs are at- tached to the feathers. Young lice resemble adults except in color and size. They differ in preferred locations on the host, and these preferences have given rise to the common names applied to various species. In general the incubation period of lice eggs is 4 to 7 days, and development of the lice from hatching to the adult stage requires 17 to 21 days. Mating takes place on the fowl, and egg laying be- gins 2 or 3 days after lice mature. The number of eggs probably ranges from 50 to 300 per female louse. The Head Louse As the name suggests, this species (Lipeurus heterographus) is found mainly on the head, al- though it occurs occasionally on the neck and else- where. It usually is located near the skin in the down or at the base of the feathers on top and back of the head and beneath the bill. In fact, the head of the louse often is found so close to the skin that poultrymen may think it is attached to the skin or is sucking blood. Although it does not suck blood, the louse is very irritating and ranks first among lice as a pest of young chickens and turkeys, which often become infested within a few hours after hatching by lice from the mother. Heavily infested chicks soon become droopy and weak and may die before they are a month old. When the chickens be- come faily well feathered, head lice decrease, but they may increase again when the fowls reach ma- turity. This louse is oblong, grayish, and about 1/10 inch long. The pearly-white eggs are attached sin- gly to the down or at the base of the small feathers 42 PARASITIC DISEASES 0I1 the head. They hatch in 4 or 5 days into min ; pale, translucent lice, resembling adults in sha i The Body Louse The body louse (Menacanthus stramineus) chickens prefers to stay on thézskin rather than the feathers, and it chooses parts of the body I are not densely feathered, such as the area be the vent. In heavy infestations it may be found‘ the breast, under the wings, and on other p I the body, including even the head. ’ When the feathers are parted, straw-col body lice may be seen running rapidly on the in search of cover. Eggs are deposited in clus near the base of small feathers, particularly vfl the vent, or in young fowls, frequently on the l or along the throat. Eggs hatch in about a e-_ and lice reach maturity in 17 to 20 days. This is the most important louse infes grown chickens. When present in large num the skin is irritated greatly, and scabs may res especially below the vent. a The Shaft Louse The shaft louse, or small body louse (Men _ gallinae) , is similar in appearance to the I louse, but smaller. It has a habit of resting on body feather shafts of chickens, where it may, seen running rapidly toward the body when f A ers are parted suddenly. Sometimes as many --» dozen lice may be seen scurrying downward alo feather shaft. Since the shaft louse apparently feeds on r? of the feathers, it is much less important than‘: relative, the body louse. It is found in limited n _ bers on turkeys, guinea fowl and ducks kept = close association with chickens. It does not i young birds until they become well feathered. * Other Kinds of Chicken Lice Four other kinds of lice usually are found‘. chickens, but they are less abundant and impo than the ones previously discussed. The wing 0; (Lipeurus caponis) , a slender gray species res n1 ing the head louse, is the most widely distrib _ and is found in the greatest numbers. It is slu and usually is seen resting between the barbul the wing and tail feathers, or occasionally on ' neck hackles and back feathers. A ' The fluff louse (Goniocotes hologaster) , =7 is found, as the common name implies, on the y’ of the body feathers, is small, rather broad, ye. and inactive. As it stays mostly in the fluff, it é little irritation or other injury. ° large chicken louse (Goniocotes gigas) is a i], dark, smoky-gray species of striking appear- I\It is seldom abundant or of much import- brown chicken louse (Goniodes dissimilis) , 'ng mainly in the southern states, is large idish brown. It seldom occurs in large _ numbers to cause serious damage. , POULTRY MITES classes of poultry are susceptible to mite at- isome of which are blood-suckers, while others a -in the skin or live on or in the feathers. thers occur in the air passages and in the sliver and other internal organs. 5 ltry mites cause retared growth, reduced roduction, lowered vitality, damaged plum- d even death. Much of the injury, consisting Jstant irritation and loss of blood, is not ap- gt without careful examination. A Common Chicken Mite . is mite (Dermanyssus gallinae) is probably 0st common mite found in all types of poul- is a blood-sucker, and when present in large _~ rs loss of blood and irritation is sufficient to ' anemia. Egg production is reduced seriously. _. is mite is a night feeder, and usually remains _, in cracks and crevices during the day and ‘é - birds at night while on the roosts. In very infestations some mites may remain on the during the day. About a day after feeding, male lays eggs in cracks and crevices. The atch and the mites develop to adults in about k. During cold weather the cycle is slower. ' ltry house remains infested 4 to 5 months aft- is vacated. nce the mite will feed on wild birds, they may ~ ponsible for some infestations, but spread " likely is caused by using contaminated coops. carriers are important. Since these mites ‘t stay on the birds during the day, apply treat- _, to the houses and equipment, not on the Feather Mite p is mite (Leponyssus sylviaruns) is an occa- , but serious pest of chickens. Heavy infesta- result in lowered condition of the birds and ' d egg production as well as a scabby skin ition. This mite remains on the bird and does . damage than the‘ common chicken mite. It re- les the common chicken mite, but can be dif- l-tiated in that it is present on birds in large rs during the day. It prefers the feathers be- e vent and around the tail, but can be found l 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 to birds is necessary to destroy the mites. Sculy-Leg Mite This mite (Cnemidosoptes 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 birds, and spreads from bird to bird, mainly by direct contact. Depluming Mite This mite (Cnemidocoptes gallinae) causes se- vere irritation by burrowing in the skin near the base of feathers, and frequently causes feathers to be pulled out or broken. The mite is barely visible to the naked eye and can be found in follicles 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 persicas) is one of the most serious parasites of poultry when it becomes numer- ous in poultry houses or on a poultry range. The tick is a blood-sucker, and when present in large numbers results in weakened birds, reduced egg production, emaciation and even death. The fowl tick is found throughout most of the South and is extremely hardy. Ticks have been kept alive without food for more than 3 years. Ticks will feed on all types of fowls. The ticks spend most of their life in cracks 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 batch of eggs. The female may lay several batches with a blood meal between each. In warm weather the eggs hatch in l0 to l4 days. In cold weather they may take up to 3 months. Larvae that hatch from the eggs crawl around until they find a host fowl. They remain attached to the birds for 3 to 10 days. Then they leave the birds and find a hiding place. After a few days they molt, then seek another blood 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 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. Nor- 43 , mally these small mites feed on wild animals, birds, snakes and lizards. Only the larvae of chiggers at- tack poultry or animals, adult mites feed on plants. Larvae usually attach to the wings, breasts and necks of poultry. They inject a poisonous substance that sets up local irritation and itching. After a few days it becomes engaged and drops off. Injury to grown fowl may not be apparent or noticed until the bird is dressed; then the lesion shows up and greatly reduces carcass value. Young chickens or turkeys may become droopy, refuse to eat and die. Due to methods of raising poultry, turkeys are af- fected more frequently than chickens. LARGE ROUNDWORMS One of the most common parasitic roundworms of poultry (Ascaridia galli) occurs in chickens and turkeys. Adult worms are about 11/2 to 3 inches long, and about the size of lead in an ordinary pen- cil. Thus they can be seen easily with the naked eye. Birds heavily infected may show droopiness, emaciation and diarrhea. Death may occur in very heavy infections, but the primary damage is re- duced efficiency. Chickens 3 to 4 months old show resistance to infection. Specimens of this parasite are found occasional- ly in eggs. The worm apparently wanders from the intestine up the cloaca and is incorporated in the egg as it is formed. The life history of this parasite is simple and direct. Females lay thick heavy shelled eggs in the intestine and these pass in the feces. A small em- bryo develops in the egg. They do not hatch. Two to 3 weeks are required for the larvae in the egg to reach infective stage. These embryonated eggs are very hardy and under laboratory conditions may remain alive for 2 years. Under ordinary conditions, probably not many live more than l year. Disin- fectants and other cleaning agents do not kill eggs under farm conditions. Birds become infected by eating eggs after they have reached the infective stage. Available drugs will remove only the adult par- asite. The immature form probably produces the most severe damage. Now the treatment of choice is piperazine. Many forms o-f piperazine are pro- duced, and all are effective if administered proper- ly. Follow the manufacturer's instructions exactly. The parasite can be controlled by strict sanita- tion. If the birds are confined, thoroughly and completely clean the house before a new group is brought in. Segregate birds by age groups, with articular care applied to sanitation of young birds. If birds are on range, use a clean range for each new groupgof birds. 44 CECAL WORMS This parasite (Heterakis gallinae) is found the ceca of chickens, turkeys and other birds. Th worms are small, white and measure % to 1/2 inch, in length. . This parasite, probably the most common wo {j parasite of poultry in the United States, apparen ‘I does not seriously affect the health of the bird. ‘ i least no marked symptoms or pathology may F blamed on its presence. The main importance a that it has been incriminated as a vector of Hispfv monas meleagridis, the agent that causes blackhié: or infectious enterohepatitis. This protozoan p ‘ site is apparently carried in the cecal worm egg a g is transmitted from bird to bird through the egg. The life history of this parasite is similar to of the common roundworm. The eggs are produc p, in the ceca and pass in the feces. They reach the if fective form in about 2 weeks. In cooler weath this may take longer. The eggs are very resistant f_ environmental conditions and will remain for lo periods. A The cecal worm can be removed by treatm u; with any of the piperazine compounds. Since r worm itself produces no observable damage, an the eggs live for long periods, it is advisable w» ’ necessary to keep chickens and turkeys separat to prevent spread of infectious enterohepatitis. Y‘ TAPEWORMS _ Tapeworms or cestodes are flattened or ribbon shaped worms composed of numerous segments r_ divisions. Tapeworms vary in size from very sm to several inches in length. The head or anteri end is much smaller than the rest of the body. Sin the tapeworm may be very small, careful exami tion often is necessary to find them. A portion l1? the intestine may be opened and placed in wati to assist in finding the tapeworms. The pathology or damage tapeworms produf in poultry is controversial. In young birds, hea infections result in reduced efficiency and slow, growth. Young birds are more severely affect g than older birds. I All poultry tapeworms apparently spend pa ' of their life in an intermediate host, and birds --{ _ come infected by eating the intermediate hos L’ These hosts include snails, slugs, beetles, ants, ; . ' i hoppers, earthworms, houseflies and others. _ intermediate host becomes infected by eating p I eggs of tapeworms that are passed in the feces. ‘A No effective drugs to remove tapeworms f o g poultry are known. The tapeworms can be v trolled by preventing the birds from eating the i_ fected intermediate hosts. SECTION 8. GLOSSARY OF TERMS Active immunity — immunity or resistance to disease that has been acquired by host response to a disease agent. It can be acquired by having a dis- ease and recovering or by vaccination. Acute — as applied to disease, one which has a short and relatively severe course. Anemia -— a condition in which the blood is deficient in quantity or quality. lf deficient in quality there is a reduction in the hemoglobin con- tent of the blood or in the number of circulating red blood cells, or both. Anemia is characterized by paleness of skin and mucous membranes and loss of energy. Antibody — an immune substance found in the blood produced in response to stimulation by an antigen. Antigen — a suspension of microorganisms. A substance which, when taken or injected into the body, will stimulate antigen production. Diagnostic Antigen — used to detect the presence of specific antibodies in the blood of an animal; used in sero- logical tests. Antiserum — serum containing specific anti- body used to treat a specific disease. Antitoxin — a specific kind of antibody that will neutralize toxin. Bacteria — microscopic, single - celled plant forms widely distributed in nature. Those capable 0f producing disease are referred to as pathogenic bacteria. Bacterin — killed suspension of bacterial organ- isms used as an immunizing agent. Bipolar —- as applied to a bacterial cell, one which will stain deeply at the cell ends and takes little stain centrally. Bivalent — as applied to antigens or bacterins, one which is made up of two strains of organisms. Carrier -— an apparently healthy animal that harbors disease organisms and is capable of trans- mitting them to other susceptible animals. Catarrhal — describes an inflammatory process . F . . involving the mucous membranes characterized by an increased flow of mucous. Chronic — as applied to disease, one of long duration. Cocci — bacterialiflgforms which, when fully de- veloped and free, are spherical. Coccidiostat — drug incorporated into the feed at low levels and fed continuously to prevent coc- cidiosis. APPENDIX 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 propagat- ed 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. 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 dis- ease 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 patho- genic organisms resulting in a disease state. Infectious —— as applied to disease, one produced by livingorganisms. As applied to living organisms, those which are capable of producing disease. Inflammation — response of tissues to an in- jury or other irritant. “Itis” — suffix denoting an inflammatory state, such as enteritis —— inflammation of the intestines, air sacculitis — inflammation of the air sacs. Lesion — visible change in size, shape, color or structure of an organ. Listless — indifferent to surroundings. Microscopic — invisible to the naked eye, visible only by the aid of a microscope. 45 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 ani- mal form that lives onior within a bird to the detri- ment 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 applied to organisms, one cap- able 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 to dis- ease that has extremely sudden onset and a short, severe course. Petechial — as applied to hemorrhage, char- acterized by small hemorrhagic spots. Polyvalent —- as applied 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 — abnonnal respiratory sound; rattling, wheezing. Rickettsial - a group of microorganisms inter- mediate between the bacterin and the viruses, some of which are pathogenic to man and animals. Rod — as applied to bacteria, a cylindrical shaped organism. Serological 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 occuring here and there; not widely diffused. Spore- as applied to bacteria and fungi, a re- productive element capable of resisting unfavor- able environmental conditions. 46 Stress — factor tending to lower resistance of a I animal to disease, such as chilling, moving, etc. A Symptom -— detectable signs of disease. Toxin -— poison produced by microorganism. Tumor — neoplasm; a mass of new tissue whi i persists and grows independently of its surroundin’ structures, and which has no physiologic use. Vaccine — suspension of large amounts of d’) ease organisms used to produce immunity in animals to which it is administered. * Virulence — as applied to a pathogenic mic -. scopic organism, its ability to overcome the u: defenses of the host. "Y Virus — ultramicroscopic microorganisms; so “If capable of producing disease. -‘ TABLES OF WEIGHTS AND MEASURES Weights l gram (g) I 1000 milligrams (mg) l kilogram (kg) I 1000 grams 1 ounce (oz) I 38.35 grams l pound (lb) I 16 ounces I 0.4536 kilogra i" I 453.6 grams ~ Liquid Measure l Liter (L) I 1000 milliliters (ml) I 33.8] ounces l gallon I 4 quarts I 8 pints I 231 cu’ inches I 3.785 liters ’ gallon of water I 8.34 pounds teaspoon I 4.93 milliliters v tablespoon I 3 teaspoons I 14.79 millilitf fluid ounce I 2 tablespoons 3 cup I 8 fluid ounces I l6 tablespoons I 236.6 milliliters l pint I 2 cups I 16 fluid ounces I 473.2 milliliters ¢_4-_4u—n_-nv_a Working Tables of Weights and Measures (Approximate Values) Parts per million (p.p.m.) l gram in l ton (2000 lb.) I 1 p.p.m. l pound in 500 tons I l p.p.m. l 2 milligrams in l gallon of water I l p.p.i Thus, if feed is to be medicated at a level 200 p.p.m., add the medicant at the rate of g grams per ton. l Thus, if water is to be medicated at a level-l’ 200 p.p.m., add the medicant at the rate of milligrams per gallon. * Dilutions To make a l-2000 dilution of a drug in dri ing water, add l ounce of drug to l6 gallons? water. ' ” [Blank Page in Original Bulletin] o; é Texas Agricultural Experiment Station, R. E. Patterson, Director, College Station, Texas