Handbook of poultry diseases Improved biosecurity and an awareness of the need for appropriate vaccination programs, reduces the

potential losses caused by both catastrophic and erosive infections on commercial-scale farms, village cooperatives and in integrated operations.
Conceptual Biosecurity: Structural Biosecurity:

CYCLE de gestion dans un levage

valuation des risques et des consquences des maladies

analyse et bilan de production et de performance financire

planification des stratgies de prvention contre les maladies ainsi que la prvention

implentation de la bioscurit ainsi que de la vaccination

Physiological Effects of High Ambient Temperature

Exposure of poultry flocks to ambient temperature above the zone of minimum metabolism results in an increase in endogenous heat production. Exposure to high environmental temperature for extended periods will suppress the humoral immune response of chickens, reducing antibody titer. It is presumed that a reduction in circulating antibody is associated with a corticosteroid-induced change in serum ions. Cellular immunity is also suppressed by prolonged exposure to temperatures in excess of 36C. This effect is mediated through T-cell or regulatory amplifier cell response. PREVENTION OF DISEASE Prevention of disease in commercial poultry operations requires the

application of a coordinated program of biosecurity, vaccination and hygiene. Mechanisms of Disease Transmission In order to develop control procedures it is important to understand the mechanisms by which pathogens are introduced into commercial poultry farms and how disease agents are disseminated among units. Mechanical transmission involves transfer of a pathogen from an infected source or reservoir host to a susceptible flock by contaminated personnel, equipment, insect vectors, rodents, wild birds, or dust carried by wind. Transovarial Route (Salmonella pullorum, Mycoplasmosis, Salmonella Enteritidis) Transmission on the Egg Shell(E. coli and paratyphoid Salmonella spp) Direct Transmission (salmonellosis, coryza, mycoplasmosis, laryngotracheitis and pasteurellosis.) Dissemination by Wind(vvND and ILT has been documented) Indirect Transmission((IBDV Salmonella spp Biological Vectors Wild birds avian influenza and Pasteurella spp. Rodents carry a wide range of diseases including pasteurellosis and salmonellosis Pox, West Nile and Highland J arbovirus may be transmitted by mosquitoes spirochetosis by Argas ticks Alphitobius diaperinus (ordre des coloptres) House flies transmit campylobacteriosis. Feed Contamination of ingredients or manufactured feed with pathogens such as Salmonella spp, or IBD and paramyxovirus virus can result in infection of susceptible flocks Vaccines Contaminated poultry vaccines prepared in eggs derived from non-specific pathogen free (SPF) flocks may contain pathogens including adenoviruses, reoviruses, or the agents responsible for chicken anemia and reticuloendotheliosis. Pathogens may also be transmitted among flocks as a result of contaminated vaccination equipment or personnel used to administer vaccine Biosecurity 4.2.1 Conceptual Biosecurity Location of the complex in relation to concentrations of poultry of the same or different species.

 Distance among breeder and growout farms and facilities such as hatcheries, feed mills, and processing plants or packing units. Location of major and minor roads and the movement of commercial and backyard poultry in relation to company facilities. Proximity to large lakes or waterways or migratory flyways. For commercial egg production consider the implications of multi-age on-line units or single-age, company-owned or contractor-operated facilities. 4.2.2 Structural Biosecurity Fenced farm area with notices to prevent trespass. Fencing of house area, with secured gates. Water supply free of pathogenic bacteria, and chlorinated to a level of 2 ppm. Farm service module comprising an office, storage, and change roomshower facilities. Concrete apron with a suitable water and power supply to permit decontamination of vehicles entering the farm. All-weather roads within secured perimeter to facilitate cleaning and to prevent dissemination of disease agents by vehicles and footwear. Appropriate location of bulk bins or secure, vermin-free storage areas for bagged feed. Installations for disposal of dead birds (incinerators, composters, pits). Secure housing with appropriate bird and rodent proofing. Concrete floors for breeding stock at the grandparent level. In many countries with endemic salmonellosis, concrete floors are required in both rearing and laying housing for breeders. Correct positioning of extractor fans to prevent airborne transmission of pathogens to flocks in adjacent houses. Impervious apron adjacent to the door of each house and installation of drains.

 Feed, unused litter and cleaned equipment should be stored in a module separated from the live-bird area of the house to prevent contamination of flocks by delivery and maintenance workers. 4.2.3 Operational Biosecurity Operational manuals should be developed for routine procedures carried out in feed mills, hatcheries, breeding and grow out facilities. Manuals should incorporate contingency plans in the event of a deviation from normal production parameters or outbreaks of disease on company farms or in units located in close proximity to the operation. Manuals should be developed for appropriate levels of management including company veterinarians and health maintenance professionals, service personnel, contractors, and employees. Standardized procedures should address specific aspects of operation including: o Decontamination and disinfection of units following depletion of flocks. o Storage, reconstitution and administration of vaccines according to recommended route. o Specific procedures on entering and leaving farms should be designated for managers, supervisors, authorized visitors, work crews and permanent and part-time employees. o Controls required to prevent contact with exotic avian species, and backyard poultry.

Salmonella pullorum 20.2 Occurrence and Economic Significance Pullorum disease (or bacillary white diarrhea, BWD) is potentially world-wide in distribution but in practice is confined to non-commercial flocks in many countries. Infection results in high mortality in young chicks. 20.3 Transmission Vertical transmission occurs by the transovarial route. Horizontal transmission takes place by direct contact between clinically affected and recovered carriers and by indirect contact with contaminated equipment, housing, litter, and clothing of personnel. The pathogen can

remain viable in soil for up to a year. 20.4 Clinical Appearance Morbidity in affected batches of chicks often exceeds 40% with corresponding mortality commencing at hatch and extending through 21 days. Affected chicks are depressed and anorexic and tend to huddle under brooders. Birds may show copious white diarrhea and accumulation of fecal material adherent to the plumage surrounding the vent. From 14 days of age onwards affected birds show stunting, poor feathering and frequently lameness due to arthritis. 20.5 Pathology Chicks show enlargement of the spleen and liver. Omphalitis is often present. Chronic cases show abscessation of the viscera (heart, internal serosa, lungs, liver) and chronic caseous typhlitis characterized by grey casts in the ceca. 20.6 Diagnosis Isolation and identification of S. pullorum from liver, intestine or yolk sac using appropriate enrichment culture and standard microbiological techniques. Recovered carriers can be identified using the rapid whole blood plate agglutination test. 113 20.7 Treatment None is recommended. Affected flocks should be depleted to eliminate chronic carriers. 20.8 Prevention Breeding stock and chicks should be purchased from suppliers and hatcheries certified free of S. pullorum by a responsible government agency. Breeder flocks can be monitored using the rapid whole-blood plate agglutination test.

Strict biosecurity should be enforced to prevent introduction of the pathogen from backyard flocks which serve as reservoirs. Rodent eradication is an important component of control.

SALMONELLOSIS-PARATYPHOID 22.1 Etiology Salmonella spp other than S. pullorum and S. gallinarum. 22.2 Occurrence A world-wide problem in integrated commercial-egg and broiler operations and also on small-scale farms. 22.3 Economic Significance Some Salmonella spp including S. enteritidis, phage type 4, may result in high chick mortality consistent with S. Pullorum infection. Generally paratyphoid Salmonella spp will result in up to 3% losses during the first 14 days. Paratyphoid Salmonella spp are responsible for food-borne infection in consumers of eggs (S. Enteritidis) and poultry meat (S. typhimurium, S. agona, S. heidelberg and possibly up to 50 other frequently encountered serotypes). 22.4 Transmission S. enteritidis is transmitted vertically by the trans-ovarial and transoviductal routes. Other Salmonella spp may be transmitted mechanically by fecal contamination of egg shells, or in cases of immunosuppressed flocks, infrequently by the transovarial route. Feed containing contaminated ingredients of animal-origin is often responsible for introduction of paratyphoid salmonellosis into integrations or entire countries. The condition can be perpetuated by recycling contaminated by-product meal from infected broilers and commercial laying flocks. Rodents and litter beetles serve as reservoirs of infection. Paratyphoid salmonellosis can be introduced by contaminated equipment, personnel

and wild birds. 22.5 Clinical Signs Elevated chick mortality and unevenness in brooding flocks are observed. No specific signs are associated with paratyphoid infection in mature flocks. Vertically transmitted S. enteritidis pt 4 infection resembles pullorum disease in chicks. 22.6 Pathology Acute cases show enlargement of the spleen and liver and occasionally enteritis and peritonitis. Chicks may show omphalitis. 117 22.7 Diagnosis Confirmation is based on isolation and identification of Salmonella spp from liver, spleen, intestine, or heart blood. Routine microbiological screening of liver/spleen/intestinal pools from post mortem submissions to laboratories is strongly recommended. Specific ELISA-based test kits are available for assaying for S. enteritidis antibody. 22.8 Treatment Furazolidone if allowed will suppress mortality but will not eliminate infection. 22.9 Prevention Reduction in prevalence in breeding flocks is possible (absolute elimination of S. Enteritidis and progressively S. typhimurium carriers) by implementing intensive programs of microbiological screening together with appropriate biosecurity procedures. Salmonella enteritidis is controlled in commercial level stock using live, modified S. typhimurium vaccines alone or in combination with inactivated S. enteritidis emulsion boosters at point of lay.

RUNTING SYNDROME synonyms Malabsorption; Infectious Stunting Syndrome 27.1 Etiology: The specific causal agents responsible for Stunting Syndrome have not been identified, although most poultry health professionals accept that specific reovirus strains (including 1733) are responsible for the condition, possibly in association with as yet unidentified viruses or anaerobic bacteria in the intestinal tract. It is noted that the condition can be reproduced by infecting specific-pathogen free chicks with intestinal homogenates from affected birds. It is not possible to reproduce the typical stunting syndrome by administering reovirus isolates from field cases, suggesting a multifactorial etiology. 27.2 Occurrence and Economic Significance The condition has been diagnosed in most broiler-raising areas and is responsible for decreased growth rate and elevated mortality in broiler chicks usually derived from young parent flocks. The severity and prevalence of the condition generally abates within 1 to 2 years after initial appearance in an area. 27.3 Transmission The reovirus presumed to be responsible for the condition is transmitted by the vertical route from infected hens to progeny in addition to lateral infection among broiler chicks. It is known that reovirus infection can remain latent in replacement pullets during the rearing stage with viremia appearing at the onset of production and persisting for approximately 4 to 6 weeks thereafter. 27.4 Clinical Signs Affected chicks show decreased growth rate which is evident by the 5th to 7th day of brooding. Feather abnormalities are obvious in affected chicks and include breakage of the shafts of the primary feathers of the wings and persistence of yellow down on the head, through 30 days of age.

Abnormal wing feathering gives rise to the term helicopter disease since the abnormal feathers resemble rotor blades. By 4 weeks of age, affected chicks which may comprise up to 25% of the flock may weigh only 250 g and are less than half the size of normal pen mates. Examination of the orange-colored, loose droppings from infected birds shows the presence of undigested grain particles. A high proportion of affected birds show a disinclination to walk due to a rickets-like syndrome characterized by osteopenia. In extreme cases fracture of the proximal epiphysis of the 131 femur occurs. Affected birds show decreased pigmentation of the skin which is evident on the shanks and beak. 27.5 Pathology Stunting syndrome attributed to malabsorption is characterized by a wide range abnormalities including: A rickets-like syndrome involving decreased skeletal density, beading of the ribs, osteopenia resulting in fracture of the proximal epiphysis of the femur (incorrectly termed femoral head necrosis). Pale colored skin and feather abnormalities. These changes which are observed clinically are confirmed on post-mortem examination. Despite obvious malabsorption, enteritis is not a primary lesion although affected birds may be concurrently infected with coccidiosis or may undergo secondary bacterial infection. Enlargement of the pancreas may be noted. There are no characteristic gross or histological lesions associated with the stunting syndrome. 27.6 Diagnosis A diagnosis of stunting syndrome is based on the history of young parent flocks producing affected chicks and the appearance of up to 20% stunting in a flock with typical clinical presentation in affected birds ranging in age from 7 to 35 days. A wide range of pathogens can be isolated from

affected flocks. Since the range of etiologic agents have not been identified, there is no definitive laboratory diagnostic procedure. 27.7 Treatment There is no specific treatment for stunting syndrome. Affected chicks can be gathered from the flocks at approximately 10 days of age and placed in a common pen where they can be provided with feed and water and protected from competition from normal pen-mates. Stunted chicks will grow slowly, and can be salvaged for live-bird sale or processing as lowweight birds. Isolation of affected chicks may reduce the probability of lateral transmission of virus. Evaluation of dietary formulations is advised to ensure nutritional adequacy. The following components should be considered: levels of methionine and lysine should attain or exceed breed specifications 132 selenium level should range from 0.1 to 0.3 ppm, with at least half of this dietary contribution in the form of selenomethionine. vitamin E supplementation should conform to NRC levels for stressed flocks (20 IU/kg) All supplementary fats and animal byproducts should be stabilized with 300-600 ppm ethoxyquin or an equivalent compound. 27.8 Prevention It is recommended that parent-level pullets receive an attenuated reoviral arthritis vaccine at 7 days followed by a multivalent live vaccine during the 14 to 30 day period consistent with the immunization program for the area. Inactivated reoviral vaccines administered during the late rearing period should contain antigenic components which are known to be protective against the reovirus strains (1733) considered responsible for stunting-malabsorption syndrome.

COCCIDIOSIS 28.1 Etiology Various Eimeria spp which parasitize specific portions of the intestinal tract of chickens. 28.2 Occurrence and Economic Significance Coccidiosis occurs world-wide and is a major cause of mortality and suboptimal growth and feed conversion efficiency in immature flocks unless appropriate preventive measures are implemented. The cost of anticoccidial feed additives and treatment is estimated to exceed $400 million annually in all poultry producing areas of the world. 28.3 Transmission The sporulated oocyst is the infective stage of the life-cycle. Infected, recovered chickens shed oocysts representing a problem in multi-age operations. Oocysts can be transmitted mechanically on the clothing and footwear of personnel, contaminated equipment, or in some cases, by wind spreading poultry-house dust and litter over short distances. Factors contributing to outbreaks of clinical coccidiosis include: litter moisture content exceeding 30% due to ingress of rain or leaking waterers. immunosuppression (Mareks disease, IBD, mycotoxins) suboptimal inclusion of anticoccidials or incomplete distribution (poor mixing) in feed. environmental and managemental stress such as overstocking, inoperative feeding systems, inadequate ventilation. 28.4 Clinical Signs Coccidiosis is generally acute in onset and is characterized by depression, ruffled plumage, and diarrhea. Birds infected with E. tenella show pallor of the comb and wattles and blood-stained cecal droppings. 28.5 Lesions E. acervulina and E. mivati: 1-2mm areas of hemorrhage interspersed

with white foci visible through the serosa of the distal duodenum and proximal jejunum. E. necatrix: severe distention of the mid-jejunum with hemorrhages in the mucosa and red-stained fluid in the lumen. E. maxima: distention of the mid-jejunum with hemorrhages in the mucosa. E. tenella: hemorrhagic typhlitis (inflammation of the cecum). 135 E. brunetti: hemorrhages of the mucosa of the distal jejunum and colon. Fibrinonecrotic enteritis may occur in chronic cases. 28.6 Diagnosis Gross lesions of E. tenella, E. necatrix and E. brunetti are diagnostic. Microscopic examination of intestinal and cecal scrapings reveals oocysts. To confirm a diagnosis in a commercial operation the following specimens should be submitted to a laboratory: Intestine from a sacrificed, affected bird preserved in 5% potassium dichromate for culture and identification of Eimeria sp. Intestine showing gross lesions in 10% formalin for histological examination. Representative feed samples for anticoccidial assay. Litter samples for oocyst counts. 28.7 Treatment Administration of amprolium solution, 0.024% of the active ingredient in drinking water for 3 - 5 days. Sulfonamides (sulfamethazines , 0.1% for 2 days, 0.05% for 4 days or commercial combinations of sulfa drugs) in drinking water. Administration of water dispersable vitamin A and K supplements may enhance recovery. 28.8 Prevention Management procedures which limit saturation of litter include:

 Appropriate installation and management of watering systems. Nipple drinkers reduce spillage of water onto litter compared to bell and trough drinkers. Acceptable ventilation rate. Maintaining recommended stocking density. Providing adequate feeding space. Inclusion of anticoccidials in diets at recommended levels will prevent clinical infection. Chemical and ionophoric anticoccidials for broilers in shuttle programs. Synthetic coccidiostats for breeders and floor-reared commercial eggproduction flocks which allow the development of premunity. Anticoccidial vaccines are appropriate for replacement breeding stock and roasters. This approach is cost-effective but requires experienced and 136 diligent management and monitoring especially if the vaccine is applied over feed. Intraocular administration by spray or the insertion of a gelatine cylinder impregnated with oocysts in the chick delivery box contributes to an even distribution of vaccine through the flock. Future control measures will include in ovo vaccination of broiler embryos with a highly purified oocyst suspension (Inovocox). Administration of a vaccine (Coxabic) derived from gametocytes to replacement pullets has been shown to confer immunity to progeny, obviating the need for anticoccidials CLOSTRIDIAL ENTEROTOXEMIA 29.1 Etiology Clostridium perfringens is the principal pathogen responsible for necrotic enteritis (NE) although the condition is multi-factorial in origin and is usually preceded by mild intestinal coccidiosis. Necrotic enteritis is often initiated by an alteration in the feeding program (commencing skip-a-day feeding of replacement breeder pullets or accidental starvation)

environmental stress, overstocking, withdrawing anti-coccidial growthstimulating feed additives, vaccination, movement or weighing of flocks, or saturation of litter. Clostridium botulinum is responsible for botulism, an enterotoxemia resulting in progressive paralysis. 29.2 Occurrence and Economic Significance Both NE and botulism can occur world-wide, in areas where chickens are reared on litter. Successive flocks in some regions show frequent or persistent outbreaks possibly due to high levels of Clostridium spp in soil or the presence of drug-resistant strains. The economic significance of clostridial enterotoxemia varies, but erosive losses of up to 4% can occur in broiler and immature breeder flocks due to direct mortality or concurrent infection with systemic bacteria. 29.3 Transmission Clostridium perfringens and C. botulinum are ubiquitous soil contaminants. Pathogenic strains of C. perfringens may be introduced onto farms by deficiencies in hygiene and biosecurity. Ingestion of the vegetative form of the organisms invariably result in colonization of the intestinal tract. 29.4 Clinical Signs Mortality is acute with no specific prodromal or clinical signs. Chickens affected with NE develop rigor (stiffness) within 1 hour of death. Chickens with botulism show ascending paresis and then paralysis extending craniad from the legs, impairing locomotion. Terminally affected birds are in sternal recumbency with flaccid necks, ruffled plumage and extension of the nictitating membrane over the cornea. 29.5 Pathology The mucosa of the intestine shows changes ranging from focal hyperemia (redness) to mucosal ulceration. In extreme cases NE is characterized by extensive pseudomembranous enteritis which resembles a coarse yellow coating. Focal hepatic necrosis may be observed. There are no characteristic lesions associated with botulism.

139 29.6 Diagnosis Histological examination of affected mucosa will demonstrate the presence of characteristic clostridial organisms applying Gram stain. Cl. perfringens can be isolated and identified by a suitably equipped laboratory using anaerobic culture. Botulinum toxin can be identified in the blood of severely affected broilers by injecting 0.5 ml of serum into susceptible mice using the intraperitoneal route. Toxin results in paralysis and death within 24 hours. 29.7 Treatment Administration of flocks with water soluble zinc bacitracin, lincomycin , virginamycin or penicillin for 72 hours reduces morbidity and mortality. Losses may reoccur following withdrawal of treatment. 29.8 Prevention Addition of zinc bacitracin, lincomycin, or virginamycin to feed at levels approved by local regulatory authorities will suppress the clinical occurrence of clostridial infections. Botulism and NE can be prevented by the management procedures recommended to prevent coccidiosis. ENDOPARASITES 30.1 Capillariasis Infection of the crop (Capillaria contorta) and the intestine (Capillaria obsignata) will result in severe emaciation and mortality in both immature and producing flocks. In floor-housed breeders and commercial layers reduction in egg production occurs. Ingluvitis (inflammation of the crop) is associated with C. contorta. Mucosal thickening and focal enteritis occurs with C. obsignata. Parasitism can be diagnosed by examination of mucosal scrapings and fecal flotation, which reveal characteristic bi-operculated ova. Treatment

Fenbendazole in feed or levamisole or ivermectin (where permitted) in drinking water. 30.2 Ascaridiasis Ascaridia galli occurs in the jejunum and Heterakis gallinarum in the cecum. Extensive A. galli infection may reduce egg production in floorhoused breeders and commercial layers. Death may occur due to intestinal obstruction in birds which are immunosuppressed or are affected by an intercurrent debilitating condition. Other nematodes which may be encountered in subsistence or small-scale flocks include: Oxyspirum mansoni a 1.5 cm ( ) nematode beneath the nictitating membrane of the eye. Syngamus trachea a 2 cm ( ) nematode in the trachea. Tetrameres americana a 3 mm ( ) spherical nematode beneath the mucosa of the proventriculus. Cheilospirura hamulosa a 2.5 cm nematode beneath the mucosa (koilin layer) of the ventriculus. Treatment Piperazine, levamisole, or ivermectin (where permitted) in drinking water. 30.3 Cestodiasis Numerous cestode species may occur in the intestinal tract and can be diagnosed at postmortem or by examination of feces. Cestodiasis results in emaciation in mature flocks, especially if severe infestation is exacerbated by malnutrition or immunosuppression. 142 The most commonly diagnosed cestodes include: Davainea proglottina - a 4 mm cestode located in the duodenum. Choanotaenia infundibulum - a 25 cm cestode located in the distal duodenum and jejunum. Raillietina tetragona - a 25 cm cestode located in the distal jejunum.

Raillietina echinobothridia - a 30 cm cestode of the jejunum resulting in nodular granulomas and catarrhal enteritis. Treatment Niclosamide in feed.

183 41.3 DIFFERENTIAL DIAGNOSES OF AVIAN DISEASES & CONDITIONS ASSOCIATED WITH SPECIFIC AGE GROUPS & TYPES OF COMMERCIAL POULTRY Diseases & Conditions characterized by:1. Mortality in chicks day old - 10 days Arenavirus infection Paratyphoid including Aspergillosis Salmonella enteritidis Avian encephalomyelitis Pullorum disease Mismanagement: Smothering (temperature, water, feed) Toxicity Omphalitis 2. Mortality & morbidity in chicks 10 - 30 days with nervous signs Argas persicus infestation Newcastle disease Avian encephalomyelitis Pyridoxine deficiency Encephalomalacia Thiamine deficiency Infectious bursal disease Toxicity Mycotoxicosis 3. Mortality & morbidity in chicks 20-50 days with locomotory abnormalities Arthritis - Staphylococcus sp. Mareks disease Mycoplasma synovia Mechanical injury Reovirus Niacin & choline deficiency Botulism Phosphorus deficiency Calcium deficiency Riboflavin deficiency Cholecalciferol (D3) deficiency Spondylolisthesis

Congenital deformities Tibial dyschondroplasia Manganese deficiency 4. Mortality & morbidity in chickens with respiratory signs Adenovirus Type-1 Infectious laryngotracheitis Avian infectious bronchitis Mycoplasmosis Avian influenza Newcastle disease Avian pox Pneumoviral,\ Swollen Head Coli-septicemia Syndrome Infectious coryza Vaccine reaction 184 5. Mortality & morbidity in broilers & pullets (other than with locomotory, respiratory & nervous signs) Adenoviral hydropericardium Liver & kidney syndrome - Hepatitis syndrome Pasteurellosis Ascites complex Salmonellosis Coccidiosis Spirochetosis Coli-septicemia Sudden death syndrome Conjunctivitis (Right heart failure) Histomoniasis Toxicity Infectious bursal disease Ulcerative & necrotic enteritis 6. Decline in egg production Asymptomatic or with mild signs & low or inapparent mortality Adenovirus Type-1 Newcastle disease Avian encephalomyelitis Nutrititional (Ca; P; Na; Avian influenza Cl deficiency) Infectious bronchitis Water & feed deprivation 7. Decline in egg production with mortality & morbidity Avian influenza Infectious laryngotracheitis Avian pox Newcastle disease Coryza Pasteurellosis

Infectious bronchitis Salmonellosis 8. Conditions resulting in mortality & morbidity encountered predominantly in caged layers Infectious conditions as above:(ILT, ND, IB, Salmonellosis, Coryza, Pasteurellosis, Adenovirus, Avian encephalomyelitis) Ectoparasitism Mycotoxicosis Endoparasitism Nutritional deficiencies (Ca; P) Fatty liver syndrome Vent peck Leucosis complex Water deprivation 185 9. Conditions affecting the integument Avian pox Ectoparasites Avitaminosis A; Biotin; Gangrenous dermatitis/Staph. E (Transudative diathesis); complex Pantothenic acid deficiency Managemental factors Cannibalism/trauma Mareks disease Dermatomycosis Pasteurellosis - wattle lesion 10. Conditions associated with subsistence & free-ranging flocks Arthritis Mycotoxicosis Avian pox Pasteurellosis Candidiasis Pendulous crop Cannibalism Pododermatitis Coccidiosis Predator loss Coli-septicemia Salmonellosis Ectoparasites Spirochetosis Emphysema (trauma) Thermal injury Endoparasite Toxicity Histomoniasis Traumatic ventriculitis Lymphoid leucosis Tuberculosis

Mareks disease Visceral gout Mycoplasmosis 11. Conditions associated with waterfowl Aspergillosis Coccidiosis Avian influenza Ectoparasites Botulism Endoparasite Chlamydiosis Lead poisoning Colibacillosis Mytotoxicosis Duck viral enteritis Nutritional deficiencies Duck virus hepatitis & Pasteurellosis food-borne infections Salmonellosis Erysipelas