Adenovirus-induced inclusion body hepatitis in four-day-old broiler breeders.

Two separate parent broiler flocks originating from the same grandparent flock experienced mortalities of 23% and 40%, respectively, in chicks between 1 and 14 days of age. Chicks affected at 4 days of age had tremors, depression, and hypoglycemia. They had pale yellow, swollen, friable livers. Pancreata were discolored and hemorrhagic. Spleens were swollen and sightly darkened. Microscopic lesions consisted of multifocal areas of acute hepatic and pancreatic necrosis with numerous basophilic intranuclear inclusions with karyomegaly. Splenic sections had severe lymphoid depletion and reticular cell and macrophage hyperplasia. An adenovirus from affected livers was isolated in chicken embryo liver cells. Serologic evidence suggests that the grandparent flock began egg production seronegative to adenovirus antibodies, was exposed during production, and, subsequently, shed adenovirus vertically to its progeny. The clinical syndrome was reproduced by injecting the isolated adenovirus into 1-day-old antibody-negative chicks. Histologic lesions in the experimentally reproduced disease cases were identical to those in the naturally occurring cases.

Deletrocephalus dimidiatus infestation in an adult rhea (Pterocnemia pennata).

Infection with the nematode Deletrocephalus dimidiatus was found in the distal small and proximal large intestines of a 30-month-old female rhea that had died after a prolonged illness. Numerous strongyle-like eggs were found on fecal flotation. Possible treatments include fenbendazole (60 ppm in water) and ivermectin (200 mg/kg). Preventive measures such as artificial incubation, segregation of chicks from adults, and placing chicks in uncontaminated environments may help slow or stop the transmission of the parasite.

Incidence of Pasteurella multocida in poultry house cats used for rodent control programs.

Cats used as mousers in commercial poultry breeder farms were tested for the presence of Pasteurella multocida. Of the cats tested, 72.7% were positive for P. multocida serotypes common to both farm cats and commercial broiler breeders. Thirty-one percent were type 1, 19% were type 4, and 6% were type 3.4.

Diazinon toxicity in broilers.

Ten 3-day-old chicks were submitted from a flock experiencing high mortality. Necropsy revealed lacrimation, diarrhea, pleural effusion, hemorrhage and ulceration of the proventriculus, and swollen, hemorrhagic livers. Numerous yellow granules were present in the crop. Assayed crop contents contained 39 ppm diazinon [O,O-diethyl O-(2-isopropyl-4-methyl-6-pyrimidyl)phosphorothioate]. The insecticide had been applied to the litter to control fire ants. The high mortality abated after new litter was added on top of the old litter. Diazinon toxicosis was traced to ingestion of diazinon-impregnated granules and was reproduced experimentally.

Acute hemorrhagic enterocolitis in ratites: isolation of eastern equine encephalomyelitis virus and reproduction of the disease in ostriches and turkey poults.

Two emus died with acute hemorrhagic enterocolitis. Eastern equine encephalomyelitis (EEE) virus was isolated in Vero cells from non-pooled samples of brain and intestine. Enterocolitis with splenic and hepatic necrosis was reproduced by intramuscular or oral inoculation of this isolate in two ostriches and three turkey poults.

Experimental exposure of broiler chickens to boric acid to assess clinical signs and lesions of toxicosis.

One-day-old broiler chicks were housed on litter treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.3 m2 of floor space. After 15 days, average body weights were 340.7 g, 278.1 g, and 213.2 g for chickens exposed to 0, 3.6, and 7.2 kg boric acid/9.3 m2, respectively (P < or = 0.05). Feed conversion was 1.68 and 2.29 in chickens exposed to 0 and 7.2 kg boric acid/9.3 m2 (P < or = 0.05). In a second experiment, after birds ingested feed treated with 2500 and 5000 ppm of boric acid for 2 weeks, body weights were 254.8 g and 149.6 g, respectively. The chickens in the control group weighed an average of 285.0 g (P < or = 0.05). The 5000 ppm treatment group had a feed conversion of 1.70, vs. 1.45 in the controls (P < or = 0.05). A dose-related feathering abnormality was evident in treated chickens. No significant histopathologic changes were observed. Livability, weight gain, and feed conversion were not adversely affected in broilers as a result of exposure to litter treated with boric acid at recommended levels of 0.4-0.9 kg/9.3 m2.

Acute toxicity of boric acid and boron tissue residues after chronic exposure in broiler chickens.

The acute oral mean lethal dose of boric acid in 1-day-old chickens was found to be 2.95 +/- 0.35 g/kg of body weight, which classifies this product as only slightly toxic to chickens. One-day-old broiler chicks were housed in floor pens in which litter had been treated with 0, 0.9, 3.6, or 7.2 kg of boric acid per 9.9 m2 of floor space. Boron residue levels in brain, kidney, liver, and white muscle were not statistically elevated following a 15-day exposure period. Boron residue levels in the same types of tissue were not significantly elevated in chicks fed 500 ppm or 1250 ppm boric acid in feed ad libitum for 3 weeks; however, residues were significantly higher in chicks fed 2500 ppm or 5000 ppm boric acid. These data indicate that broilers grown on boric acid-treated litter do not consume enough boric acid to cause elevated boron levels in tissues.

Marek's disease virus-induced transient paralysis in chickens. 3. Differentiation of field cases from classical Marek's disease by central nervous system lesions.

Vasculitis with intramural pseudocyst formation primarily in the cerebellar white matter, but also in nuclei of the medulla, resulted in leakage of IgG and albumin and vacuolation of the neuropil (vasogenic oedema) in brains from chickens with clinical signs of Marek's disease virus (MDV)-induced transient paralysis (TP). Demyelination was absent. Chickens that had recovered from TP had a restored blood-brain-barrier, indicated by the rarity of vasculitis and vascular intramural pseudocysts in the cerebellum. In addition, the vacuolation and protein leakage were greatly decreased. The minor vacuolation resulted primarily from intramyelinic (cytotoxic) oedema. The small quantity of extravascular protein was being removed by microglial cells and astrocytes. In one chicken which failed to fully recover from TP (TP-prolonged) there was neither vasogenic oedema, cytotoxic oedema, nor vasculitis in the cerebellum. The medulla of the TP-prolonged chicken had a severe lymphocytosis, swollen axons, neuronal degeneration, secondary demyelination and some associated serum protein leakage. All TP-affected and TP-recovered chickens, and the TP-prolonged chicken, had perivascular mononuclear cell cuffs within all brain sections. Chickens with classical Marek's disease (MD) generally lacked CNS vacuolation, perivascular mononuclear cell cuffs, vasculitis and serum protein leakage. However, in a few cases of MD with severe perivascular mononuclear cell cuffs, focal demyelinating plaques were seen. These plaques had associated vacuolation, serum protein leakage, axonal spheroids and neuronal degeneration.

'Cage clutch' in a flock of commercial White Leghorns.

Five commercial White Leghorn chickens were presented to the laboratory from a flock which was experiencing a mortality problem after transfer to the laying house. About 4 or 5% of the birds were 'squatting' in their cages and appeared nervous. Localized, ulcerative lesions were noted on the toes and shanks of the layers. The flock was placed on antibiotics and electrolytes, and the affected birds were removed from their cages and placed on the floor. The problem subsided, and the flock came into production on schedule. Aetiology of the disorder remains unknown.

Necrotic enteritis in cage-reared commercial layer pullets.

Necropsy of five 12-week-old pullets from a flock of 99,300 suffering from an increased mortality rate revealed enlarged, gas-filled intestines, the mucosal surfaces of which had the "dirty turkish towel" appearance typical of necrotic enteritis. Although the pullets had been raised entirely in cages, intestinal scrapings revealed the presence of Eimeria maxima. Histopathological findings were compatible with necrotic enteritis. Clostridium perfringens was isolated by anaerobic culture from the intestines. Mortality returned to normal after bacitracin and amprolium were added to the feed.

Newcastle disease vaccination of broilers with high- and low-titered commercial vaccines.

The virus titers of seven commercial B1 strain Newcastle disease vaccines were evaluated. A 2 log difference in virus content was found between the vaccine with the highest titer (10(8.8) EID 50/ml) and the one with the lowest titer (10(6.8) EID 50/ml). Broiler chickens were vaccinated with the high- and low-titered vaccines to compare hemagglutination-inhibition (HI) antibody and challenge responses. The effect of vaccination at different ages on the HI titers was also examined. There were no significant differences between vaccine groups in HI antibody response or resistance to challenge. However, the high-titered vaccine may provide a margin of safety with the currently used methods of mass vaccination.

Studies on orthoreoviruses isolated from young turkeys. III. Pathogenic effects in chicken embryos, chicks, poults, and suckling mice.

The pathogenicity of four clone-purified reoviruses (81-51, 81-68, 81-311, and 82-88) was studied in experimentally infected specific-pathogen-free (SPF) chicken embryos and chicks. SPF and specific-antigen-and-antibody-negative (SAAN) turkey poults, and suckling mice. In SPF embryos, all four viruses caused death or lesions characteristic for avian reoviruses. SPF chicks inoculated orally with isolate 81-68 showed no signs of overt disease but did develop antibodies to reovirus. In some experiments, poults inoculated orally with isolate 81-68 exhibited increased mortality, abnormal feather development, lower body weight gain, and pasted vents. Body tremors, uncoordinated motor movement, and oily hair coats were seen in suckling mice inoculated intracerebrally with isolates 81-51, 81-68, and 82-88. Mice inoculated intracerebrally with isolates 81-68 and 82-88 exhibited retarded growth.

Viral arthritis in fryers related to reovirus infection in breeders.

In 1983, twenty-two outbreaks of viral arthritis/tenosynovitis were diagnosed in a 6-month period on 18 fryer farms of one commercial operation located in western Washington. The main source of the reovirus infection was traced to a breeder flock that supplied progeny chicks to all of the affected farms.

Subcutaneous clostridial infection in broilers.

A flock of 12,500 broilers 36 days of age experienced a sudden increase in mortality. Post-mortem lesions were emphysema, severe enteritis, and a serosanguineous fluid in the subcutaneous tissue of the breast and thighs; there was no evidence of a loss in the integrity of the skin. Clostridium perfringens and C. septicum were isolated from the affected subcutaneous tissue. Histopathological and serological examination indicated previous infection with infectious bursal disease virus. The subsequent immunosuppression and severe enteritis may have permitted the clostridia access to the circulatory system, with localization in the subcutaneous areas of the breast and thighs. Mortality returned to normal 48 hours after potassium penicillin G was administered via the drinking water.

The response of broiler chickens to the addition of bacitracin methylene disalicylate to diets containing salinomycin and roxarsone.

Two experiments were conducted to evaluate the response of broiler chickens to addition of bacitracin methylene disalicylate (BMD) to diets containing salinomycin. In each experiment, five tests were conducted at different locations. In Experiment 1, all diets contained 66 mg salinomycin/kg of diet for the first 42 days and either 0 or 33 mg BMD/kg of diet for the entire 49-day feeding period. In Experiment 2, all diets contained 66 mg salinomycin and 50 mg roxarsone/kg of diet for the first 42 days and either 0, 11, 33, or 55 mg BMD/kg of diet for the entire 49-day feeding period. In Experiment 1, addition of 33 mg BMD/kg of diet significantly (P less than .05) improved body weights and feed utilization. Results were similar in all five tests. In Experiment 2, addition of 11, 33, or 55 mg BMD/kg of diet significantly (P less than .05) increased body weights. In one location the addition of 55 mg BMD/kg of diet resulted in no significant difference in body weight compared with those fed the unsupplemented diet, but in all other locations the response was similar. Addition of 33 or 55 mg BMD/kg of diet resulted in improved (P less than .05) feed utilization when all tests were combined. Feed utilization was not improved in all locations by the addition of BMD.

Studies on orthoreoviruses isolated from young turkeys. II. Virus distribution in organs and serological response of poults inoculated orally.

Day-old specific-antibody-negative turkey poults were inoculated orally with cloned turkey reovirus isolate 81-68. Virus reisolations from 11 different tissues revealed widespread distribution at 3, 5, and 7 days postinoculation (PI). Virus was isolated from the intestines until 21 days PI. Virus was isolated from tendons until day 7 PI and again at day 28 PI. Reovirus serum-neutralization antibodies appeared as early as 7 days PI. All inoculated birds showed positive VN serum titers (greater than or equal to 1:20) by day 21 PI. No reovirus was isolated from control poults, and they remained antibody-negative during the entire experiment.

Suspected mycotoxicosis in laying hens.

A flock of 15,000 leghorn-type hens experienced a 10% drop in egg production. Enlarged, blue combs and diarrhea were also present. Clinical signs, postmortem and histopathological lesions, and response to therapy were compatible with a diagnosis of mycotoxin intoxication. However, all feed samples submitted were negative for mycotoxins, so the diagnosis could not be confirmed.

The effect of aflatoxin on complement activity in broiler chickens.

Groups of broiler chickens were fed rations containing .625, 1.25, or 2.5 micrograms total aflatoxin/g of feed from one day to 42 days of age. Treatment groups were segregated according to sex and control groups were maintained. The chickens were bled at 14-day intervals, and serum was collected for assay of total complement (C) activity using a radial hemolytic procedure. No significant differences were found in C titers between males and females of the same age group. For the sexes combined, mean C titers of chickens fed aflatoxin were compared to mean titers of controls. For each age group, significant differences in C titers existed only between the control group and those chickens fed 2.5 micrograms/g aflatoxin. Complement is a major component of the humoral immune response and this study adds to the evidence that aflatoxin can be immunosuppressive to chickens.

Sinusitis in turkeys associated with respiratory cryptosporidiosis.

An outbreak of sinusitis due to cryptosporidial infection is described in 7-week-old turkeys. Infection of 3-week-old turkeys subsequently placed in the same environment is documented.