Botulism was diagnosed in 3-week-old broilers from clinical signs, absence of postmortem and histopathological lesions, and demonstration of toxin in the serum of comatose birds. Passive immunization of mice with Clostridium botulinum type-C antitoxin protected against a challenge with serum from comatose birds containing the Cl. botulinum toxin. Total mortality for the grow-out period exceeded 27% and was not altered by water medication with penicillin. Bacitracin at 100 g per ton reduced mortality to 5-7 birds per day.

Animals↗

PubMedDate not supplied

Plastic embedding of avian tissues for diagnostic histopathology.

A series of photomicrographs show the histologic features of avian tissues embedded in plastic and sectioned on glass knives. The techniques described gave superior resolution, less cell shrinkage, and fewer sectioning artifacts than sections prepared with conventional paraffin methods.

Acrylates↗

PubMedDate not supplied

Influence of strain of Mycoplasma synoviae and route of infection on development of synovitis or airsacculitis in broilers.

Two strains of Mycoplasma synoviae (WVU 1853 and F10-2AS) were compared for their relative pathogenicity in terms of airsacculitis and synovitis. Both strains produced air-sac lesions after aerosol exposure of chickens vaccinated against Newcastle disease and infectious bronchitis; both produced synovitis when inoculated into the foot pad. The WVU 1853 strain was more likely to result in synovitis, whereas the F10-2AS strain was more apt to produce air-sac lesions.

Aerosols↗

PubMedDate not supplied

Cryptosporidiosis of the bursa of Fabricius of chickens.

Light-microscope and electron-microscope studies of a coccidial organism found in the bursa of Fabricius from 3 chickens clearly established the parasite as belonging to the family Cryptosporiidae. Hyperplasia and heterophil infiltration were associated with the presence of organisms attached to the microvillus border of epithelial cells lining the plicae of the bursa of Fabricius. Although there were no clinical signs or gross lesions common to the 3 cases described, all had similar histologic lesions in the epithelium lining the bursa of Fabricius.

Animals↗

PubMedDate not supplied

Myopathy of the deep pectoral muscle in broiler breeder hens.

Myopathy of the pectoralis profundus and ambiens muscles was found in chickens from 5 flocks of broiler breeder hens. Histological lesions in the muscles varied from steatosis to loss of striations, fragmentation of fibers, and mineral deposition. A clinical response followed oral medication with vitamin E and selenium although analysis showed that selenium and vitamin E levels in the feed were normal. The possible relation between myopathy and Cassia seed in the feed is discussed.

Animals↗

PubMedDate not supplied

Relationship of complement resistance and selected virulence factors in pathogenic avian Escherichia coli.

Complement resistance, antibiotic resistance profiles, and virulence profiles of 80 Escherichia coli isolates from the intestines of normal chickens (40 isolates) and chickens diagnosed as having colisepticemia (40 isolates) were compared. Differences were observed between the two groups for antibiotic resistance, siderophore production, presence of type 1 pili, complement resistance, motility, and size of plasmids. The systemic isolates were more likely to have siderophores and type 1 pili, and to be complement-resistant and motile than were the intestinal isolates. No differences between the two groups were observed for colicin production. Further comparison of the 10 most complement-resistant isolates from the systemic group and 10 most complement-sensitive isolates from the intestinal group revealed a correlation between an isolate's resistance to complement and its ability to kill embryos, express type 1 pili, and be motile. Virulence of avian E. coli strains appears to be correlated with complement resistance and the interaction of this resistance with the ability to produce type 1 pili and be motile.

Animals↗

PubMedDate not supplied

Effect of infectious bursal agent on the response of chickens to Newcastle disease and Marek's disease vaccination.

White Leghorn chickens raised from one day old in an environment contaminated by the infectious bursal agent (IBA) had lower geometric mean titers (GMT) as measured by the hemagglutination-inhibition (HI) test to the Newcastle disease virus (NDV), than control Leghorns reared in an uncontaminated environment. Immunosuppression, defined as a reduction in GMT, was most pronounced at 35-56 days old for Leghorns vaccinated with NDV at 1 and 28 days or at 28 days. In a separate trial with broilers, immunosuppression was similar at 42-56 days old. This study also demonstrated that IBA infection in chickens increased susceptibility to Marek's disease (MD). The unvaccinated control chickens infected with IBA averaged 56.3% MD lesions, whereas unvaccinated controls not exposed to IBA averaged only 18.1% macroscopic lesions. It was also found that 20.7% of the HVT-vaccinated chickens exposed to IBA had gross MD lesions, whereas those HVT-vaccinated chickens reared in an environment free of IBA had 2.99% gross MD lesions.

Animals↗

PubMedDate not supplied

Demonstration of Eimeria tenella in bursa of Fabricius of chickens.

Coccidial life-cytle stages were detected in the bursa of Fabricius of broiler chickens inoculated with Eimeria tenella, whether or not the chickens had previously been infected with infectious bursal disease virus (IBDV). Chickens infected only with E. tenella had developing parasites in the lining epithelium, whereas chickens with both infections had gametocytes also in the epithelial cells surrounding numerous degenerating bursal cysts.

Animals↗

PubMedDate not supplied

Involvement of a type-8 avian adenovirus in the etiology of inclusion body hepatitis.

Type-8 avian adenoviruses were isolated from chickens in a commerical flock suffering an outbreak of inclusion body hepatitis. Serum-neutralizing titer to this type, but not to 7 other types of avian adenovirus, was more than 4 times as high in convalescing chickens as in chickens from the flock bled 2 weeks previously, during the disease outbreak. A disease similar to that in the commercial flock and to inclusion body hepatitis as described in the literature was produced by intra-abdominal inoculation of a type-8 isolant, AMG 5 (2a), into 1-day-old specific-pathogen-free chicks. Pathologic features of the disease included necrotizing hepatitis, pancreatitis, and severe lymphoid depletion of the bursa of Fabricius, thymus, and spleen. It was concluded that type-8 avian adenoviruses were involved in the etiology of the naturally occurring outbreak of inclusion body hepatitis.

Adenoviridae Infections↗