Parvovirus-associated cerebellar hypoplasia and hydrocephalus in day old broiler chickens.

Cerebellar hypoplasia and hydrocephalus were identified in day old broiler chickens showing nervous signs, impaired mobility, and diarrhea. At postmortem examination, brains of chickens were misshapen and cerebellums were smaller than normal. Microscopically, cerebellar folia were reduced in size and irregularly shaped, and the ventricles were widely distended. Affected cerebellums had focal areas along the base of folia where the internal granular cell layer had been lost, and Purkinje cells were disorganized and located within the molecular layer. Parvovirus DNA was detected by polymerase chain reaction in three of nine brains with oligonucleotide primers designed for amplification of chicken and turkey parvoviruses. On the basis of phylogenetic analyses, the detected virus was most closely related to chicken parvoviruses. These findings suggest that a chicken parvovirus might cause a neurologic disease of young chickens characterized by cerebellar hypoplasia and hydrocephalus; however, its role as the cause of the disease remains to be confirmed.

Serum sensitivity and apathogenicity for chickens and chick embryos of Escherichia coli J5 strain.

Escherichia coli J5 strain was assessed for its serum resistance and pathogenicity for both chickens and chick embryos. Pathogenicity for chickens was assessed by intravenous inoculation into three-week-old broiler chickens. Pathogenicity for chick embryos was determined by inoculation of 12-day-old chick embryos into the allantoic cavity. Chicken serum was used to determine the serum resistance status. E coli J5 strain was found to be serum-sensitive and apathogenic for chickens and chick embryos. No mortality and no gross lesions occurred in the chickens inoculated with this strain. The chick embryos inoculated with this strain remained alive. It is worth trying this strain as a live vaccine to immunize chickens against infection from different serotypes of E coli.

Hydropericardium syndrome in broiler chickens: its contagious nature and pathology.

Twenty-five-day-old broiler chickens were inoculated intramuscularly or orally with a suspension prepared from the livers of chickens naturally affected with hydropericardium syndrome (HPS), and uninoculated chickens were kept in the same room with the inoculated birds. The mortality rates in the chickens inoculated intramuscularly or orally were 100 per cent and 30 per cent, respectively. The corresponding groups of uninoculated chickens had mortality rates of 60 per cent and 53.3 per cent, respectively. Hydropericardium was a consistent and prominent lesion in the dead birds, and there were gross lesions in the liver and kidney. Microscopical lesions were present in the liver, kidney, bursa of Fabricius and spleen. Some hepatocytes contained basophilic, intranuclear inclusion bodies.

Pathogenicity of Enterococcus hirae for chicken embryos and betamethasone-treated chicks.

An isolate Enterococcus hirae was used to determine its pathogenicity for chicken embryos and for chicks treated with betamethasone. E hirae was inoculated intravenously into four-day-old chicks which had been treated for three consecutive days with betamethasone, and chick embryos were inoculated into the allantoic cavity with 10(2) and 10(3) bacteria. E hirae was not pathogenic for the chicks or for the embryos.

Progression of tracheal lesions in turkeys exposed by aerosol to LaSota strain of Newcastle disease virus.

Five-week-old turkeys were exposed by aerosol to the LaSota strain of Newcastle disease virus. Poults were killed on days 2, 4, 6, 8, 10, 12, and 14 postexposure, and tracheas were processed for virus quantitation and histologic examination. Newcastle disease virus was recovered at a high titer from all tracheas collected 2, 4, and 6 days postexposure. The initial tracheal lesion observed on day 2 was swelling of ciliated columnar and mucous gland cells. Some of the affected cells contained intracytoplasmic inclusions. Cell swelling and degeneration were followed by epithelial cell proliferation, fibrinopurulent exudation, and lymphocytic infiltration. Epithelial cell proliferation was most severe on days 4 and 6, when tracheas were lined with several layers of immature cells. Lymphoid nodules appeared on day 6 and persisted up to day 14. From day 8 on, there was regression of the proliferative lesion accompanied by differentiation of the immature epithelium. By day 14, the tracheal mucosa regained its normal histologic appearance.

Pathology of the trachea in turkeys exposed by aerosol to lentogenic strains of Newcastle disease virus.

Five groups of 4-week-old turkey poults were each infected by aerosol with a different lentogenic strain of Newcastle disease virus. Four days postinfection, sections of tracheas were collected for histopathologic characterization and virus titration. The most prominent lesions were fibrinopurulent exudate in tracheal lumens, hyperplasia of epithelial cells, and infiltration by lymphocytes. All strains multiplied to high titers and produced similar microscopic lesions, but the number of poults with severe microscopic lesions varied among groups.