Viral encephalomyelitis of pigeons. IV. Growth of the virus in tissue cultures.

Growth and cytopathogenicity of pigeon herpes encephalomyelitis virus (PHEV) in avian and mammalian cell cultures were investigated. The virus was cytopathogenic to all avian primary cell cultures tested and produced large syncytia with intranuclear inclusions. Viral antigen was detected in the nuclei of infected cells 6 hr postinoculation.

Viral encephalomyelitis of pigeons. V. Comparative studies of virulent and cell-culture-adapted virus.

Two strains of pigeon herpes encephalomyelitis virus BVC 78, a virulent field strain, and BVC 78 T7, a cell-culture-adapted strain, were assayed in embryonated chicken eggs and in chicken-embryo-fibroblast (CEF) cell culture to investigate their cytopathogenicity, growth kinetics, plaque characters, and virulence. In CEF the BVC 78 induced syncytia 24-48 hr postinoculation (PI), while the BVC 78 T7 induced only cell rounding 72 hr PI. The strains differed in growth patterns in CEF.

Role of Coccidia in the occurrence of necrotic enteritis of chickens.

Clostridium perfringens type A, Eimeria acervulina, and Eimeria necatrix were used to produce necrotic enteritis in chickens. The disease was produced in all groups of birds that received feed contaminated with C. perfringens.

Viral encephalomyelitis of pigeons: pathology and virus isolation.

A previously unrecorded nervous disease in pigeons was investigated. The disease, characterized by paresis, paralysis of the extremities, head-shaking, and torticollis, is contagious and spreads slowly. The mortality rate of affected pigeons was very high.

Inclusion body hepatitis in broiler chickens in Iraq.

Eighteen outbreaks of inclusion body hepatitis (IBH) were identified in broiler chickens in Baghdad in 1977 and 1978. The disease was seen mainly in 4-to-6-week-old broiler chickens. The mortality rate did not exceed 1% in any outbreak investigated.