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American Journal of Pathology, Vol 89, 649-666, Copyright © 1977 by American Society for Investigative Pathology

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Newcastle disease as a model for paramyxovirus-induced neurologic syndromes. II. Detailed characterization of the encephalitis

SP Wilczynski, ML Cook and JG Stevens

All chickens infected by intranasal and conjunctival routes with a neurovirulent strain of Newcastle disease virus (NDV) developed pneumonitis by 4 days after infection. This was followed 6 to 12 days later by the appearance of severe encephalitis in a significant number of survivors. Histologically, the encephalitis was characterized by neuronal degeneration and perivascular inflammation. In addition, a proliferative vasculitis in the molecular layer of the cerebellum was noted after 30 days, and this persisted for at least 200 days. Although CNS signs were absent during the pneumonic stage, significant amounts of virus were present in the brains of all birds at this time, and viral antigens were easily demonstrable in neurons, glial cells, and endothelial cells. However, when the CNS disease became apparent, viral antigens could not be detected in brains and NDV could regularly be recovered only by application of cocultivation techniques. At this time, the agent was selectively present in birds exhibiting neurologic signs. No evidence for immunopathologic processes was obtained, although hemagglutination inhibiting antibody levels to NDV were elevated in birds with CNS disease. Studies of an avirulent strain of NDV that replicated in the CNS but produced no disease provided evidence that the histologic lesions and the neurologic disease were related to virus multiplication in the brain parenchyma. A mechanism of the pathogenesis of NDV encephalitis is proposed and the disease is discussed relative to other paramyxovirus-induced encephalitic syndromes.

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