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Veterinary Pathology, Vol 16, Issue 6 650-660, Copyright © 1979 by American College of Veterinary Pathologists
ARTICLES |
J. A. Lisiak and M. Vandevelde
Eight dogs with severe neurologic signs, including seizures, had polioencephalomalacia of the pyriform cortex, Ammon's horn and deep structures in the temporal lobe. The polioencephalomalacia was considered to be a consequence of canine distemper virus infection based on clinical signs, typical inclusions, the demonstration of viral antigens in the lesions and of characteristic paramyxovirus nucleocapsids by electron microscopy. Little evidence for neuronal destruction by direct viral activity was found. Selective nerve cell necrosis was attributed to ischemia (vascular lesions and seizure induced consumptive anoxia) and immune mechanisms. The selective involvement of the rhinencephalic structures was thought to be related to the mode of entry and spread of the virus.
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P. A. Rudd, R. Cattaneo, and V. von Messling Canine Distemper Virus Uses both the Anterograde and the Hematogenous Pathway for Neuroinvasion J. Virol., October 1, 2006; 80(19): 9361 - 9370. [Abstract] [Full Text] [PDF] |
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