Abstract
Intracranial infection of neonatal dogs with canine parainfluenza virus (strain 78–238) progressed from an acute phase of encephalitis to a chronic phase of internal hydrocephalus. Acute encephalitis was characterized ultrastructurally by laminar cortical necrosis, neuronal degeneration, neocapillary formation, reactive gliosis, and ependymitis. Viral nucleocapsids were seen in the cytoplasm of neurons.
Ultrastructural lesions in hydrocephalic dogs were restricted to ventricular surfaces. The earliest light microscopic change in ependymal cells occurred four weeks post-infection and consisted of segmental loss of ependymal cells. Dogs killed at three and six months postinfection had quantitatively similar ultrastructural alterations in ependymal cells regardless of the extent and severity of hydrocephalus. The shape of these cells changed from cuboidal to squamous. There was progressive loss of cilia and cell organelles along with a concomitant increase of cytoplasmic filaments. Viral nucleocapsids and inflammatory cells were not present in convalescent hydrocephalic dogs. These results suggested that virus-associated hydrocephalus can occur in the absence of obvious viral persistence in ependymal cells and in the absence of inflammation in the ventricular system.