Abstract
Newborn hamsters and kittens infected with vaccinia virus developed communicating hydrocephalus without fibrotic changes in the meninges. Following intracerebral viral inoculation, a transient inflammation of the meninges, ependyma and choroid plexus was found. One month later, 70% of hamsters infected with the WR [mouse-adapted] strain of vaccinia virus and 35% infected with the vaccine strain developed hydrocephalus. The mechanism of hydrocephalus production is unclear, but differs from other models in which it is associated with stenosis of the aqueduct of Sylvius or fibrosis of the subarachnoid space.