Primary demyelination in Theiler's virus infection. An ultrastructural study

Theiler's virus infection in SJL/J mice was studied ultrastructurally at subsequent intervals after intracerebral inoculation. Extensive spinal cord lesions consisting of leptomeningeal and white matter mononuclear cell infiltrates with concomitant primary demyelination were seen by 15 days. Stripping of myelin lamellae by invading mononuclear cell processes and vesicular disruption of myelin were demonstrated to be the patterns of myelin breakdown. Oligodendrocytes in the vicinity of demyelinating lesions never showed degenerative changes, and viral inclusions could not be found in any cells in the central nervous system. Remyelinating axons, first detected 21 days after infection, were more frequently seen in the late phase of the disease when conspicuous gliosis was also present. Active demyelination could still be observed as late as one year after infection at which time inflammation was decreased. However, plasma cells were relatively more numerous at later times after infection. These ultrastructural findings are similar to experimental allergic encephalomyelitis, and suggest an immune mediated mechanism of demyelination in Theiler's virus infection.