Experimental infection of gnotobiotic Beagle dogs at 21 days of age with neurovirulent R252 strain of canine distemper virus (R252-CDV) resulted in a non-suppurative encephalomyelitis. Segmental internodal primary demyelination was found in almost 90% of the dogs from 27 days post inoculation (DPI). Ultrastructurally demyelination was initiated by the insertion of CDV-infected astrocytic processes at nodes of Ranvier with subsequent cleavage of well-preserved myelin from the axolemma. CDV-infected macrophages were consistently involved in myelin phagocytosis. Some remyelination of denuded axons occurred after 35 DPI. Persistent productive infection of the choroid plexus and ependyma in the fourth ventricle was consistently associated with subependymal foci of demyelination. Primary demyelination occurred without detectable CDV-specific virus-neutralizing (CDV-VN) antibody in either serum or cerebrospinal fluid (CSF). There were no immunoglobulin deposits or inflammatory cells within the lesions. These findings indicate that both direct CDV antibody-dependent and CDV antibody-dependent cell-mediated immune mechanisms of cytolysis or myelin destruction are not involved in the genesis of initial primary demyelination. The sequential morphologic and serologic findings in this model of demyelinating encephalomyelitis indicate that direct virus-induced injury has a major role in both the initiation and early progression of primary demyelination.
- Canine distemper virus
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Clinical Neurology
- Cellular and Molecular Neuroscience