The proposal that the biting attacks which occur during furious rabies infection are due to selective infection of CNS neurons was studied in skunks (a species important in naturally occurring disease). In this model, skunk street rabies virus infection generally produces furious rabies (characterized by increased activity and biting attacks) while Challenge virus standard (CVS) infection results in dumb rabies (absence of biting and marked depression). A detailed immunohistochemical study of brains of skunks experimentally infected with either CVS or skunk street rabies virus revealed only trace amounts of viral antigen in limbic system neurons and marked differences in viral distribution between skunk street rabies and CVS rabies viruses. These data were collected during early stage rabies when behavioral changes occur. Areas which contained heavy accumulation of street virus but low amounts of CVS rabies virus were the neuronal perikarya and processes of the dorsal motor nucleus of the vagus, dorsal raphe nucleus of the midbrain, hypoglossal and red nuclei. In contrast, large accumulations of CVS rabies virus were found in the Purkinje cells of the cerebellum, the habenular nuclei, and in the pyramidal cells throughout the cerebral cortex, while corresponding areas in all street virus-infected skunks contained minimal antigen. These findings were very consistent for animals of the same experimental group and between skunks inoculated both intramuscularly and intranasally with skunk street rabies virus. Skunks inoculated intramuscularly with CVS rabies virus failed to develop rabies. The correlation between virus infection of neurons and a possible pathogenesis of neural dysfunction was further studied using immunoperoxidase staining for the evaluation of CNS serotonin and met-enkephalin in skunks infected with either CVS rabies virus or skunk street rabies virus. There was no difference in the intensity of serotonin immunoperoxidase staining between uninfected control skunks or those infected with CVS or street rabies viruses. However, there was a reduction in the intensity of immuno-peroxidase staining for the neurotransmitter met-enkephalin, for rabid (both CVS and street rabies viruses) as compared to uninfected control skunks. These data showed that differences in the distribution of CVS rabies virus as compared to skunk street rabies virus in the CNS of experimentally infected rabid skunks, may account for the different clinical syndromes associated with these two viruses. The correlation of rabies virus accumulation within neurons to neurotransmitter imbalances during rabies disease requires further investigation to determine the mechanism by which this may occur.
| Identifer | oai:union.ndltd.org:uottawa.ca/oai:ruor.uottawa.ca:10393/7839 |
| Date | January 1992 |
| Creators | Smart, Nora (Nonie) Louise. |
| Publisher | University of Ottawa (Canada) |
| Source Sets | Université d’Ottawa |
| Detected Language | English |
| Type | Thesis |
| Format | 152 p. |
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