Abstract
Studies of the furious and paralytic forms of canine rabies at the early stage of disease have shown a more rapid viral colonization of the cerebral hemispheres in the furious form, as measured by viral antigen within neuronal cell bodies and viral RNA levels. Measurement of cellular processes separate from neuronal cell body provides a visual record of the spread of rabies virus which occurs across synapses. In this study, the amount of rabies viral antigen within cell processes was quantitatively assessed by image analysis in a cohort of naturally rabies infected non-vaccinated dogs (5 furious and 5 paralytic) that were sacrificed shortly after developing illness. Measurements were taken at different levels of the spinal cord, brain stem, and cerebrum. Results were compared to the amount of rabies viral antigen in neuronal cell bodies. Generally, the amount of rabies viral antigen in cell processes decreased in a rostral direction, following the pattern for the amount of rabies viral antigen in neuronal cell bodies and the percentage of involved cell bodies. However, there was a delay in cell process involvement following cell body involvement, consistent with replication occurring in the cell body region and subsequent transport out to cell processes. Greater amounts of antigen were seen in cell processes in dogs with the furious compared to paralytic form, at all anatomic levels examined. This difference was even evident when comparing (1) neurons with similar amounts of antigen, (2) similar percentages of involved neurons, and (3) anatomic levels that showed 100% positive neurons. These findings suggest that intracellular transport of the virus may be slower in the paralytic form, resulting in slower viral propagation. Possible mechanisms might involve host-specific differences in intracellular virus transport. The latter could be cytokine-mediated, since previous studies have documented greater inflammation in the paralytic form.
Highlights
Rabies is an almost uniformly fatal infectious disease of the central nervous system (CNS), caused by a neurotropic RNA virus in the family Rhabdoviridae, genus Lyssavirus [1]
Studying cell processes separate from cell body provides a visual record of the spread of rabies virus
The amount of viral protein in cell processes decreased from spinal cord to brain, as did the amount of viral protein in cell bodies and the percentage of involved cell bodies
Summary
Rabies is an almost uniformly fatal infectious disease of the central nervous system (CNS), caused by a neurotropic RNA virus in the family Rhabdoviridae, genus Lyssavirus [1]. Furious and paralytic clinical forms of rabies occur in both humans and dogs in a ratio of approximately 2:1 [3]. While limbic symptoms dominate the clinical picture in the furious form, paralysis of lower motor neuron type is the major clinical feature of the paralytic form [3, 4]. Differences between these two forms of rabies cannot be explained by postmortem histopathological studies. Spinal cord anterior horn cell dysfunction with central chromatolysis of the neurons at corresponding bite level (but without clinical weakness) has been demonstrated in the furious form of rabies while dysfunction of peripheral nerves, axon- or myelinopathy has been found in the paralytic form [3, 4]. Functional alteration of muscarinic acetylcholine receptors has been observed in rabid dog brains, especially in the brainstem and hippocampus [7]
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