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Rabies is a complex disease. We still do not understand the mechanisms of clinically diverse furious and dumb types and its fatal course. Moreover clinical symptomatology, once believed to be unique, may be variable, particularly in those patients who develop disease after exposure to virus of the insectivorous or frugivorous bat origin. This review summarizes classic and nonclassic clinical features associated with canine and bat rabies variants and also atypical presentations of rabies survivors. Differences in cellular tropism either at the inoculation site or in the central nervous system or differences in route of spread, or both, may account for these discrepancies. Furthermore, these may affect different sets of neurotransmitters that in turn modulate variable neurobehavioural patterns and neuroendocrine-immune cascades.

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