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