Abstract
BackgroundRabies virus preferentially involves brainstem, thalamus and spinal cord in human furious and paralytic rabies beginning in the early stage of illness. Nevertheless, rabies patient remains alert until the pre-terminal phase. Weakness of extremities develops only when furious rabies patient becomes comatose; whereas peripheral nerve dysfunction is responsible for weakness in paralytic rabies.MethodsEvidence of apoptosis and mitochondrial outer membrane permeabilization in brain and spinal cord of 10 rabies patients was examined and these findings were correlated with the presence of rabies virus antigen.ResultsAlthough apoptosis was evident in most of the regions, cytochrome c leakage was relatively absent in spinal cord of nearly all patients despite the abundant presence of rabies virus antigen. Such finding was also noted in brainstem of 5 patients.ConclusionCell death in human rabies may be delayed in spinal cord and the reticular activating system, such as brainstem, thus explaining absence of weakness due to spinal cord dysfunction and preservation of consciousness.
Highlights
Rabies virus preferentially involves brainstem, thalamus and spinal cord in human furious and paralytic rabies beginning in the early stage of illness
Regional central nervous system (CNS) distribution of rabies virus antigen and apoptosis Rabies virus antigen The overall regional distribution of rabies viral antigen was roughly similar in terms of number and location to
There was no significant correlation between short or long survival period, amount of rabies antigen positive neurons and degree of apoptosis in various CNS regions
Summary
Rabies virus preferentially involves brainstem, thalamus and spinal cord in human furious and paralytic rabies beginning in the early stage of illness. Clinical presentations of rabies in humans can be categorized as classic (furious and paralytic) and non-classic rabies [1,2] The latter is almost always associated with bat and some dog variants whereas the classic forms are associated with dog variants. Rabies virus antigen preferentially localizes in the spinal cord and brainstem and thalamus, basal ganglia if the survival period is 7 days or less regardless of the clinical forms [4]. Such brainstem and thalamus predilection is evident in animals [5]
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