Once introduced, the initial infection and multiplication occur with local monocytes for the first 48 to 96 h. Subsequently, the virus spreads across the motor end-plate, and ascends and replicates along peripheral nervous axoplasm to the dorsal root ganglia, the spinal cord, and the central nervous system (CNS). Following CNS replication in the gray matter, the virus spreads outward by peripheral nerves to virtually all tissues and organ systems. Viral infection of the salivary glands engenders infectivity of saliva; the infectivity of other body fluids is less well established.
Histologically, rabies is similar to other forms of encephalitis: diffuse and extensive monocellular infiltration with focal hemorrhage and demyelination, predominantly in perivascular areas in the gray matter of the CNS, basal ganglia, and the spinal cord. Negri bodies are the characteristic histologic finding for rabies, which is the site of CNS viral replication. They are eosinophilic intracellular lesions found within cerebral neurons and are highly specific for rabies. Negri bodies are encountered in about 75 percent of proven animal rabies; thus, although their presence is pathognomonic for rabies, their absence does not exclude rabies as a diagnostic possibility.
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