Rabies

Transmission is through the saliva of an infected mammal, usually a bite; in the United States the reservoirs are bats, raccoons, skunks, and foxes, with bats the commonest source and often without a recognized bite, while worldwide the dog dominates. The virus binds nicotinic acetylcholine receptors at the neuromuscular junction and travels retrograde by dynein along axons to the spinal cord and brain, then centrifugally to salivary glands. The long and variable incubation, weeks to months depending on the distance from the brain, is what makes post-exposure prophylaxis possible. Prodromal fever and paraesthesia at the bite site are followed by encephalitic rabies with hydrophobia, aerophobia, pharyngeal spasm, agitation, and autonomic instability, or by paralytic rabies. Negri bodies are eosinophilic cytoplasmic inclusions, classically in Purkinje cells and hippocampal neurons. Post-exposure prophylaxis is immediate wound washing plus rabies immune globulin infiltrated around the wound and vaccine on days 0, 3, 7, and 14; once symptoms appear, death is nearly universal.