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disease is useful in assessing risk As indicated in the introductory section, the virus spreads along peripheral nerves to reach the nervous system Rare cases have been caused by inhalation of the virus shed by bats; in a few cases the source of the infection may not be identi able The epidemiology and public health aspects of rabies have been reviewed by Fishbein and Robinson Clinical Features The incubation period is usually 20 to 60 days but may be as short as 14 days, especially in cases involving multiple deep bites around the face and neck Tingling or numbness at the site of the bite, even after the wound has healed, is characteristic This is thought to re ect an in ammatory response that is incited when the virus reaches the sensory ganglion The main neurologic symptoms (following a 2- to 4-day prodromal period of fever, headache, and malaise) consist of severe apprehension, dysarthria, and psychomotor overactivity, followed by dysphagia (hence salivation and frothing at the mouth ), spasms of throat muscles induced by attempts to swallow water or in rare cases by the mere sight of water (hence hydrophobia ), dysarthria, numbness of the face, and spasms of facial muscles This localization indicates the involvement of the tegmental medullary nuclei in the rabid form of the disease Generalized seizures, confusional psychosis, and a state of agitation may follow A less common paralytic form ( dumb rabies of older writings, in distinction to the above described furious form) due to spinal cord infection, may accompany or replace the state of excitement The paralytic form is most likely to follow bat bites or, in the past, the administration of rabies vaccination Coma gradually follows the acute encephalitic symptoms and death ensues within 4 to 10 days, or longer in the paralytic form With modern intensive care techniques, there have been a number of survivors In addition to mechanical respiratory support, several secondary abnormalities must be addressed, including raised intracranial pressure, excessive release of antidiuretic hormone, diabetes insipidus, and extremes of autonomic dysfunction, especially hyper- and hypotension Pathologic Features The disease is distinguished by the presence of cytoplasmic eosinophilic inclusions, the Negri bodies They are most prominent in the pyramidal cells of the hippocampus and the Purkinje cells but have been seen in nerve cells throughout the CNS In addition there may be widespread perivascular cuf ng and meningeal in ltration with lymphocytes and mononuclear cells and small foci of in ammatory necrosis, such as those seen in other viral infections The in ammatory reaction is most intense in the brainstem The focal collections of microglia in this disease are referred to as Babes nodules (named for Victor Babes, a Romanian microbiologist) Treatment Bites and scratches from a potentially rabid animal should be thoroughly washed with soap and water and, after all soap has been removed, cleansed with benzyl ammonium chloride (Zephiran), which has been shown to inactivate the virus Wounds that have broken the skin also require tetanus prophylaxis After a bite by a seemingly healthy animal, surveillance of the animal for a 10-day period is necessary Should signs of illness appear in the animal, it should be killed and the brain sent, under refrigeration, to a government-designated laboratory for appropriate diagnostic tests Wild animals, if captured, should be killed and the brain examined in the same way If the animal is found by uorescent antibody or other tests to be rabid or if the patient was bitten by a wild animal that escaped,.

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