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This very severe illness with an almost universally fatal outcome requires intensive care with attention to the airway, maintenance of oxygenation, and control of seizures Universal precautions are essential Other modalities of therapy that may be beneficial include a combination of rabies vaccine, rabies immune globulin, monoclonal antibodies (investigational), ribavirin, interferon- , and amantadine Corticosteroids are of no use
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Prognosis
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If postexposure prophylaxis is given expediently, before clinical signs develop, it is nearly 100% successful in prevention of disease Once the symptoms have appeared, death almost inevitably occurs after 7 days, usually from respiratory failure Most deaths occur in persons with unrecognized disease who do not seek medical care The induction of coma by ketamine in evolved cases, reported helpful in one case, is not universally accepted as a mode of care
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CDC National Center for Infectious Diseases Rabies http:// wwwcdcgov/ncidod/dvrd/rabies Goudsmit J et al Comparison of an anti-rabies human monoclonal antibody combination with human polyclonal antirabies immune globulin J Infect Dis 2006 Mar 15;193(6): 796 801 [PMID: 16479514] Hemachudha T et al Rabies Curr Neurol Neurosci Rep 2006 Nov;6(6):460 8 [PMID: 17074280] Krebs JW et al Rabies surveillance in the United States during 2004 J Am Vet Med Assoc 2005 Dec 15;227(12): 1912 25 [PMID: 16379626] Rupprecht CE et al Prophylaxis against rabies N Engl J Med 2004 Dec 16;351(25):2626 35 [PMID: 15602023] Suwansrinon K et al Is injecting a finger with rabies immunoglobulin dangerous Am J Trop Med Hyg 2006 Aug;75(2): 363 4 [PMID: 16896149]
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2 Arbovirus Encephalitides
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ESSENTIALS OF DIAGNOSIS
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Fever, malaise, stiff neck, sore throat, and nausea and vomiting, progressing to stupor, coma, and convulsions
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Viral & Rickettsial Infections
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Signs of an upper motor neuron lesion (exaggerated deep tendon reflexes, absent superficial reflexes, pathologic reflexes, and spastic paralysis) Cerebrospinal fluid protein and opening pressure often increased, with lymphocytic pleocytosis
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CMDT 2008
General Considerations
The arboviruses are arthropod-borne pathogens that produce clinical manifestations in humans The mosquitoborne pathogens include three alphaviruses (causing Western, Eastern, and Venezuelan equine encephalitis), five flaviviruses (causing West Nile fever, St Louis encephalitis, Japanese B encephalitis, dengue, and yellow fever), bunyaviruses (the California serogroup of viruses [in particular, California encephalitis caused by the Lacrosse agent]), and some causes of viral hemorrhagic fever (Rift Valley fever) The tick-borne causes of encephalitis include the flavivirus Powassan (northeastern United States and Canada) and tick-borne encephalitides of Europe Pathogens associated with viral hemorrhagic fever are discussed below, and only those viruses causing primarily encephalitis in the United States will be discussed here Infection with West Nile virus was first identified in the United States in the New York City area in 1999 The virus spread rapidly, with initial cases reported along the Atlantic seaboard Current cases are reported throughout the continental United States Along with West Nile fever, the leading causes of arbovirus encephalitis in the United States are St Louis encephalitis and California encephalitis Pathogen-specific reservoirs (typically small mammals or birds) are responsible for maintaining the encephalitis-producing viruses in nature Birds are the main reservoir for West Nile virus and substantial avian mortality accompanies West Nile fever outbreaks, a fact that is used to monitor disease patterns Outbreaks tend to occur in late summer and early fall Transplacental transmission is documented for the viruses that cause Western and Venezuelan equine encephalitis and West Nile fever The virus that causes West Nile fever is also transmissible via blood donation, organ transplantation, breast-feeding, and laboratory and possibly aerosol exposures The human incubation period is 2 14 days The proportion of patients in whom the disease develops after acquiring the virus is unknown Estimates were reported from serologic surveillance from the New York epidemic; fever developed in 1 of 5 infected patients and severe neurologic disease developed in 1 of 150
50% of patients in the United States with West Nile virus infection with symptoms severe enough to warrant hospitalization had significant muscle weakness This weakness can cause diagnostic confusion with the Guillain Barr syndrome and may evolve into a poliomyelitis-like syndrome Rash is reported in less than one-third of cases Among 3830 cases of West Nile virus disease reported in 2006 in the United States, 61% were reported as West Nile fever (milder disease without any neuroinvasion), about 35% were reported as West Nile meningitis or encephalitis (neuroinvasive disease), and the case fatality rate was about 3% Age older than 50 years seems to be the main risk factor for severe meningoencephalitis and death Immunosuppression appears to be a risk factor for death, especially with encephalitis cases The outcome of encephalitis is also age-dependent with residual damage principally in older patients St Louis encephalitis occurs among adults; Western, Venezuelan, and Japanese encephalitides occur primarily among children, while the Eastern encephalitis is a disease of both children and the elderly The disease manifestations associated with West Nile fever are strongly age-dependent with the acute febrile syndrome and mild neurologic symptoms more common in the young, aseptic meningitis and poliomyelitis-like syndromes in the middle aged, and frank encephalopathy in the elderly
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