From Other Journals
West Nile Virus: A Review for Family Physicians
Am Fam Physician. 2002 Dec 15;66(12):2317-2321.
The West Nile virus was previously restricted to the Eastern Hemisphere, notably Israel, Eastern Europe, and Africa, until 1999, when cases of infection were first documented in New York City. Since then, the United States has documented fewer than 100 annual cases, mostly encephalitis and meningitis. Peak incidence occurs in late August and early September, with human infections occurring from mid-July to early December. The virus is maintained in an enzootic cycle in which a mosquito vector transfers the virus from infected birds to humans and back to birds. Increasing bird deaths, especially crows, often herald the local development of human cases. The virus itself is related to several other human encephalitis viruses, including St. Louis encephalitis and Japanese encephalitis. Petersen and Marfin discuss the clinical features and prevention of West Nile virus infection (see Table 1).
Key Clinical Facts About West Nile Virus in North America
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Human infection is generally subclinical and follows an incubation period of three to 14 days. When symptoms are present, they most commonly include myalgia, fatigue, headache, and arthralgia. Neurologic disease occurs in approximately one out of 150 cases, most commonly manifesting as meningitis or encephalitis. Older age is the most common risk factor for significant neurologic disease. Severe muscle weakness in hospitalized patients in the setting of encephalitis symptoms is an important clue to West Nile virus infection. Other neurologic presentations can include ataxia and extrapyramidal signs, cranial nerve abnormalities, myelitis, optic neuritis, polyradiculitis, and seizures. Cerebrospinal fluid examination shows pleocytosis, with leukocyte cell counts ranging from zero to 1,782 per mm3 (1.8 × 106 per L), with lymphocyte predominance.
The most effective diagnostic method is detection of IgM antibody to West Nile virus in serum or cerebrospinal fluid (the latter suggesting neurologic involvement). False-positive results, which may occur because of prior exposure to a related flavivirus, can be further evaluated using the plaque reduction neutralization test that is highly specific for arthropod-borne flaviviruses. Clinical and laboratory testing guidelines are available, as well as descriptions of reporting mechanisms (see Table 2). All cases should be reported to local authorities.
TABLE 2 Web Resources for Information Related to West Nile Virus
Web Resources for Information Related to West Nile Virus
Clinical and laboratory testing guidelines:
Information on reporting mechanisms: www.cdc.gov/ncidod/dvbid/westnile/city_states.htm
Information on mosquito-control measures and pesticides: www.ace.orst.edu/info/npic/wnv
At present, treatment of infection is supportive. The use of antiviral agents, such as ribavirin and interferon, is being studied. Case fatalities are higher among persons older than 70. Many patients who survive infection have persistent symptoms such as fatigue, memory loss, difficulty walking, muscle weakness, and depression.
The authors recommend two strategies in the prevention of West Nile virus infection: reducing the mosquito population, and preventing bites by avoiding mosquito-infested areas and using insect repellents and barriers such as window screens and long-sleeved clothing. Products containing 10 to 50 percent DEET (N,N-diethyl-3-methylbenzamide) can be directly applied to skin, pets, clothing, tents, bedrolls, and screens. Children should use preparations containing no more than 10 percent DEET. Citronella may be used, but it is not as effective as DEET. Information about mosquito control measures and pesticides is available from the U.S National Pesticide Information Center (see Table 2).
Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med. August 6, 2002;137:173–9.
Copyright © 2002 by the American Academy of Family Physicians.
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