2002, Volume 13, Number 3
D. L. Wiedbrauk, Ph.D.
West Nile virus (WNV) is a mosquito-borne virus that was first identified in 1937 from an infected person in the West Nile district of Uganda. Until 1999, the WNV was found only in Africa, Asia, the Middle East, and Europe. The appearance of WNV in the United States and its rapid spread have alarmed physicians, public health officials and the general public.
The symptomatology of West Nile fever is poorly defined because surveillance activities have chiefly focused on patients with neurological disease. Approximately one in four infected persons will have malaise, anorexia, nausea, vomiting, eye pain, headache, myalgia, lymphadenopathy and rash lasting 3 to 6 days. Among the 6 symptomatic persons identified in the 1999 New York City serosurvey, 6/6 reported myalgia, 5/6 had headache, fatigue, and headache and 4/5 had arthralgia. Approximately half of the hospitalized U.S. patients had severe muscle weakness and approximately 10% of patients had complete flaccid paralysis. These symptoms may provide a clinical clue to the presence of WNV, particularly in the setting of encephalopathy.
Routine laboratory findings are often unremarkable in WNV infections and total leukocyte counts in peripheral blood are usually normal or elevated. Lymphocytopenia and anemia may also occur. Hyponatremia is sometimes present, especially in patients with encephalitis. CSF testing will often show pleocytosis with leukocyte counts ranging from 0 to 1782 cells/mm3, and a preponderance of lymphocytes. CSF protein levels are elevated (51 to 800 mg/dL) and glucose levels are normal. Computed tomography of the brain will usually show no evidence of acute disease. However, magnetic resonance imaging will show enhancement of the leptomeninges and/or the periventricular areas in about one third of patients.
Serologic detection of WNV IgM is the most efficient method for detecting WNV infections. IgM is usually present in serum samples within 8 days of the onset of symptoms and WNV IgM may persist for 6 months or longer. Submission of acute and convalescent sera are recommended. Since IgM does not cross the blood-brain barrier, the presence of WNV IgM in CSF can suggest central nervous system involvement. PCR viral culture are not recommended at this time.
Two serosurveys conducted in New York City in 1999 and 2000 showed that approximately 1 in 150 infections resulted in meningitis or encephalitis. Advanced age is the most significant risk factor for severe neurologic disease. This risk increases markedly among persons 50 years of age or older. Compared with persons 0 to 19 years of age, the incidence of severe neurological disease was 10 times higher in persons aged 50 to 59 years and 43 times higher in those over 79 years old. Overall case fatality rates were 12% in New York City and persons over 74 years of age were nearly nine times more likely to die than younger persons.
WNV is transmitted by the bite of an infected mosquito. Person-to-person spread has not been documented. There is no evidence that WNV can be spread directly from birds to people.
Only one in five infected persons will have a febrile illness. Febrile illness usually occurs 3-15 days after being bitten by an infected mosquito.
Human vaccines for West Nile Virus are under development but for the foreseeable future, prevention will depend upon two broad strategies:
1. reducing the number of mosquitoes and,
2. preventing mosquitoes from biting humans.
More information about prevention of WNV infection can be found at http://www.michigan.gov/mdch