Written by L. L.
Briceland, PharmD
Professor and Director Experiential Education, Department of Pharmacy
Practice, Albany College of Pharmacy, Albany, New York.
West Nile virus (WNV) infection is caused by a mosquito-borne
flavivirus, which is transmitted to humans through the bite of an
infected mosquito, with birds acting as the primary amplification host.
WNV is endemic to Israel and parts of Europe and Asia; since 1999, WNV
has emerged as an important human and avian disease in the United
States.[1]
Following a bite from an infected mosquito, the virus enters the
person's bloodstream and may cross the blood-brain barrier in the
central nervous system. About 80% of infected people will remain
asymptomatic. Following a 3- to 14-day incubation period, the remaining
individuals will develop an influenza-like illness, characterized by the
sudden onset of fever and/or chills, headache, malaise, and
lymphadenopathy. Fewer than 1% of patients will exhibit severe
neurologic symptoms, including meningitis, encephalitis, or acute
flaccid paralysis, which may lead to permanent impairment. Typically,
symptoms of milder WNV infection resolve over several days; however,
long-term sequelae, including numerous somatic complaints, tremor,
neuropsychological abnormalities, and motor skill deficits, have
recently been shown to exist for at least 12 months post-infection.[2]
There is no specific treatment for WNV. Supportive and symptomatic
care remains the mainstay of therapy, based on the clinical
presentation; this includes ventilatory support and intravenous
rehydration fluids. There are case reports noting some success with the
use of ribavirin and interferon alfa-2b, corticosteroids, antiepileptics,
intravenous immunoglobulin as adjuvant therapy, and/or osmotic agents.[3,4]
Given the lack of definitive therapy for WNV, preventive measures
against mosquito bites are encouraged.
