Most persons infected with WNV are asymptomatic. A seroepidemiologic study of 677 people who lived in New York City during the 1999 outbreak found that 80% of seropositive subjects never developed symptoms (Mostashari et al. 2001). After an incubation period of 2-14 days, 20% of infected subjects developed a nonspecific febrile illness that lasted 3-6 days. Nausea, vomiting, myalgia, and headache are typical symptoms. A generalized maculopapular rash may occur in up to 20% of patients.
About 1 in 150 symptomatic patients in New York City developed WNND (Mostashari et al. 2001), which is often manifested as meningitis (WNM) or encephalitis (WNE) and sometimes as acute flaccid paralysis (AFP). Patients with WNND frequently have movement disorders with tremor, myoclonus, or Parkinsonism (Sejvar et al. 2003). Muscle weakness is also common. Investigators have reported paresis in about 50% of WNND cases and complete flaccid paralysis in 10%; the latter cases lack deep tendon reflexes and mimick GBS. Seizures and focal neurologic findings have been uncommon.
The development of WNND has been directly correlated with age. Of those over 65 years old, 1 in 50 developed WNM or WNE vs 1 in 300 of those under 65 (Mostashari et al. 2001). In fact, in those over 80 years old, the risk of symptomatic neurologic disease was 43 times higher than in those under 19.
West Nile fever without meningitis is more likely in younger patients. Among those with neurologic involvement, meningitis is more common in younger patients (mean age, 35 years), and encephalitis is more common in older patients (mean age, 70 years) (Sejvar et al. 2003).
Patients with West Nile fever who do not have neurologic manifestations might have residual fatigue, muscle weakness, and headache that can persist for months after resolution of the acute febrile illness (Watson et al. 2004). Of 98 patients with laboratory-confirmed West Nile infection but no clinical evidence of WNM, WNE, or AFP, 96% had fatigue for a median of 36 days, 61% had muscle weakness for a median of 28 days, and 71% had headache for a median of 10 days. The median time for recovery to a point that the patients considered “back to normal” was 60 days.
For patients with acute symptomatic WNV infection, relative lymphocytopenia (less then 20%) is common. The cerebrospinal fluid (CSF) reveals a mild lymphocytic pleocytosis with a mean of 38 white cells/mm3 (range, 0-525) (Nash et al. 2001). Up to one-third may have more then 50% neutrophils on initial evaluation of the CSF. Increased protein with a mean of 104 mg/dL (range, 38-899) can be found. CSF glucose is usually normal.
Imaging studies of the brain usually are normal on computed tomography without evidence of inflammation. Even magnetic resonance imaging scan reveals enhancement of the meninges or periventricular areas in only about 30% of people (Nash et al. 2001). Electromyography reveals a motor axonal polyneuropathy with sparing of the sensory fibers very similar to the findings in poliomyelitis. WNV has a propensity to involve the anterior horn cells of the spinal cord in a manner very similar to poliomyelitis.
Acute infection is diagnosed by demonstration of WNV IgM in serum, which has been found in close to 100% of patients (Tardei et al. 2000). In one study, CSF samples from 94% of patients were WNV-IgM positive (Nash et al. 2001). No cases had virus isolation from CSF, and