Neurologic Infections in Travelers

Malveeka Sharma, MD, MPH; Joseph R. Zunt, MD, MPH


Semin Neurol. 2019;39(3):399-414. 

In This Article

West Nile Virus


West Nile virus (WNV) is a zoonotic arbovirus transmitted from infected birds to humans via mosquitos. The virus was first described in 1937 in Uganda. Since the first description, the virus has been identified worldwide and become an important cause of encephalitis.[55] The first documented case in the United States occurred in 1999 in New York City.[56] The virus is now endemic in the United States. There are rare cases of transmission of WNV via organ transplantation, blood transfusion, and breast milk.[57]

Life Cycle, Ecology, and Species

WNV is a flavivirus transmitted primarily by Culex mosquitoes.[58]

Clinical Manifestations

Up to 80% of human WNV infections are asymptomatic.[56] The incubation period is 3 to 6 days. About 20% of individuals develop mild symptoms consisting of fever, headache, myalgia, nausea, and anorexia.[2] Neuroinvasive disease occurs in less than 1% of all cases. However, infection is associated with mortality between 10 and 30% and high morbidity. The three major manifestations of neuroinvasive disease are meningitis, encephalitis, and acute flaccid paralysis.[56] Other manifestations include cognitive impairment, motor neuron disease, cranial nerve palsies (usually facial nerve), GBS, and movement disorders. Older age and medical comorbidities are associated with higher mortality, and presence of coma at presentation or cranial nerve palsy is highly predictive of poor outcome.[56] Most people with meningitis without focal neurological deficits tend to recover fully; however, encephalitis and flaccid paralysis are typically associated with poor prognosis.[59]


A clinical presentation of meningitis, encephalitis, or flaccid paralysis with a history of exposure to a mosquito bite or travel through endemic areas should prompt further investigation into WNV. CSF analysis will typically show elevated protein and a lymphocytic pleocytosis.[2] Detection of IgM antibody in serum and CSF via ELISA is the standard diagnostic test. Other options include viral culture, RT-PCR, and immunohistochemistry to detect viral antigens, although these tests are not as specific. Neuroimaging can reveal leptomeningeal enhancement or abnormalities in the basal ganglia, thalamus, cerebellum, or brainstem, depending on the clinical presentation, but these may also be normal.[56]


There is no specific treatment for WNV. There are numerous case reports and series evaluating the use of polyclonal immune globulin, monoclonal immune globulin, interferon, ribavirin, and corticosteroids, with no clear benefit.[58] Supportive care is the mainstay of management. Severe cases necessitate hospitalization with fluid resuscitation, respiratory support, pain control, and monitoring and management of elevated intracranial pressure and seizures.[56] Prevention is targeted to vector control, personal protective measures, and screening of blood and organ donors. No vaccine is currently available, although there are some trials underway on HydroVax-001, WN/DEN4delta30 vaccine, WN/DEN4delta30 vaccine, ChimeriVax-WN02 vaccine, and VRC-WNVDNA020–00-VP vaccine (