Neurologic Infections in Travelers

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

Disclosures

Semin Neurol. 2019;39(3):399-414. 

In This Article

Zika Virus

Epidemiology

Zika virus belongs to the Flavivirus genus and is transmitted through the bite of an infected Aedes mosquito.[49] Zika virus was first identified in 1947 in monkeys living in the Zika Forest of Uganda. Since 2007, outbreaks have occurred in Southeast Asia and the Western Pacific. In 2015, a large outbreak in Brazil marked the first occurrence in the Western Hemisphere; the introduction of the virus hypothesized to have occurred during the 2014 soccer World Cup or the 2014 World Spring Canoe championship.[50] Transmission has now been identified via intrauterine, perinatal, and sexual routes, as well as through laboratory errors and contaminated transfusions.[51]

Life Cycle, Ecology, and Species

Zika virus is a single-stranded RNA virus in the genus Flavivirus. The main vector is the Aedes mosquito.

Clinical Manifestations

Most symptomatic Zika virus infections present with a nonspecific mild febrile illness such as fever, arthralgia, myalgia, headache, and maculopapular rash, but 80% of infections are asymptomatic.[50,51] Zika has been associated with severe congenital disease, specifically microcephaly. The neurological manifestations of Zika include virus-associated myelitis, encephalitis, meningoencephalitis, GBS, and acute disseminated encephalomyelitis.[49] The most common manifestation is GBS. It has been postulated that prior infection with dengue or chikungunya may promote or be necessary to lead to the development of Zika immune-mediated GBS.[52]

Diagnosis

Zika virus infection should be suspected in patients who live in or have recently traveled through endemic regions within 2 weeks of the onset of symptoms. Because of high rates of co-infection, evaluation for other flaviviruses should also be assessed at the time of diagnosis. CSF assays are available to detect viral RNA or antibodies.[49] Due to the transient nature of viremia, real-time reverse transcription PCR (rRT-PCR) of the Zika virus can be detected in serum <7 days after onset of symptoms, but viremia persists in urine up to 14 days after onset of symptoms.[51] Detection of serum IgM antibodies or a significant rise in IgG in samples collected 2 weeks apart can support the diagnosis as well. Another confirmatory test includes the plaque reduction neutralization test, which can discriminate anti-Zika virus antibodies from other cross-reacting antibodies.[53] For evaluation of neurological manifestations, electromyography and nerve conduction studies should demonstrate a typical pattern to confirm GBS.

Treatment

As there is no specific treatment for Zika virus infection, supportive management is the mainstay of treatment.[51] For patients with GBS manifestations, close monitoring of respiratory and cardiac systems in intensive care settings and the use of plasmapheresis or IV immunoglobulins should be used.[54] Pregnant patients diagnosed with Zika virus infection should be educated and monitored for adverse outcomes.[51] There is no vaccine or postexposure prophylaxis available. Vector control and personal protective measures are the best ways to prevent infection.[51]

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