Zika virus belongs to the Flavivirus genus and is transmitted through the bite of an infected Aedes mosquito. 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. Transmission has now been identified via intrauterine, perinatal, and sexual routes, as well as through laboratory errors and contaminated transfusions.
Life Cycle, Ecology, and Species
Zika virus is a single-stranded RNA virus in the genus Flavivirus. The main vector is the Aedes mosquito.
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. 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.
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. 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. 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. For evaluation of neurological manifestations, electromyography and nerve conduction studies should demonstrate a typical pattern to confirm GBS.
As there is no specific treatment for Zika virus infection, supportive management is the mainstay of treatment. 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. Pregnant patients diagnosed with Zika virus infection should be educated and monitored for adverse outcomes. There is no vaccine or postexposure prophylaxis available. Vector control and personal protective measures are the best ways to prevent infection.
Semin Neurol. 2019;39(3):399-414. © 2019 Thieme Medical Publishers