Zika virus is a mosquito-borne infection that was initially discovered in Uganda in 1947 in Rhesus macaque monkeys which then led to spread and infection to humans in the early 1950s. Throughout the 1960 to 1980s, Zika was predominantly detected in Asia and Africa. In 2015, a Zika epidemic erupted in Brazil, spreading throughout South America, Central America, and the Caribbean through the Aedes aegypti mosquito. During this outbreak, an association with Zika and microcephaly was first identified, along with evidence of sexual transmission and other neurological symptoms including Guillain–Barre Syndrome [28]. Since 2017, Zika transmission has remained prevalent throughout most countries in the Americas and Caribbean [29].

Most people infected with Zika are asymptomatic. In those who do develop symptoms, they typically present 3–14 days after infection and are mild, including rash, conjunctivitis, muscle and joint pain, headache, and malaise. Symptoms can last between 2 and 7 days. Given symptomatology parallels with other arboviruses, diagnosis must be confirmed with laboratory testing.

There are several complications of Zika that have been reported and continue to be studied. Zika virus during pregnancy has led to several complications in infants including microcephaly, limb contractures, increased muscle tone, eye abnormalities, and hearing loss, which have since been defined as congenital Zika syndrome [29]. The risk of congenital malformations following infection during pregnancy is still being studied, but to date, an estimated 5–15% of infants born to women infected with Zika have demonstrated Zika-related complications [30••]. Congenital malformations can occur following either symptomatic or asymptomatic infection of a pregnant woman, leading to insidious outcomes including fetal loss, stillbirth, and preterm birth [31].

Zika-associated Guillain–Barre syndrome is estimated to affect 2–3 people per 10,000 ZIKV infections, which is similar to the risk associated with campylobacter infection [32]. Symptom onset is usually within 5–10 days, and management is the same as for classic GBS, with therapeutic plasma exchange or intravenous immune globulin.

For the general population who present with uncomplicated ZIKV infection, PCR and serology testing is not recommended. Given that Zika and dengue are closely related, for symptomatic patients present with < 7 days of symptoms, dengue and Zika nucleic acid amplification tests will confirm acute viral infections. For patients presenting > 7 days post symptom onset, Zika and dengue IgM serology is recommended (Table 1) [33]. If neurological symptoms are present, serum testing is recommended with consideration of cerebral spinal fluid testing. Lastly, if there is concern for ZIKV exposure or asymptomatic infection of ZIKV in a pregnant patient, serum testing is recommended up to 12 weeks after onset of illness, with serial ultrasonography to monitor for congenital ZIKV [30••]. Management of Zika continues to be supportive through rest, IV fluids, and analgesics. For patients with active infections, education is important. Use of barrier protection and contraceptives is recommended for at least 2 months in women and 3 months in men as the virus has shown to last longer in semen compared to other bodily fluids [34].

In conjunction with many arboviruses endemic to the Caribbean and Americas, there is no confirmed vaccine or specific treatment option for Zika. Treatment is supportive with emphasis on fluid resuscitation, analgesics, and avoiding aspirin or NSAIDs until dengue has been ruled out. In severe cases, hospitalization may be indicated for fluid replacement, fever control, and symptom management.