Congenital Zika virus infection is caused by maternal infection with Zika virus, a mosquito-borne single-stranded RNA virus of the Flaviviridae family, spread by mosquitoes. Zika virus is closely related to the dengue virus. Human infection is primarily acquired via bites from infected Aedes aegypti or Aedes albopictus mosquitoes in endemic areas: the tropical regions of Africa, Southeast Asia, the South Pacific islands, and more recently, the Americas. In 2015, a Zika virus outbreak was first reported in Brazil, Colombia, and Suriname. Travel-related cases have since been reported in the United States; sexually transmitted cases are suspected to have occurred, and Zika virus has been found in the semen of infected men. Viral shedding has also been documented in vaginal secretions of infected women. A small number of cases of likely local mosquito-borne Zika virus transmission have been reported in Miami, Florida, and Brownsville, Texas. Since late 2016, Zika virus transmission in the Americas has dropped significantly. There have been rare cases of person-to-person nonsexual transmission. There is no apparent sex or age predilection for Zika virus infection.

In 2015, Zika virus infection in Brazil was accompanied by an increase in the number of cases of microcephaly and intracranial calcifications seen in infants. There are also cases of fetal loss in women who were infected with Zika virus. It is thought that these outcomes are the result of congenital infection with Zika virus. Additionally, a study found that over 65% of infants with congenital Zika virus had onset of epilepsy at approximately 5 months of age.

Maternal symptoms include fever, maculopapular rash, arthralgia, and conjunctivitis.

Newborns of women infected with Zika virus during pregnancy have a 5%-14% risk of congenital Zika syndrome. The risk is greatest when the mother is infected during the first trimester, although infection during any trimester can cause congenital Zika syndrome. First-trimester infection may also be associated with higher risks of pregnancy loss, preterm birth, and brain or eye defects in the infant.

Intrapartum transmission of Zika virus from an infected mother to her infant at the time of delivery has been described. Intrauterine transmission has also been described, and it is this mode of transmission that is thought to result in fetal loss or in fetal abnormalities including microcephaly, intracranial calcifications, and eye abnormalities (alterations in the macular region). Zika virus RNA has been identified in fetal tissue, placenta, and amniotic fluid in some cases. Zika virus RNA has been isolated from human breast milk, but transmission through breastfeeding has not been demonstrated. The Centers for Disease Control and Prevention (CDC) recommends testing for Zika virus in the following situations:

• Infants born to mothers with laboratory evidence of Zika virus infection during pregnancy, and
• Infants who have abnormal clinical or neuroimaging findings suggestive of congenital Zika syndrome and a maternal epidemiologic link suggesting possible transmission, regardless of maternal Zika virus test results.

The latest information regarding congenital Zika virus infection can be found online (https://www.cdc.gov/zika).