Abstract
Zika virus (ZIKV) is a mosquito-borne flavivirus recognized as teratogenic since the 2015 to 2016 epidemic. Antenatal ZIKV exposure causes brain anomalies, yet the full spectrum has not been delineated. To characterize the clinical features of ZIKV infection at a pediatric referral center in Rio de Janeiro, Brazil, among children with antenatal ZIKV exposure. Retrospective cohort study conducted from May to July 2019 of a prospective cohort of 296 infants with antenatal ZIKV exposure followed up since December 2015 at a tertiary maternity-pediatric hospital. Zika virus infection during pregnancy. Characterization of clinical features with anthropometric, neurologic, cardiologic, ophthalmologic, audiometric, and neuroimaging evaluations in infancy and neurodevelopmental assessments (Bayley Scales of Infant and Toddler Development, Third Edition) from 6 to 42 months of age, stratified by head circumference at birth (head circumference within the reference range, or normocephaly [NC] vs microcephaly [MC]). Antenatal exposure to ZIKV was confirmed for 219 of 296 children (74.0%) referred to Instituto Fernandes Figueira with suspected ZIKV infection through positive maternal or neonatal polymerase chain reaction analysis or IgM serology results. Of these children, 110 (50.2%) were boys, ages ranged from 0 to 4 years, and 53 (24.2%) had congenital microcephaly. The anomalies observed in ZIKV-exposed children with MC or NC were failure to thrive (MC: 38 of 53 [71.7%]; NC: 73 of 143 [51.0%]), cardiac malformations (MC: 19 of 46 [41.3%]; NC: 20 of 100 [20.0%]), excess nuchal skin (MC: 16 of 22 [72.7%]; NC: 35 of 93 [37.6%]), auditory abnormalities (MC: 13 of 50 [26.0%]; NC: 14 of 141 [9.9%]), and eye abnormalities (MC: 42 of 53 [79.2%]; NC: 28 of 158 [17.7%]). Although they experienced fewer neurologic abnormalities than children born with MC, those with NC also had frequent neurologic abnormalities (109 of 160 [68.1%]), including hyperreflexia (36 of 136 [26.5%]), abnormal tone (53 of 137 [38.7%]), congenital neuromotor signs (39 of 93 [41.9%]), feeding difficulties (15 of 143 [10.5%]), and abnormal brain imaging results (44 of 150 [29.3%]). Among 112 children with NC with Bayley-III evaluations, 72 (64.3%) had average or above-average scores; 30 (26.8%) scored 1 SD below average in at least 1 domain; and 10 (8.9%) scored 2 SD below average in at least 1 domain. Among 112 children with NC, a smaller head circumference at birth was significantly associated with subsequent below-average cognitive scores (U = 499.5; z = -2.833; P = .004) and language scores (U = 235.5; z = -2.491; P = .01). Children without MC who were exposed to ZIKV in utero had a high frequency of anatomical and neurodevelopmental abnormalities. The head circumference at birth for children with NC was associated with neurocognitive development. Recognition of the wide spectrum of clinical phenotypes is critical to ensure early referral to rehabilitative interventions.
Highlights
A Zika virus (ZIKV) epidemic in northeastern Brazil starting in May 2015 quickly spread to Rio de Janeiro between September 2015 and June 2016,2,21-26 with the virus identified by real-time reverse transcriptase–polymerase chain reaction (RT-PCR) in blood samples obtained from neonates with severe microcephaly and in amniotic fluid or tissue samples obtained from fetuses of women with rash during pregnancy.[14]
Between September 2015 and June 2017, 296 children were referred to Instituto Fernandes Figueira (IFF) for suspected antenatal ZIKV exposure
The present study sought to describe the wider spectrum of clinical manifestations in children with in utero exposure to the virus who were born in the aftermath of the Rio de Janeiro ZIKV epidemic
Summary
Exposure to Zika virus (ZIKV) during pregnancy may lead to devastating brain damage in the infant, resulting in congenital ZIKV syndrome (CZS) and other clinical manifestations.[1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17] Zika virus harms the developing brain by infecting human cortical neural progenitor cells and interfering with multiplication and migration of nervous system cells.[18,19,20] A ZIKV epidemic in northeastern Brazil starting in May 2015 quickly spread to Rio de Janeiro between September 2015 and June 2016,2,21-26 with the virus identified by real-time reverse transcriptase–polymerase chain reaction (RT-PCR) in blood samples obtained from neonates with severe microcephaly and in amniotic fluid or tissue samples obtained from fetuses of women with rash during pregnancy.[14]. Infants seemingly asymptomatic at birth may eventually develop abnormalities detected by brain imaging or in subsequent neurodevelopmental evaluations.[35,36] microcephaly at birth is the hallmark of CZS, a wide spectrum of postnatal abnormalities have not yet been fully characterized.[28,35,36,37,38,39,40] The primary objective of this study was to report the range of clinical manifestations in children with confirmed ZIKV antenatal exposure followed up at a large pediatric referral center in Rio de Janeiro
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