Abstract

Little is known about the long-term neurological development of children diagnosed with congenital Zika infection at birth. Here, we report the imaging and clinical outcomes up to three years of life of a cohort of 129 children exposed to Zika virus in utero. Eighteen of them (14%) had a laboratory confirmed congenital Zika infection at birth. Infected neonates have a higher risk of adverse neonatal and early infantile outcomes (death, structural brain anomalies or neurologic symptoms) than those who tested negative: 8/18 (44%) vs 4/111 (4%), aRR 10.1 [3.5–29.0]. Neurological impairment, neurosensory alterations or delays in motor acquisition are more common in infants with a congenital Zika infection at birth: 6/15 (40%) vs 5/96 (5%), aRR 6.7 [2.2–20.0]. Finally, infected children also have an increased risk of subspecialty referral for suspected neurodevelopmental delay by three years of life: 7/11 (64%) vs 7/51 (14%), aRR 4.4 [1.9–10.1]. Infected infants without structural brain anomalies also appear to have an increased risk, although to a lesser extent, of neurological abnormalities. It seems paramount to offer systematic testing for congenital ZIKV infection in cases of in utero exposure and adapt counseling based on these results.

Highlights

  • Little is known about the long-term neurological development of children diagnosed with congenital Zika infection at birth

  • Infants included in these cohorts were mostly affected by congenital Zika Syndrome (CZS) with cerebral anomalies or neurological impairments at birth

  • Among 129 children tested for ZIKV at birth, 18 (14.0%) had a laboratoryconfirmed congenital infection and 111 (86.0%) tested negative

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Summary

Introduction

Little is known about the long-term neurological development of children diagnosed with congenital Zika infection at birth. Long-term disabilities, including cerebral palsy, epilepsy, and neurosensory alterations have been described in infants from the American and Brazilian cohorts[6,7,8,9] Infants included in these cohorts were mostly affected by congenital Zika Syndrome (CZS) with cerebral anomalies or neurological impairments at birth. The evolution of those with a laboratory-confirmed congenital infection but who were asymptomatic and without cerebral anomalies at birth remains poorly described. Using a subset of these infants, we show that those with a laboratory-confirmed congenital Zika infection at birth have higher risks of imaging and clinical adverse outcomes at 2 months, 2 years, and 3 years of life than those tested negative at birth

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