Abstract
ObjectivesTo describe and estimate the frequency of pregnancy outcomes, clinical and laboratory characteristics of vertical transmission of CHIKV in the neonate.Study designWe performed a systematic review evaluating the clinical presentation of perinatally-acquired CHIKV infection in neonates. The search was performed using Medline (via PubMed), LILACS, Web of Science, Scielo, Google Scholar and Open grey to identify studies assessing vertical transmission of CHIKV up to November 3, 2020. There were no search restrictions regarding the study type, the publication date or language. Studies with no documented evidence of CHIKV infection in neonates (negative RT-PCR or absence of IgM) were excluded.ResultsFrom the 227 studies initially identified, 42 were selected as follows: 28 case reports, 7 case series, 2 cross-sectional studies and 5 cohort studies, for a total of 266 CHIKV infected neonates confirmed by serological and/or molecular tests. The vertical transmission rate was 50% in the Reunion Island outbreak, which was the subject of the majority of the studies; the premature delivery were reported in 19 (45.2%) studies; the rate of fetal distress was 19.6% of infected babies and fetal loss occurred in 2% of the cases. Approximately 68.7% of newborns were diagnosed with encephalopathy or encephalitis after perinatally acquired CHIKV. Most of the infected neonates were born healthy, developing CHIKV sepsis clinical syndrome within the first week of life.ConclusionsWe alert neonatologists to the late manifestations of neonatal CHIKV infection, relevant to the management and reduction of morbidity. A limitation of our review was that it was not possible to carry out meta-analysis due to differences in study design and the small number of participants.
Highlights
The vertical transmission rate was 50% in the Reunion Island outbreak, which was the subject of the majority of the studies; the premature delivery were reported in 19 (45.2%) studies; the rate of fetal distress was 19.6% of infected babies and fetal loss occurred in 2% of the cases
Chikungunya virus (CHIKV) is an arthropod-borne virus of the alphavirus genus (Togaviridae family) that is believed to have originated in Africa, where it was known to circulate in sylvatic and urban cycles involving female mosquito vectors of the genus Aedes and non-human or human primates [1,2]
Since 2006, four lineages have been recognized: the West African, the East/Central/South African (ECSA), the Asian genotypes plus the Indian ocean lineage (IOL) that has diverged from the ECSA [3,4,5]
Summary
Chikungunya virus (CHIKV) is an arthropod-borne virus (arbovirus) of the alphavirus genus (Togaviridae family) that is believed to have originated in Africa, where it was known to circulate in sylvatic and urban cycles involving female mosquito vectors of the genus Aedes and non-human or human primates [1,2]. Intrapartum transmission without placental infection, a direct consequence of maternal viremia and fetal or neonatal susceptibility to a given arbovirus, has been well documented for CHIKV in mouse models [8]. Evidence of transplacental infection by the recovery of the genome of CHIKV in the amniotic fluid, the placenta and the fetal brain of stillborn fetuses in Reunion Island, when fetal loss occurred before 16 weeks of gestational age was reported. The mother’s chikungunya diagnosis was confirmed by RT-PCR detection of the viral genome in maternal blood two weeks before diagnosis of fetal loss; viral genome in the placenta and amniotic fluid confirmed transplacental transmission of CHIKV and its persistence after fetal death. Humans transplacental CHIKV transmission though seems likely, but its pathophysiology remains unknown [6,10]
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