Zika-Related Effects Can Occur Months After Normal Birth
Infants with laboratory-confirmed congenital Zika virus infection but
who do not have microcephaly at birth may experience slow postnatal
head growth that can develop into microcephaly. Therefore, the absence
of microcephaly in a neonate does not rule out Zika virus infection or
its potential teratogenic effects, according to an article published online November 22 in Morbidity and Mortality Weekly Report.
From October 2015 to January 2016, researchers at two Brazilian referral centers evaluated 13 babies (nine male) who tested positive for congenital Zika virus infection. The infants had normal head size at birth; circumferences ranged from 0.30 to 2.00 standard deviations below the mean for gestational age and sex.
By age 5 months, however, they had experienced decelerated head growth, and 11 developed microcephaly, defined as a head circumference greater than 2 standard deviations below the mean for age and sex.
"These findings provide evidence that among infants with prenatal exposure to Zika virus, the absence of microcephaly at birth does not exclude congenital Zika virus infection or the presence of Zika-related brain and other abnormalities," write researchers led by Vanessa van der Linden, MD, from the Association for Assistance of Disabled Children in Recife, Brazil.
Clinical evaluation included neurologic and orthopedic evaluation; brain imaging; hip radiography, to identify congenital dislocation; assessment of dysphasia; ophthalmologic and auditory assessment; and confirmatory electroencephalogram in infants suspected of having seizure activity.
The infants had significant neurologic complications consistent with congenital Zika syndrome. These included cortical malformations, subcortical calcifications, decreased brain volume, dysphagia, epilepsy, hypertonia, dystonia, and dyskinesia. Some babies had no voluntary hand movements and showed a persistent primitive grasp reflex.
"These findings demonstrate the importance of early neuroimaging for infants exposed to Zika virus prenatally and the need for comprehensive medical and developmental follow-up," the authors write.
They add that although the precise etiology of Zika-related postnatal microcephaly is not known, it could result from the destruction of neuroprogenitor cells and other neural cells during gestation, from molecules related to inflammatory response, or, less likely, through persistent infection of neural cells.
They call for a fuller description of the clinical manifestations associated with congenital Zika infection.
In a media statement, the CDC stressed the relevance of its recent recommendations on developmental evaluations for potentially affected infants.
The CDC continues to recommend that mothers-to-be avoid areas with reported Zika cases, and if that is not possible, to take strict measures to prevent mosquito bites. The CDC also recommends that strict measures be taken to avoid the sexual transmission of Zika virus.
From October 2015 to January 2016, researchers at two Brazilian referral centers evaluated 13 babies (nine male) who tested positive for congenital Zika virus infection. The infants had normal head size at birth; circumferences ranged from 0.30 to 2.00 standard deviations below the mean for gestational age and sex.
By age 5 months, however, they had experienced decelerated head growth, and 11 developed microcephaly, defined as a head circumference greater than 2 standard deviations below the mean for age and sex.
"These findings provide evidence that among infants with prenatal exposure to Zika virus, the absence of microcephaly at birth does not exclude congenital Zika virus infection or the presence of Zika-related brain and other abnormalities," write researchers led by Vanessa van der Linden, MD, from the Association for Assistance of Disabled Children in Recife, Brazil.
Clinical evaluation included neurologic and orthopedic evaluation; brain imaging; hip radiography, to identify congenital dislocation; assessment of dysphasia; ophthalmologic and auditory assessment; and confirmatory electroencephalogram in infants suspected of having seizure activity.
The infants had significant neurologic complications consistent with congenital Zika syndrome. These included cortical malformations, subcortical calcifications, decreased brain volume, dysphagia, epilepsy, hypertonia, dystonia, and dyskinesia. Some babies had no voluntary hand movements and showed a persistent primitive grasp reflex.
"These findings demonstrate the importance of early neuroimaging for infants exposed to Zika virus prenatally and the need for comprehensive medical and developmental follow-up," the authors write.
They add that although the precise etiology of Zika-related postnatal microcephaly is not known, it could result from the destruction of neuroprogenitor cells and other neural cells during gestation, from molecules related to inflammatory response, or, less likely, through persistent infection of neural cells.
They call for a fuller description of the clinical manifestations associated with congenital Zika infection.
In a media statement, the CDC stressed the relevance of its recent recommendations on developmental evaluations for potentially affected infants.
The CDC continues to recommend that mothers-to-be avoid areas with reported Zika cases, and if that is not possible, to take strict measures to prevent mosquito bites. The CDC also recommends that strict measures be taken to avoid the sexual transmission of Zika virus.
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