This article is more than 5 years old. Information may no longer be current.
Researchers discover late-onset Zika-associated microcephaly
Click Here to Manage Email Alerts
Researchers have found the first-ever association between congenital Zika virus infection and the onset of microcephaly in infants a few months old, suggesting an infant born without microcephaly could still develop it and other neurologic conditions later in life. The findings were reported in MMWR.
The researchers said the discovery serves as a reminder that mothers exposed to Zika during pregnancy should have their infant thoroughly screened by doctors for potential development and medical complications.
“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,” Vanessa van der Linden, MD, of the Association for Assistance of Disabled Children in Recife, Brazil, and colleagues wrote.
Van der Linden and colleagues studied 13 infants in Brazil, nine of them boys. None had microcephaly at birth, but tested positive for Zika virus-specific immunoglobulin M and later had brain abnormalities related to congenital Zika syndrome, including decreased brain volume, cortical malformations, ventriculomegaly and subcortical calcifications. Their head growth had slowed as early as age 5 months, and 11 of the infants later developed microcephaly.
According to the researchers, two of the babies were preterm, 11 were at term, and all had birth weights appropriate for gestational age. Three infants had hip dysplasia and redundant skin on the scalp at birth and six had craniofacial disproportion. Other characteristics noted in some of the infants included good eye contact and head control, arthrogryposis, involuntary hand movement, grasp reflexes, chorioretinal abnormalities, dysphagia, epilepsy and various stages of hemiparesis. Six of the 13 mothers had a cutaneous rash during their second and fifth months of pregnancy.
“The pathogenesis of postnatal microcephaly from congenital Zika virus infections is not known. The decrease in head growth might be the consequence of earlier in utero destruction of neuroprogenitor or other neural cells, persistent inflammatory response-associated molecules, or continued infection of neural cells,” according to the researchers. “The last seems less likely given the negative Zika virus RT-PCR results in all seven tested [cerebrospinal fluid] samples.
“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 researchers wrote. – by Janel Miller
- Reference:
- van der Linden V, et al. MMWR Morb Mortal Wkly Rep. 2016:doi:10.15585/mmwr.mm6547e2.
Disclosure: The researchers report no relevant financial disclosures.