RESUMO
PURPOSE: The purpose of this review is to comprehensively review Congenital Zika Syndrome in regard to their epidemiology and clinical manifestations. METHODS: This subject review of congenital Zika syndrome was composed after conducting a thorough review of the available literature on this topic using PubMed and other primary sources. RESULTS: The first epidemic of Zika virus infection in Brazil was followed by an unexpected sharp increase in the incidence of infants born with microcephaly and the description of a new disease, the congenital Zika syndrome. This review focuses on the epidemiological and clinical aspects of Zika infection in children. We conducted a brief historical account of the virus description in 1947, the rare cases of Zika infection occurring up to 2007, and the first epidemics in the Pacific between 2007 and 2014. We also discussed the isolation of the virus in Brazil in 2015 and its spread in the Americas, the microcephaly outbreak in Brazil and its association with Zika virus, and the current epidemiological panorama. We address the known clinical spectrum of Zika virus infection in the pediatric population, including manifestations of acute infection and congenital Zika syndrome, with emphasis on cranial, ophthalmic, and orthopedic abnormalities. CONCLUSION: While much has been learned about congenital Zika syndrome, the full spectrum of this infection is not yet known. This review is based on current, limited data about Zika vírus infection. As more information becomes available, we will have a more accurate picture of this new disease.
Assuntos
Infecção por Zika virus/epidemiologia , Infecção por Zika virus/terapia , Adulto , Brasil/epidemiologia , Surtos de Doenças , Anormalidades do Olho/etiologia , Feminino , Humanos , Incidência , Recém-Nascido , Microcefalia/etiologia , Gravidez , Complicações Infecciosas na Gravidez , Infecção por Zika virus/diagnósticoRESUMO
During the Zika epidemic in Brazil, a baby was born at term with microcephaly and arthrogryposis. The mother had Zika symptoms at 10 weeks of gestation. At 17 weeks, ultrasound showed cerebral malformation and ventriculomegaly. At 24 weeks, the amniotic fluid contained ZIKV RNA and at birth, placenta and maternal blood were also positive using RT-qPCR. At birth the baby urine contained ZIKV RNA, whereas CSF at birth and urine at 17 days did not. Seizures started at 6 days. EEG was abnormal and CT scan showed cerebral atrophy, calcifications, lissencephaly, ventriculomegaly, and cerebellar hypoplasia. Bacterial sepsis at 2 months was treated. A sudden increase in head circumference occurred at 4 months necessitating ventricle-peritoneal shunt placement. At 5 months, the infant died with sepsis due to bacterial meningitis. Neuropathological findings were as severe as some of those found in neonates who died soon after birth, including hydrocephalus, destructive lesions/calcification, gliosis, abnormal neuronal migration, dysmaturation of nerve cells, hypomyelination, loss of descending axons, and spinal motor neurons. ZIKV RNA was detected only in frozen brain tissue using RT-qPCR, but infected cells were not detected by in situ hybridization. Progressive gliosis and microgliosis in the midbrain may have contributed to aqueduct compression and subsequent hydrocephalus. The etiology of progressive disease after in utero infection is not clear and requires investigation.