Persistence of Zika Virus After Birth: Clinical, Virological, Neuroimaging, and Neuropathological Documentation in a 5-Month Infant With Congenital Zika Syndrome

dc.creatorChimelli, Leila
dc.creatorPone, Sheila Moura
dc.creatorAvvad-Portari, Elyzabeth
dc.creatorVasconcelos, Zilton Farias Meira de
dc.creatorZin, Andrea A.
dc.creatorCunha, Daniela Prado
dc.creatorThompson, Nathalia Raposo
dc.creatorMoreira, Maria Elisabeth Lopes
dc.creatorWiley, Clayton A.
dc.creatorPone, Marcos Vinicius da Silva
dc.date2018-12-17T17:35:13Z
dc.date2018-12-17T17:35:13Z
dc.date2018
dc.date.accessioned2023-09-26T22:10:31Z
dc.date.available2023-09-26T22:10:31Z
dc.identifierCHIMELLI, Leila et al. Persistence of Zika Virus After Birth: Clinical, Virological, Neuroimaging, and Neuropathological Documentation in a 5-Month Infant With Congenital Zika Syndrome. ournal of Neuropathology and Experimental Neurology. v. 77. n. 3. mar. 2018
dc.identifier0022-3069
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/30639
dc.identifier10.1093/jnen/nlx116
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8875784
dc.descriptionDuring 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.
dc.description2019-03-01
dc.formatapplication/pdf
dc.languageeng
dc.publisherOxford University Press
dc.rightsopen access
dc.subjectArtrogripose
dc.subjectCalcificação
dc.subjectHidrocefalia
dc.subjectMicrocefalia
dc.subjectNeuropatologia
dc.subjectRT-qPCR
dc.subjectZika Virus
dc.subjectArthrogryposis
dc.subjectCalcification
dc.subjectHydrocephalus
dc.subjectMicrocephal
dc.subjectNeuropathology
dc.subjectRT-qPCR
dc.subjectZika Virus
dc.titlePersistence of Zika Virus After Birth: Clinical, Virological, Neuroimaging, and Neuropathological Documentation in a 5-Month Infant With Congenital Zika Syndrome
dc.typeArticle


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