Details

Autor(en) / Beteiligte

• Melo, Adriana Suely de Oliveira
• Aguiar, Renato Santana
• Amorim, Melania Maria Ramos
• Arruda, Monica B
• Melo, Fabiana de Oliveira
• Ribeiro, Suelem Taís Clementino
• Batista, Alba Gean Medeiros
• Ferreira, Thales
• Dos Santos, Mayra Pereira
• Sampaio, Virgínia Vilar
• Moura, Sarah Rogéria Martins
• Rabello, Luciana Portela
• Gonzaga, Clarissa Emanuelle
• Malinger, Gustavo
• Ximenes, Renato
• de Oliveira-Szejnfeld, Patricia Soares
• Tovar-Moll, Fernanda
• Chimelli, Leila
• Silveira, Paola Paz
• Delvechio, Rodrigo
• Higa, Luiza
• Campanati, Loraine
• Nogueira, Rita M R
• Filippis, Ana Maria Bispo
• Szejnfeld, Jacob
• Voloch, Carolina Moreira
• Ferreira, Jr, Orlando C
• Brindeiro, Rodrigo M
• Tanuri, Amilcar

Titel

Congenital Zika Virus Infection: Beyond Neonatal Microcephaly

Ist Teil von

• JAMA neurology, 2016-12, Vol.73 (12), p.1407

Ort / Verlag

United States

Erscheinungsjahr

2016

Quelle

MEDLINE

Beschreibungen/Notizen

• Recent studies have reported an increase in the number of fetuses and neonates with microcephaly whose mothers were infected with the Zika virus (ZIKV) during pregnancy. To our knowledge, most reports to date have focused on select aspects of the maternal or fetal infection and fetal effects. To describe the prenatal evolution and perinatal outcomes of 11 neonates who had developmental abnormalities and neurological damage associated with ZIKV infection in Brazil. We observed 11 infants with congenital ZIKV infection from gestation to 6 months in the state of Paraíba, Brazil. Ten of 11 women included in this study presented with symptoms of ZIKV infection during the first half of pregnancy, and all 11 had laboratory evidence of the infection in several tissues by serology or polymerase chain reaction. Brain damage was confirmed through intrauterine ultrasonography and was complemented by magnetic resonance imaging. Histopathological analysis was performed on the placenta and brain tissue from infants who died. The ZIKV genome was investigated in several tissues and sequenced for further phylogenetic analysis. Description of the major lesions caused by ZIKV congenital infection. Of the 11 infants, 7 (63.6%) were female, and the median (SD) maternal age at delivery was 25 (6) years. Three of 11 neonates died, giving a perinatal mortality rate of 27.3%. The median (SD) cephalic perimeter at birth was 31 (3) cm, a value lower than the limit to consider a microcephaly case. In all patients, neurological impairments were identified, including microcephaly, a reduction in cerebral volume, ventriculomegaly, cerebellar hypoplasia, lissencephaly with hydrocephalus, and fetal akinesia deformation sequence (ie, arthrogryposis). Results of limited testing for other causes of microcephaly, such as genetic disorders and viral and bacterial infections, were negative, and the ZIKV genome was found in both maternal and neonatal tissues (eg, amniotic fluid, cord blood, placenta, and brain). Phylogenetic analyses showed an intrahost virus variation with some polymorphisms in envelope genes associated with different tissues. Combined findings from clinical, laboratory, imaging, and pathological examinations provided a more complete picture of the severe damage and developmental abnormalities caused by ZIKV infection than has been previously reported. The term congenital Zika syndrome is preferable to refer to these cases, as microcephaly is just one of the clinical signs of this congenital malformation disorder.