Instituto de Pesquisa Professor Amorim Neto (IPESQ), Campina Grande, Paraíba, Brazil2Instituto de Saúde Elpidio de Almeida, Campina Grande, Paraíba, Brazil3Faculdade de Ciências Médicas de Campina Grande, Campina Grande, Paraíba, Brazil4Hospital Municipal Pedro I, Campina Grande, Paraíba, Brazil.
Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
JAMA Neurol. 2016 Dec 1;73(12):1407-1416. doi: 10.1001/jamaneurol.2016.3720.
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.
DESIGN, SETTING, AND PARTICIPANTS: 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.
最近的研究报告称，在怀孕期间感染寨卡病毒（ZIKV）的孕妇所生的胎儿和新生儿中，小头畸形的数量有所增加。据我们所知，迄今为止的大多数报告都集中在母体或胎儿感染和胎儿影响的某些方面。
描述巴西 11 名患有与寨卡病毒感染相关的发育异常和神经损伤的新生儿的产前演变和围产期结局。
设计、地点和参与者：我们观察了巴西帕拉伊巴州的 11 名患有先天性寨卡病毒感染的婴儿，从妊娠到 6 个月。本研究中包括的 11 名妇女中有 10 名在妊娠前半年出现寨卡病毒感染症状，所有 11 名妇女均通过血清学或聚合酶链反应在多个组织中证实存在感染。通过宫内超声检查确认脑损伤，并通过磁共振成像进行补充。对死亡婴儿的胎盘和脑组织进行组织病理学分析。对来自多个组织的寨卡病毒基因组进行了调查，并进行了进一步的系统发育分析。
描述寨卡病毒先天性感染引起的主要病变。
11 名婴儿中，7 名（63.6%）为女性，分娩时母亲的中位（SD）年龄为 25（6）岁。11 名新生儿中有 3 名死亡，围产期死亡率为 27.3%。出生时的中位（SD）头围为 31（3）cm，低于考虑小头畸形病例的下限。所有患者均存在神经损伤，包括小头畸形、脑容量减少、脑室扩大、小脑发育不良、无脑回伴脑积水和胎儿运动障碍变形序列（即关节挛缩症）。对其他导致小头畸形的原因（如遗传疾病和病毒及细菌感染）的有限检测结果为阴性，寨卡病毒基因组存在于母体和新生儿组织中（如羊水、脐血、胎盘和大脑）。系统发育分析显示，病毒在宿主内发生变异，包膜基因存在一些与不同组织相关的多态性。
临床、实验室、影像学和病理学检查的综合结果提供了比以前报告更完整的寨卡病毒感染引起的严重损伤和发育异常情况。与微小头症相比，“先天性寨卡综合征”一词更能准确描述这些病例，因为小头畸形只是这种先天性畸形疾病的一种临床体征。
