美国神经病理学家协会第92届年会摘要2016年6月16-19日,马里兰州巴尔的摩

F. Rodriguez, D. Hill, Cheng-Ying Ho, A. Melo, F. Tovar-Moll, P. Oliveira-Szejnfeld, A. Camacho, G. C. Gomes, F. O. Melo, A. G. M. Batista, H. N. Machado, E. Awad, Thales A. Ferreira, R. Andrade, R. Mello, M. Arruda, R. Brindeiro, Rodrigo Delvechio, A. Tanuri
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引用次数: 4

摘要

先天性寨卡病毒感染是一种正在发展中的突发公共卫生事件,可导致小头畸形、脑内钙化,并经常导致胎儿死亡。在这里,我们介绍了一名20周胎儿的尸检结果,其中先天性寨卡病毒感染在子宫内被诊断出来。虽然小头畸形或脑内钙化尚未确定,但胎儿超声和MRI结果显示轻度脑积水伴皮质边缘明显变薄和部分胼胝体发育不全。终止妊娠后,尸检显示胎儿的大脑重量在胎龄正常范围内,但大脑皮层明显变薄。脑组织组织学检查显示大量细胞凋亡弥漫性累及新皮层“中分化”神经元。脑室下区和白质表现出严重的体积损失,伴轴突损伤和巨噬细胞浸润。此外,在电子显微镜下发现的细胞内颗粒聚集与病毒感染一致。发育成熟的深灰质核和边缘区相对较少,仅显示罕见的小胶质细胞聚集。同样,神经节隆起的生发基质形态完整,无炎症。我们的影像学和病理学结果表明,寨卡病毒相关的脑损伤可能是直接病毒损伤和中枢神经系统细胞亚群感染后炎症损伤的结果。病毒感染是否对发育序列有影响尚不清楚。未来跨孕期多个时间点的研究将更好地了解寨卡病毒感染在大脑发育中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
American Association of Neuropathologists, Inc. Abstracts of the 92nd Annual Meeting June 16–19, 2016 Baltimore, MD
Congenital Zika virus infection is a developing public health emergency, leading to microcephaly, intracerebral calcifications, and often fetal death. Here we present the neuropathological findings from an autopsy of a 20week fetus in which congenital Zika virus infection was diagnosed in utero. Though microcephaly or intracerebral calcification was not yet identified, fetal ultrasound and MRI findings revealed mild hydrocephalus with a markedly thinned cortical rim and partial corpus callosum agenesis. Following pregnancy termination, autopsy revealed a brain within the normal weight range for gestational age, however the thinned cortex was grossly notable. Histologic evaluation of the brain showed abundant apoptosis diffusely involving the “intermediately differentiated” neurons in neocortex. The subventricular zone and white matter demonstrated severe volume loss with axonal injuries and macrophage infiltrates. Additionally, an aggregate of intracellular particles identified on electron microscopy was consistent with viral infection. There was relative sparing of the developmentally mature deep grey matter nuclei and limbic regions, which showed only rare microglial aggregates. Similarly, the germinal matrix of the ganglionic eminence was morphologically intact and void of inflammation. Our imaging and pathologic findings suggest that the Zika virus-associated brain injury is likely a consequence of direct viral injury and post-infectious inflammatory damage to a subpopulation of central nervous sytemsystem cells. Whether the viral infection has an effect on the developmental sequence remains unclear. Future studies across multiple time points of pregnancy will offer better insight into the role of Zika virus infection in brain development.
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