ika virus (ZIKV) is a neurotropic flavivirus spread to humans by Aedes genus mosquitos. Zika virus was first isolated in the Zika Forest in Uganda in a nonhuman primate in 1947. 1,2 Five years later, Nigeria reported the first cases of ZIKV transmission to humans, and subsequent ZIKV outbreaks have been reported outside Africa. [1][2][3] The first autochthonous case was confirmed in 2015 in Brazil, with a subsequent increase in the number of cases. This event coincided with reports of newborns with microcephaly, congenital malformations, and neurologic syndromes. 1,2 The spread of ZIKV to other parts of Latin America, the Caribbean, and the United States brought epidemiologic concern because of the clinical manifestations, including those associated with congenital Zika syndrome (CZS). [4][5][6] Although microcephaly is considered to be the characteristic feature of CZS, other central nervous system abnormalities and ocular findings have been described as part of this entity. [7][8][9][10] Despite having clinical evidence of the association between CZS and ocular findings, [11][12][13][14][15][16] only a few studies 17,18 have identified the presence of ZIKV in mouse ocular tissues and cultured human cells. Ritter et al 19 described the presence of ZIKV antigen within the neural retina in 1 case of CZS by immunohistochemical analysis, but the histopathologic findings were not described. The only study to date that has provided valuable clinical information regarding the retinal layers affected in CZS in human eyes was performed using optical IMPORTANCE Congenital Zika syndrome (CZS) is known to be associated with severe malformations in newborns. Although microcephaly is the hallmark of this disease, the ocular findings are important given the severe visual impairment that has been observed in these patients. Regardless of the increased number of CZS cases reported, to date, no studies have described the ocular histopathologic findings of this entity.OBJECTIVES To evaluate the presence of Zika virus (ZIKV) antigens and describe the associated ocular histopathologic features of 4 cases of CZS.
Objective To evaluate fetal ultrasound and magnetic resonance imaging findings among a series of pregnant women with confirmed Zika virus infection to evaluate the signs of congenital Zika syndrome with respect to timing of infection. Methods Retrospective case series of pregnant women referred to two perinatal clinics in Barranquilla and Ibagué, Colombia with findings consistent with congenital Zika syndrome and Zika virus infection confirmed in maternal, fetal, or infant samples. Serial ultrasound measurements, fetal magnetic resonance imaging results, laboratory results, and perinatal outcomes were evaluated. Results We describe 17 cases of confirmed prenatal maternal Zika virus infection with adverse fetal outcomes. Among the 14 symptomatic women, the median gestational age for maternal Zika virus symptoms was 10 weeks (range 7–14). The median time between Zika virus symptom onset and microcephaly (head circumference less than 3 standard deviations below the mean) was 18 weeks (range 15–24). The earliest fetal head circumference measurement consistent with microcephaly diagnosis was at 24 weeks of gestation. The earliest sign of congenital Zika syndrome was talipes equinovarus, which in two patients was noted first at 19 weeks. Common findings on fetal magnetic resonance imaging were microcephaly, ventriculomegaly, polymicrogyria, and calcifications. Conclusion Our analysis suggests a period of at least 15 weeks between maternal Zika virus infection in pregnancy and development of microcephaly, and highlights the importance of serial and detailed neuroimaging.
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