2013
DOI: 10.1002/jmv.23531
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Second trimester fetal death caused by varicella‐zoster virus infection

Abstract: A 31-year-old woman contracted acute varicella at 13 weeks of gestation. Severe hydrops fetalis, hepatomegaly, and intrauterine fetal death were detected at 16 weeks of gestation by ultrasound examinations. An examination at autopsy, histopathology, and polymerase chain reaction (PCR) provided evidence of varicella-zoster virus (VZV) infection of the fetus. Second trimester intrauterine fetal death caused by mother to fetus infection of VZV is extremely rare.

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Cited by 5 publications
(3 citation statements)
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“…Varicella is unlike other TORCH infections in that the highest level of transmission to the fetus occurs in the second trimester, with 2% risk at 13-20 weeks (76). First-or thirdtrimester infection rarely leads to hydrops and demise (76)(77)(78). However, new onset of varicella at term can lead to neonatal demise.…”
Section: Varicellamentioning
confidence: 99%
“…Varicella is unlike other TORCH infections in that the highest level of transmission to the fetus occurs in the second trimester, with 2% risk at 13-20 weeks (76). First-or thirdtrimester infection rarely leads to hydrops and demise (76)(77)(78). However, new onset of varicella at term can lead to neonatal demise.…”
Section: Varicellamentioning
confidence: 99%
“…22 Because of the implementation of Rubella vaccination programs, Coxsackie viruses (particularly B3 23 and B4 24 ) have since emerged as relatively more commonly reported viruses, particularly in cases with early cardiac dysfunction and NIH 24 if not as major attributable causes of intrauterine fetal demise. 25 Other viral etiologies such as Varicella Zoster 26,27 and Adenovirus 28,29 have remained extremely rare. Coxsackie, Varicella Zoster, and Adenovirus have never been encountered by the authors.…”
Section: Infectious Causes Of Nonimmune Hydropsmentioning
confidence: 99%
“…In a rat model of LCMV, pups introduced to the virus early in gestation (days 1-10) had more frequent and severe neuropathologies compared to pups exposed later in gestation [10]. In part, this effect has been attributed to the teratogenic impact of infection during early fetal development—most evident after early transplacental rubella and varicella infections [11, 12]. However, maternal-fetal immune interactions evolve throughout pregnancy [13], possibly changing the placental response to viral pathogens as pregnancy progresses.…”
Section: Introductionmentioning
confidence: 99%