Antenatal Diagnosis of Intrauterine Infection WithCoxsackievirus B3 Associated With Live Birth

Ouellet, Annie; Sherlock, Rebecca; Toye, Baldwin; Fung, Karen Y.

doi:10.1080/1064744042000210357

Cited by 30 publications

(18 citation statements)

References 9 publications

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“…Fetal hydrops is the only finding described in a case of unequivocal transplacental fetal infection [Ouellet et al, 2004]. In this report we describe for the first time detailed fetal pathology following intrauterine transplacental transmission of a coxsackie B3 virus.…”

Section: Discussionmentioning

confidence: 94%

“…Indirect epidemiological evidence reviewed by Ornoy and Tenenbaum [2006] points toward an association of maternal enterovirus infection in pregnancy and congenital heart defects. Hydrops fetalis detected antenatally by ultrasonography was found in a single case of coxsackie B3 intrauterine fetal infection [Ouellet et al, 2004]; however, detailed fetal pathology has not been determined to date. This is the first report to describe fetoplacental autopsy findings in a 30-week fetus with coxsackie B3 transplacental infection.…”

Section: Introductionmentioning

confidence: 98%

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Transplacental infection of coxsackievirus B3 pathological findings in the fetus

Konstantinidou

Anninos

Spanakis

et al. 2007

Journal of Medical Virology

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Coxsackievirus intrauterine infection has been documented mostly on the basis of indirect evidence of transplacental transmission, with neonatal manifestations ranging from asymptomatic infection to meningoencephalitis, myocarditis, and generalized sepsis. This is the first report of prenatal findings and fetoplacental pathology in a third trimester fetus with coxsackie B3 transplacental infection confirmed by molecular techniques. Prenatal ultrasound detected severe reduction of fetal movements at the 27th week. Late onset fetal akinesia deformation sequence with mild arthrogryposis, necrotic meningoencephalitis with vascular calcifications, interstitial pneumonitis, mild myocardial hypertrophy, and chronic monocytic placental villitis were the cardinal findings at fetal autopsy following interruption of the pregnancy.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 98%

Transplacental infection of coxsackievirus B3 pathological findings in the fetus

Konstantinidou

Anninos

Spanakis

et al. 2007

Journal of Medical Virology

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“…Enteroviruses have evolved mechanisms to subvert the placental protective barrier, as incidences of fetal disease and death have been reported (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28). Here we utilized the BeWo trophoblast cell line as a model of placental trophoblasts to delineate the key cellular components that facilitate CVB entry into the trophoblast monolayer.…”

Section: Discussionmentioning

confidence: 99%

“…Maternal CVB infection and consequential fetal transmission have been associated with severe pathological outcomes, including congenital skin lesions (15), the development of type I diabetes (16,17) and thyroiditis (18) later in life, hydrops fetalis (19), fetal myocarditis (20)(21)(22), meningoencephalitis (23), neurodevelopmental delays (24), fetal sepsis (25), miscarriage (26), and stillbirth (27,28). Currently, testing for enterovirus infections during pregnancy is not routine, and thus there is a lack of data regarding their prevalence.…”

mentioning

confidence: 99%

Lipid Raft- and Src Family Kinase-Dependent Entry of Coxsackievirus B into Human Placental Trophoblasts

Delorme-Axford

Sadovsky

Coyne

2013

J Virol

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bMaternal-fetal transmission of group B coxsackieviruses (CVB) during pregnancy has been associated with a number of diverse pathological outcomes, including hydrops fetalis, fetal myocarditis, meningoencephalitis, neurodevelopmental delays, congenital skin lesions, miscarriage, and/or stillbirth. Throughout pregnancy, the placenta forms a critical antimicrobial protective barrier at the maternal-fetal interface. Despite the severity of diseases accompanying fetal CVB infections, little is known regarding the strategies used by CVB to gain entry into placental trophoblasts. Here we used both a trophoblast cell line and primary human trophoblasts to demonstrate the mechanism by which CVB gains entry into polarized placental trophoblasts. Our studies revealed that the kinetics of CVB entry into placental trophoblasts are similar to those previously described for polarized intestinal epithelial cells. Likewise, CVB entry into placental trophoblasts requires decay-accelerating factor (DAF) binding and involves relocalization of the virus from the apical surface to intercellular tight junctions. In contrast, we have identified a divergent mechanism for CVB entry into polarized trophoblasts that is clathrin, caveolin-1, and dynamin II independent but requires intact lipid rafts. In addition, we found that members of the Src family of tyrosine kinases were required for CVB entry. Our studies highlight the complexity of viral entry into human placental trophoblasts and may serve as a model for mechanisms used by diverse pathogens to penetrate the placental barrier.

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“…75 Congenital malaria and tuberculosis are also associated with fetal anemia and thrombocytopenia. 63,76,77 …”

Section: Hematological Abnormalities In Neonates With Transplacental mentioning

confidence: 99%

Disorders of the Fetomaternal Unit: Hematologic Manifestations in the Fetus and Neonate

Black

Maheshwari

2009

Seminars in Perinatology

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Histoarchitectural characteristics of the human placenta place the fetus at a high risk of growth restriction, abnormal fetomaternal cell traffic, and vertical transmission of pathogens. These abnormalities of the fetomaternal unit are frequently associated with hematological abnormalities in the fetus/neonate, and may be the first, most common, or the only clinical manifestations of these conditions. This article reviews the pathophysiology and characteristic hematological manifestations of these conditions in the fetus and the neonate.

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Antenatal Diagnosis of Intrauterine Infection WithCoxsackievirus B3 Associated With Live Birth

Cited by 30 publications

References 9 publications

Transplacental infection of coxsackievirus B3 pathological findings in the fetus

Transplacental infection of coxsackievirus B3 pathological findings in the fetus

Lipid Raft- and Src Family Kinase-Dependent Entry of Coxsackievirus B into Human Placental Trophoblasts

Disorders of the Fetomaternal Unit: Hematologic Manifestations in the Fetus and Neonate

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