Placental and fetal pathology in Coxsackie virus A9 infection: a case report

Batcup, G.; Holt, P.A.; Hambling, M.H.; Gerlis, Leon M.; Glass, M. R.

doi:10.1111/j.1365-2559.1985.tb02802.x

Cited by 44 publications

(22 citation statements)

References 9 publications

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“…In addition, our observations were not similar to those in cases of congenital infections with echoviruses or coxsackieviruses. The pathological features of echovirus or coxsackievirus infection are evident intravascular coagulation, focal hemorrhage, and necrosis in the virus-infected organs, such as the heart, kidney, brain, spleen, and liver [18][19][20][21].…”

Section: Discussionmentioning

confidence: 99%

Congenital Enterovirus 71 Infection: A Case Study with Virology and Immunohistochemistry

Chow¹,

Lee²,

Lin³

et al. 2000

Clinical Infectious Diseases

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Previously reported enterovirus 71 (EV71) infections associated with hand-foot-mouth disease, aseptic meningitis, encephalitis, polio-like myelitis, and paralysis all have involved young children. We report a 28-year-old woman who possibly contracted EV71 infection during pregnancy. Obstetric ultrasonograms at 25 weeks of gestation revealed an abnormal placenta, as well as hepatosplenomegaly, liver calcification, excessive ascites, and mild hydrocephalus of the fetus. Presence of EV71 was determined by immunodot blotting, virus culture, and partial sequencing of the amplified product of nested reverse transcription-polymerase chain reaction. Postmortem immunohistochemistry further identified EV71 in the fetal midbrain and liver. The findings indicate that intrauterine EV71 infection is possible during pregnancy.

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Section: Discussionmentioning

confidence: 99%

Congenital Enterovirus 71 Infection: A Case Study with Virology and Immunohistochemistry

Chow¹,

Lee²,

Lin³

et al. 2000

Clinical Infectious Diseases

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“…For example, a case report described a woman with Coxsackie virus A9 meningitis at 33 weeks' gestation. 36 She was delivered of a stillborn infant at 35 weeks whose placenta showed perivillous fibrin deposition and villous necrosis with inflammatory cell infiltration. Coxsackie virus A9 was cultured from the placenta.…”

Section: Viral Diseasesmentioning

confidence: 99%

Infection and stillbirth

McClure

Goldenberg

2009

Seminars in Fetal and Neonatal Medicine

112

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Summary Infection may cause stillbirth by several mechanisms, including direct infection, placental damage, and severe maternal illness. Various organisms have been associated with stillbirth, including many bacteria, viruses, and protozoa. In developed countries, between 10% and 25% of stillbirths may be caused by an infection, whereas in developing countries, which have much higher stillbirth rates, the contribution of infection is much greater. In developed countries, ascending bacterial infection, both before and after membrane rupture, with organisms such as Escherichia coli, group B streptococci, and Ureaplasma urealyticum is usually the most common infectious cause of stillbirth. However, in areas where syphilis is prevalent, up to half of all stillbirths may be caused by this infection alone. Malaria may be an important cause of stillbirth in women infected for the first time in pregnancy. The two most important viral causes of stillbirth are parvovirus and Coxsackie virus, although a number of other viral infections appear to be causal. Toxoplasma gondii, leptospirosis, Listeria monocytogenes, and the organisms that cause leptospirosis, Q fever, and Lyme disease have all been implicated as etiologic for stillbirth. In certain developing countries, the stillbirth rate is high and the infection-related component so great that achieving a substantial reduction in stillbirth should be possible by reducing maternal infections. However, because infection-related stillbirth is uncommon in developed countries, and because those that do occur are caused by a wide variety of organisms, reducing this etiologic component of stillbirth much further will be difficult.

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“…Placental lesions have been described in infections caused by echoviruses 11,13,15,17,18,19,21,23,24,25,27, and 33, and coxsackie viruses A9, B2, and B6 [43][44][45]. They present the usual gross features of hematogenous placentitis, and the microscopic lesions are identical in both infections.…”

Section: Enterovirosesmentioning

confidence: 99%

“…L. Bittencourt and A. G. P. Garcia nuclear in¢ltration is a common ¢nding in the stem vessels. In some cases, a mild mononuclear and neutrophilic in¢ltration is seen in the chorionic plate [43][44][45]. Although transplacental infection by poliovirus had been demonstrated through isolation of the virus from the placenta, there are no references to placental pathology [13].…”

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confidence: 99%

The Placenta in Hematogenous Infections

Bittencourt

Garcia

2002

Pediatric Pathology & Molecular Medicine

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Although congenital infections have been known since ancient times, at present they constitute an evolution due to the broadening of diagnostic methods. Also, the histopathological examination of selected placentas has increased in perinatal pathology. All placentas should be examined grossly by the obstetrician or the neonatologist who must select the specimens to be sent for pathologic examination. The indications for selection at delivery to detect hematogenous infection are listed in Table 1. The placentas that do not meet guidelines for pathologic examination must be kept stored at 40 degrees C for at least 72 h. This routine ensures that the placentas of asymptomatic newborns who might present early manifestations suggestive of infection would be submittedfor pathologic examination.

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Placental and fetal pathology in Coxsackie virus A9 infection: a case report

Cited by 44 publications

References 9 publications

Congenital Enterovirus 71 Infection: A Case Study with Virology and Immunohistochemistry

Congenital Enterovirus 71 Infection: A Case Study with Virology and Immunohistochemistry

Infection and stillbirth

The Placenta in Hematogenous Infections

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