Congenital Skin Lesions Caused by Intrauterine Infection with Coxsackievirus B3

Sauerbrei, Andreas; Glück, Brigitte; Jung, Kwang Yoon; Bittrich, Hans-Jörg; Wutzler, Peter

doi:10.1007/s150100070029

Cited by 54 publications

(26 citation statements)

References 8 publications

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“…The host CNS seems to be particularly susceptible during early development; enteroviruses can infect the fetus, with serious consequences, including neurodevelopmental defects (Gear and Measroch, 1973;Daley et al, 1998;Sauerbrei et al, 2000;Euscher et al, 2001), and this vulnerability is retained in newborns (Ratzan, 1985;Hsueh et al, 2000). Coxsackieviruses, members of the enterovirus genus and picornavirus family, are the single most common cause of enteroviral CNS infection in neonates, and we have recently developed an animal model system that allows us to evaluate coxsackievirus B3 (CVB3) infection and pathogenesis in the neonatal CNS (Feuer et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Feuer¹,

Pagarigan²,

Harkins³

et al. 2005

J. Neurosci.

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Type B coxsackieviruses (CVB) frequently infect the CNS and, together with other enteroviruses, are the most common cause of viral meningitis in humans. Newborn infants are particularly vulnerable, and CVB also can infect the fetus, leading to mortality, or to neurodevelopmental defects in surviving infants. Using a mouse model of neonatal CVB infection, we previously demonstrated that coxsackievirus B3 (CVB3) could infect neuronal progenitor cells in the subventricular zone (SVZ). Here we extend these findings, and we show that CVB3 targets actively proliferating (bromodeoxyuridine ϩ , Ki67 ϩ ) cells in the SVZ, including type B and type A stem cells. However, infected cells exiting the SVZ have lost their proliferative capacity, in contrast to their uninfected companions. Despite being proliferation deficient, the infected neuronal precursors could migrate along the rostral migratory stream and radial glia, to reach their final destinations in the olfactory bulb or cerebral cortex. Furthermore, infection did not prevent cell differentiation, as determined by cellular morphology and the expression of maturation markers. These data lead us to propose a model of CVB infection of the developing CNS, which may explain the neurodevelopmental defects that result from fetal infection.

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Section: Introductionmentioning

confidence: 99%

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Feuer¹,

Pagarigan²,

Harkins³

et al. 2005

J. Neurosci.

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“…A vesicular rash or bullae present at birth or within a few days have been observed with congenital HSV infections 7 . Intrauterine transmission of coxsackievirus during the late pregnancy may also lead to varicella-like congenital skin lesions 8 . The treatment of varicella pneumonia in newborns is intravenous acyclovir at 20 mg/kg/every 6 hourly for 5 days.…”

Section: Discussionmentioning

confidence: 99%

Neonatal Varicella Pneumonia: A Rare Presentation

Garg¹

2017

jmscr

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“…The alternative is to use amniocentesis to confirm ultrasonographic findings of anomalies, although it must be remembered that ultrasonography is not very sensitive or specific, and so it does not detect all malformations [169,498] . Some authors recommend following-up mothers who have contracted varicella during pregnancy by means of ultrasonography, and then searching for viral DNA in the case of malformations [19,159] , insisting on always searching for VZV DNA because other micro-organisms such as Coxsackie B and HSV can cause congenital lesions similar to those of CVS [502][503][504] . There is a report of a case of fetal malformations due to HSV2 and not VZV in a mother who contracted varicella during pregnancy [502] , and conditions such as microphthalmia dermal aplasia scleroderma (MIDAS) or microphthalmia with linear skin defects (MLS) may also lead to malformations, with maternal varicella being just a coincidence [505,506] .…”

Section: Prenatal Infection and The Diagnosis Of Cvsmentioning

confidence: 99%

“…Molecular biology tests are also indicated in the case of rare or uncharacteristic malformations, or when the relationship between maternal infection and congenital malformations is doubtful [513] . Consideration should be given to differential diagnoses of congenital varicella with rubella, cytomegalovirus, HSV, Coxsackie virus, Toxoplasma gondii, and MIDAS or MLS [165,[502][503][504]514] .…”

Section: Diagnosis In Newbornsmentioning

confidence: 99%

Microbiology laboratory and the management of mother-child varicella-zoster virus infection

Paschale

Clerici

2016

WJV

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Varicella-zoster virus, which is responsible for varicella (chickenpox) and herpes zoster (shingles), is ubiquitous and causes an acute infection among children, especially those aged less than six years. As 90% of adults have had varicella in childhood, it is unusual to encounter an infected pregnant woman but, if the disease does appear, it can lead to complications for both the mother and fetus or newborn. The major maternal complications include pneumonia, which can lead to death if not treated. If the virus passes to the fetus, congenital varicella syndrome, neonatal varicella (particularly serious if maternal rash appears in the days immediately before or after childbirth) or herpes zoster in the early years of life may occur depending on the time of infection. A Microbiology laboratory can help in the diagnosis and management of mother-child infection at four main times: (1) when a pregnant woman has been exposed to varicella or herpes zoster, a prompt search for specific antibodies can determine whether she is susceptible to, or protected against infection; (2) when a pregnant woman develops clinical symptoms consistent with varicella, the diagnosis is usually clinical, but a laboratory can be crucial if the symptoms are doubtful or otherwise unclear (atypical patterns in immunocompromised subjects, patients with post-vaccination varicella, or subjects who have received immunoglobulins), or if there is a need for a differential diagnosis between varicella and other types of dermatoses with vesicle formation; (3) when a prenatal diagnosis of uterine infection is required in order to detect cases of congenital varicella syndrome after the onset of varicella in the mother; and (4) when the baby is born and it is necessary to confirm a diagnosis of varicella (and its complications), make a differential diagnosis between varicella and other diseases with similar symptoms, or confirm a causal relationship between maternal varicella and malformations in a newborn. Core tip: Although varicella during pregnancy is infrequent and congenital varicella syndrome (CVS) is rare, every available means should be used to prevent and diagnose them. Microbiology laboratories can be crucial in these situations: Evaluating a mother's immune status with sensitive and specific tests for the detection of antibodies; allowing a rapid diagnosis with molecular biology tests when a clinical manifestation may be due to different etiologies; following pregnant women with varicella for the prenatal diagnosis of CVS with close collaboration between molecular biology investigators and specialists in imaging diagnostics.De Paschale M, Clerici P. Microbiology laboratory and the management of mother-child varicella-zoster virus infection. World

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Congenital Skin Lesions Caused by Intrauterine Infection with Coxsackievirus B3

Abstract: Intrauterine transmission of CVB3 during late pregnancy may lead to varicella-like congenital skin lesions.

Cited by 54 publications

References 8 publications

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Coxsackievirus Targets Proliferating Neuronal Progenitor Cells in the Neonatal CNS

Neonatal Varicella Pneumonia: A Rare Presentation

Microbiology laboratory and the management of mother-child varicella-zoster virus infection

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