Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 2: Varicella-zoster virus infections

Sauerbrei, Andreas; Wutzler, Peter

doi:10.1007/s00430-006-0032-z

Cited by 132 publications

(109 citation statements)

References 39 publications

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“…The crossing of the placental barrier seems to occur both viremic phases of incubation, but secondary viremia seems to play a greater role in fetal transmission [21,22,26] . Furthermore, infection arising from a lesioned birth canal can cause intrauterine infection [165] .…”

Section: Consequences Of An Infection Contracted During Pregnancymentioning

confidence: 99%

“…If the maternal varicella appears 20-7 d before the birth, the varicella in the newborn (if it develops) generally has a benign and non-fatal course because newly born infants have their mothers' antibodies and the risk of complications is low [5,26,131,165,[191][192][193] . In the case of maternal varicella between seven days before and seven after delivery, 2/3 of the infants become infected and 50% have severe symptoms because they do not have maternal antibodies and their cell-mediated response is insufficiently mature [26,145,169,191,194,195] .…”

Section: Neonatal Varicellamentioning

confidence: 99%

“…In the case of maternal varicella between seven days before and seven after delivery, 2/3 of the infants become infected and 50% have severe symptoms because they do not have maternal antibodies and their cell-mediated response is insufficiently mature [26,145,169,191,194,195] . During this period, the most dangerous situation is when maternal varicella appears between five days before and two days after delivery because, in the absence of adequate therapy, the neonatal mortality rate may be as high as 20%-30% and, even with therapy, may still be 7% [5,153,157,159,165,191,[196][197][198] . Maternal varicella may be transmitted transplacentally, or by means of ascending infection during birth, or by means of respiratory droplets or direct contact with infectious lesions after birth, and neonatal disease may manifest itself with skin lesions, ulcerated…”

Section: Neonatal Varicellamentioning

confidence: 99%

“…Microbiology laboratory in mother-child VZV infection necrotic or hemorrhagic lesions, and/or systemic disease (pneumonia, liver failure, encephalitis or coagulopathy) [16,26,53,159,165] . As the incubation period of varicella transmitted in utero from the initial maternal rash is 10-12 d (but may be as short as four days), the varicella observed in infants in the first 10-12 d of life is considered of intra-uterine origin, and that appearing later as probably post-natal [53,90,145,159,165] .…”

Section: Neonatal Varicellamentioning

confidence: 99%

“…The course of the disease is normally uncomplicated, but it is recommended to check children with herpes zoster for other clinical signs of intra-uterine infection especially at ophthalmological signs [147,203] . The incidence of herpes zoster is 4%-20% in the case of documented in utero infection but, if this is not the case and the mother had varicella during the pregnancy, the incidence decreases to 0.8%-1.7% depending on whether the maternal varicella appeared in the second or third trimester [145,159,164,165,203] . Herpes zoster may also occur after 2-41 mo of life in 15% of newborns with CVS if the onset of maternal varicella was between the eighth and twenty-fourth week of gestation [147] .…”

Section: Herpes Zoster In the First Years Of Lifementioning

confidence: 99%

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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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Section: Consequences Of An Infection Contracted During Pregnancymentioning

confidence: 99%

Section: Neonatal Varicellamentioning

confidence: 99%

Section: Neonatal Varicellamentioning

confidence: 99%

Section: Neonatal Varicellamentioning

confidence: 99%

Section: Herpes Zoster In the First Years Of Lifementioning

confidence: 99%

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

Paschale

Clerici

2016

WJV

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The Treatment of Herpes Simplex Infections<subtitle>An Evidence-Based Review</subtitle>

Cernik¹

2008

Arch Intern Med

171

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enital and labial herpes simplex virus infections are frequently encountered by primary care physicians in the United States. Whereas the diagnosis of this condition is often straightforward, choosing an appropriate drug (eg, acyclovir, valacyclovir hydrochloride, or famciclovir) and dosing regimen can be confusing in view of (1) competing clinical approaches to therapy; (2) evolving dosing schedules based on new research;(3) approved regimens of the Food and Drug Administration that may not match recommendations of the Centers for Disease Control and Prevention or of other experts; and (4) dissimilar regimens for oral and genital infections. The physician must first choose an approach to treatment (ie, intermittent episodic therapy, intermittent suppressive therapy, or chronic suppressive therapy) based on defined clinical characteristics and patient preference. Then, an evidence-based dosing regimen must be selected. In this review, data from all sources are tabulated to provide a handy clinical reference.

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Herpes Simplex: Viruses and Infections

Hal

Dwyer

2009

Encyclopedia of Life Sciences

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Human herpes viruses 1 and 2 (HSV‐1 and HSV‐2) are among the most common human viral pathogens. Various epidemiological factors determine the infecting HSV type with significant changes in the epidemiology of genital herpes and HSV‐1 infections especially in developed countries. Following transmission of HSV to a susceptible person, symptomatic or asymptomatic infection may result with localized disease, the most common manifestation. HSV then establishes latency in the dorsal root ganglia which enables subsequent reactivation. The risk and rate of reactivation are dependent on numerous host factors and the infecting viral subtype. The number of diagnostic tests has increased with molecular methods improving our understanding of asymptomatic viral shedding. Antiviral therapy ameliorates the clinical manifestations and improves survival in neurological disease. Prophylactic antiviral strategies have been formulated for recurrent disease, but vaccine trials do not yet show clinically relevant benefit. Key concepts Classification of human herpes viruses Structure and replication of HSV Pathogenesis of HSV Latency Immunological responses to HSV Epidemiology of HSV Interaction between HSV and HIV infection Clinical manifestations and complication Diagnostic modalities for HSV detection Antiviral therapy and strategies used in the treatment of HSV Preventative strategies and vaccines

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Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 2: Varicella-zoster virus infections

Cited by 132 publications

References 39 publications

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

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

The Treatment of Herpes Simplex Infections<subtitle>An Evidence-Based Review</subtitle>

Herpes Simplex: Viruses and Infections

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