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INTRODUCTION

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Varicella-zoster virus (VZV) is a member of the herpesvirus family. Primary maternal VZV infection (chickenpox) can result in fetal or neonatal infection. Other rare complications include spontaneous abortion, fetal demise, and premature delivery. Reactivation infection (zoster) does not result in fetal infection. Primary maternal VZV infection during the last trimester can cause pneumonia with significant morbidity and mortality. The overall incidence of maternal and neonatal varicella has decreased over the past 10–15 years, presumably due to varicella vaccination. Active surveillance among adults has shown that the incidence of varicella declined 74% during 1995–2005, despite vaccination rates among adults of only 3%. Herd immunity is the likely explanation for this phenomenon. Varicella immunization is recommended for all nonimmune women as part of prepregnancy and postpartum care. Varicella vaccine should not be administered to pregnant women, because the possible effects on fetal development are unknown, although no cases of congenital varicella syndrome or patterns of malformation have been identified after inadvertent immunization of pregnant women. When postpubertal females are immunized, pregnancy should be avoided for at least 1 month after immunization. Reporting of instances of inadvertent immunization with a varicella-zoster–containing vaccine during pregnancy is encouraged (1-800-986-8999, www.merckpregnancyregistries.com/varivax.html).

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There are three forms of varicella-zoster infections involving the neonate: fetal, congenital (early neonatal), and postnatal.

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FETAL VARICELLA SYNDROME

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I. DEFINITION

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This form occurs when the mother has her first exposure to VZV during the first half of pregnancy. It is also recognized in the literature as congenital varicella syndrome (CVS).

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II. INCIDENCE

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This form is fortunately rare; only ∼5% of women of childbearing age are susceptible to VZV. The incidence of varicella during pregnancy is estimated at 1–5 cases per 10,000 pregnancies. The incidence of embryopathy and fetopathy after maternal varicella infection in the first 20 weeks is ∼1%. Recent evidence suggests that the incidence is much lower than previously estimated.

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III. PATHOPHYSIOLOGY

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Maternal transmission of the virus probably occurs via respiratory droplets or direct contact with chickenpox or zoster lesions. The virus replicates in the oropharynx, and viremia results, before the onset of rash, with transplacental passage to the fetus. Almost all cases reported have involved exposure between the 8th and 20th weeks of pregnancy. The pathogenesis of fetal varicella syndrome (FVS) may reflect disseminated infection in utero or as a consequence of failure of virus–host interaction to result in establishment of latency, as normally occurs in postnatal VZV infection. Since VZV is a lymphotropic virus, it has the potential to spread to all fetal organs by the hematogenous route. Pathology specimens from aborted fetuses with VZV infection have shown the virus to be distributed throughout fetal tissues. Microcephaly can be attributed to VZV encephalitis and irreversible damage to growth of the developing brain. Of interest, the virus does not appear to ...

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