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Congenital varicella syndrome (CVS) is a rare disorder resulting from maternal–fetal VZV transmission, usually between 8 and 20 weeks' gestation.1,2 The incidence of maternal VZV infection has been estimated to be between 5 and 7 cases per 10 000 pregnancies.2 Fetus-specific factors play a crucial role, and fetal consequences of maternal exposure may be highly variable.3 Given that up to 2% of fetuses infected between 8 and 20 weeks' gestation may exhibit pathogenetic effects of VZV,4 we estimate the CVS incidence rate to be about 2.8–4 cases per 100 000 pregnancies.
Since the description of CVS by Laforet and Lynch in 1947,5 embryopathy following fetal infection with VZV has been well described in case reports.1,2,6 More recently, a number of reports have focused on the complications of VZV reactivation.7,8 Although zoster infection may develop in the neonatal period, descriptions of intrauterine reactivation are very rarely reported.
CVS manifests as cutaneous scars, limb hypoplasia, muscle atrophy, malformation of the digits, psychomotor retardation, microcephaly, cortical atrophy, Horner's syndrome and various eye abnormalities, including cataracts, chorioretinitis and microphthalmos. Intrauterine growth retardation as well as motor and sensory deficits have also been described
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