Abstract
IU/mL (positive VZV IgG titer, >1 IU/mL). Both the mother and the newborn had a VZV IgM titer of 1 IU/mL). The IgG titers of the mother and the newborn child showed no change after 3 months. IgM antibodies against herpes simplex virus (HSV) and hepatitis C virus (HCV) were not detected either the mother or the newborn. VZV DNA was detected a liquor specimen by PCR. Vesicle swab specimens failed to reveal VZV, and the Tzanck test showed neither polynuclear giant cells nor intranuclear inclusions the vesicle fluid. In our opinion, these findings indicate that the vesicles and the exudative blistery erythema spanning the axillary cavum are associated with a delayed in utero healing process, and that the vesicles are not an expression of the florid, active rash typical of infection. The mother was treated with acyclovir, 700 mg iv q8h for 7 days, within 2 days after the onset of vesiculopapular exanthema. Soon after birth, the newborn was treated with acyclovir, 30 mg/kg/day, given 3 divided doses for 20 days. The term varicella embryopathy refers to the spectrum of fetal anomalies associated with maternal VZV infection during the first trimester of pregnancy. VE manifests as cutaneous scars, limb hypoplasia, muscle atrophy, malformation of the digits, psychomotor retardation, microcephaly, cortical atrophy, Horner syndrome, and various eye abnormalities, including cataracts, chorioretinitis (figure 2), and microphthalmos. Intrauterine growth retardation, motor and sensory deficits, as well as other minor abnormalities have also been described [1, 2]. Approximately 30% of affected infants die during the first months of life, and infants who survive may present with a variety of sequelae, including early leukemia or other malig-
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