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Data on the incidence and severity of congenital and neonatal varicella in australia from 1995 to 1997. It includes case studies of affected infants and their mothers, as well as statistics on the annual incidence and gender, age, and severity of the cases. The document also discusses the potential benefits of vaccinating non-immune women prior to pregnancy.
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Table 12 Neonatal varicella in Australia, 1997 Time of mother’s varicella contact Gender Rash onset (days of age) Disease severity Age baby given ZIG Time mother given ZIG Acyclovir for baby Before delivery* M F F F F
at birth 13 1
at birth day 1 at birth
day 2 at infection at contact At term M 21 ++ – Yes After delivery (^) F F F F M M
day 1 day 2 day 5 day 3 day 11 day 2 Yes Yes No known source of infection (^) NA 21 + – Severity of disease: + mild ++ moderate ZIG zoster immune globulin NA not available Overview 1995- Over this three year period, 75 notifications were received and 71 (95%) questionnaires were returned. From these, 51 confirmed cases of congenital and neonatal varicella infection, including one termination, were identified. The annual incidence, shown in Table 13, is expressed per 100,000 live births and excludes the termination of pregnancy. Of the 50 incident cases, 20 were males, 26 females and the sex of four remains unknown. Maternal ages ranged from 18 to 39 years. No cases were reported from Tasmania. Table 13 Annual incidence of congenital and neonatal varicella, 1995- Congenital varicella Incidence (95% CI) Neonatal varicella Incidence (95% CI) 1995* 3 1.2 (0.3-3.7) 15 5.9 (3.4- 9.9) (^1996) 1 0.4 (0.02-2.6) 16 6.3 (3.7-10.5) (^1997) 2 #^ 0.8 (0.3-1.8) 13 5.2 (2.9- 9.1) Total 6 0.8 (0.3-1.8) 44 5.8 (4.3- 7.8)
Congenital varicella The incidence of congenital varicella did not vary over the study period (Table 13). Clinical severity of cases varied (Table 14). Severe malformations were seen both following maternal infection in the first 13 weeks as well as later in the pregnancy. Timing of maternal infection ranged from eight to 26 weeks gestation. There were too few cases to determine whether the risk of congenital malformation was significantly lower after maternal infection in the first 13 weeks than between 13 and 20 weeks gestation, as has been shown in larger series. In the literature, there are few reported cases of congenital varicella following maternal infection after 20 weeks’ gestation. It is therefore interesting that the infant exposed to maternal infection at 26 weeks gestation was severely affected. Conversely, two infants whose mothers had varicella at 13 and 18 weeks were born without defects. They developed zoster at five and four months of age respectively, with complete recovery. One child with defects, whose mother was infected at 12 weeks gestation, also developed herpes zoster at the age of 10 weeks.