The most common characteristic abnormalities associated with congenital rubella include ophthalmologic (cataracts, retinopathy, and glaucoma), cardiac (patent ductus arteriosus and peripheral pulmonary artery stenosis), auditory (sensorineural hearing loss), and neurologic (behavioral disorders, meningoencephalitis, and mental retardation) conditions. In addition, infants can present with growth retardation, hepatosplenomegaly, early-onset jaundice, thrombocytopenia, radio-lucent bone disease, and purpuric skin lesions (“blueberry muffin” appearance from dermal erythropoiesis).
Detection of rubella-specific IgM antibody usually indicates recent infection. Measurement of rubella-specific IgG over several months can be confirmatory. Rubella virus can be isolated from blood, urine, CSF, and throat swab specimens. Infants with congenital rubella are chronically and persistently infected and tend to shed live virus in urine, stools, and respiratory secretions for 1 year. Infants should be isolated while in the hospital and kept away from susceptible pregnant women when sent home.
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CMV is the most common congenital infection and the leading cause of sensorineural hearing loss, mental retardation, retinal disease, and cerebral palsy. Congenital CMV occurs in about 0.5% to 1.5% of births. When primary infection occurs in mothers during a pregnancy, the virus is transmitted to the fetus in approximately 35% of cases. Rates of CMV infection are three to seven times greater in infants born to adolescent mothers compared to others. The risk of transmission of CMV to the fetus is independent of gestational age at the time of maternal infection. The earlier in gestation that the primary maternal infection occurs, the more symptomatic the infant will be at birth. The most common sources of CMV for primary infections occurring in mothers during pregnancy are sexual contacts and contact with young children. It is well known that CMV can be transmitted to the fetus even when maternal infection occurred long before conception. This transmission can occur as the result of virus reactivation, chronic infection, or reinfection with a new strain.
More than 90% of infants who have congenital CMV infection exhibit no clinical evidence of disease at birth. Approximately 10% of infected infants are small for gestational age and have symptoms at birth. Findings include microcephaly, thrombocytopenia, hepatosplenomegaly, hepatitis, intracranial calcifications, chorioretinitis, and hearing abnormalities. Some infants can present with a blueberry muffin appearance as the result of dermal erythropoiesis. Skull films may reveal periventricular calcifications. An additional 10% of infected infants may not present until later in infancy or early childhood, when they are found to have sensorineural hearing loss and developmental delays. Mortality is 10% to 15% in symptomatic newborns. Perinatal CMV infection acquired during birth or from mother’s milk is not associated with newborn illness or CNS sequelae.
Congenital CMV infection is diagnosed by detection of virus in the urine or saliva. Detection is often accomplished by traditional virus culture methods but can take several weeks to obtain a result. Rapid culture methods using centrifugation to enhance infectivity and monoclonal antibody to detect early antigens in infected tissue culture can give results in 24 hours. PCR also can be used to detect small amounts of CMV DNA in the urine. Detection of CMV within the first 3 weeks after birth is considered proof of congenital CMV infection.
Trial studies in severely symptomatic newborns of the antiviral agent ganciclovir have shown a lack of progression of hearing loss.