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Approximately 1% of all neonates are infected with CMV in utero and excrete CMV at birth. Although the majority of CMV infec-tions are asymptomatic, 5% of infected neonates show symptoms at birth. A DNA herpesvirus, CMV may be transmitted insaliva, semen, cervical secretions, breast milk, blood, or urine. CMV infection is often asymptomatic, although it can cause a short febrile illness. Similar to HSV, CMV may have dormant periods, only to reactivate at a later time. There are multiple serotypes and the presence of anti-CMV IgG does not confer immunity; recurrent infection may occur with a new strain of virus. The prevalence of antibodies to CMV is inversely proportional to age and socioeconomic status.
The risk of neonatal infection is significantly higher with primary maternal infection than with recurrent infec-tion; with recurrent infection the risk of neonatal infection is much lower, at 2% or less. Intrauterine growth restric-tion is sometimes noted. Most infants are asymptomatic at birth; when signs occur, they include petechiae, hepato-splenomegaly, jaundice, thrombocytopenia, microcephaly, chorioretinitis, or nonimmune hydrops fetalis. Long-term sequelae include severe neurologic impairment and hear-ing loss.
There is no effective vaccine or treatment for maternal or fetal infection. Therefore, routine serologic screening for CMV in pregnancy is not recommended. Testing is gener-ally limited to women in whom CMV infection is suspected and is done by culture or PCR. Antiviral agents have been used to treat neonate infection but remain experimental.
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