CYTOMEGALOVIRUS
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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