CMV disease is widespread in the general population. Although cervicitis is common, the virus is probably transmitted to the fetus transplacentally. Infection of the fetus usually occurs in the first trimester of pregnancy, sometimes later, by way of an inapparent maternal viremia and infection of the placenta. The newborn can also be infected in the course of delivery or afterward by the mother’s milk or by transfusions. However, only a small proportion of women known to harbor the virus give birth to infants with active infection. The likelihood of the fetus being infected is much greater if the seronegative mother becomes infected for the first time during pregnancy. In one study, 18 percent of infants born to such mothers were symptomatic at birth, and 25 percent became blind, deaf, or cognitively impaired within a few years (Fowler et al). In mothers with recurrent CMV infection, the infants were asymptomatic at birth, and only a few developed serious sequelae. Evidently, the presence of maternal antibodies before conception protects against congenital CMV infection.
Early infection of the fetus may result in a malformation of the brain; later, there is only inflammatory necrosis from encephalitis in parts of the normally formed brain. Disseminated inflammatory foci have been observed in the cerebrum, brainstem, and retinae. Here there were aggregates of lymphocytes, mononuclear cells, and plasma cells. The mononuclear histiocytes (microglia cells) contain inclusion bodies; some astrocytes are similarly affected. Granulomas form and later calcify, particularly in the periventricular regions. Often there is hydrocephalus. In the low-birth-weight or full-term infant, the clinical picture is one of jaundice, petechiae, hematemesis, melena, direct hyperbilirubinemia, thrombocytopenia, hepatosplenomegaly, microcephaly, mental defect, and convulsions. Cells in the urine may show cytomegalic changes. There is a pleocytosis and an increased protein in the CSF.
Congenital CMV infections pose a much greater problem than does rubella. There is no way of identifying the infected fetus prior to birth or to prevent inapparent infections in the pregnant woman. As indicated above, if the pregnant woman has measurable titers of antibodies to CMV at the time of conception, her infant is relatively protected. Moreover, some infected infants (with viruria) may appear normal at birth but develop neural deafness and developmental delay several years later. Viral replication in infected organs continues after the first year and health workers are at risk. A second child may be infected.
There is no known treatment. The difficulties in prenatal diagnosis of maternal infection preclude planned abortion. Routine serologic testing should be done on every young woman of childbearing age. Until an effective vaccine becomes available, pregnancy should be avoided if a sexual partner is infected.
In the United States, approximately 10 percent of cases of AIDS have occurred in women, almost all of them of childbearing age, and the rate of new cases is increasing at a faster rate among them than among men. The numbers are higher in many developing countries. In children, practically all instances of AIDS come from an HIV-infected mother (“vertical transmission”). The infection may be acquired in utero, during delivery, or from breast-feeding. The relative importance of each of these modes of transmission has not been settled.