The overall incidence of CMV infection in adults estimated from large studies of blood donors, hospital workers, and pregnant women is around 1-2% per year (17,19,20). Higher rates of primary CMV infection have been documented in women of lower socioeconomic status. In developing countries, most people acquire CMV during early childhood. Studies have clearly shown the importance of both sexual activity and close contact with CMV-infected children as sources of maternal CMV infection (11). Evidence for sexual transmission of CMV is provided by studies that showed higher rates of CMV seropositivity in young women with other indicators of sexual activity, such as sexually transmitted diseases, greater number of sex partners, or young age at sexual debut (21,22). The results of a case-control study showed that history of sexually transmitted disease in the mother was an independent risk factor for the birth of a newborn with congenital CMV infection (23).
A dramatic rise in age-related prevalence of CMV infection in children attending child care centers compared with those kept at home has been demonstrated. Furthermore, the transmission of CMV strains among children in this setting has been documented by molecular epidemiology (24). Studies of parents of children attending day care centers and child care workers demonstrated a high rate of seroconversion and a strong association between care of younger CMV-shedding children and seroconversion (25-27). Molecular analysis of the isolates provided further evidence for transmission of CMV strains from child to caregiver (26-28).
CMV can be transmitted from mother to child transplacentally, during birth, and in the postpartum period via breast milk. Congenital CMV infection rates are directly related to maternal seroprevalence rates. Rates of congenital CMV infection are higher in developing countries and higher for low-income groups in developed countries (7,10,29). The mechanisms for this increased rate of congenital CMV in populations with high seroprevalence rates are not clear. Studies of risk factors for congenital CMV infection have also documented an association between young maternal age and increased rates of congenital CMV infection (30). Preece at al. also found that non-white race and single marital status were independently associated with increased risk of congenital CMV infection (31). Fowler et al. reported an increased risk of congenital CMV infection in women with sexually transmitted diseases, single mothers, and those younger than 20 years (32).
Intrapartum transmission of CMV occurs in around 50% of infants born to mothers shedding CMV from the cervix or vagina at the time of delivery (33). Genital tract shedding of CMV is more common in younger women, declining from around 15% in young teenagers to less than 1% in women over 30 years of age (34,35). Rates of CMV excretion from the cervix and vagina also change during gestation, with low rates early in gestation increasing to rates that equal or exceed those in nonpregnant women late in gestation. Cervical shedding of CMV has also been associated with other sexually transmitted diseases and with a greater number of sexual partners (36). In the United States, approx 10% of women shed CMV at the time of delivery; rates as high as 40% have been reported in Taiwanese women (36,37).
Breast milk is a principal route of transmission of CMV from mother to the child during infancy. Between 27 and 70% of seropositive women shed CMV in breast milk (38,39). It was reported that transmission of CMV to nursing infants of seropositive mothers was related to duration of breastfeeding and detection of CMV in milk by virus isolation (40). The proportion of infants acquiring CMV is directly related to maternal seroprevalence rates and the frequency of breastfeeding.
Vertical transmission of CMV plays an important role in the epidemiology of human CMV infection. In countries where a high proportion of infants acquire CMV from a maternal source, the majority of children are infected in early childhood. Aside from the medical significance of congenital CMV infection, infants who acquire CMV in utero, during delivery, or from mother's milk shed virus for years and serve as a source of the virus for other children and caregivers with whom they have close contact.
Blood products and transplanted organs are the most important vehicles of transmission of CMV in the hospital setting; the latter are unlikely to be of concern during pregnancy. Transmission of CMV through packed red blood cell, leukocyte, and platelet transfusions poses a risk of severe disease for seronegative small premature infants and immunocompromised patients (41). The risk of transmission of CMV with blood products increases with the number of units transfused, the presence of white blood cells, and the lack of serum antibody in the recipient (42). Prevention of blood product transmission of CMV can be achieved by using seronegative donors or by special filters that remove white blood cells (41,43,44). Another potential source of nosocomial CMV infection of particular concern to those in reproductive medicine is semen donated for artificial insemination (45,46). Although no cases of congenital CMV infection attributed to donor insemination have been reported, the fact that sexual activity is clearly a risk for CMV infection and that virus can commonly be recovered from semen suggests a need for caution. The American Fertility Society has recommended serological screening of semen donors for antibody to CMV (47). Person-to-person transmission of CMV requires contact with infected body fluids and therefore should be prevented by routine hospital infection control precautions. Studies in health care settings found no evidence of increased risk of CMV infection in settings in which patients shedding CMV are encountered (19,48).
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