Primary CMV infection in pregnancy is shown by seroconversion of CMV-specific IgG antibodies from negative to positive concomitantly with positive IgM antibody and very low-avidity IgG detection. The fetus may be usually infected within 4 to 8 weeks from viremia, but transmission may occur more rapidly in the last months of pregnancy. IgG avidity, which measures the capacity of antibodies of binding CMV antigen, is very low in the first weeks after a primary infection and allows to exclude a recurrent infection.
Congenital CMV infection occurs in approximately 40% of infants born to mothers with primary infection. The highest risk of severe sequelae (up to 50%) concerns a primary maternal infection occurring during the first 4 months of pregnancy.

Fetal infection and disease

Fetal CMV infection should be closely monitored by ultrasound examination for evidencing IUGR, hepatosplenomegaly, hyperechogenicity of bowel, liver or periventricular area, cerebral ventriculomegaly, ascites or hydrops, cystic lesions in the brain, liver or placenta. Magnetic resonance imaging (MRI) is an essential tool for revealing cerebral abnormalities caused by migrational disorders, vascular diseases and genetic factors, starting from 20 weeks’gestation.

Neonatal infection

In neonates, congenital CMV infection is diagnosed by CMV DNA detection from urine or blood within three weeks from birth, to differentiate congenital from postnatal infection. In symptomatic as well as asymptomatic infants, testing of brain stem auditory evoked responses should be performed as soon as possible to reveal profound hearing abnormalities which cannot be detected by acustic otoemissions. The ophtalmoscopic examination and visual evoked potentials could reveal retinal involvement.