Cytomegalic inclusion disease (CID) usually occurs as a subclinical infection followed by periodic reactivation revealed by shedding of the virus. It may be serious in the neonate when infection is transmitted to the fetus in utero.

Clinical Manifestations and Pathology

Cytomegalic infection is characterized histologically by the presence of large cells containing inclusion bodies in the midst of an infiltration of mononuclear cells that may be present in any of the body organs.

In prenatal infections most infants are born without clinical evidence of disease, although some 10 to 15 percent may show microcephaly, retardation of growth or mental development, hepatosplenomegaly, jaundice, and calcifications in the brain. There may be abnormalities in liver function tests and in hematopoiesis. Some 10 to 30 percent of infants with symptomatic disease die in early life. Evidence of involvement of the central nervous system can develop in the early years of life, even though the child may appear normal. The evidence is manifested as impaired intellect, neuromuscular abnormalities, chorioretinitis, optic atrophy, or hearing loss.

Neonatal infection acquired at birth from an infected cervix or later from the mother’s milk usually goes unnoticed but can be identified by the development of antibodies. In addition, respiratory symptoms including pneumonia, as well as petechial rash and enlargement of the liver and the spleen, may occur. In these cases, however, acute involvement of the central nervous system is rare. Infection in children is generally asymptomatic and is evidenced only by the development of antibodies and the shedding of virus. Occasionally hepatosplenomegaly and abnormal liver function are found. There is no proof that pharyngitis occurs at the presumed portal of entry.