Cytomegalovirus (CMV) is the most frequent known cause of perinatally acquired infections. Congenital acquisition occurs in 0.5% to 2.7%1-3 and natal acquisition occurs in 4% to 10%3,4 of all deliveries. More than 90% of congenitally and natally acquired CMV infections are subclinical. Of infants infected in utero, a substantial percentage have late neurologic sequelae, such as decreased mentation and auditory impairment.2,3 Not enough studies exist to permit an accurate prediction of eventual outcome among these infants. Nevertheless, CMV is rapidly emerging as the infectious agent most frequently responsible for congenital abnormalities.
The first human strains of CMV were isolated in 1955 by Smith,5 from autopsy material of two infants described by Rowe et al,6 and by Weller and associates, who isolated the virus from hepatic tissue and/or urine of three living infants with cytomegalic inclusion disease (CID).7 Prior to this time, CID was