S. Shershab  ( Department of Obstetrics and Gynecology, St. James’s Hospital & Trinity College, Medical School, Dublin-8. )
R.F. Harrison  ( Department of Obstetrics and Gynecology, St. James’s Hospital & Trinity College, Medical School, Dublin-8. )

Man is the only reservoir of cytomegalovir­us.¹ 13% of the general population are carriers of this virus with a high incidence of intra uterine infection. A wide variety of abnormalities has been observed, including hearing loss, mental retarda­tion, cerebral palsy, seizures, blindness, defects in tooth structure and poor school performance². Congenital CMV infection is usually due to transplacental spread of the virus³, however, the mother is usually asymptomatic and may have either a primary or reactivated latent infection⁴.

This 32 years old lady was in her second pregnancy. She had blood group 0 rhesus positive. Her TPHA was negative and she was rubella im­mime at the time of her booking in the ante-natal clinic. Her first pregnancy was normal and she was delivered of a normal male babywho weighed 4.080 kg. She was first seen in the ante-natal clinic at 10 weeks gestation. She attended the ante-natal clinic regularly until 39 weeks. Her diastolic blood pressure was slightly raised in the last trimester. Other parameters of ante-natal care were normal in each visit. She hada normal delivery ofa live male infant after a labour of 4 hours and 40 minutes. The baby responded to suction and 02. The baby was small for dates and transferred to the speeial care baby unit after paediatric consultation. The clinical fea­tures of bilateral cataracts, microcephaly and facial dysmorphism were noted. The baby weighed 2.010 kgs and died 2 days after developing marked jaun­dice despite exchange transfusions. Serological tes­ting revealed a CMV titre of 128 i.u. and Igm positive, but the mother showed no significant amount of antibodies.

The baby had facial dysmorphism with hy­pertelorism, microcephaly associated with prema­ture fusion of sutures, partial collapse of liver parenchyma associated with bile staining and a normal bihary tract, a wide spread petechial rash and massive splenomegaly. Histological examination of liver, spleen, kid­ney and lungs revealed the presence of CMV in­clusion bodies. The overall features were charac­teristic of generalized cytomegalic inclusion dis­ease.

CMV infection is endemic throughout the world with marked geographical variation in the incidence of infection. InAfrica andAsia over 90% of the population become infected and most of them acquire antibodies in childhood. In contrast in western countries more than 60% acquire infec­tion later in life⁵, particularly in higher socio­economic groups in whom the major exposure oc­curs in adolescence and early adult life. In the recent study of Griffiths and Baboonian (1984), it was shown that one woman in every 133 ex­perienced primary CMV infection duringpregnan­cy, which is twice as frequent as rubella infection during pregnancy⁶. It is now evident that the two viruses present quite different problems and only by prospective studies can the risk be assessed⁷. It is shown that 1st trimester infection will definitely cause congenital abnormalities⁸, and the infection early in pregnancy is associated with a sevenfold excess of fetal loss⁶. In one study it is noticed that fetal immune responses, both humoral and cell mediated are more vigorous in late gestation than early in pregnancy while maternal immune res­ponse is diminished in all stages of pregnancy and the most striking decrease occurred in the third trimester⁹. In the same study it was found that pregnant women with CMV infection are at in-creased risk of giving birth to congenitally infected infants particularly if active infection occurs late in pregnancy. These findings of infant damage due to third trimester infection are confirmed by Griffiths and Baboonian in humans and by Kumar in guinea pigs^9,6,10. Neonatal CMV infection is multisystem disease and new born babies may either be normal or show manifestations of disease as in the above case, or be still born⁴. 1-2% of all live births have C.M.V. and 10-20% of these infected neonates have some degree of handicap attributable to CMV^2,6,11. Perinatal and neonatal management is still not satisfactory. Two attenuated strains of live virus (AD-169 and TOWNE 1) are available but vaccination is still controversial. Therapy with in­terferon is under trial at the moment¹². Recently a case is reported in which a3 month old boywith life threatening CMV infection was successfully trea­ted with high titre anti CMV plasma¹³.

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