MORE than two decades have elapsed since Gregg1 and Swan et al2 observed the relationship of antecedent maternal rubella infection during pregnancy to the birth of anomalous infants. Unequivocal diagnosis of rubella and its virological differentiation from other, clinically similar, diseases were first reported in 1962.3-5 The subsequent epidemics of 1963 and 1964 provided abundant evidence of the ravages of this infection among the unborn. In the laboratory, newly available diagnostic tools permitted an accurate recording of the extent and distribution of the disease, particularly its protean manifestations when rubella begins in utero. The classic postrubella syndrome of cataracts, cardiac anomalies, nerve deafness, and mental defect was expanded to comprise diverse anomalies. A persistent state of chronic antenatal infection also emerged which was reflected in viscera, neural, and osseous tissues, and often continued postnatally, throughout infancy.6
Mechanisms operative in rubella teratogenesis are not clear. The generalized