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Shirley G. Driscoll, MD

Am J Dis Child. 1969;118(1):49-53.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Boston

From the departments of pathology and obstetrics and gynecology, Harvard Medical School, and Boston Hospital for Women (Lying-in Division), Boston.

Footnotes
Received for publication March 4, 1969.

Read before the International Conference of Rubella Immunization, Bethesda, Md, Feb 18, 1969.

Reprint requests to Boston Hospital for Women (Lying-in Division), 221 Longwood Ave, Boston 02115.

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