In:

Epidemiology and Infection

Author:

J. E. Cradock-Watson

Fifty years ago in New South Wales the late Sir Norman Gregg [1] described congenital cataracts in 78 babies, 67 of whose mothers had had clinical rubella in early pregnancy; he concluded that the disease in the mother caused the abnormality in the baby. Gregg [1-3] and Swan [4, 5] and their colleagues reported that deafness, heart disease and microcephaly were also major components of the congenital rubella syndrome. The need to prevent this tragic outcome stimulated intensive work on laboratory diagnosis and vaccine development, leading to the isolation of rubella virus in 1962 and then to methods for antibody detection. These complementary advances established the two traditional pillars of virological diagnosis and opened the way to immunization, with the result that some countries are now on the verge of eliminating a disease which for over 100 years was regarded as no more than a mild and harmless exanthem of childhood.

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