Twenty years after Norman Gregg, in 1941, discovered the association between intrauterine rubella and congenital cataracts, a rubella pandemic occurred, with devastating consequences. During the 1962–1965 global pandemic, an estimated 12.5 million rubella cases occurred in the United States, resulting in 2000 cases of encephalitis, 11,250 therapeutic or spontaneous abortions, 2100 neonatal deaths, and 20,000 infants born with congenital rubella syndrome (CRS), a constellation of birth defects that often includes cataracts, heart defects, and deafness [1]. The economic impact of this epidemic in the United States was estimated to be $1.5 billion [1].

The global epidemic spurred the development of rubella vaccines and emphasized the need to develop and implement strategies for using these vaccines to prevent this devastating health burden. In 1969, live attenuated rubella vaccines were licensed in the United States. The goal of the rubella vaccination program was to prevent congenital infections, including CRS. The initial strategy used to achieve the public health goal was to target chil-