it was too little, too late to slow the progression of the epidemic across the United States. By mid-November, numbers of new cases and deaths from influenza and pneumonia had leveled off and begun to decline. Following a return to normal levels in December, a second wave of excess mortality due to respiratory illness began in January 1958 and peaked the following month.
Henderson et al. (2009) note several similarities in epidemiologic behavior between the 1957 H2N2 pandemic and the 2009 H1N1 pandemic: both arose early in the year and spread widely during the spring, both abated over the early summer months in the Northern Hemisphere while major epidemics developed in the Southern Hemisphere (as is also typical of seasonal influenza), and both (to date) were marked by relatively mild illness with low case-fatality rates.
Pandemic H3N2 emerged in Hong Kong in 1968 and spread rapidly across the globe. During the winter of 1968-1969, the virus caused an estimated 40,000 deaths in the United States, but in Europe, it inexplicably smoldered until the following winter before causing significant morbidity and mortality (Simonsen et al., 2005). That this pandemic was the least deadly of the three twentieth-century pandemics may be due to the fact that only the H antigen in H3N2 had “shifted” with respect to the previous pandemic H2N2 strain. In people born before 1891, the presence of H3 antibodies may have also afforded this otherwise vulnerable population some degree of protective immunity against the H3N2 influenza A virus. In the United States, people between the ages of 45 to 64 were shown to have a threefold higher risk of death from pandemic H3N2 than from epidemic influenza during the years prior to and following the pandemic (Simonsen et al., 2005).
Early in 1976, an outbreak of swine-origin influenza among military personnel at Fort Dix, New Jersey, resulted in 13 confirmed cases, including one death (CIDRAP, 2009). Serologic studies suggested that more than 200 soldiers had been infected with an H1N1 virus and that person-to-person transmission had occurred (Sencer and Millar, 2006). The outbreak, however, never spread beyond Fort Dix. Its origin remains unknown (CIDRAP, 2009). The major events in the swine flu vaccination campaign, adapted from Neustadt and Feinberg (1978), are presented in Box WO-2.
Similarities between the 1976 H1N1 virus and the 1918 H1N1 pandemic strain prompted concern that a similarly devastating pandemic was imminent, recalled keynote speaker David Sencer, who in 1976 was the director of the Centers for Disease Control (CDC). He reviewed the process by which the decision was made to start a mass vaccination program to protect the American public from