1916

In U.S., summer outbreak of polio epidemic in 26 states, especially mid-Atlantic states: 27,000 cases and 6,000 deaths; in Newark & NYC, about 80% of cases were children under five years old (Rogers, 10ff.). Scientific understanding of polio, guided by Simon Flexner’s work at Rockefeller Institute for Medical Research, was that polio resulted from a filterable virus that entered the body through the nose and mouth (and was spread by sneezing and kissing) and traveled directly to the brain and spinal cord along nerve pathways (21-25, 173). By the 1950s, this model was supplanted by one in which the polio virus entered the body through the mouth, traveled to the intestines via the blood, and only occasionally affected the nervous system (24, 173-176). This followed from the culture work of John Enders and his team at Children’s Hospital in Boston in 1948; they cultivated the Lansing strain of polio (unlike Flexner’s mixed MV strain) (173; Galambos & Sewell, 59). It was also found that polio antibodies in blood were a “defining sign of exposure to polio and that such exposure might provide lasting immunity” (174). In 1916, germ theory (the “New Public Health”) continued to be interpreted in the context of political demands and cultural prejudices; physicians and health officials “did not believe that germs spread disease randomly. Disease germs were associated with specific kinds of places and people. . . . In practice, most official quarantine measures [19th c. “sanitary science”] sought to regulate the behavior of immigrant families as the most effective way to control the spread of the epidemic” (32, 33, 42-43, 46-47, 57). “Polio was explained in both terms of the traditional filth theory and the concepts of modern bacteriology. Even the most up-to-date scientists, who tended to support a theory of personal contact in disease transmission, mixed their analyses of the epidemic with dust and fomites, older symbols of disease” (70, 143-45, 163-64). “A traditional environmental model underlay epidemiologists’ questions but proved inadequate to explain the patterns they found, for researchers were only willing to associate the disease with the presence – not absence – of poverty and dirt” (150). Therefore, appearance of polio among middle-class, nonimmigrant children explained in terms of an insect theory (150-54) and other external factors such as infected milk (157-59), infected food, careless parents. “Despite contradictory evidence, in epidemiological study as in public health work, polio remained firmly linked to filth and poverty” (143), even though “The discrepancy between dirt and disease was the most difficult break from the traditional epidemiological past…. The bacteriological model allowed investigators to transform dirt into infected filth, a sign that individuals, through carelessness and ignorance, had abdicated their responsibility for preventing disease” (162).