- Rheumatic Fever and Streptococcal Infection: Unraveling the Mysteries of a Dread Disease
In 1931, Benedict Massell joined the medical staff of the House of the Good Samaritan, a hospital that specialized in treating children with rheumatic fever, and for the next four decades he was an ardent student of the disease. This volume represents his understanding of rheumatic fever; as such, it is a mix of history, memoir, and medical lecture.
Few diseases have undergone changes as profound as those experienced by rheumatic fever in the twentieth century. When Massell first encountered it, rheumatic fever was a leading cause of disease and death in children. In the [End Page 519] 1930s, many estimates from both sides of the Atlantic recorded that nearly 2 percent of children suffered from rheumatic heart disease; rheumatic fever, thus, formed part of every physician’s practice. By the time of Massell’s retirement in 1973, it hardly concerned practicing physicians at all. During the span of his career, rheumatic fever inspired an enormous amount of medical research. Despite Massell’s promise in the preface to consider four hundred years of the disease’s history, most of his book is reserved for the years of his active participation in the scientific debates.
As the title of his book indicates, Massell believes that physicians’ appreciation of streptococcal infection as the “trigger” in rheumatic fever was the cardinal event in the history of the disease. He provides an overview of many other aspects, but he devotes most of the volume to the streptococcus and to current views of the bacterium’s role in rheumatic fever. His grasp of the literature is impressive. His notes run to ninety pages, and every paragraph exudes details of countless research studies.
Rheumatic fever was one of medicine’s most intriguing illnesses. Massell starts with the historical record of its six clinical components: migratory arthritis, heart disease, chorea, erythematous rashes, tonsillitis, and subcutaneous nodules. In the 1880s, British pediatricians Thomas Barlow and Walter Cheadle pulled together these components into the clinical entity of rheumatic fever. Medical attention next shifted to causes. Cheadle suggested that tonsillitis often preceded the other symptoms, leading physicians to explore tonsillar infection. Massell is careful to credit many observant physicians, but several stand out in his account: Arthur Newsholme, J. Alison Glover, Alvin Coburn, and William Collis. Published the year that Massell joined the staff at “Good Sam,” Coburn’s epidemiological evidence—which argued that infection with one particular tonsillar germ, the Group A streptococcus, had to precede rheumatic fever—cemented the relationship between bacterium and disease and served to ignite an explosion of streptococcal research. For example, Rebecca Lancefield grouped streptococci according to polysaccharides and M-proteins; and Edgar Todd identified antistreptolysins, providing serologic confirmation of prior streptococcal infection.
The arrival of sulfonamide in clinical practice shortly after Coburn’s discovery furnished physicians with a preventive drug. After World War II, penicillin emerged as a treatment for the prior streptococcal infection. It was a crowded research field: Massell’s index includes the names of more than seven hundred participants. (This enumeration points to one of the major problems in writing a history of twentieth-century medicine: coming to grips with the immense biomedical enterprise in a readable historical format.) Not all researchers immediately accepted the streptococcal hypothesis. Massell carefully documents the doubts that Homer F. Swift, May G. Wilson, and T. Duckett Jones—his contemporaries—entertained about the streptococcal trigger.
Toward the end of the volume, there are chapters on “contributing factors” (chap. 11) and “susceptibility factors” (chap. 12). Here readers may take issue with Massell’s historical interpretation. In the decades before streptococcal infection dominated research, physicians explored rheumatic fever’s preference for [End Page 520] crowding, northern latitudes, dampness, and poverty, and its tendency to run in families. Eventually insights from streptococcal/human ecology made sense of these preferences, but until then each had vocal and persuasive proponents. Only in the context of this broader debate about the nature of rheumatic fever do...