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Despite the fact that acute rheumatic fever has become rare almost everywhere in the United States (except in the Salt Lake City area) and in most of the rest of the developed world, interest in this historically important and clinically fascinating disorder is great. This interest is demonstrated by the recent publication of several books on this subject and related topics. Acute rheumatic fever has bestowed a great legacy on many health care institutions. One example is the hospital at which I work, the Children's Memorial Hospital in Chicago, founded by Julia Foster Porter in 1882 after her 13-year-old son, Maurice, died of acute rheumatic fever. For decades, like similar institutions, this hospital had a large ward for patients with rheumatic fever, but the need for such facilities has almost disappeared.
Peter English, the author of this most recent interpretation of the history of acute rheumatic fever in the United States and Britain, brings unique credentials to his task: he is the Josiah Charles Trent Associate Professor of the History of Medicine at Duke University as well as a primary care pediatrician. His history begins at the very end of the 18th century and encompasses all of the 19th and part of the 20th centuries, ending quite abruptly and somewhat disappointingly in 1965.
English puts forth several hypotheses, which, if proved correct, would break new ground in our comprehension of this still poorly understood disorder. He posits that the biologic entity we now call acute rheumatic fever changed — he uses the term "mutated" — beginning around 1800, from a disorder affecting only joints ("acute articular rheumatism") to one that involved the brain and heart. This change resulted, he proposes, in the addition of the features of chorea, pericarditis, and, somewhat later, endocarditis in patients with acute rheumatism. English further suggests that another biologic change in rheumatic fever in the late 19th and early 20th centuries resulted in myocarditis — another new manifestation, and one that often remained undetected but produced chronic debility that was evident at autopsy decades after an attack of acute rheumatic fever.
These rather startling claims demand close scrutiny. To accept the concept that a complex disorder such as acute rheumatic fever has, in fact, changed biologically, one must be convinced that technological advances during the period in question did not create the illusion that the disease itself had "mutated." Such an artifact or illusion could come about from the use of new tools that revealed phenomena that were previously not apparent. If English is right, one would expect that cardiac disease compatible with rheumatic heart disease or self-limited chorea did not exist before "mutation" of the disease. If such conditions did exist, alternative causes should be apparent to explain them.
The relevant technological changes of the 19th century were, of course, truly revolutionary. Laënnec invented the stethoscope in 1816, and, as English acknowledges, Bouillaud used it by 1837 in examining patients with rheumatic fever. Stille indicated in 1839 that cardiac auscultation had become routine in the diagnosis of acute rheumatism. Thus, the recognition of pericardial and valvular disease was greatly facilitated by this technological innovation. Electrocardiography, first developed by Einthoven in 1903, was available routinely for clinical use by the 1920s and greatly facilitated the demonstration of rheumatic myocardial involvement in ways previously not possible in living patients. Thus, it is not at all surprising that cardiac involvement would be recognized increasingly in patients with acute rheumatism during the era encompassed by English's work, even in the absence of a change in the fundamental character of the illness.
English has chosen to focus particularly on the important observations of Wells in 1810 and briefly notes that Pitcairn in 1788 and Baillie in 1797 first associated heart disease with acute rheumatism. However, as detailed nicely in the history by Benedict Massell (Rheumatic Fever and Streptococcal Infection. Cambridge, Mass.: Harvard University Press, 1997), Lancisi (1707), Vieussens (1715), and Morgagni (1761) had all earlier described autopsy features compatible with rheumatic heart disease. Morgagni observed such findings in some patients with acute rheumatism, even though the heart disease was not explicitly connected to the rheumatic illness. Similarly, Pulteney's report in 1761 of a young man with severe acute rheumatism, obliteration of the pericardial space, and marked cardiomegaly is not referred to by English.
It is my view that, in the end, English does not make a convincing case to support his main hypotheses. Nevertheless, much of this book makes interesting reading, and it portrays well the sense of confusion and the conflicting "expert" opinions surrounding acute rheumatic fever through the 19th and 20th centuries. Particularly interesting is the discussion of the evolution of therapy. Relatively minor technical disappointments include the consistent failure to capitalize the "S" in Streptococcus pyogenes and the inappropriate use of streptococcus viridans (the former species name for 
-hemolytic streptococci). Students of the history of group A streptococcus, rheumatic fever, and the history of medicine should find this a provocative and challenging book.
Stanford T. Shulman, M.D.
Northwestern University Medical School
Chicago, IL 60611
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