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Communication
A letter to the editor will be considered only if it relates to an article or review published in this journal; publication is solely at the editors' discretion. The AHA disclaims responsibility for statements, of either fact or opinion, made by the writers. Letters should not exceed one thousand words for articles and seven hundred words for reviews. They can be submitted by e-mail to ahr@indiana.edu, or by postal service to Editor, American Historical Review, 914 E. Atwater Ave, Bloomington, IN 47401. For detailed information on the policies for this section, see http://www.historycooperative.org/ahr/communpo.html.
ARTICLES
To the Editors:
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| In "The Black Death: End of a Paradigm" (AHR, June 2002, 703–738), Professor Samuel K. Cohn, Jr. presents an intriguing hypothesis, that the disease responsible for the Black Death is not the same as contemporary epidemic plague, caused by Yersinia pestis. However, his assertion that humans do not develop immunity to this pathogen is incorrect. The fact that available vaccines require frequent booster shots notwithstanding, people exposed to plague develop long-lasting immunity and are not susceptible to reinfection for many years, if ever. The multiphasic pattern of recrudescence observed by Dr. Cohn, with lower peaks with each outbreak, is actually consistent with the observed facts about plague. Since the flea vector is not an efficient means of disease transmission, many remain uninfected during the initial outbreak. Subsequent outbreaks result in lower peak incidence of infection, since, with each recurrence, fewer are susceptible, as an ever-greater portion of the population becomes immune. A century or two later, the plague can recur in full efflorescence, as subsequent generations lack immunity. These facts do not detract from Dr. Cohn's more persuasive arguments. Lack of predominance of inguinal buboes over lymphatic swellings in other locations would rule out flea-borne plague as a cause of the Black Death. Although some of the medieval descriptions of skin lesions could reflect disseminated intravascular coagulation—which causes the "blackness" associated with "Black Death," if Yersinia is indeed the causative agent—multiple and various skin lesions also suggest the possibility of a pathogen other than Yersinia pestis. |
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