3 Medieval and Modern Bubonic Plague: Some Clinical Continuities

In his book The Black Death transformed,1 Samuel K Cohn claims that the epidemic disease described in western European historical sources from ad 1347 to the mid-seventeenth century under the names plague, pestis, pestilence, plagen and the like must have been a disease other than the modern plague that reached Hong Kong in May 1894 from other parts of China, and later spread first to India and then to all inhabited continents. Alexandre Yersin showed that the disease in Hong Kong was caused by a bacterium, later named Yersinia pestis. It was also Yersin who claimed that he had found not only the cause of plague in China, but also the cause of the medieval and early modern plague epidemics. Four years after the discovery of the bacillus, Paul-Louis Simond proposed the transmission route from the rat (Rattus rattus) via the flea (Xenopsylla cheopis) to humans, although the scientific community was not fully convinced until ten years later, since this hypothesis did not explain all observations. The problems with the hypothesis were forgotten, which is easy to understand when we remember that the doctors and epidemiologists who were working in India at that time were facing a worsening and very serious epidemic. The simple preventive message to public health workers and the public was: exterminate the rats. The identification of medieval plague as the same disease as modern plague was accepted within thirty years, first by medical scientists and later by historians. Cohn writes, “Without argument, historians and scientists have taken the epidemiology of the modern plague and imposed it on the past, ignoring, denying, even changing contemporary testimony, both narrative and quantitative, when it conflicts with notions of how modern bubonic plague should behave.”2 I agree to some extent with Cohn's criticism of how historians have imposed a modern understanding of plague epidemics in India on historical epidemics, and especially how historians have invented large populations of rats in the medieval towns and countryside of northern Europe without any support from contemporary historical sources or archaeology.3 However, I strongly disagree with his main point, which is that the medieval and modern plague epidemics must have involved different diseases in medical and bacteriological terms. Thus, I argue that Yersinia pestis is the cause of both medieval bubonic plague and modern bubonic plague, and that the symptoms, signs, pathology and pathophysiology are very similar. On the other hand, the two series may have differed in speed of transmission, population mortality and some other epidemiological characteristics because of differences in climate, housing conditions, the availability and population density of flea species and other possible insect vectors, and the availability of susceptible mammals other than rats. Cohn's main arguments are as follows: There is a lack of evidence of involvement of rats and fleas (Xenopsylla cheopis) in late-medieval/early-modern plagues. The speed of transmission is different (medieval being rapid, modern being slow). The mortality and the age and sex distribution of victims are different (e.g. high mortality in Europe in medieval times, low mortality in modern times in India). Acquired immunity is different (long-lasting immunity in medieval times, no lasting immunity in modern times). The signs and symptoms are different (e.g., boils mainly in the neck and armpits in medieval plagues, and in the groin in modern plague). Cohn also claims that when Yersin and his contemporary medical doctors identified plague in Hong Kong with late medieval and early modern plague epidemics, no recent medical knowledge about plague was available to European doctors, and that the medical information available dated back to the last plague epidemic in London in 16654 or to earlier epidemics, even though it was generally known that there had been epidemics of plague in 1722 in Marseilles, in 1743 in Messina and in 1771–2 in Moscow.