3 Medieval and Modern Bubonic Plague: Some Clinical Continuities

L. Walløe
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引用次数: 31

Abstract

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.
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3中世纪和现代腺鼠疫:一些临床连续性
在他的书《黑死病的转变》中,1 Samuel K Cohn声称,从公元1347年到17世纪中叶,在西欧历史资料中被描述为鼠疫,鼠疫,瘟疫,plagen和类似的流行病必须是一种疾病,而不是1894年5月从中国其他地区传到香港的现代瘟疫,后来首先传播到印度,然后传播到所有有人居住的大陆。亚历山大·耶尔辛指出,香港的鼠疫是由一种细菌引起的,后来被命名为鼠疫耶尔森氏菌。也是耶尔辛声称他不仅发现了中国鼠疫的原因,而且还发现了中世纪和近代早期鼠疫流行的原因。在发现这种芽孢杆菌四年后,保罗-路易斯·西蒙德提出了从老鼠(Rattus Rattus)通过跳蚤(Xenopsylla cheopis)传播给人类的途径,尽管科学界直到十年后才完全相信,因为这个假设并不能解释所有的观察结果。这个假设的问题被遗忘了,当我们记得当时在印度工作的医生和流行病学家面临着日益恶化和非常严重的流行病时,这就很容易理解了。给公共卫生工作者和公众的简单预防信息是:消灭老鼠。中世纪鼠疫与现代鼠疫是同一种疾病,这一观点在30年内被医学科学家和历史学家接受。Cohn写道:“毫无疑问,历史学家和科学家们将现代鼠疫的流行病学强加于过去,忽视、否认甚至改变当代的证词,无论是叙述上的还是数量上的,当这些证词与现代黑死病应该如何表现的观念相冲突时。在某种程度上,我同意科恩的批评,他认为历史学家把对印度鼠疫流行的现代理解强加于历史上的流行病,尤其是历史学家在没有任何当代历史资料或考古学支持的情况下,虚构了北欧中世纪城镇和乡村的大量老鼠然而,我强烈不同意他的主要观点,即中世纪和现代的鼠疫流行在医学和细菌学方面一定涉及不同的疾病。因此,我认为鼠疫耶尔森菌是中世纪黑死病和现代黑死病的病因,它们的症状、体征、病理和病理生理学都非常相似。另一方面,由于气候、住房条件、蚤类和其他可能的昆虫媒介的可得性和种群密度以及鼠以外易感哺乳动物的可得性不同,这两个系列可能在传播速度、种群死亡率和其他一些流行病学特征方面存在差异。Cohn的主要论点如下:缺乏证据表明老鼠和跳蚤(Xenopsylla cheopis)参与了中世纪晚期/现代早期的瘟疫。传播的速度是不同的(中世纪是快的,现代是慢的)。死亡率以及受害者的年龄和性别分布是不同的(例如,中世纪欧洲死亡率高,现代印度死亡率低)。获得性免疫是不同的(中世纪的持久免疫,现代的没有持久免疫)。体征和症状是不同的(例如,在中世纪瘟疫中,疮主要在颈部和腋窝,而在现代瘟疫中,疮在腹股沟)。科恩还声称当Yersin和他的当代医生确定鼠疫在香港与中世纪晚期和近代早期瘟疫流行,最近没有医学知识对鼠疫提供给欧洲医生,医学信息追溯到去年早些时候在伦敦在16654年或瘟疫流行流行,尽管一般都知道,1722年在马赛有瘟疫流行,在1743年在莫斯科在梅西纳和1771 - 2。
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