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Black Death

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Lisa Wolfe
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« Reply #15 on: June 24, 2012, 06:07:00 pm »

Walløe complains that all of these authors "take it for granted that Simond's infection model, black rat → rat flea → human, which was developed to explain the spread of plague in India, is the only way an epidemic of Yersinia pestis infection could spread", whilst pointing to several other possibilities.[42]

A variety of alternatives to the Y. pestis have been put forward. Twigg suggested that the cause was a form of anthrax and N. F. Cantor (2001) thought it may have been a combination of anthrax and other pandemics. Scott and Duncan have argued that the pandemic was a form of infectious disease that characterise as hemorrhagic plague similar to Ebola. Archaeologist Barney Sloane has argued that there are insufficient evidence of the extinction of large number of rats in the archaeological record of the medieval waterfront in London and that the plague spread too quickly to support the thesis that the Y. pestis was spread from fleas on rats and argues that transmission must have been person to person.[43][44] However, no single alternative solution has achieved widespread acceptance.[36] Many scholars arguing for the Y. pestis as the major agent of the pandemic, suggest that its extent and symptoms can be explained by a combination of bubonic plague with other diseases, including typhus, smallpox and respiratory infections. In addition to the bubonic infection, others point to additional septicemic (a type of "blood poisoning") and pneumonic (an airborne plague that attacks the lungs before the rest of the body) forms of the plague, which lengthen the duration of outbreaks throughout the seasons and help account for its high mortality rate and additional recorded symptoms.[28]
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