Alternative explanations

This interpretation was first significantly challenged by the work of British bacteriologist J. F. D. Shrewsbury in 1970, who noted that the reported rates of mortality in rural areas during the 14th century pandemic were inconsistent with the modern bubonic plague, leading him to conclude that contemporary accounts were exaggerations. In 1984, zoologist Graham Twigg produced the first major work to challenge the bubonic plague theory directly, and his doubts about the identity of the Black Death have been taken up by a number of authors, including Samuel K. Cohn, Jr. (2002), David Herlihy (1997), and Susan Scott and Christopher Duncan (2001).

It is recognized that an epidemiological account of the plague is as important as an identification of symptoms, but researchers are hampered by the lack of reliable statistics from this period. Most work has been done on the spread of the plague in England, and even estimates of overall population at the start vary by over 100% as no census was undertaken between the Domesday Book and 1377. Estimates of plague victims are usually extrapolated from figures from the clergy.

In addition to arguing that the rat population was insufficient to account for a bubonic plague pandemic, sceptics of the bubonic plague theory point out that the symptoms of the Black Death are not unique (and arguably in some accounts may differ from bubonic plague); that transference via fleas in goods was likely to be of marginal significance and that the DNA results may be flawed and might not have been repeated elsewhere, despite extensive samples from other mass graves. Other arguments include the lack of accounts of the death of rats before outbreaks of plague between the 14th and 17th centuries; temperatures that are too cold in northern Europe for the survival of fleas; that, despite primitive transport systems, the spread of the Black Death was much faster than that of modern bubonic plague; that mortality rates of the Black Death appear to be very high; that, while modern bubonic plague is largely endemic as a rural disease, the Black Death indiscriminately struck urban and rural areas; and that the pattern of the Black Death, with major outbreaks in the same areas separated by five to fifteen years, differs from modern bubonic plague, which often becomes endemic for decades, flaring up on an annual basis.

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.

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. However, no single alternative solution has achieved widespread acceptance 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 septicemia (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.