Contratrombone64
Admiral of Fugues
Fascinating: (taken from Wikipedia, so a fair amount of verification I guess is apt).
Not bubonic plague?
Recent scientific and historical investigations have led some researchers to doubt the long-held belief that the Black Death was an epidemic of bubonic plague. For example, in 2000, Gunnar Karlsson pointed out that the Black Death killed between half and two-thirds of the population of Iceland, although there were no rats in Iceland at this time. Rats were accidentally introduced in the nineteenth century, and have never spread beyond a small number of urban areas attached to seaports. In the fourteenth century there were no urban settlements in Iceland. Iceland was unaffected by the later plagues which are known to have been spread by rats. However, without a rodent reservoir, pneumonic plague can be transmitted from human to human by respiratory transmission, and bubonic and septicemic plague can be transmitted from human to human by human-biting fleas.
In addition, it was previously argued that tooth pulp tissue from a fourteenth-century plague cemetery in Montpellier tested positive for molecules associated with Y. pestis. Similar findings were reported in a 2007 study,[49] but other studies have yielded negative results. In September 2003, a team of researchers from Oxford University tested 121 teeth from sixty-six skeletons found in fourteenth-century mass graves. The remains showed no genetic trace of Y. pestis.
In 2002, Samuel K. Cohn published the controversial article, The Black Death: End of the Paradigm.[50] In the article Cohn argues that the medieval and modern plagues were two distinct diseases differing in their symptoms, signs and epidemiologies.[51] Cohn asserts that the agent causing the bubonic plague, Yersinia pestis, was first cultured at Hong Kong in 1894. In turn, the medieval plague that struck Europe, according to Cohn, was not the bubonic plague carried by fleas on rats as traditionally viewed by scientists and historians alike.[18]
Cohns argument that medieval plague was not rat-based is supported by his claims that the modern and medieval plagues hit in different seasons, had unparalleled cycles of recurrence, and varied in the manner in which immunity was acquired. The modern plague reaches its peak in seasons with high humidity and a temperature of between 50 °F (10 °C) and 78 °F (26 °C), as rats fleas thrive in this climate.[52] In comparison, the Black Death is recorded as hitting in periods where rats fleas could not survive, i.e. hot Mediterranean summers above 78 °F (26 °C).[18] In terms of recurrence, the Black Death on average did not resurface in an area for between five and fifteen years after it hit.[53] Contrastingly, modern plagues often hit an affected area yearly for an average of eight to forty years. Last, Cohn presents evidence displaying that individuals gained immunity to the Black Death during the fourteenth century, unlike the modern plague. He states that in 1348 two-thirds of those suffering from plague died in comparison to one-twentieth by 1382.[18] Statistics contrastingly display that immunity to the modern plague has not been acquired.
Cohn also points out that in the latter part of the nineteenth century buboes appeared mostly on an infected person's groin, while medieval primary sources indicate that the Black Death caused buboes to appear on necks, armpits, and groins. This difference, he argues, ties in with the fact that fleas caused the modern plague and not the Black Death. Since flea bites do not usually reach beyond a person's ankles, in the modern period the groin was the nearest lymph node that could be infected. As the neck and the armpit were often infected during the medieval plague, it appears less likely that these infections were caused by fleas on rats.[54]
In 1984, Graham Twigg published The Black Death: A Biological Reappraisal, where he argued that the climate and ecology of Europe and particularly England made it nearly impossible for rats and fleas to have transmitted bubonic plague. Combining information on the biology of Rattus rattus, Rattus norvegicus, and the common fleas Xenopsylla cheopis and Pulex irritans with modern studies of plague epidemiology, particularly in India, where the R. rattus is a native species and conditions are nearly ideal for plague to be spread, Twigg concludes that it would have been nearly impossible for Yersinia pestis to have been the causative agent of the plague, let alone its explosive spread across Europe. Twigg also shows that the common theory of entirely pneumonic spread does not hold up. He proposes, based on a re-examination of the evidence and symptoms, that the Black Death may actually have been an epidemic of pulmonary anthrax caused by Bacillus anthracis.
Not bubonic plague?
Recent scientific and historical investigations have led some researchers to doubt the long-held belief that the Black Death was an epidemic of bubonic plague. For example, in 2000, Gunnar Karlsson pointed out that the Black Death killed between half and two-thirds of the population of Iceland, although there were no rats in Iceland at this time. Rats were accidentally introduced in the nineteenth century, and have never spread beyond a small number of urban areas attached to seaports. In the fourteenth century there were no urban settlements in Iceland. Iceland was unaffected by the later plagues which are known to have been spread by rats. However, without a rodent reservoir, pneumonic plague can be transmitted from human to human by respiratory transmission, and bubonic and septicemic plague can be transmitted from human to human by human-biting fleas.
In addition, it was previously argued that tooth pulp tissue from a fourteenth-century plague cemetery in Montpellier tested positive for molecules associated with Y. pestis. Similar findings were reported in a 2007 study,[49] but other studies have yielded negative results. In September 2003, a team of researchers from Oxford University tested 121 teeth from sixty-six skeletons found in fourteenth-century mass graves. The remains showed no genetic trace of Y. pestis.
In 2002, Samuel K. Cohn published the controversial article, The Black Death: End of the Paradigm.[50] In the article Cohn argues that the medieval and modern plagues were two distinct diseases differing in their symptoms, signs and epidemiologies.[51] Cohn asserts that the agent causing the bubonic plague, Yersinia pestis, was first cultured at Hong Kong in 1894. In turn, the medieval plague that struck Europe, according to Cohn, was not the bubonic plague carried by fleas on rats as traditionally viewed by scientists and historians alike.[18]
Cohns argument that medieval plague was not rat-based is supported by his claims that the modern and medieval plagues hit in different seasons, had unparalleled cycles of recurrence, and varied in the manner in which immunity was acquired. The modern plague reaches its peak in seasons with high humidity and a temperature of between 50 °F (10 °C) and 78 °F (26 °C), as rats fleas thrive in this climate.[52] In comparison, the Black Death is recorded as hitting in periods where rats fleas could not survive, i.e. hot Mediterranean summers above 78 °F (26 °C).[18] In terms of recurrence, the Black Death on average did not resurface in an area for between five and fifteen years after it hit.[53] Contrastingly, modern plagues often hit an affected area yearly for an average of eight to forty years. Last, Cohn presents evidence displaying that individuals gained immunity to the Black Death during the fourteenth century, unlike the modern plague. He states that in 1348 two-thirds of those suffering from plague died in comparison to one-twentieth by 1382.[18] Statistics contrastingly display that immunity to the modern plague has not been acquired.
Cohn also points out that in the latter part of the nineteenth century buboes appeared mostly on an infected person's groin, while medieval primary sources indicate that the Black Death caused buboes to appear on necks, armpits, and groins. This difference, he argues, ties in with the fact that fleas caused the modern plague and not the Black Death. Since flea bites do not usually reach beyond a person's ankles, in the modern period the groin was the nearest lymph node that could be infected. As the neck and the armpit were often infected during the medieval plague, it appears less likely that these infections were caused by fleas on rats.[54]
In 1984, Graham Twigg published The Black Death: A Biological Reappraisal, where he argued that the climate and ecology of Europe and particularly England made it nearly impossible for rats and fleas to have transmitted bubonic plague. Combining information on the biology of Rattus rattus, Rattus norvegicus, and the common fleas Xenopsylla cheopis and Pulex irritans with modern studies of plague epidemiology, particularly in India, where the R. rattus is a native species and conditions are nearly ideal for plague to be spread, Twigg concludes that it would have been nearly impossible for Yersinia pestis to have been the causative agent of the plague, let alone its explosive spread across Europe. Twigg also shows that the common theory of entirely pneumonic spread does not hold up. He proposes, based on a re-examination of the evidence and symptoms, that the Black Death may actually have been an epidemic of pulmonary anthrax caused by Bacillus anthracis.
