Theories of the Black Death are a variety of explanations that have been advanced to explain the nature and transmission of the Black Death (1347–51). A number of epidemiologists from the 1980s to the 2000s challenged the traditional view that the Black Death was caused by plague based on the type and spread of the disease. The confirmation in 2010 and 2011 that Yersinia pestis DNA was associated with a large number of plague sites has led researchers to conclude that "Finally, plague is plague."
Plague
Several possible causes have been advanced for the Black Death; the most prevalent is the bubonic plague theory. Efficient transmission of Yersinia pestis is generally thought to occur only through the bites of fleas whose mid guts become obstructed by replicating Y. pestis several days after feeding on an infected host. This blockage results in starvation and aggressive feeding behaviour by fleas that repeatedly attempt to clear their blockage by regurgitation, resulting in thousands of plague bacteria being flushed into the feeding site, infecting the host. However, modelling of epizootic plague observed in prairie dogs, suggests that occasional reservoirs of infection such as an infectious carcass, rather than "blocked fleas" are a better explanation for the observed epizootic behaviour of the disease in nature.
One hypothesis about the epidemiology—the appearance, spread, and especially disappearance—of plague from Europe is that the flea-bearing rodent reservoir of disease was eventually succeeded by another species. The black rat (Rattus rattus) was originally introduced from Asia to Europe by trade, but was subsequently displaced and succeeded throughout Europe by the bigger brown rat (Rattus norvegicus). The brown rat was not as prone to transmit the germ-bearing fleas to humans in large die-offs due to a different rat ecology. The dynamic complexities of rat ecology, herd immunity in that reservoir, interaction with human ecology, secondary transmission routes between humans with or without fleas, human herd immunity, and changes in each might explain the eruption, dissemination, and re-eruptions of plague that continued for centuries until its unexplained disappearance.
Signs and symptoms of the three forms of plague
The plague comes in three forms and it brought an array of signs and symptoms to those infected. The classic sign of bubonic plague was the appearance of buboes in the groin, the neck, and armpits, which oozed pus and bled. Most victims died within four to seven days after infection. The septicaemic plague is a form of "blood poisoning", and pneumonic plague is an airborne plague that attacks the lungs before the rest of the body.
The bubonic plague was the most commonly seen form during the Black Death. The bubonic form of the plague has a mortality rate of thirty to seventy-five percent and symptoms include fever of 38–41 °C (101–105 °F), headaches, painful aching joints, nausea and vomiting, and a general feeling of malaise. The second most common form is the pneumonic plague and has symptoms that include fever, cough, and blood-tinged sputum. As the disease progressed, sputum became free flowing and bright red and death occurred within 2 days. The pneumonic form of the plague has a high mortality rate at ninety to ninety-five percent. Septicemic plague is the least common of the three forms, with a mortality rate close to one hundred percent. Symptoms include high fevers and purple skin patches (purpura due to DIC). Both pneumonic and septicemic plague can be caused by flea bites when the lymph nodes are overwhelmed. In this case they are referred to as secondary forms of the disease.
David Herlihy identifies from the records another potential sign of the plague: freckle-like spots and rashes. Sources from Viterbo, Italy refer to "the signs which are vulgarly called lenticulae", a word which bears resemblance to the Italian word for freckles, lentiggini. These are not the swellings of buboes, but rather "darkish points or pustules which covered large areas of the body".
The uncharacteristically rapid spread of the plague could be due to respiratory droplet transmission, and low levels of immunity in the European population at that period. Historical examples of pandemics of other diseases in populations without previous exposure, such as smallpox and tuberculosis transmitted by aerosol amongst Native Americans, show that the first instance of an epidemic spreads faster and is far more virulent than later instances among the descendants of survivors, for whom natural selection has produced characteristics that are protective against the disease.