This is a continuation of the first part in a series about what caused the Black Death in 12th-17th century Europe, and part of Plague Week here at Retro, which is looking like it might become Plague Fortnight.
The first appearance of the Black Death in Europe was sometime in the 14th century, however major bouts of Plague recurred almost every generation until the 1700s when sanitation improved dramatically. Rare “modern-day” bouts of the plague still occur occasionally in livestock and people, but the invention and standardization of anti-bacterial drugs drastically improved the chance to quell the infection and survive.
In Part One, I mentioned that the main scientific consensus regarding the cause of the Black Death was a particularly nasty (and fast-acting) bacteria called Y. pestis, which is responsible for bubonic plague. However, there exist a few alternative theories that scientists have offered over the years. Specifically, that while the modern-day bouts of plague are indeed Y. pestis, the widespread deaths in the 14th century were not from bubonic plague but from anthrax or an Ebola-like virus..
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Several historians have noted that if what caused the Black Death was truly transmitted by fleas, as Y. pestis is, then areas which had no rats or fleas would not have had great losses due to the plague. However, about two-thirds of Iceland’s population was wiped out during the 14th century, despite it having no rats at the time. And many areas with hot summers above 82 degrees F, which is too hot for fleas to transmit Y. pestis, were hit equally hard by the Black Death. The medieval plague and the modern plague seem to peak in different seasons–the modern plague in temperate weather and the medieval plague in quite hot weather. Symptoms also vary somewhat, as the location of the “buboes” in the medieval plague were in the lymph nodes in the groin, armpits, and neck while the modern plague buboes are mostly limited to the groin. Another issue is the rate and depth of transmission of the disease. Y. pestis has a brief incubation and high rate of fatality to the infected patient, so how did the Black Death spread so rapidly and so far? Most people would be bed-ridden in a few days, and dead in a few more. Perhaps another pathogen is to blame.
These questions led some scientists, Graham Twigg and Norman Cantor in particular, to theorize that the Black Death may have been attributed to anthrax (Bacillus anthracis) or the “cattle anthrax” murrain rather than Y. pestis. Anthrax is also spread by a bacteria and often fatal. In this case, the disease would have been spread by grass-eating livestock like cows or pigs, and people could become infected by eating meat from an anthrax-infected animal. This theory was bolstered somewhat by the discovery of anthrax spores in a plague pit (burial site for plague victims) in Scotland as well as the discovery of recorded symptoms during the Black Death not indicative of Y. pestis. Others claim that the Black Death was actually many separate contagions, with anthrax being one of them.
In addition, Susan Scott and Christopher Duncan believed that the Black Death might have been attributed to a virus as opposed to bacteria, and proposed an Ebola-like virus as the culprit. They claimed that this would have solved the problem as to how the plague spread far and fast, as this virus would have had a much longer incubation period therefore allowing more people to become infected in the meantime. They noted that church records from the 14th century listed sometimes 30 days incubation before death, which may have been too slow for a Y. pestis infection. In addition, they claim that a virus would have been much more efficient in human-to-human transfer and infection than a bacterial infection would have, and better explains the widespread nature and high contagion of the disease. It is interesting to note that Europeans do have an increased immunity to Ebola-like viruses, higher than the rest of the world, and this may be explained by its emergence during the Black Death.
Probably still Pestis
Despite these theories, most epidemiologists and plague historians agree that Y. pestis is still the best explanation of the widespread deaths during the Black Plague of medieval Europe. The remains of some of the victims of the plague have confirmed that Y. pestis was active during that time– dental pulp from a plague cemetery in Montpellier, France confirmed DNA from Y. pestis and were negative for anthrax. As for the “Iceland problem,” it is quite likely that European rats infected with the plague stowed away on ships bound for Iceland. In such closed quarters there was a high probability of infecting a high proportion of the crew (who then transmitted it to people in Iceland). Furthermore, infected rats survived longer than infected humans and may have lived to see Iceland, breed, and infect other mammals. As for the transmission of Y. pestis from human-to-human, this was quite possible as the bacteria became aerosolized in coughed-up water droplets which others breathed in. A ship could be the ideal place for that to occur.
So, in summary, while there are still a few mysteries to work out as to how the plague was definitively transmitted and why/how it incubated and spread, it seems safe to say that Y. pestis was indeed the cause of the Black Death.
Close up of a 14th century talisman against the plague.
 Plague is transmitted while the infected flea is feeding, by regurgitation of the bacillus from the flea’s alimentary tract through the proboscis into the new host. Yersinia pestis is rapidly eliminated from the proventriculus of the oriental rat flea when the mean monthly ambient temperature exceeds 28 degrees C (82 degrees F), and plague epidemics decline with the advent of hot weather (Cavanaugh, 1971).