Centuries after the Black Death devastated Europe, modern science is filling gaps in our knowledge about the pandemic – and trying to find out why it has yet to return to full strength.
The plague of Florence in 1348, as described in Boccaccio's Decameron Wellcome Trust/Wikimedia Commons (CC BY 4.0)
Sampling Eras is a column by Rubee Dano that explores the intersection of science and history. Rubee is a history and philosophy student, with a particular interest in the history of science and academia.
It is surprising that there are still 2,000 cases of the plague every year. As common belief would have it, rats in the Middle Ages boarded trading ships to Europe from Asia and the disease ominously also known as the Black Death subsequently wiped out a third of the population. That’s not necessarily incorrect—but there’s much more to the story of this long-spanning disease. It seems inconceivable that the same disease can be around after seven hundred years, but the plague has evolved since the 14th century. So much so that, until very recently, there was much debate over whether or not the modern plague was even the same disease as the one that ravaged Europe in the Middle Ages.
Scientists and historians debated for a long time over the cause of the Black Death, and whether or not it is the same disease as the modern bubonic plague. In fact, some wondered if the plague was caused by a haemorrhagic fever, similar to Ebola. But in 2011, scientists of the University of Tubingen and the University of Canada examined the remains of plague victims using new molecular techniques and confirmed that the medieval plague was caused by Yersinia pestis, a bacterium that still exists today.
Y. pestis is a member of the Enterobacteriaceae family, which also includes bacteria responsible for other human diseases such as salmonella and shingles, as well as the ubiquitous bacterium E. coli, famously found in the human digestive tract and science labs all over the world. Y. pestis seems to have existed since at least the medieval period, specifically around the 14th century, however recent discoveries have demonstrated that the species was alive long before then.
Colonies of Yersinia pestis, grown on chocolate agar. Yum. US Department of Health and Human Services/Wikimedia Commons (public domain)
The reason there was ever a debate about the link between the ancient and modern plagues is fairly simple: the symptoms of modern disease and the Black Death don’t match. These days, the bubonic plague tends to have flu-like symptoms, including a fever, chills, headache, muscle ache and seizures, and of course swollen lymph glands, known as buboes. Meanwhile, historical accounts describe the Black Death’s symptoms as including the swelling of the lymph glands followed by the emergence of similar swollen lumps all over the body, along with black and purple spots. Bleeding from the nose and other orifices was also common, and taken as a sure sign that death was coming.
Modern cases of the plague are generally treated with strong antibiotics, including streptomycin, gentamycin and chloramphenicol, according to the World Health Organisation, though there is evidence to suggest some antibiotic-resistant strains can emerge. Effective treatment must be paired with a quick diagnosis, and if the patient shows pneumatic symptoms, they must be isolated, as the pneumatic form of the plague can be transmitted via the air from an infected person’s cough. The pneumatic plague refers to the infection of one’s respiratory system with the Y. pestis bacterium, and the bubonic plague is a lymphatic infection, and less severe. The bubonic plague is the most common type, and both bubonic and pneumatic plagues may turn septicaemic if not properly treated: That is, they may result in a Y. pestis infection of the blood. Without treatment, the plague is still incredibly likely to lead to death, though in most cases where treatment is available, the patient will recover.
Allen Cheung of Monash University says of the modern plague that antibiotic resistance is relatively rare. Cheung’s analysis of the possibility of the emergence of an epidemic or pandemic of the modern plague for The Conversation is fairly optimistic—Cheung believes it unlikely that a modern pandemic will emerge, and if it does, treatment is effective. Modern Y. pestis is no more virulent than previous epidemic strains, Cheung says, therefore it is unlikely that new strains of the plague will emerge and become pandemic based solely on virulence factor.
Another wrinkle in the story of the plague is that the Middle Ages outbreak was not the first occurrence of the disease. The first wave of the plague, in the commonly accepted three-wave theory, came in 511 A.D., and was known as the Plague of Justinian. It affected areas in the Mediterranean, specifically parts of the Byzantium Empire such as Constantinople (modern-day Istanbul), and killed large numbers in both Europe and Asia. This weakened the Byzantium and Persian empires considerably, and may have contributed to their eventual fall to the Muslim conquests in later centuries.
Human remains have been instrumental in discovering the microbiological causes of ancient disease. S. Tzortzis/Wikimedia Commons (public domain)
Analysis of Y. pestis DNA from 6th century teeth has confirmed the bacteria was responsible for the Plague of Justinian. The particular strain, however, was considerably different to those associated with medieval plague victims and modern cases. Evolutionary analysis of the strains support the idea that the rodent population acts as a “reservoir” for bacteria, from which new emergences of the plague into human populations can spring. It is also possible that Y. pestis caused earlier plagues, such as those in Athens in the 5th century BC and the Antonine Plague of the 2nd century AD, but as we do not currently have disease samples from this period, this remains a difficult idea to test.
The concept of a rodent-reservoir is that of a persistence of the Y. pestis bacterium within the European rodent population and their associated fleas. The theory states that due to climate change, the bacteria would either dwindle in numbers or increase; colder weather resulted in the death of more of the bacterium’s hosts, while warmer weather allowed them to breed. Until recently, this theory was believed to have accounted for the continuing re-emergence of the plague in Europe. That is, the cause of the plague remained in Europe during periods of little infection, spreading later on in ideal conditions and causing the historic epidemics.
The rodent-reservoir theory has been heavily debated, however it seems a compromise between this theory and a recent theory on climate change better explains the re-emergence of the plague in waves over a long period of history. Earlier this year, a paper suggesting the cause of the plague to be climate change in Asia, rather than in Europe, was published. In the paper, scientists Boris Schmidt and Nils Christian Stenseth of the University of Oslo show a connection between climate-driven outbreaks of the plague in Asia and the re-emergence of the plague in Europe. These findings suggest fault in the reservoir theory that European rat populations acted as a sink for the plague and allowed its re-emergence. Instead, Schmidt and Stenseth’s findings link the European plague to Asian rodent reservoirs, stating that Asian rodent reservoirs were the original source of all European plagues, and that the plague was simply imported to Europe in each occurrence, rather than the bacterium remaining dormant in European rodent populations as the previous theory suggested.
Are rodents really to blame for the bubonic plague? Wellcome Trust/Wikimedia Commons (CC BY 4.0)
Schmidt and Stenseth also note, in an article for The Conversation, that while there are many narratives about the spread of the plague, it is not necessarily true that black and brown rats were the cause of the medieval plague, as some scientists and historians believe. Though the re-emergence of the plague in London centuries later seemed to stem from these rats, “there is poor archaeological evidence there were many rats across much of northern Europe in the Middle Ages aside from small populations of black rats in harbour towns, and no historic records that rats played a role in the disease.” It is possible that rather than black rats, the plague originally spread from gerbils. The most compelling argument against the belief that European black rats were the original source of its spread to Europe is that there are no reports of the large numbers of dead rats that would appear in the instance of a Y. pestis infection within the rat population.
While the precise cause of the spread of various occurrences of the medieval European plague remain debated, marmots and other varieties of Asian squirrels still carry Y. pestis in modern day China, contributing to the reservoir that Schmidt and Stenseth cite as the source of climate-driven plague emergences in Asia.
It seems that while most of us have heard of the Black Death, and might have studied it in history class or even at university, there is still much debate about the plague that generally doesn’t come up in discussion outside the academic community. As Schmidt and Stenseth point out in their dialogue about their study and the common narratives of the plague, there is not only much we don’t know about the disease but much we presume to know. They end their comments by suggesting that we should be asking how exactly the plague was introduced and reintroduced to Europe, and why, it seems, the disease stopped spreading to Europe but remained endemic in Asia, as well as the Middle East and Northern Africa. This not only provides an interesting new line of inquiry, but also could help us understand more about what is still a prevalent disease today.
