ive here. Here we have what is taken as an established fact, that rats were the biggest culprits in the spread of the Black Death, which is likely to be false. Among other reasons, it spread too quickly…. Which suggests that human- and human-borne insects such as fleas are likely the prime suspects.
Written by Samuel Cohn, Professor of History, University of Glasgow, and Philip Slavin, Associate Professor of History, University of Stirling. Originally published in The Conversation
The Black Death swept across Europe between 1347 and 1353, killing millions. Then the outbreak of plague continued in Europe until the nineteenth century.
One of the most popular facts about the plague in Europe is that it was spread by rats. In some parts of the world, the bacteria that cause plague, Yersinia pestis-Maintains a long-term presence in wild rodents and fleas. This is called an animal “reservoir”.
While the plague begins in rodents, it is sometimes transmitted to humans. Europe may once have hosted animal reservoirs that caused epidemics of the plague. But the plague could also have spread again and again from Asia. Which of these scenarios was present remains a matter of scholarly debate.
Our recent research, published in the Proceedings of the National Academy of Sciences (PNAS), shows that environmental conditions in Europe would have prevented the plague from remaining in continuous, long-term animal reservoirs. How, then, did the plague persist in Europe for so long?
Our study presents two possibilities. First, the plague was being reintroduced from Asian reservoirs. Secondly, there may have been temporary short- or medium-term tanks in Europe. In addition, the two scenarios may be mutually supportive.
However, the rapid spread of the Black Death and subsequent outbreaks in the next few centuries also suggests that slow-moving rats may not have played the critical role in transmitting the disease they are often portrayed.
To find out whether plague could survive in long-term animal tanks in Europe, we examined factors such as soil properties, climatic conditions, terrain types, and rodent species. All of these factors seem to affect the ability of plague to survive in reservoirs.
For example, higher concentrations of certain elements in the soil, including copper, iron, and magnesium, as well as higher soil pH (whether acidic or alkaline), cooler temperatures, higher elevations, and lower precipitation appear to develop Fixed cabinets, though it’s not entirely clear why, at this point.
Based on our comparative analysis, centuries-old plague reservoirs of wild rodents were less likely to have existed from the Black Death of 1348 to the early 19th century than they are today, when exhaustive research ruled out any such reservoirs within Europe.
This contrasts sharply with regions throughout China and the western United States, where all of the above conditions persist Yersinia pestisReservoirs are found in wild rodents.
In Central Asia, long-term, continuous rodent tanks may have existed for thousands of years. As ancient DNA and textual evidence hints, once plague crossed into Europe from Central Asia, it appears to have implanted short- or medium-term seedings or reservoirs in European wild rodents. The most likely place for this was in Central Europe.
However, as local soil and climatic conditions do not favor long-term, continuous reservoirs, the disease has had to be re-imported, at least in some cases. Importantly, the two scenarios are not mutually exclusive.
To delve deeper into the role of rats in spreading the plague in Europe, we can compare different outbreaks of the disease.
The first plague pandemic began in the early sixth century and lasted until the late eighth century. The second pandemic (which included the Black Death) began in the 1330s and lasted five centuries. A third pandemic began in 1894 and is still with us today in places like Madagascar and California.
These pandemics largely included the bubonic form of the plague, in which the bacteria infect the human lymphatic system (which is part of the body’s immune defences). In pneumonic plague, the bacteria infect the lungs.
Epidemics of the second pandemic differed radically in their nature and transmission from modern epidemics. First, there were strikingly different levels of mortality, with some second epidemic outbreaks reaching 50%, while third epidemic outbreaks rarely exceeding 1%. In Europe, the numbers for the third pandemic were even lower.
Second, there were different rates and patterns of transmission between these two eras of plague. There were huge differences in the pace and speed of moving goods, animals, and people between the late Middle Ages and today (or the late nineteenth century). However, the Black Death and many of its subsequent waves spread with astonishing speed. On the ground, it raced nearly as fast every day as a modern outbreak over the course of a year.
As described by modern historians, physicians, and others—and as quantitatively reconstructed from archival documents—pandemics of the second pandemic spread faster and more widely than any other disease during the Middle Ages, even faster than any period until the cholera outbreaks of 1830 or the great influenza of 1918-2020.
No matter how the various European waves of the second pandemic begin, wild and non-wild rodents — rats, first of all — move much more slowly than they move around the continent.
Third, the seasonality of plague also shows wide variations. Third pandemic epidemics (except in rare cases, mainly pneumonic plague) followed the fertility cycles of rat fleas. These rise in relatively humid conditions (although low precipitation is important for the first establishment of plague reservoirs) and within a temperature range between 10°C and 25°C.
By contrast, second pandemic epidemics can cross the winter months in bubonic form, as was seen across the Baltic regions from 1709-13. But in a Mediterranean climate, from 1348 until the 15th century the plague was a summer infection that peaked in June or July – during the hottest and driest months.
This deviates strikingly from the plague seasons in these regions in the twentieth century. Because of the low relative humidity and high temperatures, these months were the times least likely for plague to spread among rats or humans.
These differences raise the crucial question of whether the bubonic form of plague relied on slow-moving rodents for its transmission, when instead it could spread more efficiently directly, from person to person. Scientists have speculated that this may be caused by external parasites (fleas and possibly lice), or through people’s respiratory systems and through touch.
Questions such as the exact roles humans and rats played in previous plague epidemics need more work to be resolved. But as this study and others have shown, great strides forward can be made when scholars and historians work together.