The Black Death ravaged Europe between 1347 and 1353, killing millions. Plague outbreaks in Europe then continued into the 19th century.
One of the most recited facts about the plague in Europe was that it was spread by rats. In some parts of the world, the bacterium that causes plague, Yersinia pestis, maintains a long-term presence in wild rodents and their fleas. This is called an animal reservoir.
While plague begins in rodents, it sometimes spreads to humans. Europe may once have hosted animal reservoirs that triggered plague pandemics. But plague could also have been repeatedly reintroduced from Asia. Which of these scenarios was present remains a topic of scientific controversy.
Our recent research, published in Proceedings of the National Academy of Sciences (PNAS), have shown that environmental conditions in Europe would have prevented the plague from surviving in persistent, long-term animal reservoirs. How did the plague persist in Europe for so long?
Our study offers two possibilities. One, the plague was reintroduced from Asian reservoirs. Second, there could have been short- or medium-term temporary reservoirs in Europe. In addition, the two scenarios may have been mutually supportive.
However, the rapid spread of the Black Death and subsequent outbreaks in the following centuries also suggest that slow-moving rats may not have played the critical role in the transmission of the disease that is often portrayed.
To find out whether plague could survive in long-term animal reservoirs in Europe, we examined factors such as soil properties, climatic conditions, terrain types and rodent varieties. These all seem to affect whether the plague can stay in the reservoirs.
For example, high concentrations of some elements in soil, including copper, iron, and magnesium, as well as a high soil pH (whether acidic or alkaline), cooler temperatures, higher elevations, and lower rainfall appear to favor the development of persistent reservoirs , although it’s not entirely clear why at this stage.
Based on our comparative analysis, it was even less likely that hundreds of reservoirs of wild rodent plague had existed from the Black Death in 1348 to the early 19th century than today, as extensive research rules out such reservoirs in Europe.
This is in stark contrast to regions across China and the western United States, where all of the above conditions persist Yersinia pestis reservoirs in wild rodents exist.
In Central Asia, long-term and persistent rodent reservoirs may have existed for millennia. As ancient DNA and textual evidence suggests, it appears that once the plague crossed into Europe from Central Asia, it seeded a short- or medium-term reservoir or reservoirs in European wild rodents. The most likely place for this to have been was in Central Europe.
Since local soils and climatic conditions did not favor long-term and persistent reservoirs, the disease had to be re-imported, at least in some cases. It is important that the two scenarios are not mutually exclusive.
To go deeper into the role of rats in the spread of 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 later eighth century. The second pandemic (which included the Black Death) began in the 1330s and lasted for five centuries. A third pandemic began in 1894 and remains with us today in places like Madagascar and California.
These pandemics overwhelmingly involved the bubonic form of plague, in which the bacteria infect the human lymphatic system (which is part of the body’s immune system). In pneumonic plague, the bacteria infect the lungs.
The plagues during the second pandemic differed radically in character and transmission from more recent outbreaks. First, there were strikingly different levels of mortality, with some other pandemic outbreaks reaching 50 percent, while for the third pandemic they rarely exceeded 1 percent. In Europe, the figures for the third pandemic were even lower.
Second, there were different rates and patterns of transmission between these two plague eras. There were huge differences in the frequency and speed of transport of goods, animals and people between the late Middle Ages and today (or the late 19th century). Yet the Black Death and many of its subsequent waves spread with astonishing speed. Over land, it ran almost as fast every day as the modern eruptions do over a year.
As described by contemporary chroniclers, physicians and others – and as reconstructed quantitatively from archival documents – the plagues of the Second Pandemic spread faster and more widely than any other disease during the Middle Ages. They were actually faster than in any period until the cholera outbreaks of 1830 or the great influenza of 1918 to 1920.
Regardless of how the various European waves of the second pandemic began, both wild and non-wild rodents—primarily rats—moved much more slowly than the rate of transmission around the continent.
Thirdly, the plague’s seasonal variations also show large deviations. The plagues of the third pandemic (apart from the rare ones, mainly of pneumonic plague) have closely followed the fecundity cycles of rat fleas. These rise with relatively moist conditions (although less rainfall is important for the plague reservoirs to first establish) and within a temperature band between 10 and 25 degrees Celsius.
In contrast, plagues from the second pandemic could cross the winter months in bubonic form, as seen over the Baltic regions from 1709 to 1713. But in the Mediterranean climate from 1348 to the 15th century the plague was a summer contagion that peaked in June or July — in the hottest and driest the months.
This differs strikingly from the plague seasons in these regions in the 20th century. Because of the low relative humidity and high temperatures, these months were the least likely times for plague to break out among rats or humans.
These differences raise a crucial question as to whether the bubonic form of the plague relied on slow-moving rodents for its transmission when it could instead spread much more efficiently directly, from person to person. Researchers have speculated that this may have occurred due to ectoparasites (fleas and possibly lice) or through human airways and through touch.
Questions such as the exact roles played by humans and rats in past plague pandemics need further work to resolve. But as shown by this study, and others, great strides forward can be made when researchers and historians work together.
This article was originally published on The conversation of Samuel Cohn on University of Glasgow and Philip Slavin on University of Stirling. Read the original article here.