To the editors:
Monica Green’s essay is an extremely interesting and important review of a great study, Bruce Campbell’s The Great Transition: Climate, Disease and Society in the Late-Medieval World. In his book, Campbell explains why the Black Death of the fourteenth century happened when it did, a pandemic he once described as the “single most important environmental event of the last 1,000 years.” He sees a clear link between an increasingly humid climate, the insect and animal population, and outbreaks of Yersinia pestis. Campbell tells a fascinating story that spans approximately eighty years, during which the plague spread from western China to Europe’s Atlantic seaboard.
Unlike many medievalists, who are often dismissive of climatic questions, Campbell sees climate change as crucial to the reemergence of the plague. The ecosystem, viewed by Campbell as an abstract socioecological complex, is influenced, but not determined by climate. The returning plague, according to Campbell, was a game-changer. In the mid-fourteenth century, European society had already been weakened by events such as the Great Famines (1312–1322), the Great Cattle Panzootic (1316–1321), and the Tuscan Famines (1328–1330). The Black Death saw the population and economic output plummet, killing both producers and consumers.
In his book, Campbell does not settle upon a straightforward relationship between climate and society, simply overlaying different data and different methods. Instead, he identifies a number of factors that help to explain the influence of climate change on the plague: the supply of food to sylvatic rodent hosts and the density of the local population; the host-dependent vector population growth rates; the effects of temperature and humidity on the bacterium itself; and the effects of temperature and humidity on flea activity. Groundbreaking studies by archeologists and biologists are also included in Campbell’s study. Inspired by the work of the Dutch ecologist Marten Scheffer, The Great Transition explains the downturn in global growth between 1341 and 1354 in terms of mounting ecological and economic stresses, culminating in commercial and financial recession while the Black Death spread across all the commercialized trading areas in Europe.
It is the aspects of this scenario for which there are still no reasonable explanations that are the focus of Green’s essay. Of particular concern are the current estimates for the amount of time required for the bacterium to spread over such great distances. According to Campbell, the bacterium began spreading westwards along the caravan routes from semi-arid China to Issyk Kul, a lake in modern-day eastern Kyrgyzstan, at a rate of less than a kilometer each week. The plague’s progress thereafter increased rapidly, covering one and a half kilometers per day. How did the plague spread across the landscape? And is the route described by Campbell the right one? Did the plague spread in a unidirectional manner, as Campbell suggests, or are a series of radiating epizootics, as described by Green, a more plausible explanation? “The problem,” Green writes, “is that this fulminating epizootic happened either too far back in time, or too far away from the Black Sea.” Campbell’s argument draws upon climatic influences and economic history. Green, on the other hand, seeks to reconcile the genetic narrative with that of a global disease.
The history of Y. pestis, according to the most recent research, begins in the late Stone Age and is marked by genetic turnover at times of great migration. The very first outbreak, the Neolithic Plague in Asia and Europe, was, it seems, due to an extinct evolutionary branch. The second outbreak was the famous Justinianic Plague. The third historical pandemic that can be attributed to Y. pestis was the late medieval Black Death. Campbell’s study of the third outbreak is based on data gleaned from France, Italy, southern Germany, the Netherlands, and England. Recent studies have also identified 18 deaths from the plague in Barcelona (fourteenth century), 93 deaths in Bolgar, a city in modern-day Tatarstan (late fourteenth century), and 67 deaths in Ellwangen in southern Germany (sixteenth century). The outbreaks in Barcelona, London, and Bolgar all belong to the same branch, which leads to the nineteenth century pandemic in China. The outbreak in Ellwangen, on the other hand, belongs to a different branch that was European rather than global, and that leads to the 1720–22 outbreak in Marseille.
According to the paleoscientists who reconstructed the Y. pestis genome, it remains unclear whether its origins are to be found in China. It may have come instead from somewhere in the central Eurasian steppe. Nonetheless, the historical impact and high mobility of Y. pestis is now well established. “We are only now learning,” Green writes, “how to read genetic lineages as rough maps that show us both the geography and the chronology of evolving diseases.” The spread of the disease between China and Europe is still not fully explained. More data is needed. The same is true for its branches and their routes through history. The Black Death shaped the history of humanity throughout the centuries that followed. It is not a story that begins and ends in the middle of the fourteenth century.
The bacterium responsible for the Black Death builds a biofilm that blocks the stomach of an infected flea. The starving flea then attempts to feed repeatedly in a short period of time. Yet fleas cannot be the main transmitter of the disease. Y. pestis is, in fact, a rodent-borne pathogen. For this reason, understanding the impact of the disease on the rodent population is crucial. Were there, for example, biological changes to the pathogen that led to the outbreaks of the Black Death? As it stands, the research suggests this is implausible. Despite it being a rodent-borne pathogen, a biological explanation is also needed for the high mobility of Y. pestis.
The emerging molecular evidence can only serve to enrich our reading of the historical sources. In his book, Campbell draws upon an extraordinary range of climatic and economic data. Yet he devotes little time to examining the written sources. Our increasing knowledge of the biology of the disease can help historians to ask new questions from these old sources. In a methodological sense, Monica Green is correct when she writes that “[w]e need to think big.” But we also need to look again at the written sources in the light of our enhanced biological understanding.
Christof Paulus
Monica Green replies:
I am pleased that my review of Professor Campbell’s important monograph, The Great Transition, has prompted such thoughtful responses. It is a sign of the speed of research that already since June, when my review appeared, new genetics evidence has appeared that further complicates the central question I raised: can climate be invoked as a causal factor in disease history if we are unsure of the timing or even the locus of the biological events we wish to explain?
