In response to “Black as Death” (Vol. 4, No. 1).

To the editors:

Monica Green has written a major review of a very important book. Green and Bruce Campbell are world authorities on the Black Death and the bubonic plague, and when they put pen to paper, we who are interested pay very close attention. Campbell’s The Great Transition is a foundational interpretation of the economy, climate, and impact of the Black Death. His command of the scholarship, long established in medieval economic and demographic history and now definitively demonstrated in his relatively recent turn to the history of climate, has produced a volume that will stand the test of time. The Great Transition has dramatically narrowed the boundaries of debate, perhaps in some cases to a point of no return.

Apparently Green agrees, because she spends relatively little time in her review discussing—or taking issue with—the great body of Campbell’s book. In particular, his account of the medieval preconditions to crisis, and the impact of the transitional shift in European climate unfolding from the 1260s: cold, wet summers that infected livestock with rinderpest, ruined crops, and set off the Great Famine, leading into the impact of the plague itself. War and religion play a not insignificant role in Campbell’s story. On this point, Green is convinced by his analysis, and she moves to the question that is hotly debated: the Inner Eurasian origins of the Black Death. This is an old debate given new urgency by new evidence and by a certain nervous anxiety about coming pandemics in the time of the Anthropocene. Here the blinding pace of new research in climate science and genomics have, as Green politely suggests, already dated some elements of Campbell’s analysis.

Campbell’s account of the Inner Asia origins of the Black Death rests upon two pillars in recent genetic and climatic science, the work of teams led by Yujun Cui and Fa-Hu Chen. In 2013, Cui et al. published a definitive map of the variants of Yersinia pestis demonstrating that the plague had ancient origins in the Qinghai Plateau and just after the beginning of the Black Death exploded into a starburst polytomy of three branches, suggesting what Green called a fulminating epidemic.1 The density of Y. pestis on Inner Asian landscapes is fundamentally shaped by their marmot hosts’ access to water. For this reason, evidence for changes in humidity has been all important. Since 2008, Chen has been developing the argument that the climate of arid Central Asia varied in tandem with the North Atlantic Oscillation (NAO) and the South Asia monsoon. Positive NAO—as was the case in the Medieval Optimum—pushed the westerlies into North Asia; Central Asia was left parched, while South Asia experienced strong monsoons. From the 1260s and the opening stages of the Little Ice Age, this pattern was reversed. Central Asia became wetter: water and grass was available for plague-bearing marmots and the horses of a vast Mongol cavalry.2

Paying close attention to swings between drought and pluvial, Campbell follows Cui and Chen to describe plague emerging somewhere near the Qinghai Plateau in the 1260s and spreading west along the Silk Road.3 Here he is in conflict with historian Robert Hymes who, as Green points out, argued in 2013 for the twenty-one-year Mongol campaign against the Xia state in the Gansu Corridor, beginning in 1205, as the critical point of origin. The Mongols spread the plague further with the subsequent campaigns against the Jurchen Jin and Song domains in the 1230s and the 1270s.4 The problem here, unfortunately, for both Campbell and Hymes, is new evidence published in 2017, as well as the locations of many of the samples presented in the 2013 paper by Cui et al. The critical plague samples from the Qinghai region are all from ancient, pre-Bronze Age lineages, but there are many more Tien Shan samples, and most of them are from younger lineages dated just before the proposed Black Death genetic starburst. Indeed, the Tien Shan, as Green mentions quickly, is the location of by far the greatest number of pre-Black Death lineages sampled from modern populations, either marmot hosts or human victims, making it, for now, the leading suspect as the point of origin for the Black Death.5

Combining these numbers, the plague identification of a Hun burial in the Tien Shan around 180 CE, and the long-established Nestorian Christian epidemic at Issuk Kul in 1338–1339 would seem to clinch the case. But a new body of work on paleo-sediments along the Tien Shan may be constraining Chen’s Little Ice Age moistening of arid Central Asia. Work published in the past few years suggests that the climatic patterns were complicated along the Tien Shan range, and south across the Taklimakan desert and Dzungaria to the east. Specifically, they point to a sharp climate boundary running along the Tien Shan peaks, and that the high alpine meadows and scree slopes—prime marmot habitat—of the north side of the range running down to Issyk Kul may have been getting drier as the Little Ice Age began. The Taklimakan and points east, on the other hand, seem to have been getting wetter.6 If this argument is accepted, a Tien Shan origin for the Black Death suddenly becomes considerably more complicated. Clearly nothing is settled, but the frame of the argument is becoming tighter and more focused.

Finally, and very briefly, I cannot end without reference to times and tribulations well before the bounds of Campbell’s Great Transition. It is now well established that the Justinian Plague of 542 to the 800s CE was indeed the bubonic plague. New work in Y. pestis genetics has not only dated the biological origins at roughly 4000 BCE, but it has also identified Y. pestis in the teeth and bones of skeletons dating from 2800 BCE forward.7 The Black Death was at least the Third Pandemic—making the Modern Pandemic of 1898 the Fourth—following the Plague of Justinian and these new Bronze Age plague appearances. In particular, it has been suggested that the early plague, carried by the Early Bronze Age Yamnaya peoples (3300–2600 BCE) of the steppe, may have been the cause of population collapse in Neolithic Europe.8 Given the identification of plague burials among the more mobile Late Bronze Sintashta and Andronovo cultures (2000–1400 BCE) of the Urals and the Altai,9 it is not out of the question that the plague may be implicated in the decline of Oxus oasis towns along the ancient trade routes though Turkmenistan and Afghanistan, and the disappearance of the Harappan city-states of the Indus valley. Green asks us to think big, and these are some of the directions that thinking big about the plague might lead us.

John Brooke

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?

A paleogenetics study of plague by Maria Spyrou et al. published in June returned to the Bronze Age, more than 3,000 years before the Black Death.10 It is significant for issues raised by John Brooke for two reasons. First, it demonstrated, from aDNA dating to about 3800 BP, that strains ancestral to Yersinia pestis as we know it today already existed, capable of transmission by flea and thus capable of causing bubonic plague. Thus, if there was a Bronze Age pandemic that merits the term, as Brooke suggests, then it was likely caused by this organism, rather than the previously identified Bronze Age plague, which did not have flea-capable properties, and which, though widely dispersed, has not, to date, been tied to any mass mortality events. Such events may yet be found in the archaeological record, of course, and in positing a recalibration of how we enumerate major disease events, Brooke puts his finger on the increasingly important issue of common nomenclature in fields where genetics is changing the known landscape.11

Second, the study by Spyrou et al. potentially pushes back the chronology of both the late medieval polytomy (the “Big Bang”) and the genesis of the strain involved in the Black Death that devastated western Eurasia. If, as they suggest,12 the emergence of the Black Death strain may have occurred in the late twelfth century, which would push the polytomy even earlier, then we will need to go back to the drawing board once again in looking for the climate events that precipitated or facilitated this sudden dispersal of Yersinia pestis.

For the biological component of explaining the Great Transition, therefore, the challenges of dating evolutionary events remains a pressing concern. The larger phenomena of what for the moment I will still call the Second Plague Pandemic remain to be defined and fixed in time (origin), space (locus), and transmission mechanisms. Until those parameters are more accurately determined, we cannot claim climatic determinants. If the major east-to-west transmission of the newly created Branch 1 lineage of Y. pestis from the Tian Shan Mountains to the Volga River Basin or the Caucasus Mountains occurred, as now seems possible, in the thirteenth century, this would render the Issyk Kul outbreak in Kyrgyzstan in the 1330s irrelevant to the larger Black Death narrative. “The frame of the argument,” as Brooke says, may be “becoming tighter and more focused” with regard to the climate of Arid Central Asia, but as long as the chronology of Y. pestis’s development is still unclear, the climate data affords us little insight. Nevertheless, something extraordinarily consequential did happen in the following century, in the 1340s in western Eurasia, and I am persuaded that Campbell is right to look at climate as a factor that pushed a precarious situation over its tipping point. Whether the weather patterns of Central Asia played a role too is a point yet to be proven.

How we reconcile the western narrative of plague (from the Caspian Sea to the Atlantic) with the still hypothetical eastern narrative (from the Tian Shan Mountains to the Pacific) remains to be seen.13 Since writing my initial draft of the Campbell review last fall, I have had the good fortune to discuss the evidence for fourteenth-century epidemics in China with Timothy Brook, a historian in Qing era China. From my reading of the currently available phylogenetic evidence, it is possible that the early thirteenth-century epidemics examined by Hymes may have been the product of the “Big Bang” and that China’s reported epidemics of the fourteenth century were also plague. As Hymes noted in 2014, the recovery of aDNA from medieval China would be transformative, and that remains a major desideratum for the field.

John Brooke is Professor of History and Anthropology and Director of the Center for Historical Research at Ohio State.

Monica Green is an American historian and Professor of History at Arizona State University.

  1. Yujun Cui et al., “Historical Variations in Mutation Rate in an Epidemic Pathogen, Yersinia Pestis,” Proceedings of the National Academy of Sciences of the United States of America 110 (2013): 577–82. 
  2. Fa-Hu Chen et al., “Moisture Changes over the Last Millennium in Arid Central Asia: A Review, Synthesis and Comparison with Monsoon Region,” Quaternary Science Reviews 29 (2010): 1,055–68; Neil Pederson et al., “Pluvials, Droughts, the Mongol Empire, and Modern Mongolia,” Proceedings of the National Academy of Sciences of the United States of America 111 (2014): 4,375–79. 
  3. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 246–52 
  4. Robert Hymes “Epilogue: A Hypothesis on the East Asian Beginning of the Yersinia pestis Polytomy,” The Medieval Globe 1 (2014): 285–308. 
  5. The Qinghai and Tien Shan have each produced ten ancient 0.PE samples, but the Tien Shan region has produced 66 0.ANT samples, the variant that immediately preceded the Black Death samples as typed from Black Death plague burials in Europe. It is possible that a wider sampling campaign will change this picture. See data from tables and supplementary information in Yujun Cui et al., “Historical Variations in Mutation Rate in an Epidemic Pathogen, Yersinia Pestis,” Proceedings of the National Academy of Sciences of the United States of America 110 (2013); Galina Eroshenko et al., “Yersinia pestis Strains of Ancient Phylogenetic Branch 0.ANT Are Widely Spread in the High-mountain Plague Foci of Kyrgyzstan,” PLOS ONE 12 (2017): e0187230. See also Yanjun Li et al., “Genotyping and Phylogenetic Analysis of Yersinia pestis by MLVA: Insights into the Worldwide Expansion of Central Asia Plague Foci,” PLOS ONE 4 (2009): e6000; Julia Riehm et al., “Yersinia pestis Lineages in Mongolia,” PLOS ONE 7 (2012): e30624; L. Kukleva, et al., “Analysis of Diversity and Identification of the Genovariants of Plague Agent Strains from Mongolian Foci,” Russian Journal of Genetics  51, no. 3 (2015): 238–44. 
  6. See especially Jens Fohlmeister et al., “Winter Precipitation Changes During the Medieval Climate Anomaly and the Little Ice Age in Arid Central Asia,” Quaternary Science Reviews 178 (2017): 24–36; and Linda Taft et al., “Sclerochronological Oxygen and Carbon Isotope Ratios in Radix (Gastropoda) Shells Indicate Changes of Glacial Meltwater Flux and Temperature since 4,200 cal yr BP at Lake Karakul, Eastern Pamirs (Tajikistan),” Journal of Paleolimnology 52 (2014): 27–41; Christian Wolff et al., “Precipitation Evolution of Central Asia during the Last 5000 Years,” Holocene 27 (2017): 142–54; Anja Schwarz et al., “Mid- to Late Holocene Climate-driven Regime Shifts Inferred from Diatom, Ostracod and Stable Isotope Records from Lake Son Kol (Central Tian Shan, Kyrgyzstan),” Quaternary Science Reviews 177 (2017): 340–56; Xiangtong Huang et al., “Dust Deposition in the Aral Sea: Implications for Changes in Atmospheric Circulation in Central Asia during the Past 2000 Years,” Quaternary Science Reviews 30 (2011): 3,661–74; Hedi Oberhänsli et al., “Variability in Precipitation, Temperature and River Runoff in W Central Asia during the Past ~2000 Yrs," Global and Planetary Change 76 (2011): 95–104; Wei Wang and Zhaodong Feng, “Holocene Moisture Evolution across the Mongolian Plateau and Its Surrounding Areas: A Synthesis of Climatic Records,” Earth-Science Reviews 122 (2013): 38–57. 
  7. Simon Rasmussen et al., “Early Divergent Strains of Yersinia pestis in Eurasia 5,000 Years Ago,” Cell 163 (2015): 571–82; Aida Andrades Valtueña, “The Stone Age Plague and Its Persistence in Eurasia,” Current Biology 27 (2017): 3,683–91. 
  8. Kristian Kristiansen et al., “Re-theorising Mobility and the Formation of Culture and Language among the Corded Ware Culture in Europe,” Antiquity 91 (2017): 334–47, 335; Volker Heyd, “Kossina’s Smile,” Antiquity 91 (2017): 348–59, at 249; Martin Furholt, “Massive Migrations? The Impact of Recent aDNA Studies on Our View of Third Millennium Europe,” European Journal of Archaeology 21 (2018): 159–91, 168. 
  9. Simon Rasmussen et al., “Early Divergent Strains of Yersinia pestis in Eurasia 5,000 Years Ago,” Cell 163 (2015): 572–73.   
  10. Maria Spyrou et al., “Analysis of 3,800-year-old Yersinia pestis Genomes Suggests Bronze Age Origin for Bubonic Plague,” Nature Communications 9 (2018): 2,234, doi:10.1038/s41467-018-04550-9. 
  11. Stefanie Eisenmann et al., “Reconciling Material Cultures in Archaeology with Genetic Data: The Nomenclature of Clusters Emerging from Archaeogenomic Analysis,” Scientific Reports 8 (2018): 13003, doi:10.1038/s41598-018-31123-z. 
  12. See Supplemental Table 9 in Maria Spyrou et al., “Analysis of 3,800-year-old Yersinia pestis Genomes Suggests Bronze Age Origin for Bubonic Plague,” Nature Communications 9 (2018): 2,234, doi:10.1038/s41467-018-04550-9. 
  13. See Robert Hymes, “A Hypothesis on the East Asian Beginnings of the Yersinia pestis Polytomy,” The Medieval Globe 1 (2014): 285–308.