Genetics / Book Review

Vol. 4, NO. 1 / May 2018

Black as Death

Monica Green

The Great Transition: Climate, Disease and Society in the Late-Medieval World
by Bruce Campbell
Cambridge University Press, 485 pp., $34.99.

Bruce Campbell’s The Great Transition chronicles an important and gloomy historical moment. The two centuries between the 1260s and 1470s witnessed the collapse of international networks of exchange, multiple wars, economic contraction, repeated famines, and demographic decline. The single most profound event was what is still considered the most devastating pandemic of human history: the Black Death of the middle of the fourteenth century. In Europe and around the Mediterranean basin, mortality levels have been estimated at between forty and sixty percent. The 1470s were only a period of stabilization. The new world that the Great Transition ushered in was colder, wetter, and more disease ridden than any humans had ever known before. Historians of the early modern period have recognized the climatic period known as the Little Ice Age (LIA) for some time.1 For the history of medicine, no agreed-upon term has arisen for this regime of intense infectious diseases, which were in full global circulation after 1492. For plague in particular, it is now recognized that instead of seeing the Black Death as a singular event, we should instead recognize the 500-year period of plague infestation that it initiated in Eurasia and Africa as the Second Plague Pandemic.

The Great Transition

Campbell’s book has twelve tables, seventy-eight figures, most of them graphs, and a bibliography running forty-six pages. Campbell has always favored data-heavy analyses; his many decades of study on English agriculture were based on massive compilations of data on crop yields, and he has recently coauthored a comprehensive survey of the British economy from the thirteenth to nineteenth centuries.2 Agriculture is always dependent on weather, which in turn depends on climate cycles; this explains Campbell’s movement into climate history about ten years ago. The devastating effects of the Black Death on England, where population loss was accompanied by a massive decline in wealth, explain his interest in the pandemic. Campbell’s efforts in attempting to master the emerging fields of paleoscience that deal with climate and infectious disease will repay the dedicated reader.

The Black Death was not the only catastrophe Europe suffered in the fourteenth century. A whole generation of readers has the title and imagery of Barbara Tuchman’s A Distant Mirror: The Calamitous 14th Century seared into their conceptions of life in the late Middle Ages.3 Famines, the Hundred Years’ War, economic disruptions, and all manner of hardship made life in Europe, at least, distinctly unpleasant. Campbell looks at this same long fourteenth century, arguing that this 200-year period should be carved out from the previous periodization in climate history, which saw the warm period of the Medieval Climate Anomaly (MCA) leading straight into the LIA. For Campbell, a variety of climate-forcing factors and economic shifts argue for designating the Great Transition as its own separate period, with four distinct phases.

  • 1260s to 1330s: This period saw the end of the MCA, a prolonged, mostly warm period that began around 900 CE which, with one exception in the first half of the eleventh century, was likely due to a high solar irradiance. In the MCA, not only Europe but much of Eurasia flourished. Rising populations, increasing urbanization, an economy growing by leaps and bounds: never had the world seen so much sustained growth and cultural flourishing. The onset of the Wolf solar minimum signaled the end of this prolonged period.4 Combined with changing weather, many years in this period experienced pronounced rainfall at levels that had not occurred since the 1250s and would not occur again until the 1980s. The late thirteenth and early fourteenth centuries saw repeated catastrophes, including a sheep-scab epizootic in the 1270s and 1280s, the Great Northern European Famine of 1315–17, and a cattle panzootic of 1319–20. This period also saw a marked reduction of international trade, with severe shortages of bullion.
  • 1340s to 1370s: The 1340s and early 1350s were, as Campbell remarks, “an almost uniquely disturbed and climatically unstable period when long-established atmospheric circulation patterns were on the cusp of lasting change.”5 The period was distinctly cold, and tree rings show a collective growth minimum. Extreme weather events stand out, such as the devastating Saint Mary Magdalene’s flood in central Germany in July 1342, which raised the Main to levels higher than have ever been documented since, and washed away the better part of topsoil in the region. Warfare, harvest failures, and famine all struck, virtually at once, followed by the great Black Death pandemic, 1346–1353. Despite a few years of climatic and economic alleviation in the 1350s, the plague’s return in the early 1360s ensured that population levels remained depressed. Campbell ventures an estimate of plague mortality of twenty-five million people in Europe, with figures in England indicating that at least one-third of the population perished, and, in certain regions, almost forty percent.6 The plague returned again around 1360, this time having a particularly pronounced effect on children born since the Black Death. It would return at least three more times before the century ended, and would, in fact, haunt most of Europe and the Mediterranean for the next three centuries. By the 1380s, Europe’s population had been reduced by half.
  • 1370s to 1470s: During this period, climate conditions continued to deteriorate. The LIA followed a brief period of solar irradiance in the late fourteenth century, the so-called Chaucerian maximum. The Spörer minimum, ca. 1416–1534, had effects on the Indian Ocean monsoon, the Nile flood, and the North Atlantic oscillation, resulting in global temperature drops of 0.4–0.8°. The aerosols produced by the eruption of Mount Kuwae off the coast of Vanuatu around 1458 reinforced these trends. Europe remained in a demographic spiral, burdened by infectious disease, a depressed economy, and war.
  • 1470s on: The Spörer solar minimum finally eased, and there was a slight alleviation of the intense cold. Campbell notes a demographic shift in Europe around 1500, when, even without any apparent cessation of the disease regime, population recovery, at least in northern Europe, led to levels approaching those before the Black Death. By this point, Portugal, allied with Genoa, had circumvented the trans-Saharan trade in gold and ivory and established its own direct ties with West Africa. It also began its expansion into the Atlantic, as did the Spanish and then the English. The Dutch, however, came out most successfully as Europe’s new economic power. This newly configured Europe, one where northern countries took over the economic power formerly wielded by Italy, had now adjusted to the new world the previous two centuries had made. In other words, the Great Transition was completed and the Old World had adjusted to the new climatic and economic balance.

The late medieval period is well-worn territory for Europeanist historians, and many of the political, economic, and cultural ruptures of the period are well-known. Yet the commonly cited signposts that medievalists and early modernists usually use to stake out their respective terrain now stand as just items in long lists of interconnected shifts, declines, and catastrophes in Campbell’s account. The fall of Constantinople to the Ottoman Turks in 1453, for example, signaling the end of Roman Byzantium, the last vestige of the Empire, is here nothing more than another falling domino. The majority of the book keeps its focus on England and the economic evidence Campbell knows best; when it ventures beyond, Europe still serves as its point of view. This narrow focus has its costs. Overall, Campbell presents a tight chronological narrative, moving between global forces that shift monsoon patterns and tree growth, and changes in the silver supply and the spice market, down to the level of microbes. Campbell often uses dramatic language: “the Rubicon had been crossed,” and, the “climatic regime had already passed the point of no return.”7 The transition Campbell is chronicling is, “big, complex, multi-faceted.”8 It was a transition, not a cycle.9 The buildup is long, and the identification of the consequences must be extended, too, because societies had to establish new socio-ecological equilibria to deal with a world that had been transformed.

The story, then, is complex and justifies the 200-year span that Campbell stakes out. But there is a climax, a tipping point, and it falls in the 1340s. Save for the eruption of the Samalas volcano in 1257, whose effects turn out to be less dramatic than initial assessments had predicted, all the changes leading up to the 1340s were gradual or iterative. Only one change seemed to be unique, and horrifically sudden, in that crucial fifth decade of the fourteenth century, and that was the arrival of plague.

The Plague

It seems a strange coincidence that the Middle Ages are bookended by two plague pandemics: the Justinianic plague, from ca. 541 to ca. 750, and the Black Death, which we usually date from 1347 to 1353 but which should now be seen as the beginning of the much longer Second Plague Pandemic. Historical periods are conventions we create, and the transition from antiquity to the Middle Ages, on the one hand, and then the Middle Ages to the early modern period, on the other, were fixed in historiography long before questions about the environment or history of disease loomed large. Yet both pandemics share more similarities than could have been imagined even a decade ago, which suggest why they should have been implicated in two of the greatest turning points in Afro-Eurasian history. Not simply were both caused by the same organism, Yersinia pestis, but climate science confirms that both emerged in periods of pronounced, and quite sudden, global cooling. Molecular genetics suggests that both issued out small pockets of long-term animal infestation in the central Eurasian steppe, or perhaps a region at the edge of the deserts of the Qinghai–Tibet Plateau, areas now part of western China and eastern Kyrgyzstan. The assumption that plague emerged out of arid central Asia is at the core of Campbell’s analysis, since he ties its emergence to a sudden period of drought in the 1250s, which followed several decades of exceptionally high moisture. Alternatively, he suggests that plague erupted during a subsequent drought in the 1290s, which in turn was reinforced by a subsequent pluvial period in the 1310s.10 The important point to note here is Campbell’s willingness to ascribe the initiation of the most devastating pandemic in history to two different points in time.

The issue is not that Campbell hasn’t been able to settle on a specific date; that would be difficult in the extreme, since we are talking about events transpiring between fleas and rodents in the wild. The issue is that, since he wishes to place these events in central Asia, it matters considerably whether they had a hundred, fifty, or only as little as thirty years to generate effects 4,500 kilometers away in the region of the Black Sea. And whether the interval was long or short, there is also the question of why the path of spread would have been unidirectional, when we would expect a radiating pattern out of a central focus. Since he believes that the spreading outbreak covered the longest part of its journey, the 3,300 miles from Kyrgyzstan to the Black Sea, in between eight and twelve years,11 both the speed and the unidirectionality become problematic. How does plague move across a landscape? How much time does it take? And how much genetic change should we expect to have occurred in relation to time elapsed? The first questions have been asked repeatedly in historiography about the Black Death; the third is one we have only been able to pose in the past few years. Clearly, the wet environment of much of the thirteenth and fourteenth centuries, which Campbell has documented persuasively for Asia and Europe and which was reinforced by the sudden cold of the 1340s, is well suited for sustaining continued plague outbreaks, and for allowing plague to focalize in adjacent areas, finding new pockets of burrowing rodents to afflict in slow-burning enzootics. But sustaining plague as a local enzootic, and accounting for locally radiating epizootics, is different from igniting a pandemic 4,500 kilometers away. The genetics is what Campbell is using to place the Black Death’s origin in central Asia.12 But the genetics is also what complicates his scenario.

The Pest

Yersinia pestis has likely been around as a distinct organism for about 28,000 years.13 It is a single-celled organism, a bacterium that doesn’t have so much as a flagellum to move itself through any medium. For at least the past three thousand of those 28,000 years, it has depended on fleas to ferry it from host to host, thus insuring its evolutionary survival. It persists primarily in rodents, particularly those that burrow and hibernate. It is not a human disease. And therein lies the paradox. Despite the many millions of people it has killed throughout history, it only affects humans as an epiphenomenon of fulminating animal outbreaks. Therein also lies the chief difficulty in tracking it historically. Humans report human outbreaks in their chronicles, they bemoan human deaths in their sermons, and they pray for divine intervention to avert future human catastrophes. Beyond a lingering terror of the disease in nonepidemic periods, plague is otherwise invisible. Most history that has been written about plague, therefore, is partial and insufficient to reconstruct its biological history as one of the deadliest pathogens in the world.

As with climate, a new kind of paleoscience can make up for a lot that humans cannot see. The differences in kind between climate reconstructions and disease reconstructions are important. In climate science, proxy data is proxy not because it is a physical substitute for something else like, say, a three-dimensional print of a dinosaur bone that might substitute for the original, but because it serves as evidence for some other historical phenomenon. The volcanic detritus in an ice-core sample, the pollen retrieved from the bottom of a lake, all these material substances do in fact date from the historical period being investigated. In paleogenetics, in contrast, two different kinds of genetic data are used, only one of which is properly historical. Ancient DNA (aDNA) is retrieved from the bones or teeth, or even the cave floor of once-living organisms.14 Rare, expensive to extract, and still challenging to sequence, aDNA is the most exiguous of data. To date, only thirty complete Y. pestis genomes have been sequenced from aDNA. To supplement them, geneticists use modern samples of the organism, collected either in the field from wild animals or in clinics from human patients, to reconstruct their evolutionary phylogenies. From these inferred family trees, it has been possible to reconstruct a surprisingly evocative history of plague. But it is not yet complete. Both aDNA and recently collected samples have embedded geographical data, which allow plotting the evolutionary progression and spread of particular strains of the pathogen across space. What neither ancient nor modern genomes have is exact clocks. Instead, they have something more akin to sundials: they can tell time relationally, but not exactly.

The issue of how one tells time with genetic evidence is crucial. In the one map Campbell gives showing the path of the Black Death,15 he overlays data from different sources. This is usually a powerful technique by which to show the larger patterns in tree-ring data or climate and crop data. Here, Campbell is collapsing two kinds of evidence for the plague’s geography. An underlay shows the zones of plague focality in the former Soviet Union from the Black Sea to nearly the Pacific in the mid-twentieth century. The overlay represents the plague’s alleged spread from Issyk Kul, a lake in modern-day eastern Kyrgyzstan, to Marseille in the fourteenth century. The figure as a whole is entitled “The spread of plague from Asia to Europe, 1338–47.” It implies that the modern-day natural history of plague fully supports the historical reconstruction of the Black Death that Campbell has just laid out. But just because the plague is somewhere now, doesn’t mean it has always been there. Many historians, Campbell among them, have rightly recognized that Y. pestis aDNA research has confirmed the bacteria’s role as the cause of the Black Death. Its additional value, once partial sequencing was supplemented by whole genome sequencing in 2011, has been that it allows differentiation among strains of the plague. We now see them as archaeological layers in a vast epidemiological reconstruction. Y. pestis may have changed very little over the past five thousand years, but those changes are enough to tell us a complicated story of the plague’s migrations.

The Sudden Divergence

All existing strains of Y. pestis that took on their distinct genetic signature prior to the late medieval period belong to a single evolutionary branch of the organism’s reconstructed phylogenetic tree, Branch 0.16 A major study of the plague’s global phylogeny published in 2010 postulated a twofold divergence in the evolution of Y. pestis occurring at an unknown point at least 728 years ago.17 For a historian, that figure is of little interpretive value. By 2013, geneticists were able to propose a much more refined understanding of this evolutionary split, and a tighter chronology.

Branch 0 had actually split into four lineages, each with its own unique genetic signature. This polytomy, or sudden divergence, has been dubbed “the Big Bang” by Yujun Cui et al., who described it in 2013.18 They took advantage of a stunning new piece of data: the complete sequence of Y. pestis that had been retrieved in 2011 from a Black Death burial ground in London.19 This genome, precisely dated because we have written documentation for the cemetery’s creation and closure, was shown to have only two single-nucleotide polymorphisms (SNPs) differentiating it from the most recent common ancestor of the four new lineages of Y. pestis. There are 2,326 SNPs across the whole Y. pestis phylogeny of Branch 0 and its descendants, Branches 1-4. This represents a period of at least three thousand years in an organism whose genome is over four million base pairs in length. This means that every SNP is potentially meaningful in reconstructing plague’s history.

In estimating the sudden divergence of the later Middle Ages, Cui et al. suggested a date between 1142 CE and 1339 CE, with 1268 CE considered the most likely. Campbell used the study by Cui et al. to test his climatic evidence, and found it consilient with the climate shift of the first phase of the Great Transition. Since his book went to press, two more Y. pestis genomes from the fourteenth century have been sequenced, one from Barcelona and another from southern Russia.20 Additionally, the discovery that one of the London genomes identified with Y. pestis in 2011 had been misidentified, and was in fact from a burial site later than the Black Death, explains why it presented a more derived state of the organism.21 Campbell, not yet aware of the misidentification and misdating of the London genome, assumes that there is evidence for the quick evolution of Y. pestis during the initial outbreak of the Black Death. The four sequenced aDNA genomes give us a much better idea of what this branch of the Y. pestis lineage looked like in the middle of the fourteenth century. There is the Black Death genome itself, identified in both Barcelona, where plague arrived in May 1348, and in London, where it arrived in December 1348 or the following month. There is, as well, the pestis secunda genome, found in a London burial ground dating to the 1360s. This genome is two SNPs further evolved from the Black Death genome.22 And there is a genome from southern Russia, with one further derived SNP common to the Branch 1 lineage, also likely dating from the 1360s. The availability of these new genomes makes it likely that, were a new estimate of the timing of the polytomy to be calculated, the numbers proposed by Cui et al. might narrow somewhat. But probably not by much. A late thirteenth- or early fourteenth-century date for the polytomy seems reasonable.

Too Far Back, or Too Far Away

The study by Cui et al. did something more than suggest a date for the polytomy. It showed a variable rate of change in Y. pestis. During epidemic events, Y. pestis seemed to change very quickly. In a strain known at the time from a single Mongolian marmot, the organism seemed barely to change.23 Cui et al. suggested how we should read the evidence. The acquisition of SNPs in a short period suggests a fulminating epidemic. The acquisition of few SNPs over a longer period likely indicates that plague is in a stable, isolated environment. Thus when we see that two SNPs, and then a third, have been acquired on Branch 1 between roughly the end of the 1340s and the 1360s, that is an indication of epidemic transmission.

What, then, of the two earlier SNPs that separate the Black Death genome of 1348–50 from the sudden divergence of the polytomy? Are they evidence of a fulminating epidemic? Or an epizootic, an epidemic in an animal population? Or were they acquired slowly, by the organism staying in a stable environment? Judging from the scenario that Campbell offers, the two earlier SNPs should be evidence of either an epidemic or an epizootic. To make his case, Campbell draws on the concept of a trophic cascade, a biological domino effect where a change at one level of a food chain causes changes at all the other levels. For plague, rising levels of moisture meant more plant food for rodents. More food meant more rodents, which meant more fleas that fed on them. In a classic spillover event, rodent populations merged and passed their fleas on to new populations. The transmission chain eventually connected to commensal rodents, those that lived in proximity to humans, who, once they died and their still-hungry fleas abandoned them, created the opportunity for the disease to pass to humans. The plague’s progress as a pandemic, Campbell remarks, may have also been aided by either human fleas or human lice. This transmission mechanism would obviate the presence of rats and potentially speed up the rate of transmission.

The problem with this scenario is not that it is implausible. Campbell effectively summarizes what most plague scientists believe to be plague’s normal cycle. The problem is that this fulminating epizootic happened either too far back in time, or too far away from the Black Sea.24

Campbell is not the first to propose an east Asian genesis of the plague. It has been a staple of historiography for over a century, though not by any means universally accepted. It has received new support from genetics, which since 2004 has indicated that China has had the widest diversity of Y. pestis strains. A basic assumption of evolutionary theory is that an organism is most diverse where it has lived longest. This would place the origin and development of Y. pestis on the Qinghai–Tibet Plateau in western China or on the border with Kyrgyzstan. Campbell also links new developments in genetics to an older piece of data. Since the 1880s, first archaeologists and then historians have suggested that the apparent plague outbreak near Issyk Kul, which lies about one-third of the distance to the Black Sea from the Qinghai–Tibet Plateau, was a prelude to the bigger pandemic to come. Nestorian Christians lived in the area, and tombstone inscriptions indicate a sudden rise in mortality during 1337 and 1338.25 An epidemic seems likely. That this epidemic was plague has not been demonstrated with aDNA—the cemeteries were excavated in the 1880s, and the current whereabouts of the bodies is unclear. A prospective diagnosis of the plague is plausible. Many strains of Y. pestis haunt the region to this day.

A great mystery continues to hang over Issyk Kul. The majority of Y. pestis strains in this area of Kyrgyzstan are ancestral to the polytomy. The few that are post-polytomy are strains that must have been imported at a later date.26 We have no evidence that the polytomy happened in or near Issyk Kul, or the Tien Shan mountains on the border between Kyrgyzstan and China. We only know that the region harbors strains suggestive of the prelude to the polytomy. In 1346, numerous reports of plague began appearing in the Golden Horde, just before the plague hit Caffa.27 Aside from the Golden Horde, historians have never demonstrated that the plague caused millions of casualties throughout the Mongol Empire. A specialist in Mongol history has recently suggested that assigning the pandemic’s origin to Mongol territory is little more than an allegation meant to discredit an already maligned foe.28

Plague is not a human disease. We should expect gaps in our documentary evidence, because outbreaks passing solely through wild animal populations would be unlikely to elicit human notice. Campbell is right that the fluctuating climate of the thirteenth and fourteenth centuries could have contributed to epizootics of plague. But there were already multiple plague strains in existence by that point, more than we can document now, and they were already scattered in various niches across the terrain of central Asia.29

The Misleading Mongols

The Italian merchants from Genoa and Venice who tapped into the Black Sea trade in the late thirteenth and early fourteenth centuries were connecting to a hive of trading activity that already existed in the region. This territory, and much beyond, had come under a single political entity in the previous century, as large as any of the climatic forces at play: the Mongol Empire.

Begun by Chinggis Khan’s conquests in the early 1200s, the Mongol Empire was expanded by his sons and grandsons, continuing as an alliance of four khanates centered in China, Iran, central Asia, and Russia until 1368. At its height, the empire stretched from Korea to Hungary, and from Siberia to Vietnam.30 Despite its enormity the Empire gets only a passing mention in Campbell’s book.31

Rinderpest is a viral disease that shares a common ancestor with measles. Descriptions in narrative sources, and the larger epidemiological pattern, suggest that an expanding Rinderpest epizootic, or panzootic, spread across Eurasia in the late thirteenth and early fourteenth centuries, reaching western Europe by the early fourteenth century. It arrived hard on the heels of the climate-induced Great Northern European Famine. By killing many herds, it reinforced the demographic impact of the famine, eliminating not only their meat and dairy products, but also their fertilizer. The apparent path and timing of this panzootic strongly implicates eastern Eurasia as the origin of the disease. Chinese chronicles report cattle disease in Mongolia beginning in 1288. Cattle mortalities are then reported in Russia and Poland in 1298. By 1300 the disease had spread to Bavaria. In 1308–10, it was reported across much of continental western Europe, and by 1320–22, it had reached the British Isles. The Mongols conquered by means of their horses, which were not susceptible to Rinderpest, but their belongings and food were transported by oxen. The slow, westward spread of a viral disease readily passing from herd to herd is thus a reasonable hypothesis, making sense of both the distance and the timing, even in the absence of aDNA.

The fulminating plague pandemic of the late 1340s, so vividly recounted by contemporary chroniclers such as Giovanni Boccaccio, Gabriele de Mussis, and Ibn al-Wardi, struck 140 years after the Mongols emerged. Why did this military expansion, with its intense traffic of troops, supplies, captives, and refugees, not set off a pandemic in the early or mid-thirteenth century? Campbell wishes to tie the plague’s emergence to climate changes in arid central Asia during this period, where pronounced shifts between droughts and pluvials had begun by the mid-thirteenth century. The trading activities of Italian merchants in the later thirteenth and early fourteenth centuries helped expand what was previously local. The Italians were tapping into trading networks across Eurasia that had already been developed by the Mongols.32 Campbell depicts a slow-burning epidemic. Our historical accounts, by way of contrast, say it was lightning fast. I believe that Campbell has documented the origins of the Black Death in the pluvial–drought shifts in central Asia.

He just had the wrong one.

The Four Branches

The polytomy created four new branches of Y. pestis. The traditional narrative recounting the story of the Golden Horde at Caffa and the spread of disease into the Mediterranean has been validated by both paleogenetics and phylogenetics; indeed, paleogenetics has confirmed the persistence in Europe of a strain seeded by the Black Death.33 That narrative only accounts for Branch 1. What happened to the other three? Judging from their living descendants, Branches 3 and 4 seem to have had only regional effects. These strains are found exclusively in Kyrgyzstan, Mongolia, Siberia, and western China.34 Branch 2, in contrast, seems to have had as explosive an effect in central and western Eurasia as Branch 1 did in western Eurasia and the Mediterranean littoral. A vast swath of Eurasia was infected by plague in the fourteenth century or later. Concentrating primarily on branch 1 and its westward spread, Campbell has neglected more than half of plague’s later medieval history across Eurasia.

This is no small point, since historians have never documented plague in the Mongol Empire, aside from the territory of the Golden Horde.35 An argument has emerged that many of the epidemics that befell Chinese cities in the thirteenth and fourteenth centuries may have been outbreaks of the plague. William McNeill advanced this thesis in the 1970s.36 Working before the advent of paleogenetics, McNeill sought to place the plague’s geographical origin in Yunnan, a province in southwest China. This is a claim now contradicted by the genetic evidence, which places the origin of the late medieval strains of plague in western China, far from both Yunnan and the eastern Chinese cities where epidemics were reported. A new tack has been taken by Robert Hymes, a historian of Song China. Mongol troops in the early thirteenth century, having picked up plague while passing through the Gansu Corridor, a long-term reservoir for the disease, transmitted plague into northern and eastern China.37 A wetter climate created lush steppe pastures for horses and was likely a factor in the expansion of the Mongol empire. A sudden increase in moisture might have also heightened plague activity.

Accepting population figures for China collected by Jean-Noël Biraben in 1979, Campbell acknowledges the marked reduction of China’s population in the thirteenth century, but he credits it to the military depredations of the Mongols.38 This is remarkable, since Chinese sources clearly ascribe the cause of tens of thousands of deaths to epidemics.39 Campbell says virtually nothing about fourteenth-century depopulations, even though another series of epidemics in the 1330s and 1340s in eastern China has long been acknowledged.40

In an essay published in 2009, entitled “Mongols as Vectors of Cultural Transmission,” Thomas Allsen demonstrated that in the 1220s the Mongols sent a thousand households of Muslims from Herat to Uighur; they also sent several thousand weavers from Turkestan to Beijing. Several thousand Alans, an Iranian speaking people from northern Caucasia, were transported 4,700 kilometers to northern China.41 To this day, a post-polytomy lineage of plague is as prevalent in the Caucasus as it is in China.42 These forced relocations were ecologically disruptive. The inhabitants of Herat may have been moving into an area where wild rodents were already infested.

Ushered in by the Great Transition, the cold and wet climate of Eurasia was clearly hospitable for the long-term maintenance of plague. Paleogenetic studies have now confirmed the existence of a new western lineage of Y. pestis. Once these methods have been applied more widely throughout Eurasia, we will better be able to tell the stories of how the Second Plague Pandemic changed the fortunes of nearly all of Eurasia.43

Beyond Human Scale

Campbell does not use the term Anthropocene in The Great Transition. Nevertheless, our own very modern dilemma haunts this book, for we, too, live with the specter of a Great Transition. If sudden climatic shifts could cause such devastation in the fourteenth century, when cities were smaller, travel was slower, and human contamination of air, water, and land was minimal, what hope do we have for today, when germs can travel around the world in less than two days, and more than half the world’s population of seven billion people live in cities? Does it matter whether our climate change is human induced? We are no more able to undo climate change than the people of the fourteenth century.

In a recent overview of the late Roman Empire, historian and archaeologist Stephen Mitchell made an evocative observation. Archaeologists see a panorama beyond the human lifespan; historians, in contrast, see events such as wars as history’s hinge-points. “No ancient writer,” Mitchell remarks, “was able to adopt a perspective that surveyed the demographic catastrophe over two centuries, a task that has to be left to modern analysis.”44 Campbell is, in spirit, among the archaeologists. In appealing to climate history, he takes the view that no unassisted human eye can perceive. In assessing the impact of the Black Death, we too must look beyond the chronicles of Boccaccio, de Mussis, and al-Wardi.

Work by archaeologist Carenza Lewis has demonstrated that England was indeed devastated by the Black Death. Some parts of England were depopulated by as much as fifty or sixty percent; some areas were completely abandoned.45 Yet England proved resilient. The monarchy held, the legal system continued to function, and the economy adapted reasonably quickly. After the plague, English people seemed healthier and lived longer than several decades earlier.46 Still, we cannot generalize from the English case. The effects of the plague in Egypt were devastating.47 The Ottoman experience has recently been examined by Nükhet Varlık, who shows that the plague actually worked to increase the strength of Ottoman rule.48 James Belich has recently claimed that, in the face of increasing mortality, Europe expanded rather than contracted. It was the repeated devastation of the plague that caused Europe to push beyond its natural borders and become the dominant colonial power.49

In bringing the paleosciences to bear on our reinterpretations of the past, something extraordinary has happened. The sciences are documenting events that historians had not previously known. The Samalas eruption in 1257 was a massive volcanic event. Its signature was first recognized in ice cores in 1999. By various measures, it seems to be the most violent volcanic event in the Holocene. Scouring documentary records, tree-ring data, and ice-core samples, geologists and climate scientists recently found evidence for strong cooling in Europe, Siberia, and Japan. Nonetheless, famines in England and Japan could not have been due to climatic changes triggered by the Samalas eruption. They had begun before its effects could have possibly been felt.50 Campbell turns a closer eye to England, which had long been known from historical chronicles to have suffered severe famine in 1258, the year after the eruption. Echoing the climate scientists, Campbell shows that global cooling effects were secondary to other climatic events: strong solar forcing, La Niña conditions in the Pacific, and a positive North Atlantic oscillation. These shrouded the effects of the volcano’s detritus as it spread around the globe in 1258.51 In treating these subjects, Campbell gives a master class on how to synthesize climatic, political, and economic history.

There is a danger in deriving causal from chronologically proximate connections. But there is also much to be gained from the daring analogical thinking that has enlivened the disciplines of climate and epidemiological history in recent years. Kyle Harper, in his study of the late Roman Empire, provides an example. From narrative sources, coins, and inscriptions, he documents a little-known epidemic in Roman history. Dubbed the Cyprianic Plague, after a North African bishop who was among the first to describe it, the disease was both excruciating and lethal. Harper judges it to have been some kind of Ebola-like hemorrhagic fever. Like Hymes with respect to the plague in China, Harper is held back by a lack of molecular evidence, and, like Campbell, he can give no persuasive account of its route into the Roman Empire. He might have toyed with a major epidemiological clue that was already in front of him. Earlier in the same chapter, Harper described the millennial celebrations for the city of Rome held in 248 CE. Animals were brought to Rome for a celebratory slaughter. The hippopotamuses, elephants, lions, leopards, giraffes, and even one rhinoceros must have come from sub-Saharan Africa. The Cyprianic Plague began in 249, the year following the Roman millennial. Either the animals themselves, or the hunters who captured and transported them, may have carried a viral disease from a previously isolated ecological niche. It is just such a scenario of zoonotic spillover that we now identify as a common feature of emerging diseases. Changes in agricultural practices, in hunting patterns, in food practices, in transport routes: if there is one great lesson we have learned in global health in the past forty years, it is that human agency is the common dominator in turning local episodes of cross-species pathogen transmissions into history-altering pandemics.52

Campbell and Harper both suggest that the people of the Roman Empire and the Middle Ages were not simply the victims of ill fortune: they were human actors faced with the reality of climate change. Campbell has succeeded in making the Great Transition a historical turning point with which all narratives of European history must now reckon. If he has been less successful in the epidemiological parts of this investigation, that is because the methods of thinking globally in disease history are not yet as advanced as they are in the field of climate history. We are only now learning how to read genetic lineages as rough maps that show us both the geography and the chronology of evolving diseases.

We need to think big.

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DOI: 10.37282/991819.18.17
  1. This later, colder world has been described in detail by books such as Geoffrey Parker, Global Crisis: War, Climate Change and Catastrophe in the Seventeenth Century (New Haven: Yale University Press, 2013); and Sam White, A Cold Welcome: The Little Ice Age and Europe’s Encounter with North America (Cambridge, MA: Harvard University Press, 2017). Timothy Brook, “Nine Sloughs: Profiling the Climate History of the Yuan and Ming Dynasties, 1260–1644,” Journal of Chinese History 1, no. 1 (2017): 27–58, is an example of an older kind of climate history that relies primarily on written accounts and engages hardly at all with the climate sciences. ↩
  2. Bruce Campbell, Three Centuries of English Crop Yields, 1211–1491; and Stephen Broadberry et al., British Economic Growth 1270–1870 (Cambridge, UK: Cambridge University Press, 2015). ↩
  3. Barbara Tuchman, A Distant Mirror: The Calamitous 14th Century (New York: Ballantine Books, 1987). ↩
  4. A period of low solar irradiance starting around 1282 and continuing until 1342. In many instances, as with the Wolf solar minimum, Campbell introduces concepts from climatology without defining them until many pages later (in this case, p. 52, the fourth reference to the phenomenon). Given that climate history is itself such a new field (see the final section of this review), a wise editor would have suggested the inclusion of a glossary. See Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 52. ↩
  5. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 277. ↩
  6. Ibid., 307. ↩
  7. Ibid., 23–24, 341. ↩
  8. Ibid., 24. ↩
  9. Ibid., 20. ↩
  10. Ibid., 249–51; see also 325–26 for a summary on his theory of the time, route, and cause of plague’s alleged spread across central Eurasia. A recent study for the Gansu (Hexi) corridor, based on tree rings in the Qilian Mountains (to the east of the Qinghai–Tibet Plateau), finds a smoother pattern, with drought in 1161–1216 and 1260–1349, and wet spells in 1217–1259, 1350–1408. See Yang Deng et al., “Tree-Ring Recorded Moisture Variations Over the Past Millennium in the Hexi Corridor, Northwest China,” Environmental Earth Sciences 76 (2017): 1–9. ↩
  11. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 302. ↩
  12. Campbell is correct in reporting (ibid., 293) that the genetics has argued for an origin for Y. pestis in China since 2004. However, other aspects of his summary of the genetics are less precise. He suggests, for example, that, “the strain responsible for the Black Death pre-dated evolution of the three main modern plague lineages, orientalis, medievalis and antiqua” (ibid., 293). Not simply is that terminology for the lineages otiose, but the whole understanding of the polytomy (the divergence into four, not three, branches I discuss here) is that it happened before the Black Death, not after—let alone, because of—it. It is unclear what Campbell means in saying that the Black Death strain was “non-identical” to the strain identified by Alexandre Yersin in Hong Kong in 1894. Y. pestis has been proven to be one of the least evolved pathogens known to science, a phenomenon of clonality that has been called “genetically monomorphic.” See Mark Achtman, “Insights from Genomic Comparisons of Genetically Monomorphic Bacterial Pathogens,” Philosophical Transactions of the Royal Society B 367 (2012): 860–67. ↩
  13. This date is suggested by Aida Andrades Valtueña et al., “The Stone Age Plague and Its Persistence in Eurasia,” Current Biology 27, no. 23 (2017): 3,683–91.e8. ↩
  14. Viviane Slon et al., “Neandertal and Denisovan DNA from Pleistocene Sediments,” Science 356, no. 6,338 (2017), 605–608. ↩
  15. See Figure 4.9 in Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 301. ↩
  16. There is another, extinct lineage of Y. pestis from the Bronze Age that has now been documented from multiple aDNA samples. See Simon Rasmussen et al., “Early Divergent Strains of Yersinia Pestis in Eurasia 5,000 Years Ago,” Cell 163 (2015), 571–82; and Aida Andrades Valtueña et al., “The Stone Age Plague and Its Persistence in Eurasia,” Current Biology 27, no. 23 (2017): 3,683–91.e8. ↩
  17. Giovanna Morelli et al., “Yersinia pestis Genome Sequencing Identifies Patterns of Global Phylogenetic Diversity,” Nature Genetics 42, no. 12 (2010): 1140–45. ↩
  18. 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, no. 2 (2013), 577–82. ↩
  19. Kirsten Bos et al., “A Draft Genome of Yersinia pestis from Victims of the Black Death,” Nature 478, no. 7,370 (2011), 506–10. ↩
  20. Maria Spyrou et al., “Historical Y. pestis Genomes Reveal the European Black Death as the Source of Ancient and Modern Plague Pandemics,” Cell Host and Microbe 19, no. 6 (2016), 874–81. ↩
  21. It was because of this misidentification, which wasn’t identified until early 2016, that Campbell assumes (Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 294) that there is evidence for Y. pestis’s quick evolution during the initial Black Death outbreak. See Monica Green and Boris Schmid, “Tiny Changes with Huge Implications: Counting SNPs in Plague’s History,” Contagions blog, ed. Michelle Ziegler, June 27, 2016 and June 29, 2016. ↩
  22. At least one of the characteristic SNPs of the second London genome was also found in a partially sequenced isolate from Bergen op Zoom (Netherlands); this isolation can only be roughly dated to the latter half of the fourteenth century. See Stephanie Haensch et al., “Distinct Clones of Yersinia pestis Caused the Black Death,” PLOS Pathogens 6, no. 10 (2010): e1001134. ↩
  23. In that case, the strain had only acquired 17 SNPs in the past 700 years. Two additional isolates of strain 4.ANT1 have since been found. See G. Odinokov et al., “Анализ полногеномной последовательности штаммов Yersinia pestis на основе ступенчатого 680-SNP алгоритма (Analysis of the Genome Wide Sequence of Yersinia pestis strains Based on the Consecutive 680-SNP Algorithm),” Problemy Osobo Opasnykh Infektsii 3 (2013): 49–54; and 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. ↩
  24. The time–distance problem of an east-Asian origin thesis was already discussed in detail, long before the genetics evidence came on the scene, in John Norris, “East or West? The Geographic Origin of the Black Death,” Bulletin of the History of Medicine 51 (1977): 1–24. ↩
  25. The Issyk Kul cemetery has been known since 1885, and was excavated in 1886 and 1887. Some bodies were removed, but it is unclear what became of them. The headstones were taken away from the original burial site, and most of them are on deposit in St. Petersburg and Moscow. See T. William Thacker, “A Nestorian Gravestone from Central Asia in the Gulbenkian Museum, Durham University,” The Durham University Journal 59 (1967): 94–107; and Uli Schamiloglu, “The Impact of the Black Death on the Golden Horde: Politics, Economy, Society, Civilization,” Golden Horde Review 5, no. 2 (2017): 325–43. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 242, adopts the Issyk Kul narrative from Norris who, however, thought it was an isolated outbreak unrelated to the main Black Death explosion in the Crimea. ↩
  26. See 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, no. 10 (2017): e0187230. ↩
  27. Through his loose phrasing describing the siege of Caffa, Campbell implies that plague first broke out in 1345. Sources are in fact consistent that the first apparent outbreak was in 1346. See Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 275. ↩
  28. Paul Buell, “Qubilai and the Rats,” Sudhoffs Archiv 96, no. 2 (2012): 127–44, even while engaging with the genetics evidence available through 2011, denies that plague ever made any significant impact on the Mongols. See also Peter Jackson, The Mongols and the Islamic World: From Conquest to Conversion (New Haven: Yale University Press, 2017), 408, who despairs that resolution of the Black Death’s origins is soluble. ↩
  29. Of the 133 unique strains of Y. pestis studied by Cui et al. 2013, 28 are pre-polytomy. Those, of course, are just the ones that have survived to the present day. We will never know how many others are now extinct. ↩
  30. It brought much of China and most of the Abbasid caliphate under its control. It might have even taken in Mamluk Egypt if events in Syria, at the Battle of Ayn Jalut in 1261, had gone differently. The state of Mongol studies is usefully summarized in Michal Biran, “The Mongol Empire: The State of the Research,” History Compass, 11, no. 11 (2013): 1,021–33; and Michal Biran, “The Mongol Empire and Inter-Civilizational Exchange,” in The Cambridge World History: Volume V: Expanding Webs of Exchange and Conflict, 500 CE–1500 CE, ed. Benjamin Kedar and Merry Wiesner-Hanks (Cambridge: Cambridge University Press, 2015), 534–55. ↩
  31. The only extended analysis, less than a full paragraph, comes in the epilogue (Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 397–98). ↩
  32. Hodong Kim, “The Unity of the Mongol Empire and Continental Exchanges over Eurasia,” Journal of Central Eurasian Studies 1 (December 2009): 15–42; Hosung Shim, “The Postal Roads of the Great Khans in Central Asia under the Mongol-Yuan Empire,” Journal of Song-Yuan Studies 44 (2014): 405–69. ↩
  33. Kirsten Bos et al., “Eighteenth Century Yersinia pestis Genomes Reveal the Long-Term Persistence of an Historical Plague Focus,” eLife 10.7554/eLife.12994 (2016); and Maria Spyrou et al., “Historical Y. pestis Genomes Reveal the European Black Death as the Source of Ancient and Modern Plague Pandemics,” Cell Host and Microbe 19, no. 6 (2016), 874–81. ↩
  34. For isolates of Branches 3 and 4, see 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, no. 2 (2013), 577–82; and 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, no. 10 (2017): e0187230. ↩
  35. Paul Buell, “Qubilai and the Rats,” Sudhoffs Archiv 96, no. 2 (2012): 127–44. ↩
  36. William McNeill, Plagues and Peoples (Garden City, NY: Anchor Press, 1976). ↩
  37. Robert Hymes, “A Hypothesis on the East Asian Beginnings of the Yersinia pestis Polytomy,” The Medieval Globe 1 (2014), 285–308, also cites the work of two Chinese scholars who have been pursuing this line of inquiry. Campbell acknowledges Hymes’s work (Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 241, 322, 398), but only in passing. ↩
  38. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 59–60. ↩
  39. Robert Hymes, “A Hypothesis on the East Asian Beginnings of the Yersinia pestis Polytomy,” The Medieval Globe 1 (2014), 295. ↩
  40. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late-Medieval World (Cambridge: Cambridge University Press, 2016), 283, makes passing reference to epidemics in China in the 1340s, but without any elaboration or speculation as to cause. ↩
  41. Thomas Allsen, “Mongols as Vectors of Cultural Transmission,” in Nicola Di Cosmo, Allen Frank, and Peter Golden, eds., The Cambridge History of Inner Asia, vol. 2: The Chinggisid Age (Cambridge: Cambridge University Press, 2009), 135–54. ↩
  42. N. Yu. Nosov et al., “[Phylogenetic Analysis of Yersinia pestis Strains of Medieval Biovar from Natural Plague Foci of the Russian Federation and Bordering Countries],” Problemy Osobo Opasnykh Infektsii 2 (2016): 75–78 (in Russian). ↩
  43. Plague’s pre-modern effects on another continent, Africa, will be explored in a forthcoming special issue of the online journal, Afriques. ↩
  44. Stephen Mitchell, A History of the Later Roman Empire, AD 284–641, 2nd edn. (Oxford: Blackwell, 2014), 490–91. ↩
  45. Carenza Lewis, “Disaster Recovery? New Archaeological Evidence from Eastern England for the Impact of the ‘Calamitous’ 14th Century,” Antiquity 90, no. 351 (2016): 777–97. ↩
  46. See most recently Sharon DeWitte, “Stress, Sex, and Plague: Patterns of Developmental Stress and Survival in Pre- and Post-Black Death London,” American Journal of Human Biology 30, no. 1 (2017), doi: 10.1002/ajhb.23073, and the literature cited therein. ↩
  47. Here, instead of marginally productive croplands returning to pasture because of the lack of people to work it, the centuries-in-the-making system of canals in the Nile delta silted up and became unusable in places, pulling the productivity of the entire country down. Stuart Borsch, “Plague Depopulation and Irrigation Decay in Medieval Egypt,” The Medieval Globe 1 (2014): 125–56. ↩
  48. Nükhet Varlık, Plague and Empire in the Early Modern Mediterranean World: The Ottoman Experience, 1347–1600 (Cambridge: Cambridge University Press, 2015). ↩
  49. James Belich, “The Black Death and the Spread of Europe,” in The Prospect of Global History, eds. James Belich et al. (Oxford: Oxford University Press, 2016), 93–107. ↩
  50. Sébastien Guillet et al., “Climate Response to the Samalas Volcanic Eruption in 1257 Revealed by Proxy Records,” Nature Geoscience 10 (2017): 123–28. See also Frank Ludlow, “Chronicling a Medieval Eruption,” Nature Geoscience 10 (2017): 77–78. ↩
  51. Bruce Campbell, “Global Climates, the 1257 Mega-Eruption of Samalas Volcano, Indonesia, and the English Food Crisis of 1258,” Transactions of the Royal Historical Society 27 (2017): 87–121. ↩
  52. Monica Green, “The Globalisations of Disease,” in Human Dispersal and Species Movement: From Prehistory to the Present, eds. Nicole Boivin, Rémy Crassard, and Michael Petraglia (Cambridge: Cambridge University Press, 2017), 494–520. ↩

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

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