Climate and Disease in Medieval Eurasia
- Monica H. GreenMonica H. GreenHistory Department, Arizona State University
When the first hominins and their successors migrated north from Africa into Eurasia, they created a new, interlinked disease environment. They brought some diseases, such as malaria, with them from Africa, and newly encountered others, such as plague, in Eurasia. Regional changes in climate played a role in human health, not simply due to their influence in determining the success of year-to-year harvests and grazing lands, but also because periods of warming or severe and sudden cooling shifted the interactions between humans and the flora and fauna that made up their environment. Exchanges of disease between the two continents would continue up through the medieval era. Whereas vast distances and low population density likely shielded Eurasian populations from frequent epidemic outbreaks up through the Neolithic period, by the beginning of the common era, with its vastly intensified trade networks, Eurasia would begin to see a new phenomenon: pandemics, including the Justinianic Plague and the Black Death, the largest mortality events in human history. The diseases of medieval Eurasia are still among the world’s leading infectious killers and causes of debilitating morbidity. Because they have all persisted to the present day (with the exception of smallpox), modern science plays an important role in their historical reconstruction.
The Climatic Diversity and Microbial Unification of Medieval Eurasia
Eurasia—the connected land space stretching from Portugal to Korea and including the major islands of Ireland, England, Japan, and the Indonesian archipelago—encompasses all the different climatic zones of the Northern Hemisphere, from the tropical climes of Indonesia to the frozen tundra of Siberia. Eurasia was never completely separated from Africa, and the land bridge connecting the two continents has been in constant use for the past million years. The disease ecologies of these two largest continents therefore need to be considered together. The geography of infectious disease is important because, as living organisms, pathogens—that is, the bacteria, viruses, and other microparasitic entities that cause disease—all have histories linked to time and place. Every widely distributed disease originated as a local outbreak. Of the main infectious diseases that circulated in Eurasia in the medieval period, at least two—malaria and perhaps smallpox—had their origins in Africa. Plague and possibly also leprosy both originated in Eurasia, and were then both transmitted to Africa.1
The presence of a pathogen is an obvious prerequisite for infectious disease, but so is the presence of susceptible hosts. A recent assessment of the disease burden in Song-era china (960–1279 ce) describes Chinese society crossing “epidemiological frontiers” in the central medieval period, with increased population and an expanded geographical footprint contributing to an increase in epidemics.2 But that was surely true of many societies across Eurasia from just before the beginning of the Common Era up through the start of regularized global contact around 1500. Population density is a critical variable in epidemiological history. Rome was the first urban concentration to reach a population level of one million people, so it is no coincidence that the Roman Empire is now said to have ushered in the Age of Pandemic Disease.3 By the late 15th century, voyages would establish regular migration and trade links between the Old and New Worlds, creating what has been described as “the microbial unification of the world.” Eurasia and Africa had long since formed their own interconnected disease landscape.4
Population levels and morbidity and mortality rates are difficult to assess with confidence in the premodern period, given the absence of regularized demographic data for any part of Eurasia. Therefore, it is likely that reliable statistical assessments of the impact of infectious diseases in medieval Eurasia will continue to elude us.5 But another important task for epidemiological history—namely, the ability to track the paths of infectious diseases geographically and possibly even pinpoint the instigating causes of particular outbreaks—can now be pursued more vigorously than has ever been possible before. This is largely due to developments in genetics since the 1990s. Having their own genetic identities, pathogenic microorganisms carry the stories of their development and proliferation in their genes.
The reconstruction of those Stories can be approached from two angles. On the one hand, on the basis of complete genome sequences from modern samples, it is possible to work out the relative relatedness of any one sample to another. Thus, for example, the huge variety of tuberculosis strains in the world today can, when fully sequenced, produce a phylogeny (that is, a family tree) that tells the story of how those thousands of different strains arose and diverged from each other.6 Since samples always have geographic data attached to them, such tree modeling also allows mapping.
On the other hand, a second development in genetics, involving fewer researchers but producing equally decisive results, has been the rise of palaeogenetics. Biologists involved in this field have developed techniques to reconstruct genetic material from historical remains. Palaeogenetics reconstructs aDNA (“ancient DNA”) from skeletal tissue or mummies, allowing the hypothetical connections proposed by the phylogenies to be tethered to actual historical samples of bacteria, and now viruses, from centuries ago. The earliest and most extensive work in this field has been done on plague (the disease caused by the bacterium Yersinia pestis), hence the length of that section in this article. But comparable work on leprosy, tuberculosis, and smallpox is allowing ever more robust stories to be told.7 Of the diseases to be addressed here, only malaria has not yet yielded complete genomes from historical samples, though its history can be supplemented (as can that of leprosy) by study of skeletal lesions produced by the organism. The as yet unequal geographic distribution of palaeogenetics studies is in part a function of comparably unequal distributions of archaeological work; palaeogeneticists cannot work without samples provided them by archaeology.
Climate plays a role in disease history in several ways. First, for obligate pathogens that have only humans as their host—such as tuberculosis, leprosy, and smallpox—ambient temperatures affect levels of human dress and the degree of indoor congregation (for warmth), which in terms of transmission either aid or reduce the success of disease generation. Tuberculosis, leprosy, and smallpox are all transmitted via respiration, sneezing, or coughing, with droplets or aerosols propelling the microscopic pathogen from one host to the next. These methods of transmission are generally more effective in colder weather. Malaria and plague, in contrast, rely on insect vectors for transmission. (Plague can also be transmitted secondarily via respiration.) Malaria and plague thus rely on environmental conditions supportive of vector replication to sustain chains of transmission. Since the linkages between climatic changes and disease are far from secure in the current state of investigation, I limit observations about both climate and disease together to my discussion of plague, which, of these several major infectious diseases, seems to be the one most closely susceptible to pronounced shifts of climate.
Many other factors affect health, of course, besides the presence or absence of infectious diseases. Nutrition, access to sunlight, and absence of social stresses are the most important. Livestock diseases have also been critical to human existence, with the cattle panzootics of the tenth and fourteenth centuries being particularly influential across Eurasia.8 In many ways, however, those animal diseases tell the same stories as human ones: namely, stories of migration, trade, and the effects of changing climates. This article, therefore, will recount some elements of the stories of four major infectious diseases to have afflicted humans in Eurasia from the Bronze Age up to the period of regular global connectivity: malaria, leprosy, smallpox, and plague. All these accounts will be altered as new results become available. The geographies, as well as the chronological turning points, might shift. But major insights have already been achieved in pinpointing the origins and epidemiological trajectories of these diseases. The role that Eurasia has played as both incubator and victim of the world’s major infectious diseases is coming more clearly into view.
Malaria’s African Origins and Asiatic Spread
A quick glance at maps showing the geographic distribution of the two main kinds of human malaria presents a striking contrast: vivax malaria (caused by Plasmodium vivax) is primarily a disease of Asia, with lesser infiltration in the Americas and the east coast of Africa. Falciparum malaria (caused by Plasmodium falciparum), in contrast, most heavily affects sub-Saharan Africa and those areas that received the heaviest human traffic out of West Africa during the trans-Atlantic slave trade.9 It has been only recently that a coherent explanation of the distribution of these two major forms of malaria has been proposed.10
In a series of three major studies conducted in the early 21st century, a team of researchers connected with the laboratory of Beatrice Hahn have established the larger continental histories of vivax and falciparum malaria.11 Both come from Africa. Vivax, in its older form, was an indiscriminate organism, moving across multiple species of primate hosts in its original context of Africa. Although the organism (a one-celled protozoan with a multistage lifecycle) was dependent on spending part of its lifecycle in mammalian hosts, it could use its mosquito vectors to readily move from host species to host species. Human infections were therefore likely intermittent, if not chronic, as long as humans remained in climates where vector mosquitoes thrived. When humans migrated from Africa into Asia, they took the proto-vivax malaria with them. (When this process actually happened, and even whether it was Homo sapiens or another hominid species that affected this transference, is still unclear.) In this new environment in Asia, however, there was not the wide diversity of other primate species for the organism to constantly cycle through, so vivax became an obligate human pathogen: one so closely adapted to its human hosts that it rarely or never could survive when human hosts were not available. Obviously, the disease still needed its mosquito vector, so when humans migrated to latitudes where mosquitoes did not thrive, the disease died out. This seems to be the reason why malaria did not travel to the Americas with the First Peoples, who would have outrun mosquitoes in their long transit through the Beringia crossing.
Those human populations who remained in Africa, however, continued to be subjected to the vivax progenitor, which was still crossing species with other primates. Yet something interesting happened. Most sub-Saharan Africans have what is called Duffy antigen negativity: even though vivax can enter their bodies through a mosquito bite, an infection will not take hold, because their blood cells will not allow the malarial pathogen to enter. Hence, because of increasing spread of this advantageous genetic characteristic, vivax became a nonissue for sub-Saharan populations.
In the meantime though, a new, and much more lethal, type of malaria was transferred to humans. This was falciparum malaria, which seems to have originated as a human obligate pathogen with only a few small genetic changes from a strain already adapted to gorillas. Because falciparum relied on a more limited range of mosquitoes, and because it had to be more regularly transmitted from human host to human host to be sustained, falciparum has remained largely confined to the African continent (vivax, which means “long-lived,” could establish latent infections in hosts’ livers, which could last up to three to four years, whereas falciparum was more quickly cleared from the body, if it did not kill its host). Traces of falciparum malaria have been found in Egyptian mummies from the 2nd millennium bce.12 And the disease would, after the medieval period, be successfully transmitted to the Americas with the massive importation of slaves from sub-Saharan West Africa. But aside from a few ecological niches where it was able to take hold (such as the swamplands surrounding Rome), falciparum “epidemics” seem to have died out quickly in the ancient and medieval Mediterranean.13 It would seem, then, that for the history of medieval Eurasia, vivax was likely the most influential form of malarial disease. Its effects in bringing increased morbidity to areas where anthropogenic land changes increased the likelihood of mosquito replication—rice cultivation being the most obvious—is a topic that will likely see more consideration in historical studies.
Of the four infectious diseases examined in this article, leprosy may well have been the most widely dispersed throughout Eurasia during the medieval period. A disease that manifests in a variety of different ways, and maims rather than kills, leprosy elicited a range of responses. No attempt has yet been made to construct a pan-Eurasian history of leprosy, however, and a comprehensive account of either its biological or social history is still many years away. For leprosy, all three disciplines involved in constructing disease history—bioarchaeology, genetics, and documentary history—have a role to play. Leprosy is documented by skeletal remains in early medieval England, Spain, and the Levant. It is documented in India as much as 2000 years before that, where the oldest palaeopathological evidence we have for leprosy in humans comes from the post-urban phase of the Indus Age.14 Genetically, leprosy presents a conundrum, because there is a wide divergence between the history of the causative organism, and its apparent history as a human pathogen. The estimated date of divergence of the two known species of leprosy pathogens, Mycobacterium leprae and Mycobacterium lepromatosis, is about 13.9 million years ago. In other words, the leprosy species predate the existence of all great apes, not simply hominin lineages. The two species of leprosy must, therefore, have come to humans through zoonotic transmissions. When and where that happened, however—or even if it happened multiple times—cannot yet be determined.15
Our still-unfolding picture of leprosy’s genetic history identifies the oldest documented evolutionary lineage of M. leprae not in India, but at the Pacific Rim of Asia.16 Lineage 0 was first identified by Schuenemann and colleagues in 2013. Modern samples that have thus far been sequenced come from Japan, China, and New Caledonia, with the latter sub-lineage having split from the former two at an estimated date of 792 bce.17 Is the Pacific Rim the site of origin of leprosy as a human disease? That is not at all clear. Schuenemann and colleagues hypothesize that Lineage 0 split off from the most recent common ancestor of all forms of Mycobacterium leprae around 5000 years ago.
But in what species did leprosy originate, and from there transmit to humans? Currently, two strains of leprosy, representing the two leprosy bacterium species, have been documented in an unlikely host: red squirrels in various parts of the United Kingdom. One strain, a type of M. leprae, is the same organism found in medieval gravesites in England and Sweden; it was also transferred to North America at some point during the past several hundred years and came to infect armadillos there. The other species of leprosy bacterium, Mycobacterium lepromatosis, which was discovered in 2008, has likewise been found in red squirrels in the United Kingdom. In that case, however, the strain found in the squirrels diverged about 27,000 years ago from the closest known strain in humans, which has been found in Central America, Canada, and Singapore.18 Red squirrels (Sciurus vulgaris) are a Palaearctic species, inhabiting all of Northern Eurasia from Ireland to Russia’s eastern Kamchatka Peninsula.19 If this species of squirrel has had a long-term relationship with the two strains of leprosy, and has not simply been infected anthropogenically in recent times, then that trans-Eurasian distribution may account for a good deal of the mystery of leprosy’s history.
As for palaeogenetics, aDNA retrieval has been particularly successful for Mycobacterium leprae. Complete genomes have been successfully extracted and sequenced from medieval gravesites in Sweden, Denmark, and England, which have allowed for construction of the geographic and chronological parameters of the disease’s history.20 The lineage currently found in West Africa (Lineage 4) is believed to have diverged from the ancestor of lineages now found across continental Eurasia in the 1st century bce. How or when it reached West Africa is unclear, though passage from Asia via the Middle East is conceivable. (The disease is first documented in written sources in the eastern Mediterranean around the 3rd century bce.) The other three lineages—called 1, 2, and 3 in genetic phylogenies—are more closely associated. Phylogenetically, they move from west to east and grow progressively younger in divergence time: Lineage 3 is associated (from aDNA samples) with England and Denmark (and, later, the Americas), and is estimated to have diverged from a common ancestor with Lineages 2 and 1 in the 1st century ce; Lineage 2 (also documented from medieval aDNA) is associated with England, Denmark, and Sweden, and diverged from its common ancestor with Lineage 1 perhaps in the 3rd century ce; and finally, Lineage 1 is associated with India and Indonesia, diverging from its common ancestor with Lineage 2 perhaps in the 7th century ce. This genetic narrative builds on decades of palaeopathological work that has documented the presence of leprosy infections in medieval samples.21
Leprosy is a very slowly replicating disease. With close to two weeks needed for an individual cell to reproduce, the leprosy bacillus can take years to establish an extensive infection in the human body. When it is in advanced stages, leprosy can have pronounced physical signs. Hence, it is likely the slow and visible destruction of the body that accounts for leprosy’s particular status as a disease that, even in widely separated cultures, has at times elicited practices of segregation and stigmatization. But leprosy does not produce “epidemics.” It moves slowly and insidiously through populations. Historically, we would expect to see it tied more to major migrations or other practices, like slavery, that moved populations around slowly.22 Slave trading manuals from both the Islamicate world and Europe identify incipient leprosy as a concern for the slave-inspecting physician or potential buyer.23
It is not yet clear to what extent either medical explanations of leprosy’s nature and disease course, or social practices of tolerance or exclusion of those afflicted by leprosy, have larger patterns or connections. All the major literate medical traditions—in India, China, the Islamicate world, and the ancient Mediterranean and medieval European worlds—produced descriptions of leprosy. But these traditions varied widely among themselves in terms of how they classified the disease (was it a skin disease or a condition of the whole body?), its etiology (was it contagious or did it develop from some inborn defect?), and its treatment (were some or all of its many manifestations amenable to treatment or cure?).24 The latter issue was critical because, if leprosy was also deemed contagious, then the presence of persons carrying the disease might be perceived as a threat. No other Eurasian society seems to have regularized the institutionalization of persons suffering from leprosy in the way that Christian, Western Europe did from the 11th century on, though practices that in some instances extended to exclusion and ostracizing of persons with leprosy can be found widely. Precisely why the foundation of European leprosaria (that is, leper houses) began in the 11th and 12th century is still unclear, since paleopathological studies demonstrate that leprosy was present in European populations well before that point.25 European leprosaria were not institutions of incarceration, but were instead religious institutions which one entered voluntarily. The proliferation of leprosaria in Europe is more accurately understood as a new vogue in charitable giving, rather than a sign of the epidemiological growth of the disease. And it is clear that, even in those urban areas where leprosaria were established, the physical presence of the disease did not necessarily override all the other social connections any given individual might have with their larger community.26
In Islamicate societies, there is no comparable evidence of institutionalization, although leprosy was generally seen as a contagious disease, prompting jurists to consider it as grounds for divorce, to recommend segregation of the afflicted individual from larger society, and to regulate the involvement of those suffering from leprosy in mercantile transactions.27 Leung similarly finds that in China, segregation was not the norm; rather, it was a practice adopted only toward the end of the medieval period. In Japan, likewise towards the end of the medieval period, we find a practice of burying persons with leprosy with an iron pot on their head. But it was perhaps not only persons with leprosy who were buried this way, and it was perhaps not a kind of stigmatization. These individuals, likely gravely disabled, were cared for in life. The iron pot may have been intended to prevent the spread of disease from the grave and to decontaminate the souls of the deceased.28 Palaeopathological analysis of a woman suffering from plague in later medieval Cyprus makes clear that, despite the advanced state of her disease, she remained a valued member of her community.29 There is, then, no universal evidence of the exclusion of persons with leprosy in medieval Eurasia.
The current understanding of the biological history of smallpox, the disease we have long ascribed to the virus Variola major, traces its origins back to a hypothetical zoonotic transfer between human, camels, and naked-soled gerbils (Gerbilliscus kempi). That event would have likely happened in the Horn of Africa, where we can locate all three species together; the date has been estimated at 3.5 to 4,000 years ago, which would coincide with the approximate domestication of dromedary camels in the Arabian peninsula.30 At what point smallpox migrated out of East Africa and into the Eurasian landmass is unclear. The famously pockmarked mummy of the Egyptian Pharoah Ramses V (d. 1157 bce) has failed repeatedly to yield persuasive genetic evidence for the smallpox virus, and we have no other records to connect the disease with Egypt. It has long been suspected that smallpox was behind the so-called Antonine Plague of 2nd-century Rome, which may have killed up to a quarter of that city’s population, then the largest city in the world with about 1 million inhabitants. But that epidemic has thus far evaded secure identification on genetic grounds even if, epidemiologically, the speed, symptoms, and geographic range of the epidemic seem to fit smallpox’s profile. Moreover, if reported epidemics in the eastern part of the Roman Empire in the 4th and early 6th centuries were likewise smallpox, as has been suggested, these would seem to form a chain with persuasive descriptions in Europe and the eastern Mediterranean going back to the 6th and 7th century, respectively.31 Narrative accounts of what seems to be smallpox go back to the 7th century or earlier in Indian records and to the 4th or 5th century in Chinese records, suggesting eastward movement of the disease.32
The origins of smallpox are, of course, important for epidemiological history. But of more importance for understanding the history of the disease in medieval Eurasia is an understanding of its persistence. Was it widespread and endemic throughout Eurasia? Or did it have a more localized, more occult profile? If the character of the early form of the virus was similar to its documented character in modern times, then it would have had three decisive features that controlled its epidemiological behavior: (1) once it transferred from African gerbils and/or camels, it became an obligate human pathogen—that is, it had no animal reservoir in which it could lurk between human outbreaks; (2) it had a fairly short disease interval, from initial infection to resolution (spontaneous cure or death), of approximately one month, meaning that it had to move fairly quickly from host to host; and (3) if patients survived, they survived with life-long immunity from reinfection. They likely also would have survived with distinctive scarring. That meant that smallpox needed one or both of the following conditions to survive: “fresh” victims (newborn children or immigrés) continually coming into large, stable populations of immunes; or it needed to be constantly on the move, spreading from settlement to settlement. The 10th-century descriptions of al-judari in al-Razi (working in Rayy and Baghdad) and of wan dou chuang in medical writers of the Chinese Song dynasty as a disease primarily of children would fit the prior scenario, while the experience of smallpox moving across wide landscapes of small nomadic or farming communities would fit the latter one.33 Researchers involved in the World Health Organization project to eradicate smallpox in the 1960s and 1970s found that the disease could be sustained in quite small populations: “at no time were more than 1 per cent of the villages (20 of 2331) involved with smallpox, and at the lowest point only seven villages (0.3 per cent) had cases of smallpox present.”34
This may account, therefore, for the fact that our evidence for smallpox’s history is so scattered and discontinuous. There is a cluster of writing about smallpox in the area between Egypt and Khwarazm (at the intersection of modern Uzbekistan, Turkmenistan, and Kazakhstan) between the 7th and 11th centuries. Al-Razi’s account of smallpox, written either in Rayy or Baghdad in the first half of the 10th century, acknowledged the earlier description of smallpox (and perhaps also measles) by the 7th-century Alexandrian physician, Aaron; even al-Razi’s account, though often called the first monograph on the disease, was preceded by a work by Thabit ibn Qurra (826–901), a Syriac-speaking translator and scholar likewise working in Baghdad. Two accounts of what appear to be smallpox survive from Constantinople in the 11th and 12th centuries, and we know that al-Razi’s Arabic text was translated into Greek in the 11th century.35 Further east, a cluster of scholars who gathered for a short time at the Khwarazmian court of the Khwarazmshah Ma’mun ibn Ma’mun included Ibn Sina (Avicenna, d. 1037), who would write the most famous medical book of the Middle Ages, the Canon of Medicine; and Abu Sahl al-Masihi (d. 999/1000), who wrote both An Investigation on the Nature of Epidemics, their Prevention and Cure, and also a detailed description of smallpox.36
Another scholar at Khwarazm was the geographer and polymath al-Biruni (d. 1048), who later travelled to India. There, he described smallpox as coming from a wind blowing off Sri Lanka.37 Al-Biruni’s testimony is particularly valuable: presumably, what he described in India was the same thing his intellectual circle knew in Khwarazm. Corroboration of al-Biruni’s account of the presence of smallpox in India in this period is the emergence in Hindu religion, between the 10th and 12th centuries, of a goddess, Shitala, who was an anthropomorphic personification of the disease.38
The most extensive evidence for smallpox in the medieval period comes from East Asia. In China, we find what seems to be smallpox described as early as the 4th century ce. If the textual tradition has been correctly interpreted, then this earliest description, by the physician and alchemist Ge Hung, writing in 340 ce, describes it as a fairly new disease, coming to China from the west. He offers a basic symptomatology and acknowledges that quick treatment can avert the worst of the disease. For Ge’s commentator, Tao Hongjing, writing around 500, in contrast, the task is to reconstruct the arrival of the disease in China, which is now placed some distance in the past, and to further elaborate on its treatment.39 By the 11th century, smallpox was being described, as it had been by al-Razi, as a disease primarily affecting children. Moreover, this is the first period when the notion of smallpox as a “fetal toxin” appears, echoing the idea common in Arabic writings that it was caused by leftover maternal menstrual blood.40 In Japan, it is believed that smallpox first arrived in epidemic fashion in 735, killing as much as one-third of the population. This initial outbreak was followed by twenty-eight epidemics over the course of the next 500 years.41
The fact that different medical traditions in several different languages established descriptive categories for what we now call smallpox strongly suggests that all these writers were describing and experiencing a common biological entity. Al-Razi’s description of the extreme pain in the limbs that sometimes preceded death by smallpox accords well with modern understandings of the virus’s clinical course.42 But the existence of such descriptions cannot be grounds for assuming that smallpox (or a smallpox-like entity) was circulating perpetually throughout all of medieval Eurasia. There are no further specialized texts on smallpox composed in Arabic after the 11th century.43 Most Western European medical textbooks from the late 11th century on would include a chapter on variola, the Latin term used by the famous 11th-century translator Constantinus Africanus to translate the Arabic al-judari. But aside from one 11th- or 12th-century skeleton in France that shows lesions characteristic of survivors of smallpox infections, there is no persuasive evidence that smallpox was present in Western Europe between the 6th century, when Gregory of Tours seems to describe a smallpox outbreak, and the 14th century.44 Carmichael and Silverstein, who survey the evidence for smallpox in Europe prior to the 17th century, find the first reported outbreaks of variola in Europe to be in Florence in 1335 and Naples in 1336; then, in Siena in 1363, in Vicenza in 1386, and Bologna in 1393.45 Those seem to have been minor outbreaks; the first incident they call a proper epidemic did not occur until 1444, in Paris. Records from the Netherlands show a similar chronology, with an initial outbreak around 1383 and another in 1444 or thereafter.46
The timing is significant. The circumstances surrounding the 1330s outbreaks in Italy are as yet unclear, but for the one in the 1360s, there might be a larger context. A register of slaves owned by Florentine citizens exists for the later 14th century, starting in 1366 and extending up to 1397. Compiled in response to a local law demanding that all slaves in Florence be registered (which means that they may have been in their master’s or mistress’s household for some time when the register starts in 1366), it lists the name and ethnicity (geographic origin) of the slave in each entry, plus distinguishing physical features. Of the 347 slaves mentioned, 58 (17 percent) are reported as having smallpox scars. All but three of these scarred slaves are identified as Tatars or “from Caffa.”47 Moreover, to judge from their ages, with only one exception, all the smallpox-scarred individuals (most of whom are women) would have been alive in the mid-1350s. Although several children aged ten and younger are listed (down to age seven), none of them are noted as having scars. Did a smallpox outbreak in the 1350s in the territory of the Golden Horde lead to outbreaks in Tuscany in subsequent decades? It is too soon to tell. But the intense trade in grain, lumber, and slaves that brought the Black Death to Western Europe could have brought other diseases as well. India had already been linked to the steppe by the Turkic expansion of the 11th century, and, under the Mongols, ties between central and eastern Eurasia grew even more intricate. To answer the question of smallpox’s late medieval history, therefore, will likely necessitate looking at forces linking the whole of Eurasia.
Genetics has not factored much in the story of smallpox thus far. Being a virus instead of a bacterium (and hence with a much smaller genome), the odds against recovering and reconstructing it are high. And an irony of the disease’s eradication in the 1970s is that there are few archived samples from which to reconstruct phylogenies.48 Nevertheless, a genetics breakthrough in smallpox history has recently been made—and as with the history of leprosy, it brings as much perplexity as enlightenment. A complete genome sequence of smallpox was assembled in 2016 from naturally mummified remains in Vilnius in Lithuania, dating from the 17th century. Researchers found that this 17th-century strain was basal to all modern archived strains of smallpox virus that were sampled.49 Normally, we should expect that an organism (and for this purpose, we can consider smallpox’s virus a biological entity unto itself) would have increasingly diverse offspring the longer it had existed in the world. Smallpox, as we have seen, was distributed across an increasingly wide geography in the late Middle Ages, and would expand even further—into Africa, the Americas, and the Pacific—in the early modern period. Yet the Vilnius sample suggested that, insofar as it could be gauged from global mid-20th-century samples, modern smallpox had emerged out of a single strain. Was this modern smallpox a recent zoonotic transfer, entirely unrelated to “smallpox” as described by medieval sources? Or had the medieval virus diversified as we would have expected but then died out, leaving just this one particularly virulent strain surviving?
There’s no way to tell at this point, but the latter interpretation seems more likely. Whatever the circumstances that moved smallpox westward in the late medieval period, it is clear that by the mid-16th century, it was expanding explosively.50 The spread of smallpox to the New World is simply part of a global pandemic that Eurasia and Africa were experiencing collectively for the first time. Importantly, the mid-1500s is also the point at which we have the first clear evidence for the development of inoculation, a term that covers a variety of techniques to artificially induce an immune response and ward off future infection.51 The simultaneous invention of these methods suggests that populations were faced with a disease far more fearsome and contagious than that al-Razi and his medical counterparts had faced. If the results from Vilnius offer us a hint of smallpox’s overall character, then it seems likely that the disease came very close to extinction on several occasions, only to be fanned into pandemic phases once again.
Plague is the disease caused by the bacterium Yersinia pestis, an organism first microbiologically identified in Hong Kong in 1894. The locus of scientific discovery, in the context of what would be called the Third Plague Pandemic, created assumptions that plague was intimately associated with East Asia, particularly Yunnan Province or south China. It is clear now that the strain of plague principally responsible for the Third Pandemic was itself a recent arrival in southern China, having come to Yunnan perhaps in the 17th or even 18th century.52 Yet that was not China’s first experience with plague. China, like virtually all of Eurasia, has had many encounters with this ruthless killer, which has been shown to be capable of rather rapid transcontinental migrations. Separating the different waves of plague’s spread is now becoming possible thanks to the development of new genetics analyses. How tightly those waves can be tied to climatic shifts is as yet unclear, but certain lines of evidence suggest a connection, at least in the major pandemic outbreaks of plague.
Evolutionary genetics has established that Y. pestis is a clone of Yersinia pseudotuberculosis, a relatively benign organism that survives in open water and soil, is transmitted between mammalian hosts through the oral-fecal route, and usually causes mild enteric distress before clearing from the body. Plague (Yersinia pestis), in contrast, has, in the absence of modern antibiotic therapy, one of the highest mortality rates known to science. Bubonic plague, the most common form, begins as a fulminating infection in the lymphatic system in response to the bite of an infected vector (flea or tick, or possibly louse), passing afterwards into the bloodstream where, once established as a septicemic infection, it quickly causes death in 40 to 60 percent of those infected. Pneumonic plague is caused when the same organism, instead of entering the mammalian host through an insect bite, is transmitted directly into the lungs by droplets coughed or sneezed out by an already infected host and inhaled by a second host. Lodged in the lungs, an even more rapid infection sets in, causing death within two to three days of onset of symptoms, as opposed to up to seven to ten days in bubonic infections. Other routes of entry are possible: gastroenteric, caused when infected animal meat is eaten; and septicemic, when Y. pestis enters directly into the bloodstream.
Y. pestis likely diverged from Y. pseudotuberculosis about 28,000 years ago, around the time of the Last Glacial Maximum. Plague is a disease of rodents—for the most part, of wild rodents that do not share their habitat with humans. The bacterium is passed from rodent host to rodent host by fleas (or occasionally, ticks). It is only when something disrupts that host-vector ecosystem that human outbreaks occur. A group of extinct strains of Y. pestis has now been widely documented across central Eurasia, in the Afanasievo and Yamnaya cultures of the Bronze Age. These findings were surprising for several reasons, one of them being that this Bronze Age plague did not seem to be capable of transmission by flea.53 In contrast, the strains of plague connected with the historic pandemics of the Middle Ages—the Justinianic Plague, from 541 to c. 750, and the Second Pandemic, whose beginning we usually connect to the devastating Black Death, starting in 1346—were clearly caused by flea-transmitted strains.
This is a critical detail of plague’s biology, because unlike malaria and smallpox, whose histories we have recounted above, plague is not an obligate human pathogen—indeed, with one important exception, humans are utterly irrelevant to plague’s successful persistence in the world today. The exception is that humans have been principally responsible for plague’s long-distance migrations, from the Bronze Age right up to the 20th century. It is now clear that strains of plague have traversed much of the Eurasian continent multiple times. And it is at least in part human activity that transforms local zoonotic transfers of plague from small-scale transactions involving a few animals into large-scale pandemics.
The new genetic understanding we have of the late antique and late medieval pandemics suggests that we should look to the Qinghai-Tibet Plateau, or areas of modern Xinjiang (China’s Uygur Autonomous Region) and Kyrgyzstan just to the west of it, as the source of the strains that caused the first two pandemics, the Justinianic and the Black Death. That, at least, is where strains closely related to the medieval pandemic strains are now found in the world today. What caused the spread of this single-celled microorganism from that original source? What routes did the organism take to reach major centers of population many thousands of kilometers away? Those questions have yet to be answered. What is becoming increasingly clear is that, for both the Justinianic Plague and the plague regime initiated by the Black Death, historians have likely underestimated the geographic extent of plague, its mortality levels, and the ensuing economic and political shifts attributable to the abandonment of farmland and general depopulation. While we cannot yet say with certainty whether the Justinianic Plague had any impact on central or eastern Eurasia, in the case of the late medieval pandemic, indications are strong that much more of Eurasia, and perhaps significant portions of Africa, was impacted than hitherto believed.
Genetics as an Epidemiological Tracker
The presence of Yersinia pestis has now been established by aDNA in crisis burials dating from the time of both the Justinianic Plague and the Black Death, as well as subsequent outbreaks.54 Most of those samples, to date, come from Western Europe. Until aDNA samples are retrieved from eastern and southern Eurasia, questions will legitimately remain concerning whether or not the many epidemics reported in Song and Yuan (Mongol) China, for example, really were plague in our modern understanding. For the time being, studies of plague strains that are currently widely distributed across China show a distinctive signature suggestive of widespread proliferation of the disease in the medieval or early modern period.
The Y. pestis phylogeny—its family tree—shows what seems to be a sudden proliferation into new strains before the Justinianic Plague. That proliferation also coincides with a host switch: all earlier strains of plague seem to have made voles—small field rodents—their major host, whereas most of the subsequent strains of plague, prior to the modern period, have persisted in marmots of various kinds. Both voles and marmots might be used for food, but marmots are also valuable for their fur. Whether some kind of “marmot economy” was involved in sparking the Justinianic Plague is not clear. Our historical evidence, from written sources, paints the plague as firmly centered in the Mediterranean region, far from marmot territory, with reports of mortality extending eastward to Persia.55 Twitchett has posited that outbreaks in China in the 7th century were also due to plague, yet at the moment, we have neither phylogenetic nor palaeogenetic evidence to confirm the presence of plague in eastern China under the Tang, and no medical descriptions sufficiently detailed to make an identification of plague.56 Sequencing of the genome of Y. pestis involved in the Justinianic Plague that reached Bavaria shows it to have 63 SNPs (single nucleotide polymorphisms), differentiating it from the main lineage off of which it branched.57 This could be compared, for example, with strains now found in East Africa, which acquired up to 104 SNPs between the time of the polytomy, the sudden genetic divergence of Y. pestis (c. 1300 ce), and the late 20th or early 21st century, when the samples were collected, or with the 82 SNPs acquired by strains that developed between the time of the Black Death and the outbreak in Marseille in 1722. In other words, even if the Justinianic Plague strain did originate in the Qinghai-Tibet Plateau or Xinjiang, it arrived in the Mediterranean a very changed organism, altered, perhaps, by passing through several different host species, as well as different ecosystems, before making its way to transalpine Germany, which is where the two genomes sequenced thus far have been retrieved.
Given the absence of any clear descriptions of plague east of Persia, and given the genetic distance of the Justinianic Plague strain from its closest Chinese relations, we cannot confidently assert that the Justinianic Plague was a pan-Eurasian phenomenon. But neither can we rule out such a possibility, since the Mediterranean basin and major parts of central and east Asia seem to have shared a common, pronounced climatic shift in the 6th century. In 536, 540, and 547, three separate but successive volcanic explosions (at least one of them in Central America) projected millions of tons of silicates into the earth’s atmosphere. The “dust veil” of 537–538 is reported in a variety of different narrative accounts, while the cooled temperatures are recorded in tree-ring data from the European Alps to the Russian Altai range.58 Did this sudden global cooling “cause” the plague pandemic? That is unlikely. As noted, the reconstructed genome of the Justinianic strain suggests that it had been evolving separately from its progenitor lineage for quite some time. But proliferation of plague has been tied in modern modeling scenarios to sudden periods of cooling and increased rainfall which, at the very least, increases the replication of a “rodent infrastructure” because of the greater availability of food.59 The onset in 541 of the first terrible impact of the plague in the eastern Mediterranean—reported most famously by the Byzantine historian Procopius—suggests that those experiencing both the gloom and the chill of these years saw their woes as connected.
The Black Death
The current lack of retrieved Y. pestis aDNA for central and eastern Eurasia also characterizes our current knowledge of the 14th-century pandemic—but in this case, there is circumstantial evidence that plague was indeed a pan-Eurasian event. For the western half of Eurasia, of course, we have long had a rich documentary record for the timing and impact of the Black Death. From Gabriele de Mussis’s famous, indelible image of the Ulus of Jochi (Golden Horde) attacking Genoese merchants with catapulted, plague-ridden bodies during the siege of the Black Sea port of Caffa in 1346, to Boccaccio’s vivid descriptions of the chaos brought on in Florence by the plague, to Ibn Khaldun’s haunting image of “oblivion and restriction” having come over the world, there has been no lack of evidence for the plague’s effects in Europe, the Levant, or North Africa from the middle of the 14th century on. Estimates of total mortality for both Western Europe and major centers of the Islamicate world usually fall between 40 and 60 percent.60
The findings from genetics have reinforced—or, at least, not contradicted—this narrative. In 2011, the complete genome of Yersinia pestis was retrieved from three bodies buried in the London Black Death Cemetery at East Smithfield, a cemetery particularly valuable for analysis because its dates of creation (late 1348 or early 1349) and closure (1350) are well documented. In fact, two genetic sequences were announced, the second one being found in a fourth body. The first sequence, evolutionarily prior to the other, could be placed almost at the center of a comprehensive phylogenetic tree for Y. pestis that had slowly been in development since 1994. This Black Death genome, it was determined, fell just two genetic changes, that is, two SNPs, beyond the polytomy, resulting in a “Big Bang” that suddenly split what had been a single-branched evolutionary tree of Y. pestis into four new lineages. The Black Death genome was near the base of Branch 1, while the second genome announced in the 2011 study fell two further SNPs along Branch 1. Although not recognized initially, the second genome came not from the Black Death Cemetery but from a later burial site associated with a second wave of plague in London in the 1360s.61
The first London genome represents the strain clearly associated with the major European mortality of the mid-14th century. It is, nucleotide-for-nucleotide, identical to a genome sequenced in 2016 from Barcelona, from a mass burial pit in one of that city’s basilicas. That strain produced further progeny within Europe in the early modern period. These later strains are known from partial genome sequences from Manching-Pichl (Bavaria) and Brandenburg; a whole genome from the German town of Ellwangen, which suffered a plague outbreak in the late 15th- or early 16th century; and five whole genomes from Marseille in 1722, the last known outbreak of plague in continental Europe. Although it cannot yet be proven that these strains developed within the confines of Europe rather than being newly imported each time, the consistency of the results does strongly suggest the creation of one or more reservoirs for plague within Western Europe itself. The creation of those reservoirs may, moreover, have been facilitated by a climatic shift that had its most pronounced effects in the 1340s, ushering in the long cool period known as the Little Ice Age. Unlike the climatic shift of the 6th century, which can be tied to volcanic activity, the climatic shifts of the 14th century have been linked to shifts in solar irradiance, oceanic atmosphere patterns, and excessive rainfall.62 The Black Death, therefore, created a new disease regime in the Mediterranean and Europe, and may itself have been fueled by a new climatic regime. It would transform the populations, the economies, and the lives of most of these societies for the next 500 years.63
But the Black Death strain affected more than just Europe and the Mediterranean. The Black Death strain must have proliferated through hundreds of thousands of rodents and perhaps millions or billions of fleas or other insect vectors to have caused the mass mortality that it did. That fulminating process had already begun in a plague reservoir near the Black and Caspian Seas—and it did not die out. That reservoir gave birth to a second strain, the pestis secunda, which would also afflict Europe. Whether this second strain took a southern route into Western Europe via the Black and Mediterranean Seas (as its predecessor had in the 1340s), or a northern route facilitated by the mercantile networks of the Hanseatic League in the North Sea, is not yet clear. The pestis secunda strain has been documented in both the Netherlands and London.64 This same reservoir seems also to have created a new epidemic trajectory, sending plague northward into Russia, where an even more evolved form of the strain has been found in a 14th-century burial in the southern Russian town of Bolgar City.65 An immediate progenitor of the Bolgar City strain likewise proved to be hardy, since—to judge from the distribution of still living strains—its direct descendants would reach sub-Saharan Africa, Tibet, and, by the 17th or 18th century, Yunnan Province, from where they would seed the Third Pandemic.66
Plague in Central and Eastern Eurasia: A Role for the Mongols?
That, then, was the fate of Branch 1, the westernmost of the four branches created by the “Big Bang” polytomy of the 13th century. Branches 3 and 4 had limited geographic range; they are found now only in Gansu Province, Mongolia, and Siberia. Branch 2, however, produced progeny that would end up being distributed across the area of the Caucasus to Uzbekistan, and across the whole of China, into Tibet, and into Nepal. In other words, its imprint was almost exactly the same as that of the Mongol Empire.
So, what was the role of the Mongols in initiating the Second Plague Pandemic? As noted earlier, humans are for the most part irrelevant to plague’s evolution, except in one respect: long-distance dissemination. It was humans who carried plague out of Caffa and across the Black Sea and Mediterranean in their ships; it was humans who must have distributed rodents, or at least their fleas, across the same routes where grains, textiles, or furs were traded via urban networks in Europe and North Africa. Indeed, it was likely only a few such acts of biological disruption that were needed to move plague across vast distances.67 The role of the Mongols in nudging plague out of its isolated, wilderness reservoirs has long been suspected but never proven. William McNeill, writing long before the breakthroughs of genetics could be envisioned, saw the Mongols’ disruptive act as occurring in Yunnan Province, where plague had broken out in the 19th century and which he thought was its natural home.68 Yet as already noted, the new genetics does not support a southern Chinese origin of the Second Pandemic. More recently, Hymes, taking into account the new genetics, has suggested that the Mongols’ first encounters between 1206 and 1221 with the Xia State in Gansu Province (on the northern edge of the Qinghai-Tibet Plateau) may have been the key disruptive act.69 Accustomed to eating marmot in their homeland, they may have continued that dietary habit when they encountered new species of this large and tasty rodent while expanding into new territories, not knowing that some of them harbored a dangerous disease. Whatever the circumstances of the epidemiological encounter, there seems to have been new transmission of the disease. Hymes notes the repeated coincidence of Mongol sieges and subsequent epidemic outbreaks, most spectacularly at Kaifeng in 1232, which suffered a 40 percent loss in population.
If it was indeed plague that caused these 13th-century epidemics, and if it was indeed the Mongols who were the disruptive force that moved plague out of its long-term, wild-rodent reservoirs in isolated areas of the northern Qinghai-Tibetan Plateau, there is, at the moment, no clear genetic signature to prove it. Palaeogenetics evidence for any pre-polytomy events, should it ever be recovered, would be decisive. Still, even if Hymes’s hypothesis that plague—and not some other, massively lethal disease—was responsible for the early 13th-century epidemics is substantiated, there is a century to account for between these first associations between the Mongols and an “emerging disease” in the 1200s, and the narratives we have of both the Black Death in western Eurasia and a new series of disease outbreaks recorded in 14th-century Chinese sources (1331, 1333, 1344, and 1345). There is one possible genetic trace to connect the 13th- and 14th-century narratives: a surviving strain of Y. pestis (0.ANT3) originated just before the polytomy. Twenty isolates have been identified; they are found only in marmots or ground squirrels in the far west of Xinjiang, or even further west, in Kyrgyzstan, the heart of the Chaghatai Khanate.70 These strains share a common ancestor with the one that led up to the polytomy, and they may be the last remaining echo of an as yet unknown event that pushed Y. pestis into a new pandemic phase.
If plague was on the move in the 13th century, why was there no “Black Death” then? Many of the same mercantile networks that existed in the 14th century also existed in the 13th, which was also the main period of Mongol military expansion and ensuing massive displacements of populations. Here is where a possible parallel with the Justinianic Plague may come into play. As noted, the Justinianic Plague was preceded by a worldwide climatic event caused by a sequence of exploding volcanoes. Importantly, there was a major volcanic event in the 13th century, too: the explosion of the Samalas volcano in Indonesia, which perhaps exceeds in the size of its output every other volcanic explosion of the Holocene. It occurred in 1257, the same year the Mongols besieged an obscure fort in Iran called Lambasar. When the siege ended, there was a plague outbreak, similar to the pattern Hymes has already documented for Jin-era China earlier in the century. As has been noted, some event or sequence of events seems to have moved a hardy lineage of Y. pestis westward from Xinjiang or the Tian Shan Mountains in the 13th century, perhaps into areas near the Caspian Sea. Was the siege of Lambasar part of that process? There is no way to tell at this point. But if the transported bacterium was indeed the match that could light a fire of plague, it still needed fuel. The volcanic event of 1257 has been shown to have had less of a climatic impact than might be predicted on the basis of its size: records from Europe and Japan show that, although it created a shift in weather patterns and atmosphere still detectable in both physical proxy records and human accounts, its duration was not especially pronounced.71
That was not true of the climate shifts that occurred in the 14th century. Economic historian Bruce Campbell calls this period “the Great Transition,” and sees it ushering in a permanent change in climate, and indeed, in the very economies and social structures of Eurasia.72 As we have seen, some event, perhaps in the third quarter of the 13th century, perhaps at the very beginning of the 14th century, suddenly split Yersinia pestis’s evolutionary line in three (and soon four) different directions. One offshoot seems to have either stayed locally in Gansu Province or returned there, splitting again almost immediately; these Branches, 3 and 4, then either stayed in Gansu or passed into Mongolia and Siberia, where the two lineages are found to this day. Another offshoot, the Black Death strain (which differs only by two SNPs from the ancestor it shared with Branches 3 and 4), “seeded” a new reservoir of plague that broke out devastatingly in the western Mongol territories (the Ilkhanate and the Golden Horde), causing plague outbreaks from at least 1346 in Tabriz, Azerbaijan, Saray, Khorazm, and, of course, in Caffa. This strain then passed into the Mediterranean and Europe, causing the pandemic we traditionally call the Black Death. Another offshoot, what we now call Branch 2, would move eastward. The evolutionarily most ancestral extant strain we have of it has been found in the central Caucasus Mountains, and other offshoots would remain in that area.73 But many other offshoots traveled further to the East, and there embedded themselves in communities of marmots, ground squirrels, and a variety of other rodents in all areas of China, Nepal, Tibet, and Mongolia. These strains may have swamped strains that were already in China, if, in fact, Hymes’s belief that the 13th-century epidemics were also the result of plague is correct.
The Mongols may, at the beginning of their military expansion out of Mongolia, have benefitted from climatic change.74 Expansive grassy fields giving fodder to their horses was their biggest boon. But climate seems to have had very different effects at the end of their moment in history. Of all the strains of Yersinia pestis that persist in the world today, close to 80 percent descend from the 13th-century dispersal of plague across northern Eurasia. Plague would terrorize societies across Eurasia and North Africa—and even sub-Saharan Africa—for centuries. Descendants of the Black Death strains would create global panic anew when they hijacked a 19th-century mode of mobility— steamships—and thus became not simply a transcontinental killer, but a transoceanic one as well.
Discussion of the Literature
There is not yet a distinct area of “climate and disease studies” in the field of Eurasian history. The two topics have distinct intellectual pedigrees, though they share the perspective that the nation-state functions poorly as a unit of analysis, since for climate as well as infectious disease, national borders are meaningless. Disease history, or historical epidemiology, in turn has two pedigrees. On the one hand, it is a subset of the history of medicine. On the other hand, disease history has been the province of the field of palaeopathology, which often now falls under the larger rubric of bioarchaeology. The two approaches to the history of disease could be seen as, on the one hand, reconstructing human views about and perceptions of disease (whether medical or lay); or on the other hand, reconstructing the material record of disease from the evidence of human bodies. The latter field did much of its work for decades at the macroscopic level: that is, by examining what could be seen in terms of lesions in teeth or bones with the naked eye. Those analyses have now broadened to encompass a variety of methods that assess physical remains on a molecular level; these now include the highly specialized field of palaeogenetics.
History of medicine developed broadly over the course of the 20th century to encompass all aspects of medical ideas and practice, as well as experiences of health and disease, from theories of physiology to anatomical practices, therapeutic techniques, and social interactions between medical practitioners or institutions and their clientele. History of medicine, particularly since the late 20th century, has emphasized the perspectives of the historical actors themselves. There is an older historiography of disease history based entirely on written accounts and formulations of disease as they were used in the past.75 Leprosy, for example, has been the subject of specialized historical studies, as well as palaeopathological research. Leung’s history of leprosy in China, for example, is comparable to work done on medieval Europe by Rawcliffe and Demaitre, all of which are written primarily from documentary records or medical treatises, with little engagement with the material record of the disease.76 There is, moreover, a strong historiographical tradition of examining ideas about the causes of disease, specifically whether it was due to the internal physiological characteristics of the individual, to environmental factors, or to actual transmissibility of some noxious property between individuals.77
A line of critique that has often divided “history of medicine” and “history of disease” approaches is the issue of retrospective diagnosis. Prior to the development of scientific methods of assessing the presence of infectious disease in the pre-germ theory past—from examination of physical lesions by palaeopathologists, on the one hand, and from reconstruction of genetic histories of pathogens by either phylogenetic or palaeogenetic methods, on the other hand—histories of disease were constructed almost entirely on the basis of written records or works of art. As products of human creativity, it has been argued, such records cannot represent disease outside of the categories and vocabularies used at the time the records were created.78 For the modern historian to impose modern disease categories onto culture-specific records is both vain and distorting.
Once this skepticism about the ability to identify diseases in the past from written or artistic sources was raised, however, it was difficult to put to rest, even if most historians were willing to believe, for example, the al-Razi’s al-judari was, in fact, smallpox. Prior to the successes identifying Yersinia pestis in human remains in the 2000s, there had been thirty years of debate whether Y. pestis was indeed the cause of the Black Death and subsequent human outbreaks. That question was never going to be resolved based on historical written documentation, for the simple fact that microbes were never observed or recorded in written accounts before the availability of modern microscopy. In one formulation of this view, absent the modern laboratory, there were no germs.79
This critique did not address the ontological reality of infectious diseases, but even for scholars who opposed the nihilism of the anti-retrospective diagnosis stance, there was little basis on which to explore that ontological reality. The late 19th-century laboratory did seem to be the ne plus ultra, the point beyond which the history of microorganisms could not go. An evolutionary approach to infectious disease history, in contrast, focuses exactly on the ontological reality of pathogen species’ histories. P. vivax and P. falciparum, M. tuberculosis and M. africanum, M. leprae and M. lepromatosis, V. major and Y. pestis (the agents of, respectively, malaria, tuberculosis, leprosy, smallpox, and plague) all existed in the pre-laboratory past, whether or not the humans alive at the time recognized their existence. Molecular genetics, both by establishing the family trees of these organisms and retrieving their genetic fossils, is beginning to give real definition to these parameters of time and space.
It is likely that disease histories in the future will follow the path already taken in climate history, which is to move toward a consilient historiography, one that takes both physical (in this case, biological) continuities and perceived experiences of disease into account.80 New interrogations of disease history will demand greater coordination between geneticists, bioarchaeologists, and historians.81 One reason is chronological and evidentiary overlap. As discussed in this article, several of the recent genetics studies have proposed radically shorter time frames for the experience of human infectious diseases than in older paradigms, placing their histories within the scope of the main developments of urban civilization. Even if they cannot help determine the presence of microbes, written and artistic historical records are still our most valuable indicators of where humans have been and what they have been doing in the past three millennia. Second, as it becomes increasingly obvious how great a role humans’ own social and cultural behaviors play in disease transmission, even in vector-borne disease it becomes increasingly necessary to study not only the microbe, but every other trophic level involved. For example, most forms of rice production create excellent breeding grounds for mosquitoes, with extensive amounts of stagnant water. Do we see changes in malarial burdens along with agricultural shifts?82
The role of climate in these interactions remains to be determined. Climate history, a richly interdisciplinary field, is a recent development. To connect to other traditions of history, climate history has had to develop greater chronological resolution. A continued weakness of climate history in relating to disease history is the difficulty of moving beyond observed correlation (say, the coincidence of the Justinianic Plague and Black Death with major cooling events in the 6th and 14th centuries, respectively) to causal effects. In the case of plague, cool temperatures, especially when combined with increased precipitation, have been documented to allow enzootic plague foci to flourish. Yet outbreaks of plague in wild rodent populations do not necessarily mean that there will be outbreaks in human populations. The increased use of mathematical modeling to work out epidemiological profiles of historical events, even if they focus on better documented recent events, will enrich the power of epidemiological history both to reconstruct the spread of infectious diseases of the past, and to help design models to face the uncertain future that lies ahead, where compromised antibiotic arsenals and global warming will likely change the interactions between humans, disease, and climate once again.83
Primary Sources, Digital Materials, and a Word of Caution
Of the diseases surveyed here, plague has generated the most specialized literature.84 For the history of disease and climate, the most telling primary sources are not written texts, but bones and teeth, pollen and trees, and other remnants of the physical world that existed in the medieval past. As explained above, the archivists and interpreters of that data are not traditional historians, but scientists of various stripes. And much of the raw data on which they base their work is being published digitally. (See “Links to Digital Materials” below.)
Traditions of medical writing in all parts of Eurasia can be used to establish modes of thinking about disease. Surveys exist for Arabic medical literature, Indian medical literature, Chinese medical literature, and Western European medical literature.85 In all these cultural traditions, however, the majority of the material remains in manuscript, unedited. Efforts are underway in a variety of cultural institutions to digitize these materials, which will make them more readily accessible to skilled researchers.
Links to Digital Materials
Aside from databases of climatological data, there are few online resources for interrogating the history of disease in the premodern era. Certain libraries have concentrated collections of digitized printed books from their collections. All the bioarchaeological data from London’s East Smithfield Black Death Cemetery and its successor cemetery, St Mary Graces, are available via the Museum of London Centre for Bioarchaeology. Other online resources are the Supplementary Materials usually published with scientific studies. Thus, for example, the landmark papers “Yersinia pestis Genome Sequencing Identifies Patterns of Global Phylogenetic Diversity”, which created a global assembly of Yersinia pestis isolates, and “Historical Variations in Mutation Rate in an Epidemic Pathogen, Yersinia pestis, which constructed a new phylogenetic tree of Yersinia pestis based on 133 complete genome sequences, have all their supporting data published online. And, of course, all complete genome sequences of Y. pestis, the MTBC, and other organisms are available in public databanks. It is important to note that most bibliographical databases in biomedicine (PubMed, SciVerse Scopus, etc.) do not index humanities publications. The majority of work published by historians of premodern medicine will therefore not be captured in such searches, nor will it necessarily be in English (as has become normative in the sciences). Instead (or in addition), humanities indices, like International Medieval Bibliography and Regesta Imperii should be consulted.
For the history of disease and history of medicine, Harvard University has a digital collection called Contagion: Historical Views of Diseases and Epidemics, a collection of older printed books (c. 1500–c. 1900) on infectious diseases. Islamic Medical Manuscripts at the National Library of Medicine is a curated online collection not only of manuscripts in the US National Library’s collections in Bethesda, MD, but also a rich encyclopedia of information of medical writers of the Islamicate world and their books. The Bibliothèque Inter-Universitaire de Santé in Paris (BIUS) has a superb digitized collection of older printed works in medical history available online (Medic@). The eTK/eVK (electronic Thorndike-Kibre/electronic Voigts-Deery-Kurtz) are digital inventories of, respectively, medieval Latin and medieval English literature in science and medicine. Because titles of texts were often unstable or missing, the habit developed in Western bibliography to use the incipit, the opening words of a text, as its identifier. Lynn Thorndike and Pearl Kibre (TK) adopted this method to survey the vast landscape of Latin scientific and medical literature.86 In preparing a comparable, born-digital survey of Old and Middle English scientific and medical literature (eVK), Linda Voigts and Patricia Deery-Kurtz digitized and updated TK (now eTK). The Selected, Annotated Bibliography of the History of Chinese Science and Medicine Sources in Western Languages is a bibliography prepared by Nathan Sivin at the University of Pennsylvania. Medicine in Medieval Egypt is an online exhibit and exploration of the medical materials collected in the Cairo Genizah, a repository of discarded materials formerly held at the Ben Ezra Synagogue in Fustat (Old Cairo).
For climate history, see the Old World Drought Atlas. Also, the Digital Atlas of Roman and Medieval Civilizations (see DARMC) includes databases on Historical Evidence of Pre-modern Climate, 100 bce–1500 ce.
Finally, a word of caution. As explained above, the advent of ancient DNA (“aDNA”) since the 1990s, together with other aspects of molecular genetics, has transformed our ability to understand the history of infectious diseases, particularly since the complete sequencing of historical genetic material became possible in 2011. Many historical studies done before 2011 have continuing value as analyses of documentary records, which remain crucial to understanding the human responses to disease. But they should be read with caution in terms of any claims they make about either the identity or antiquity of pathogenic organisms or the geography of their spread.
- Achtman, Mark. “How Old are Bacterial Pathogens?” Proceedings of the Royal Society. B: Biological Sciences 283, no. 1836 (August 2016).
- Biraben, Jean Noël. Les hommes et la peste en France et dans les pays européens et méditerranéens. Paris: Mouton, 1975–1976.
- Brooke, John L. Climate Change and the Course of Global History: A Rough Journey. New York: Cambridge University Press, 2014.
- Buikstra, Jane E. and Charlotte A. Roberts, eds. The Global History of Paleopathology. Oxford: Oxford University Press, 2012.
- Eroshenko, Galina A., Nikita Yu Nosov, Yaroslav M. Krasnov, Yevgeny G. Oglodin, Lyubov M. Kukleva, Natalia P. Guseva, Alexander A. Kuznetsov, Sabyrzhan T. Abdikarimov, Aigul K. Dzhaparova, and Vladimir V. Kutyrev. “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.
- Goldschmidt, Asaf. “Epidemics and Medicine During the Northern Song Dynasty: Revival of Cold Damage Disorders (Shanghan).” T’oung Pao 93 (2007): 53–109.
- Green, Monica H., ed. Pandemic Disease in the Medieval World: Rethinking the Black Death, special inaugural issue of The Medieval Globe 1 (2014).
- Grmek, Mirko D. Diseases in the Ancient Greek World. Translated by Mireille Muellner and Leonard Muellner. Baltimore, MD: Johns Hopkins University Press, 1989.
- Kiple, Kenneth F., ed. The Cambridge World History of Human Disease. Cambridge, UK: Cambridge University Press, 1993.
- Köhler, Kitti, Antónia Marcsik, Péter Zádori, Gergely Biro, Tamás Szeniczey, Szilvia Fábián, Gábor Serlegi, Tibor Marton, Helen D. Donoghue, and Tamás Hadju. “Possible Cases of Leprosy from the Late Copper Age (3780–3650 cal bc) in Hungary.” PLoS ONE 12, no. 10 (2017): e0185966.
- Krause, Johannes, and Svante Päabo. “Genetic Time Travel.” Genetics 203, no. 1 (May 2016): 9–12.
- Lascaratos, John, and Constantine Tsiamis. “Two Cases of Smallpox in Byzantium.” International Journal of Dermatology 41, no. 11 (2002): 792–795.
- McMichael, Anthony. Climate Change and the Health of Nations: Famines, Fevers, and the Fate of Populations. Oxford: Oxford University Press, 2017.
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1. Monica H. Green, “The Globalisations of Disease,” in Human Dispersal and Species Movement: From Prehistory to the Present, eds. Nicole Boivin, Rémy Crassard, and Michael D. Petraglia, 494–520 (Cambridge, UK: Cambridge University Press, 2017). The interpretation of leprosy’s possible Eurasian origin that I give below differs from my previously published statements, which followed the earlier theories of geneticists.
2. Stephen Boyanton, “The Treatise on Cold Damage and the Formation of Literati Medicine: Social, Epidemiological, and Medical Change in China, 1000–1400,” PhD diss., Columbia University, 2015, adopts the concept of epidemiological frontiers from Asaf Goldschmidt, “Epidemics and Medicine during the Northern Song Dynasty: Revival of Cold Damage Disorders (Shanghan),” T’oung Pao 93 (2007): 53–109.
3. Kyle Harper, “Pandemics and Passages to Late Antiquity: Rethinking the Plague of c. 249–270 Described by Cyprian,” Journal of Roman Archaeology 28 (2015): 223–260.
4. Emmanuel Le Roy Ladurie, “Un concept: l’unification microbienne du monde (XVIe–XVIIe siècles),” Schweizerische Zeitschrift für Geschichte 23, no. 4 (1973): 627–696. An abbreviated English translation is also available: Emmanuel Le Roy Ladurie, “A Concept: The Unification of the Globe by Disease,” trans. Sian Reynolds and Ben Reynolds, in The Mind and Method of the Historian, 28–83 (London: Harvester, 1981).
5. Novel methods continue to be attempted, nevertheless. See, for example, Stuart Borsch and Tarek Sabraa, “Plague Mortality in Late Medieval Cairo: Quantifying the Plague Outbreaks of 833/1430 and 864/1460,” Mamluk Studies Review 19 (2016): 57–90; and Stuart Borsch and Tarek Sabraa, “Refugees of the Black Death: Quantifying Rural Migration for Plague and Other Environmental Disasters,” Annales de Démographie Historique 2017 N°2, no. 134, 63–93.
6. For example, David Stucki et al., “Mycobacterium tuberculosis Lineage 4 Comprises Globally Distributed and Geographically Restricted Sublineages,” Nature Genetics 48 (2016): 1535–1543.
7. I have omitted a survey of tuberculosis from the present article, not because it was not present in medieval Eurasia (it clearly was), nor even because it has not seen major advances in research of late (it has), but because no clear narrative has yet emerged of its development or geographic spread. See Green 2017, 499–502. Speculative historical studies based on phylogenetics of the Mycobacterium tuberculosis. Complex include the following: Igor Mokrousov et al., “Emerging Peak on the Phylogeographic Landscape of Mycobacterium tuberculosis in West Asia: Definitely Smoke, Likely Fire,” Molecular Phylogenetics and Evolution 116 (2017): 202–212; and Mary B. O’Neill, Andrew Kitchen, Alex Zarley, William Aylward, Vegard Eldholm, and Caitlin S Pepperell, “Lineage Specific Histories of Mycobacterium tuberculosis Dispersal in Africa and Eurasia,” bioRxiv (Oct. 27, 2017).
8. Timothy P. Newfield, “A Cattle Panzootic in Early Fourteenth-Century Europe,” Agricultural History Review 57, no. 2 (2009): 155–190; Timothy P. Newfield, “Human–Bovine Plagues in the Early Middle Ages,” Journal of Interdisciplinary History 46, no. 1 (Summer 2015): 1–38; Timothy P. Newfield, “Domesticates, Disease and Climate in Early Post-Classical Europe: The Cattle Plague of c. 940 and its Environmental Context,” PCA: European Journal of Postclassical Archaeologies 5 (2015): 95–126; Bruce M. S. Campbell, “Panzootics, Pandemics and Climatic Anomalies in the Fourteenth Century,” in Beiträge zum Göttinger Umwelthistorischen Kolloquium 2010–2011, ed. Bernd Herrmann, 177–215 (Göttingen, Germany: Universitätsverlag Göttingen, 2011); and Philip Slavin, “The Great Bovine Pestilence and its Economic and Environmental Consequences in England and Wales, 1318–1350,” Economic History Review 65, no. 4 (2012): 1239–1266.
9. Peter W. Gething, et al., “A New World Malaria Map: Plasmodium falciparum Endemicity in 2010,” Malaria Journal 10, no. 378 (2011); and Peter W. Gething et al., “A Long Neglected World Malaria Map: Plasmodium vivax Endemicity in 2010,” PLoS Neglected Tropical Diseases 6, no. 9 (2012): e1814.
10. There are at least five species of plasmodia that regularly infect humans. It has been suggested that the others beside the human-adapted vivax and falciparum are of even greater antiquity. See Gavin G. Rutledge et al., “Plasmodium malariae and P. ovale genomes provide insights into malaria parasite evolution,” Nature 542 (Feb. 2, 2017): 101–104.
11. Weimin Liu et al., “Origin of the Human Malaria Parasite Plasmodium falciparum in Gorillas,” Nature 467 (September 23, 2010): 420–425; Weimin Liu et al., “African Origin of the Malaria Parasite Plasmodium vivax,” Nature Communications 5, no. 3346 (2014); and Sesh A. Sundararaman et al., “Genomes of Cryptic Chimpanzee Plasmodium Species Reveal Key Evolutionary Events Leading to Human Malaria,” Nature Communications 7, no. 11078 (2016).
12. Zahi Hawass et al., “Ancestry and Pathology in King Tutankhamun’s Family,” JAMA 303, no. 7 (2010): 638–647. Tutankhamun ruled from 1333 to 1324 BCE.
13. Kyle Harper, The Fate of Rome: Climate, Disease, and the End of an Empire (Princeton, NJ: Princeton University Press, 2017), 84–88; and Timothy P. Newfield, “Malaria and Malaria-Like Disease in the Early Middle Ages,” Early Medieval Europe 25, no. 3 (2017): 251–300.
14. Gwen Robbins et al., “Ancient Skeletal Evidence for Leprosy in India (2000 BC),” PLoS One 4, no. 5 (2009): e5669, 1–8.
15. An African origin of M. leprae was proposed as one of two hypotheses in Marc Monot et al., “On the Origin of Leprosy,” Science 308 (May 13, 2005): 1140–1142, which first established the lineage numbering system for M. leprae. In Marc Monot et al., “Comparative Genomic and Phylogeographic Analysis of Mycobacterium leprae,” 41, no. 12 (December 2009): 1282–1289, similarly based on modern genetic samples but here adding data from a partial reconstruction of genetic material from a burial in 5th-century Egypt, Monot and colleagues affirmed an East African origin of the disease. A substantial revision of the phylogeny, plus the positing of a more ancestral Lineage 0, appears in Verena J. Schuenemann et al., “Genome-wide Comparison of Medieval and Modern Mycobacterium leprae,” Science 341 (July 12, 2013): 179–183, which has, in my opinion, thrown the assumed African origin of M. leprae into question. A long-term study of leprosy in Hungary, based on ten thousand samples, found leprosy present in the late Copper Age (3800–3500 BCE), followed by a long period of absence. It reappeared in the late Roman period and continued until the later Middle Ages. See György Pálfi et al., “Osteoarchaeological and Paleomicrobiological Evidence of Leprosy in Hungary,” The 83rd Annual Meeting of the American Association of Physical Anthropologists, April 8–10, 2014, Calgary, Canada. Special Issue: S1 Supplement 58: 213; and Kitti Köhler et al., “Possible Cases of Leprosy from the Late Copper Age (3780-3650 cal BC) in Hungary,” PLoS ONE 12, no. 10 (2017): e0185966.
16. As noted above, while there are indeed two species of leprosy bacteria, the more recently discovered one, Mycobacterium lepromatosis, has not yet been confirmed to have played any role in medieval Eurasia. There is not yet any palaeopathogical method to distinguish infection of M. leprae from M. lepromatosis, and no aDNA of the latter organism has yet been found.
17. Schuenemann et al., 2013. See also Pushpendra Singh et al., “Insight into the Evolution and Origin of Leprosy Bacilli from the Genome Sequence of Mycobacterium lepromatosis,” PNAS 112, no. 14 (2015): 4459–4464.
18. Charlotte Avanzi et al., “Red Squirrels in the British Isles are Infected with Leprosy Bacilli,” Science 354, no. 6313 (Nov. 1, 2016): 744–747; Helen M. Butler et al., “Further Evidence of Leprosy in Isle of Wight Red Squirrels,” Veterinary Record 180 (April 22, 2017): 407. The suggested divergence between strains of M. lepromatosis leaves open the possibility that it entered the Americas with the First Peoples, but there is no other evidence one way or another at the time of this writing for its deeper history.
19. Encyclopedia of Life.
20. Schuenemann 2013. See also Singh 2015.
21. For example, three burial sites in the Spanish town of Pamplona yields skeletal evidence suggestive of leprosy in Roman (2nd–4th century), Visigothic (7th–9th century), and Islamic (8th century) periods. See M. P. De Miguel Ibáñez et al., “Tres posibles casos de lepra en la Plaza del Castillo (Pamplona, Navarra),” in Paleopatología: ciencia multidisciplinar, ed. A. González Martín, O. Cambra-Moo, J. Rascón Pérez, M. Campo Martín, M. Robledo Acinas, E. Labajo González, and J. A. Sánchez Sánchez, 355–365 (Madrid: Sociedad Española de Paleopatología, 2011). A summary of findings to date can be found in Sarah A. Inskip et al., “Osteological, Biomolecular and Geochemical Examination of an Early Anglo-Saxon Case of Lepromatous Leprosy,” PLoS ONE 10, no. 5 (2015): e0124282. See also Ruth I. Meserve, “A Ravaging Disease in Medieval Central Eurasia: Leprosy,” Central Eurasia in the Middle Ages: Studies in Honour of Peter B. Golden, ed. István Zimonyi and Osman Karatay, Turcologica, 104, 265–274 (Wiesbaden, Germany: Harrassowitz, 2016), though note that she has not taken into account the work of Schuenemann et al., 2013.
22. Importantly, Monot et al. 2009 (p. 1287) reported that the 5th-century individual in Dakhleh Oasis, Egypt, found to be carrying a lineage 3 M. leprae strain (which Monot and colleagues assumed should have been associated with Europe) proved, upon analysis, to have an isotopic profile different from that of others buried at the site, suggesting that he was an immigrant. Similarly, the earliest known case of leprosy in England that has been proven by aDNA likewise, dating from the 5th–6th century, likewise appears to be an immigrant; see Inskip et al., 2015.
23. Hannah Barker, “Purchasing a Slave in Fourteenth-Century Cairo: Ibn al-Akfānī’s Book of Observation and Inspection in the Examination of Slaves,” Mamluk Studies Review 19 (2016): 1–23; and Carmel Ferragud, “The Role of Doctors in the Slave Trade during the 14th and 15th Centuries within the Kingdom of Valencia (Crown of Aragon),” Bulletin of the History of Medicine 87 (2013): 143–160.
24. On India: Roland E. Emmerick, “Some Remarks on the History of Leprosy in India,” Indologica Taurinensia 12 (1984): 93–105; Robert Joseph Gallagher, “An Annotated Translation of Chapter 7 of the Carakasaṃhitā Cikitsāsthāna: Leprosy and Other Skin Disorders.” On China: Angela Ki Che Leung, Leprosy in China: A History, Studies of the Weatherhead East Asian Institute, Columbia University (New York: Columbia University Press, 2009). On Islamicate world: Michael W. Dols, “Leprosy in Medieval Arabic Medicine,” Journal of the History of Medicine and Allied Sciences 34, no. 3 (July 1979): 314–333; Michael W. Dols, “D̲j̲ud̲h̲ām,” in Encyclopaedia of Islam, 2d ed, ed. P. Bearman, Th. Bianquis, C. E. Bosworth, E. van Donzel, and W. P. Heinrichs (2012). On Europe: Luke E. Demaitre, Leprosy in Premodern Medicine: A Malady of the Whole Body (Baltimore, MD: Johns Hopkins University Press, 2007); and Carole Rawcliffe, Leprosy in Medieval England (Woodbridge, UK: Boydell & Brewer, 2006).
25. See Inskip et al., 2015.
26. Elma Brenner, “The Leprous Body in Twelfth- and Thirteenth-Century Rouen: Perceptions and Responses,” in The Ends of The Body: Identity and Community in Medieval Culture, eds. Suzanne Conklin Akbari and Jill Ross, 239–259 (Toronto: University of Toronto Press, 2013).
27. Dols, “Leprosy” 1979; Justin Stearns, “Contagion,” Encyclopedia of Islam, 3rd ed. (Leiden, Netherlands: Brill, 2010), 180–182; and Russell Hopley, “Contagion in Islamic Lands: Responses from Medieval Andalusia and North Africa,” Journal for Early Modern Cultural Studies 10, no. 2 (Fall/Winter 2010): 45–64.
28. Koichi Suzuki et al., “Paleopathological Evidence and Detection of Mycobacterium leprae DNA from Archaeological Skeletal Remains of Nabe-kaburi (Head-Covered with Iron Pots) Burials in Japan,” PLoS ONE 9, no. 2 (2014): e88356.
29. Brenda J. Baker and Katelyn L. Bolhofner, “Biological and Social Implications of a Medieval Burial from Cyprus for Understanding Leprosy in the Past,” International Journal of Paleopathology 4, no. 1 (2014): 17–24.
30. Igor V. Babkin and Irina N. Babkina, “A Retrospective Study of the Orthopoxvirus Molecular Evolution,” Infection, Genetics and Evolution 12, no. 8 (December 2012): 1597–1604. On the date of domestication of Camelus dromedarius, see Fiona B. Marshall et al., “Evaluating the Roles of Directed Breeding and Gene Flow in Animal Domestication,” Proceedings of the National Academy of Sciences 111, no. 17 (April 29, 2014): 6153–6158.
31. Elio Lo Cascio, L’Impatto della ‘Peste Antonina’ (Santo Spirito [Bari], Italy: Edipuglia, 2012). Harper 2017, 98–115 and 174–175, now offers the best assessment of the identification of the disease as smallpox on the basis of the extant textual evidence. On what seems to be smallpox in the 5th and 7th centuries, see p. 329, n. 76.
32. G. Jan Meulenbeld, A History of Indian Medical Literature, 5 vols. (Groningen, Netherlands: Egbert Forsten, 1999–2002), vol. IIA, 63–64; vol. IIB, 76–77.
33. Green 2017, 505–510; Chia-feng Chang, “Aspects of Smallpox and its Significance in Chinese History,” PhD diss., School of Oriental and African Studies, 1996; Chia-Feng Chang, “Dispersing the Foetal Toxin of the Body: Conceptions of Smallpox Aetiology in Pre-modern China,” in Contagion: Perspectives from Pre-Modern Societies, eds. Lawrence I. Conrad and Dominik Wujastyk, 23–38 (Aldershot, UK: Ashgate, 2000).
34. William H. Foege, J. Donald Millar, and J. Michael Lane, “Selective Epidemiologic Control in Smallpox Eradication,” American Journal of Epidemiology 94, no. 4 (1971): 311–315, esp. 311.
35. Pan S. Codellas, “The Case of Smallpox of Theodorus Prodromus,” Bulletin of the History of Medicine 20 (1946): 207–215; and John Lascaratos and Constantine Tsiamis, “Two Cases of Smallpox in Byzantium,” International Journal of Dermatology 41, no. 11 (2002): 792–795.
36. Lutfallah Gari, “Arabic Treatises on Environmental Pollution up to the End of the Thirteenth Century,” Environment and History 8, no. 4 (November 2002): 475–488; my thanks to Nahyan Fancy for this citation. See also Emilie Savage-Smith, “New Evidence for the Frankish Study of Arabic Medical Texts in the Crusader Period,” Crusades 5 (2006): 99−112.
37. Al-Beruni’s India, ed. E. Sachau, 2nd ed., 2 vols. (London, 1910), vol. 1, 309. My thanks to André Wink for alerting me to al-Biruni’s testimony, which has not previously been noted in smallpox historiography. On al-Biruni’s ties to the Khwarazm court, see D. J. Boilot, “al-Bīrūnī,” in Encyclopaedia of Islam, 2nd ed., eds. P. Bearman, Th. Bianquis, C. E. Bosworth, E. van Donzel, and W. P. Heinrichs (2012); for a survey of his oeuvre, see Michio Yano, “al-Bīrūnī,” in Encyclopaedia of Islam, 3rd ed., eds. Kate Fleet et al. (2013).
38. Ralph W. Nicholas, “The Goddess Śītalā and Epidemic Smallpox in Bengal,” The Journal of Asian Studies 41, no. 1 (November 1981): 21–44. My thanks to Anne Feldhaus for this reference.
39. Joseph Needham, with the collaboration of Lu Gwei‐djen, “China and the Origins of Immunology,” in Science and Civilisation in China, vol. VI, Biology and Biological Technology, Part 6: Medicine, ed. Nathan Sivin, 114–174 (Cambridge, UK: Cambridge University Press, 2000); Chang 1996; and Chang 2000. I have updated the names of Ge Hong and Tao Hongjing to standard Pinyin forms (the forms in Needham were “Ko Hung” and “Thao Hung-ching”).
40. Chang 1996, 54–55. Although the role of menstrual blood is not mentioned in al-Razi (see Rhazes, A Treatise on the Smallpox and Measles, trans. William Alexander Greenhill, London: Sydenham Society, 1848), it is found in writers such as al-Majusi; see Leven 1993, 349–350.
41. Akihito Suzuki, “Smallpox and the Epidemiological Heritage of Modern Japan: Towards a Total History,” Medical History 55 (2011): 313–318.
42. Cristina Álvarez Millán, “The Case History in Medieval Islamic Medical Literature: Tajarib and Mujarrabat as Source,” Medical History 54 (2010): 195–214, esp. 201–202.
43. Paul Richter, “Beiträge zur Geschichte der Pocken bei den Arabern,” Archiv für Geschichte der Medizin 5 (1912): 311–331; and Karl-Heinz Leven, “Zur Kenntnis der Pocken in der arabischen Medizin, im lateinischen Mittelalter und in Byzanz,” in Die Begegnung des Westens mit dem Ostens. Kongreßakten des 4. Symposions des Mediävistenverbandes in Köln 1991 aus Anlaß des 1000. Todesjahres der Kaiserin Theophanu, eds. Odilo Engels and Peter Schreiner, 341–354 (Sigmaringen, Germany: Thorbecke, 1993).
44. Yves Darton, et al., “Osteomyelitis variolosa: A Probable Mediaeval Case Combined with Unilateral Sacroiliitis,” International Journal of Paleopathology 3, no. 4 (2013): 288–293.
45. Ann G. Carmichael and Arthur M. Silverstein, “Smallpox in Europe Before the Seventeenth Century: Virulent Killer or Benign Disease?,” Journal of the History of Medicine and Allied Sciences 42 (1987): 147–168. Note that Carmichael and Silverstein’s suggestion that Variola minor, a far less lethal strain of smallpox, evolutionarily preceded Variola major, has been falsified by modern genetics studies, which locates the emergence of V. minor as late as the 19th century; see Ana T. Duggan et al., “17th Century Variola Virus Reveals the Recent History of Smallpox,” Current Biology 26, no. 24 (December 19, 2016): 3407–3412.
46. Hans van den Broek, “Genezing van blindheid na pokken of mazelen: Nederlandse mirakelverhalen, 14e-18e eeuw [Recovery from blindness following smallpox or measles: Dutch miracle stories, 14th-18th century],” Nederlands Tijdschrift voor Geneeskunde 154, no. A1853 (2010).
47. Ridolfo Livi, La schiavitù domestica nei tempi di mezzo e nei moderni (Padua, Italy: Antonio Milani, 1928). My thanks to Hannah Barker for bringing this study to my attention, and sharing with me her valuable insights about this unique register.
48. Eradication has also left some unresolved questions about the virus’s clinical manifestations. See J. Michael Lane, “Remaining Questions about Clinical Variola Major,” Emerging Infectious Diseases 17, no. 4 (April 2011): 676–680.
49. Duggan et al., 2016.
50. In addition to Carmichael and Silverstein 1987, Needham and Lu 2000, and Suzuki 2011, see Peter Boomgaard, “Smallpox, Vaccination, and the Pax Neerlandica: Indonesia, 1550–1930,” Bijdragen tot de Taal-, Land- en Volkenkunde 159, no. 4 (2003): 590–617; John C. Riley, “Smallpox and American Indians Revisited,” Journal of the History of Medicine and Allied Sciences 65 (2010): 445–477; and Günhan Börekçi, “Smallpox in the Harem: Communicable Diseases and the Ottoman Fear of Dynastic Extinction during the Early Sultanate of Ahmed I (r. 1603–1617),” in Plague and Contagion in the Islamic Mediterranean, ed. Nükhet Varlık, 135–152 (Kalamazoo, MI: ARC Humanities Press, 2017).
51. The claims made in the 1980s by Joseph Needham and Lu Gwei‐djen that inoculation was discovered in China by at least the 11th century have been challenged by their own editor, Nathan Sivin. See Needham, Lu, and Sivin, “China and the Origins of Immunology,” 169–174.
52. Giovanna Morelli et al., “Yersinia pestis Genome Sequencing Identifies Patterns of Global Phylogenetic Diversity,” Nature Genetics 42, no. 12 (2010): 1140–1145; and Yujun Cui et al., “Historical Variations in Mutation Rate in an Epidemic Pathogen, Yersinia pestis,” PNAS 110, no. 2 (2013): 577–582.
53. S. Rasmussen et al., “Early Divergent Strains of Yersinia Pestis in Eurasia 5000 Years Ago,” Cell 163 (2015): 571–582; and Aida Andrades Valtueña et al., “The Stone Age Plague and Its Persistence in Eurasia,” Current Biology 27, no. 23 (December 4, 2017): 3683–3691.e8.
54. Stephanie Haensch et al., “Distinct Clones of Yersinia pestis Caused the Black Death,” PLoS Pathogens 6, no. 10 (2010): e1001134; Kirsten I. Bos et al., “A Draft Genome of Yersinia pestis from Victims of the Black Death,” Nature 478, no. 7370 (2011): 506–510; David M Wagner et al., “Yersinia pestis and the Plague of Justinian, 541–543 AD: A Genomic Analysis,” Lancet Infectious Diseases 14, no. 4 (2014): 319–326; Kirsten I Bos et al., “Eighteenth Century Yersinia pestis Genomes Reveal the Long-Term Persistence of an Historical Plague Focus,” eLife 5 (2016): e12994; Maria A. 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 (8 June 2016): 874–881; Michal Feldman et al., “A High-Coverage Yersinia pestis Genome from a 6th-Century Justinianic Plague Victim,” Molecular Biology and Evolution 33, no. 11 (2016): 2911–2923.
55. Lester K. Little, ed., Plague and the End of Antiquity: The Pandemic of 541–750 (Cambridge, UK: Cambridge University Press, 2007).
56. Denis Twitchett, “Population and Pestilence in T’ang China,” in Studia Sino-Mongolia: Festschrift für Herbert Franke, eds. Wolfgang Bauer, Münchener ostasiatische Studien 25, 35–67 (Wiesbaden, Germany: Franz Steiner Verlag, 1979).
57. On the SNPs, see Feldman et al. 2016, Supplementary Materials, Table S9.
58. M. Sigl et al., “Timing and Climate Forcing of Volcanic Eruptions for the Past 2,500 Years,” Nature 523 (30 July 30, 2015): 543–549; Ulf Büntgen et al., “Cooling and Societal Change during the Late Antique Little Ice Age from 536 to around 660AD,” Nature Geoscience 9 (2016): 231–236.
59. Nils Chr. Stenseth et al., “Plague Dynamics are Driven by Climate Variation,” Proceedings of the National Academy of Sciences 103, no. 35 (2006): 13110–13115; Tamara Ben Ari et al., “Plague and Climate: Scales Matter,” PLoS Pathogens 7, no. 9 (2011): e1002160; and Kenneth L. Gage, “Factors Affecting the Spread and Maintenance of Plague,” in Advances in Yersinia Research, eds. Alzira Maria Paiva de Almeida and Nilma Cintra Leal, special issue, Advances in Experimental Medicine and Biology 954, no. 1 (2012): 79–94.
60. Ole Benedictow, The Black Death, 1346–1353: The Complete History (Woodbridge, UK: Boydell, 2004); and Stuart Borsch and Tarek Sabraa, “Refugees of the Black Death: Quantifying Rural Migration for Plague and Other Environmental Disasters,” Annales de Démographie Historique 2017 N°2, no. 134, 63–93.
61. See Monica H. Green and Boris Schmid, “Tiny Changes with Huge Implications: Counting SNPs in Plague’s History,” Contagions blog, ed. Michelle Ziegler, (June 27, 2016).
62. Bruce Campbell, The Great Transition: Climate, Disease and Society in the Late Medieval World (Cambridge, UK: Cambridge University Press, 2016); Chantal Camenisch et al., “The 1430s: A Cold Period of Extraordinary Internal Climate Variability During the Early Spörer Minimum With Social and Economic Impacts in North-Western and Central Europe,” Climate of the Past 12 (2016): 2107–2126.
63. James Belich, “The Black Death and the Spread of Europe,” in The Prospect of Global History, ed. James Belich, John Darwin, Margret Frenz, and Chris Wickham, 93–107 (Oxford: Oxford University Press, 2016); Stuart Borsch, “Plague Depopulation and Irrigation Decay in Medieval Egypt,” The Medieval Globe 1 (2014): 125–156; Nükhet Varlık, Plague and Empire in the Early Modern Mediterranean World: The Ottoman Experience, 1347–1600 (Cambridge, UK: Cambridge University Press, 2015); and Nükhet Varlık, ed., Plague and Contagion in the Islamic Mediterranean (Kalamazoo, MI: ARC Humanities Press, 2017).
64. This was the second genome that was announced in 2011 as coming from the London Black Death Cemetery (Bos et al., 2011), but was in fact from a later cemetery, likely from the 1360s, called St Mary Graces.
65. Spyrou et al., 2016.
66. Monica H. Green, “Putting Africa on the Black Death Map: Narratives from Genetics and History,” special issue of Afriques (forthcoming).
67. The SNPs (single nucleotide polymorphisms) that are used to track the genetic evolution of Y. pestis take their origin in a genetic change of one single cell. That single cell then must have the extraordinary good fortune to replicate many millions of times in order to “seed,” first, an animal outbreak, and then a human outbreak. So, every new lineage that is established starts with one single cell, and therefore with one single animal host.
68. William H. McNeill, Plagues and Peoples (New York: Anchor Press, 1976; rev. ed. 1998).
69. Robert Hymes, “A Hypothesis on the East Asian Beginnings of the Yersinia pestis Polytomy,” The Medieval Globe 1 (Fall 2014): 285–308.
70. Cui et al., “Historical Variations in Mutation Rate in an Epidemic Pathogen, Yersinia pestis”; Ekaterine Zhgenti et al., “Genome Assemblies for 11 Yersinia pestis Strains Isolated in the Caucasus Region,” Genome Announcements 3, no. 5 (2015): e01030–15; Galina A. 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.
71. Sébastien Guillet et al., “Climate Response to the Samalas Volcanic Eruption in 1257 Revealed by Proxy Records,” Nature GeoScience 10 (February 2017): 123–129; Sébastien Guillet, et al., “Climate Response to the Samalas Volcanic Eruption in 1257 Revealed by Proxy Records,” Nature Geoscience 10 (2017): 123–128; Frank Ludlow, “Chronicling a Medieval Eruption,” Nature Geoscience 10 (February 2017): 77–78; Bruce M. S. 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.
72. Campbell 2016.
73. N. Yu Nosov et al., “Филогенетический анализ штаммов Yersinia pestis средневекового биовараиз природных очагов чумы Российской Федерации и сопредельных стран [Phylogenetic Analysis of Yersinia pestis Strains of Medieval Biovar from Natural Plague Foci of the Russian Federation and Bordering Countries],” Problemy Osobo Opasnykh Infektsii [Problems of Particularly Dangerous Infections] 2 (2016): 75–78 (in Russian).
74. Neil Pederson et al., “Pluvials, Droughts, the Mongol Empire, and Modern Mongolia,” PNAS 111, no. 12 (2014): 4375–4379; see also Ulf Büntgen and Nicola Di Cosmo, “Climatic and Environmental Aspects of the Mongol Withdrawal from Hungary in 1242 CE,” Scientific Reports 6, no. 25606 (2016).
75. This summary of the history of medicine describes a professional discipline within history. There is another genre of history of medicine that appears within biomedical journals, but is not normally peer-reviewed by historians.
76. Angela Ki Che Leung, Leprosy in China: A History, Studies of the Weatherhead East Asian Institute, Columbia University (New York: Columbia University Press, 2009); Luke E. Demaitre, Leprosy in Premodern Medicine: A Malady of the Whole Body (Baltimore, MD: Johns Hopkins University Press, 2007); and Carole Rawcliffe, Leprosy in Medieval England (Woodbridge, UK: Boydell & Brewer, 2006).
77. For example, Lawrence I. Conrad and Dominik Wujastyk, eds. Contagion: Perspectives from Pre-Modern Societies (Aldershot, UK: Ashgate 2000); and Justin K. Stearns, Infectious Ideas: Contagion in Premodern Islamic and Christian Thought in the Western Mediterranean (Baltimore, MD: Johns Hopkins University Press, 2011).
78. Jon Arrizabalaga, “Problematizing Retrospective Diagnosis in the History of Disease,” Asclepio 54, no. 1 (2002): 51–70; Cristina Álvarez Millán, “Disease in Tenth-Century Iran and Irak According to al-Rāzi’s Casebook,” Suhayl 14 (2014): 49–88. Artistic depictions have been particularly subject to misinterpretation. See Lori Jones and Richard Nevell, “Plagued by Doubt and Viral Misinformation: The Need for Evidence-based Use of Historical Disease Images,” The Lancet Infectious Diseases 16, no. 10 (October 2016): e235–e240.
79. Andrew Cunningham, “Transforming Plague: The Laboratory and the Identification of Infectious Disease,” in The Laboratory Revolution in Medicine, ed. A. Cunningham and P. Williams, 209–244 (Cambridge, UK: Cambridge University Press, 1992).
80. Michael McCormick, “History’s Changing Climate: Climate Science, Genomics, and the Emerging Consilient Approach to Interdisciplinary History,” Journal of Interdisciplinary History 42, no. 2 (Autumn 2011): 251–273; Adam Izdebski et al., “Realising Consilience: How Better Communication Between Archaeologists, Historians and Natural Scientists Can Transform the Study of Past Climate Change in the Mediterranean,” Quaternary Science Reviews 36 (2016): 5–22.
81. It is significant that there are now five major essays, written by historians for the benefit of other historians, on the significance of the new genetics of plague: Lester K. Little, “Plague Historians in Lab Coats,” Past and Present 213 (2011): 267–290; J. L. Bolton, “Looking for Yersinia pestis: Scientists, Historians, and the Black Death,” in Society in an Age of Plague, ed. Linda Clark and Carole Rawcliffe, The Fifteenth Century 12 (2013): 15–38; Monica H. Green, “Taking ‘Pandemic’ Seriously: Making the Black Death Global,” in Pandemic Disease in the Medieval World: Rethinking the Black Death, inaugural issue of The Medieval Globe 1, no. 1–2 (Fall 2014): 27–61; George Dameron, “Identificazione di un killer: recenti scoperte scientifiche e storiche sulla natura della peste nera,” in Boccaccio 1313–2013, ed. Francesco Ciabattoni, Elsa Filosa, and Kristina Marie Olson, 57–70 (Ravenna, Italy: Longo, 2015); and Pierre Toubert, “La Peste Noire (1348), entre Histoire et biologie moléculaire,” Journal des Savants (Janvier-Juin 2016): 17–31.
82. Charlotte L. King et al., “Considering the Palaeoepidemiological Implications of Socioeconomic and Environmental Change in Southeast Asia,” Archaeological Research in Asia, 11 (2017): 27–37.
83. For example, Xavier Didelot, Lilith K. Whittles, and Ian Hall, “Model-Based Analysis of an Outbreak of Bubonic Plague in Cairo in 1801,” Journal of the Royal Society Interface 14, 20170160 (2017).
84. Rosemary Horrox, trans., The Black Death (Manchester: University of Manchester Press, 1994) is the best collection of primary sources, though it covers only Western Europe and has a pronounced focus on materials from England. John Aberth, The Black Death: The Great Mortality of 1348–1350: A Brief History with Documents, The Bedford Series in History and Culture (New York: Palgrave MacMillan, 2005), replicates some of the same materials, but usefully adds documents from al-Andalus. No collection of materials from the Islamicate world has ever been assembled, but see literature cited in Michael Dols, The Black Death in the Middle East (Princeton, NJ: Princeton University Press, 1977). Similarly, no collection of materials on plague in pre-modern China has been assembled; see Hymes 2014 for bibliography.
85. Fuat Sezgin, Geschichte des arabischen Schrifttums. III. Medizin-Pharmazie-Zoologie-Tierheilkunde bis ca. 430 A.H. (Leiden, Netherlands: Brill, 1970); Manfred Ullmann, Die Medizin im Islam (Leiden-Köln, Netherlands: Brill, 1970); A New Catalogue of Arabic Manuscripts in the Bodleian Library, Oxford, Volume 1: Medicine (Oxford: Oxford University Press, 2011); and Peter Pormann and Emilie Savage-Smith, Medieval Islamic Medicine (Edinburgh: University of Edinburgh Press, 2007). On the specific genre of the case history in Arabic medicine, see Álvarez Millán 2014. Dominik Wujastyk, Anthony Cerulli, and Karin Preisendanz, eds., Medical Texts and Manuscripts in Indian Cultural History (New Delhi: Manohar, 2013). Asaf Goldschmidt, The Evolution of Chinese Medicine: Song Dynasty, 960–1200 (New York: Routledge, 2008); Stephen Boyanton, “The Treatise on Cold Damage and the Formation of Literati Medicine: Social, Epidemiological, and Medical Change in China, 1000–1400,” PhD diss., Columbia University, 2015; and Michael Stanley-Baker, “New Digital Tools for the History of Medicine and Religion in China,” China Policy Institute: Analysis, September 27, 2016. In addition to eTK/eVK (see “Links to Digital Materials” below), the following recent surveys are of use: Monica H. Green, “Integrative Medicine: Incorporating Medicine and Health into the Canon of Medieval European History,” History Compass 7, no. 4 (June 2009): 1218–1245; and Elma Brenner, “Recent Perspectives on Leprosy in Medieval Western Europe,” History Compass 8, no. 5 (2010): 388–406.
86. Lynn Thorndike and Pearl Kibre, Catalogue of Incipits of Medieval Scientific Writings in Latin, 2nd ed. rev. (Cambridge, MA: Medieval Academy of America, 1963).