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.

Leprosy

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.

Smallpox

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

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.