Plagues and Peoples

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by William H. McNeill


  The conquests and ethnic encroachments which Turks and Mongols achieved before, and more spectacularly after, A.D. 1000 simply could not have occurred had these peoples not achieved and maintained a level of immunity to civilized diseases almost equivalent to that prevailing in the major civilized centers themselves. Everything known of the trade patterns and political structures of the steppe make this seem likely, indeed all but certain. Frequent movement across long distances, and occasional assembly into large gatherings for raids or (with the Mongols) for a great annual hunt, provided ample opportunity for infectious diseases to be exchanged and propagated among the nomads, and even, as Chinese records attest, to be sometimes communicated to less mobile civilized populations.

  Trade and Islamic missionaries penetrated much of Africa in exactly the same way as other Moslem traders and missionaries roamed the Eurasian steppe; and presumably with almost the same epidemiological effect, although in many African landscapes diseases peculiar to that continent presented barriers to alien intrusion more formidable than anything present in other parts of the earth. Hence civilized encroachment was restricted and, mayhap, African exposure to civilized diseases may have been less thoroughgoing than was true in the Asian steppes. On the other hand, when African slaves began to come to the New World after 1500, they suffered no spectacular die-off from contact with European diseases, which is sufficient demonstration that in their African habitat some exposure to the standard childhood diseases of civilization must have occurred, if not before, then soon after 1200.

  In the New World, on the contrary, the Eurasian epidemiological experience of the first Christian millennium had no echoes whatever. As population thickened and civilized centers arose in Mexico and Peru, comparatively vast human communities came into being that were highly vulnerable to Old World infections. Civilized Amerindians after 1200 were therefore like Mediterranean and Far Eastern peoples at the beginning of the Christian era: populations dense enough for epidemic decimation. But before exploring the fateful implications of this circumstance, we must first consider a second great Eurasian epidemiological upheaval, centering on the Black Death of the fourteenth century.

  IV

  The Impact of the Mongol Empire on Shifting Disease Balances, 1200–1500

  I

  f the disease history of the Old World as reconstructed in Chapter III is correct, at least in its main lines, one may conclude that epidemiological adjustments arising from the establishment of regular communication across the spaces separating one civilized community of Eurasia from another had worked themselves out by about A.D. 900 into a relatively stable pattern. That is to say, by that time human populations had adjusted to the confluence of the various infectious diseases that in earlier times had developed differently in different parts of Eurasia and Africa. In all probability, no considerable population within the ecumene remained altogether inexperienced with any of the major person-to-person epidemic infections, although in many places such diseases appeared only at intervals when an accumulation of susceptible age classes provided the tinder needed to sustain an epidemic conflagration.

  Two systematic instabilities remained. One was the persistent and cumulatively massive growth of human population in the Far East and Far West, resulting from the way in which the Chinese and Europeans had broken through older epidemiological and technological barriers shortly before A.D. 900. Eventually this development affected the macro-balances of the Old World in emphatic fashion, making first China and then western Europe critically influential in military, economic, and cultural matters. The other source of systematic instability within the Eurasian world balance, as defined between 900 and 1200, was the possibility of further altering communications patterns, both by sea and land.

  The first such change that affected both macro- and micro-parasitic patterns in far-reaching ways was the intensification of overland caravan movement across Asia that reached its climax under the Mongol empires founded by Genghis Khan (1162–1227). At the height of their power (1279–1350), the Mongol empires embraced all of China and nearly all of Russia (the distant Novgorod alone remained independent), as well as central Asia, Iran, and Iraq. A communications network comprising post messengers capable of traveling one hundred miles a day for weeks on end, and slower commercial caravans and armies, marching to and fro across vast distances, knitted these empires together until the 1350s, when rebellion flared within China, leading by 1368 to the complete expulsion of the Mongols from their richest conquest.

  Before that upheaval, however, literally thousands of persons moved to and fro across Eurasia, often leaving scant trace in written records. Marco Polo’s famous account of his travels, for instance, came into existence merely by accident. Captured in war and imprisoned in a Genoese jail, a fellow prisoner thought it worthwhile to write down Marco’s stories. Otherwise, there would be absolutely no surviving record of the Polos’ existence. Other records casually reveal how permeable the Eurasian continent became under the Mongols. When, for instance, the Flemish friar William of Rubruck, arrived as the French king’s emissary in the Mongol capital of Karakorum in 1254, he met a woman, native to a village near his own birthplace, who had been captured fourteen years before in the course of a Mongol raid into central Europe.1

  Mongol communications had another important effect. Not only did large numbers of persons travel very long distances across cultural and epidemiological frontiers; they also traversed a more northerly route than had ever been intensively traveled before. The ancient Silk Road between China and Syria crossed the deserts of central Asia, passing from oasis to oasis. Now, in addition to this old route, caravans, soldiers and postal riders rode across the open grasslands. They created a territorially vast human web that linked the Mongol headquarters at Karakorum with Kazan and Astrakhan on the Volga, with Caffa in the Crimea, with Khanbaliq in China and with innumerable other caravanserais in between.

  From an epidemiological point of view, this northward extension of the caravan trade net had one very significant consequence. Wild rodents of the steppelands came into touch with carriers of new diseases, among them, in all probability, bubonic plague. In later centuries, some of these rodents became chronically infected with Pasteurella pestis. Their burrows provided a microclimate suited to the survival of the plague bacillus winter and summer, despite the severities of the Siberian and Manchurian winters. As a result, the animals and insects inhabiting such burrows came to constitute a complex community among which the plague infection could and did survive indefinitely.

  No one knows for sure when the burrowing rodents of the Eurasian steppe first became carriers of plague. Their role in sheltering bubonic infection was discovered in 1921–24 by an international team of epidemiologists dispatched to investigate an outbreak of human plague in Manchuria. That investigation, in turn, built upon work in the Don-Volga regions of southern Russia, dating back to the 1890s, which indicated that various rodent species were plague carriers. By then, the pattern of infection was age-old and local human customs for coping with the risk of infection were immemorial. Yet it does not follow, as Russian writers have assumed, that the infection did not establish itself in historic times.2 Quite the contrary. I contend that Mongol movements across previously isolating distances in all probability brought the bacillus Pasteurella pestis to the rodents of the Eurasian steppe for the first time.

  In order to evaluate such an hypothesis, it is helpful to step outside the chronological frame of this chapter to consider more closely the nineteenth- and twentieth-century plague epidemic whose containment by international teams of doctors constitutes one of the most dramatic triumphs of modern medicine.

  The story begins deep in the interior of China, where, as we saw in the preceding chapter, plague had probably been endemic in Himalayan borderlands between China and India by a few centuries after the Christian era and perhaps long before that. Early in the nineteenth century, the upper reaches of the Salween River constituted the boundary between infected an
d uninfected areas. Then in 1855 a military revolt broke out in Yunnan. Chinese troops were sent across the Salween to suppress the rebels, and, being unfamiliar with the risks of bubonic infection, contracted the disease and carried it back with them across the river into the rest of China. Thereafter, outbreaks of plague continued to occur in various parts of the Chinese interior without attracting much attention from the outside world, until in 1894 the disease reached Canton and Hong Kong and sent a chill of fright through the European settlements in those ports.3

  Techniques of bacteriology were still in their infancy in 1894, so news of the recurrence of a disease that still loomed large in European folk memory set disciples of Pasteur and Koch eagerly to work to unravel the mystery of its propagation. International teams were therefore dispatched to the scene, and within a matter of weeks of their arrival in Hong Kong a Japanese and a French bacteriologist independently discovered Pasteurella pestis, the bacillus of plague (1894). During the following decade most of the details of how the bacillus was transmitted by fleas from rodents to men became firmly established through the work of a series of international task forces operating in such diverse places as Hong Kong, Bombay, Sydney, San Francisco, and Buenos Aires.

  International interest in the plague was intensified by the fact that within a decade of its arrival in Hong Kong, all the important seaports of the world experienced outbreaks of the dread disease. In most places, the infection was quickly contained; in India, however, plague broke through into the interior, and within a decade of its arrival in Bombay (1898) some six million persons had died of it.4 Recurrent minor outbreaks and the obvious risk of a major disaster if the infection really got going among human populations in Europe, America, and Africa spurred research in every threatened area.

  One of the most significant discoveries was this: in California, South Africa, and Argentina, burrowing communities of wild rodents picked up the plague bacillus even more readily than people. California ground squirrels were first discovered to be infected with plague in 1900, in the same year that a minor outbreak of the disease occurred among the Chinese population of San Francisco. The plague quickly disappeared among humans; but the bacillus throve among the ground squirrels, and continues to do so until the present day. Within less than a decade, similar infections were discovered among burrowing rodent communities of South Africa outside Durban, and in Argentina outside Buenos Aires soon after human plague episodes had occurred in those ports.

  The fact that the species of rodents were different in each region, and differed from burrowing rodent communities in Asia, did not make much difference. The rodent burrows, whatever the exact mix of native inhabitants, proved very hospitable to the bacillus; and in fact, each year since the infection was first observed outside San Francisco, the infected region of North America has increased. As a result, by 1975 a reservoir of infection had come into existence throughout most of the western United States and extended into both Canada and Mexico. Such a vast area of infection, in fact, is equivalent to any of the long-standing plague foci of the Old World.5

  The geographic spread of plague infection in North America occurred naturally in the sense that the life patterns of ground-burrowing rodents create conditions for the communication of the infection from one underground “city” to another. When the rodent young have attained a certain maturity, they are evicted from the familial burrow and mill around seeking a new home. Some of the young abandon the community entirely and wander across country, traveling as much as several miles. Such wanderers will readily attempt to join a new rodent community if they find one. This life pattern provides a very effectual way of exchanging genes, with the well-known evolutionary benefits such an exchange imparts; it also allows for the propagation of infection from one rodent community to another across as much as ten to twenty miles per annum. Plague propagation among North American rodents was also accelerated by human agency. Ranchers actually transported sick rodents in trucks, sometimes across hundreds of miles, with the intention of infecting local communities of prairie dogs and reducing their numbers, thus allowing cattle to find more grass. But the spread of plague in North America, while affected by such acts, did not depend on human intervention. The upshot was that by 1940 no fewer than thirty-four species of burrowing rodents were carrying plague bacilli in the United States, and thirty-five different species of fleas were also infected.6

  After 1900, human plague continued to occur sporadically in North America as well as in Argentina and South Africa. Mortality held steady at about 60 per cent for those who contracted the infection until the discovery of antibiotics in the 1940s made cure easy and sure, so long as an appropriate diagnosis was made in time. But habits of life among ranchers and other twentieth-century human occupants of the semiarid plains of America and South Africa were such as to create effectual barriers between themselves and the rodent-flea communities in which the bubonic bacillus flourished. Hence the occurrences of human plague in the newly infected regions of the world remained few in number and attracted little attention, especially since local authorities were often anxious to hush up the existence of so dread a disease within their zones of jurisdiction.

  In 1911, however, a new and large-scale outbreak of human plague occurred in Manchuria and again in 1921. Fresh international efforts were speedily organized to contain these epidemics. Investigators soon discovered that the human plague had been contracted from marmots. These are large burrowing rodents, whose skins commanded a good price on the international fur market. But, like the recently infected ground squirrels and other rodents of North America, marmot burrows sometimes housed Pasteurella pestis.

  Nomad tribesmen of the steppe region, where these animals lived, had mythic explanations to justify epidemiologically sound rules for dealing with the risk of bubonic infection from marmots. Trapping was taboo; a marmot could only be shot. An animal that moved sluggishly was untouchable, and if a marmot colony showed signs of sickness, custom required the human community to strike its tents and move away to avoid bad luck. Such customary prescriptions presumably reduced the possibility of human infection with plague to minor proportions.

  But in 1911, as the Manchu Dynasty tottered toward its final collapse, long-standing government regulations prohibiting the Chinese from moving into Manchuria broke down. As a result, swarms of inexpert Chinese emigrants went after marmot furs. Knowing nothing of local traditions, the Chinese trapped sick and healthy animals indiscriminately—with the result that plague broke out among them and then spread along the newly constructed railroad lines of Manchuria from what speedily became its urban focal center at Harbin.7

  This entire sequence of events from 1894 to 1921 occurred under the eyes of professionally sensitized medical teams whose job was to find out how best to control plague. In some instances researchers went to considerable pains to reconstruct the pattern of diffusion whereby the plague had penetrated new regions and populations. Without such study and the prophylactic measures that followed, the twentieth century might well have been inaugurated by a series of plagues reaching completely around the earth, with death tolls dwarfing those recorded from the age of Justinian and the fourteenth century, when the Black Death ravaged Europe and much of the rest of the Old World.

  Three points seem worth making on the basis of what is known of mankind’s nineteenth- and twentieth-century brush with bubonic plague.

  First, the steamship network that arose in the 1870s was the vehicle that dispersed the infection around the globe, and did so, once the epidemic broke out in Canton and Hong Kong, with a speed that was limited only by the speed with which a ship could carry its colony of infected rats and fleas to a new port. Speed was obviously decisive in allowing a chain of infection to remain unbroken from port to port. Since it creates immunities among survivors, Pasteurella pestis was, after all, certain to run out of susceptible hosts among a ship’s company of rats, fleas, and men within a few weeks. In the days of sail, the oceans had simply been too wide for the d
isease to survive on shipboard long enough to make a lodgment in the seaports and waiting rodent communities of America and South Africa. But when steamships began to travel faster and, being bigger, perhaps also carried larger populations of rats among whom the infection could circulate longer, the oceans suddenly became permeable as never before.

  Second, infected ships’ rats and their fleas not only conveyed plague bacilli to human hosts in diverse seaports, but also managed to infect their wild cousins in several semi-arid regions of the earth. Apparently in California, Argentina, and South Africa, potential wild reservoirs for bubonic infection had existed for incalculable ages. All that was needed to create new natural plague foci was a means to convey the bacillus across intervening barriers (in this case, oceans) to new regions where suitably massive populations of burrowing rodents were already in the ground. Such rodent populations proved both susceptible to the disease and capable of sus- taining an unbroken chain of infection indefinitely, despite wide local differences of habitat and speciation.

  No comparable unintended geographical transfer of an infection of importance to humanity has occurred since medical men became capable of observing such phenomena; but this does not mean that similar sudden shifts did not occur in earlier times. On the contrary, the history of the plague bacillus in the nineteenth and twentieth centuries offers a model and pattern for such transfers: not least, in the suddenness with which the infection occupied new ground when older barriers to its diffusion had been breached. The fact is that however sudden and surprising they may seem, these recent triumphs for Pasteurella pestis constitute a normal biological phenomenon. For a new ecological niche, wherever presented, tends to be occupied quickly by whatever organism—human or non-human—thereby multiplies its kind.

 

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