Plagues and Peoples

by William H. McNeill

  Whatever the reality may have been—and it clearly varied sharply from community to community and in ways no one could in the least comprehend—we can be sure that the shock to accustomed ways and expectations was severe. Moreover, the plague did not disappear from Europe after its first massive attack. Instead, recurrent plagues followed at irregular intervals, and with varying patterns of incidence, sometimes rising to a new severity, and then again receding. Places that had escaped the first onset commonly experienced severe die-off in later epidemics. When the disease returned to places where it had raged before, those who had recovered from a previous attack were, of course, immune, so that death tolls tended to concentrate among those born since the previous plague year.

  In most parts of Europe, even the loss of as much as a quarter of the population did not, at first, make very lasting differences. Rather heavy population pressure on available resources before 1346 meant that eager candidates were at hand for most of the vacated places. Only positions requiring relatively high skills—farm managers or teachers of Latin, for instance—were likely to be in short supply. But the recurrences of plague in the 1360s and 1370s altered this situation. Manpower shortages came to be widely felt in agriculture and other humble occupations; the socio-economic pyramid was altered, in different ways in different parts of Europe, and darker climates of opinion and feeling became as chronic and inescapable as the plague itself. Europe, in short, entered upon a new era of its history, embracing as much diversity as ever, since reactions and readjustments followed differing paths in different regions of the Continent, but everywhere nonetheless different from the patterns that had prevailed before 1346.30

  In England, where scholarly study of the plague has achieved by far its greatest elaboration, population declined irregularly but persistently for more than a century, and reached a low point some time between 1440 and 1480.31 Nothing comparably definite can be said about other parts of Europe, though there is no doubt whatever that plague losses continued to be a significant element in the Continent’s demography until the eighteenth century.32 If one assumes that population decay lasted about as long on the Continent as in England—an assumption liable to innumerable local exceptions but plausible overall—the period required for medieval European populations to absorb the shock of renewed exposure to plague seems to have been between 100 and 133 years, i.e., about five to six human generations.33 This closely parallels the time Amerindian and Pacific island populations later needed to make an even more drastic adjustment to altered epidemiological conditions and suggests that, as in the case of Australian rabbits exposed to myxomatosis, 1950–3, there are natural rhythms at work that limit and define the demographic consequences of sudden exposure to initially very lethal infections.34

  Parallel to this biological process, however, was a cultural one, whereby men (and perhaps rats, too) learned how to minimize risks of infection. The idea of quarantine had been present even in 1346. This stemmed from biblical passages prescribing the ostracism of lepers; and by treating plague sufferers as though they were temporary lepers—forty days quarantine eventually became standard—those who remained in good health found a public and approved way to express their fear and loathing of the disease.35 Since everyone remained ignorant of the roles of fleas and rats in the propagation of the disease until the very end of the nineteenth century, quarantine measures were not always effectual.

  Nevertheless, since doing something was psychologically preferable to apathetic despair, quarantine regulations became institutionalized, first at Ragusa (1465), then at Venice (1485); and the example of these two Adriatic trading ports was widely imitated elsewhere in the Mediterranean thereafter.36 The requirement that any ship arriving from a port suspected of plague had to anchor in a secluded place and remain for forty days without communication with the land was not always enforced, and even when enforced, rats and fleas could sometimes come ashore while human beings were prevented from doing so. All the same, in many cases such precautions must have checked the spread of plague, since, if isolation could be achieved, forty days was quite enough to allow a chain of infection to burn itself out within any ship’s company. The quarantine rules which became general in Christian ports of the Mediterranean in the sixteenth century were therefore well founded.

  Yet plague continued to filter past such barriers, and continued to constitute a significant demographic factor in late medieval and early modern times in all parts of Europe. In the Mediterranean, access to the enduring reservoir of rodent infection was especially easy via Black Sea and Asia Minor ports.37 Outbreaks of plague were therefore frequent enough to keep the quarantine administration of all major ports continuously alive until, in the nineteenth century, new ideas about contagion led to relaxation of old rules.38 The last important plague outbreak in the western Mediterranean occurred in and around Marseilles, 1720–21; but until the seventeenth century occasional plague outbreaks, carrying off anything up to a third or a half of a city’s population in a single year, were normal.39, 40 Venetian statistics, for instance, which became fully reliable by the second half of the sixteenth century, show that in 1575–77 and again in 1630–31, a third or more of the city’s population died of plague.41

  Outside the Mediterranean, European exposure to plague was less frequent and public administration in late medieval and early modern times was less expert. The result was to make visitations of plague rarer and, at least sometimes, also more catastrophic. A particularly interesting case was the outbreak of plague in northern Spain, 1596–1602. One calculation holds that half a million died in this epidemic alone. Subsequent outbreaks in 1648–52 and 1677–85 more than doubled the number of Spaniards who died of plague in the seventeenth century. Pasteurella pestis must thus be considered as one of the significant factors in Spain’s decline as an economic and political power.42

  In northern Europe the absence of well-defined public quarantine regulations and administrative routines—religious as well as medical—with which to deal with plague and rumors of plague, gave scope for violent expression of popular hates and fears provoked by the disease. In particular, longstanding grievances of poor against rich often boiled to the surface.43 Local riots and plundering of private houses sometimes put the social fabric to a severe test.

  After the Great Plague of London, 1665, Pasteurella pestis withdrew from northwestern Europe, though it remained active in the eastern Mediterranean and in Russia throughout the eighteenth and nineteenth centuries. Quarantine and other public health measures probably had less decisive overall effect in limiting the outbreaks of plague, whether before or after 1665, than other unintended changes in the manner in which European populations co-existed with fleas and rodents. For instance, in much of western Europe, wood shortages led to stone and brick house construction, and this tended to increase the distance between rodent and human occupants of the dwelling, making it far more difficult for a flea to transfer from a dying rat to a susceptible human.44 Thatch roofs, in particular, offered ready refuge for rats; and it was easy for a flea to fall from such a roof onto someone beneath. When thatch roofs were replaced by tiles, as happened generally in London after the Great Fire of 1666, opportunities for this kind of transfer of infection drastically diminished. Hence the popular notion that the Great Fire somehow drove the plague from the city probably had a basis in fact.

  The spread of a new species of house rat through most of Europe in the eighteenth century is also believed to have increased the distance between rats and humans, since the invading gray rat was a wilder, warier animal, and preferred to burrow in the ground instead of infesting roofs and house walls as the black rat—a better climber—was wont to do. There is, however, no ground for the common assertion that the invading gray rat was not susceptible to the plague bacillus; hence the argument that attributes the disappearance of plague to the supplanting of black by gray rats in most of Europe is epidemiologically faulty—as well as anachronistic, since the new rat species only reached western Europe
toward the close of the eighteenth century.45

  Perhaps more important but far more obscure were changes in infectious patterns among the populations of northwestern Europe. There is a possibility, for example, that a mutant form of Pasteurella pestis known as Pasteurella pseudo-tuberculosis may have established itself as a common person-to-person infection in the cooler, moister parts of Europe where conditions for droplet infection were better than in drier climates. “Pseudo-tuberculosis” was seldom fatal. Symptoms resembled typhoid; but the disease does confer at least a partial immunity to plague. Unfortunately, since its symptoms are readily confused with other fevers arising from infections of the digestive tract, there is no possibility of disentangling its history as a human disease from other afflictions. In addition, there are uncertainties as to the correct way to describe the relationship between the plague bacillus and Pasteurella pseudo-tuberculosis. Some bacteriologists claim to have observed mutation of Pasteurella pestis into pseudo-tuberculosis; others doubt their results.

  Until these matters achieve better definition, it is therefore premature to jump to the conclusion that a mutation from Pasteurella pestis to Pasteurella pseudo-tuberculosis did in fact establish itself in Europe. One can, however, recognize that this is exactly the sort of adjustment that is to be expected when an initially very lethal infection has time to achieve a more stable relationship with its hosts. And it is clear that the pneumonic form of the plague, dispensing as it did with any intermediate host, and achieving 100 per cent lethal consequences for those affected within little more than a single day, could only survive as a human infection by undergoing such a mutation.46

  Whatever combination of factors may have been responsible, the upshot for western Europe is not in doubt: the disappearance in the latter part of the seventeenth century of a disease which had haunted the European imagination for three centuries. This geographically modest retreat of Pasteurella pestisy range later provoked a grand theory to the effect that plague has appeared among humankind in three great pandemics: in the sixth century, in the fourteenth century, and, abortively, in the twentieth century. This idea developed among the medical teams concerned with plague control in the twentieth century—understandably enough since it gave their work special significance.47 Yet the fact is that plague did not disappear among populations living closer to the Eurasian steppe reservoir, nor did it diminish in virulence, as the pandemic theory assumes, in those regions where it continued to manifest itself. It seems more likely therefore that changes in housing, shipping, sanitary practices, and similar factors affecting the way rats, fleas, and humans encountered one another were the decisive regulators, both in the advance and in the retreat of plague. The effort to structure scanty available evidence into three global pandemics seems to be a mistaken attempt to project the plague experience of western Europe onto the whole of Eurasia.48

  Other significant changes in disease patterns also occurred in Europe, either as a result of the heavy incidence of the plague after 1346 or because other new infections besides the bubonic bacillus flooded westward with the altered pattern of human movement that the Mongol empire established within Eurasia. The most notable phenomenon was the decline in the incidence of leprosy, which had been a significant disease in medieval Europe up to the time of the Black Death. Leprosy, of course, was a generic term used to describe a number of different infections that affected the skin in conspicuous and horrible ways. The specific disease known by that name today arises from a bacterial infection that was first identified in 1873 by a Norwegian medical man, Armauer Hansen; and to distinguish this infection from others formerly termed “leprosy,” the term “Hansen’s disease” is sometimes used.

  Hansen’s disease appears to have established itself in Europe and the Mediterranean coastlands in the sixth century A.D.49 Thereafter, together with other infections classified as leprous, it remained of major importance until the fourteenth century. Leprosaria were established outside thousands of medieval towns. By the thirteenth century one estimate puts their number in all of Christendom at 19,000.50

  The die-off incident to the Black Death certainly depopulated many leprosaria, but the notion that all infected individuals died, so that the disease therefore disappeared, is clearly wrong. Hansen’s disease did continue to exist, on a significant scale, in Scandinavia and more sparsely in other parts of Europe as well. The fundamental fact, nevertheless, was that the number of lepers never again became anything like what it had been before 1346, and leprosaria had to be put to other uses—often converted into hospitals for the sick or, as in Venice, assigned as a quarantine station for suspected plague carriers.

  Needless to say, the ecological circumstances that led to the remarkable decrease of leprosy in Europe cannot be reconstructed. Recent medical research suggests that the amount of vitamin C in the diet might be of importance, since that vitamin has the power to repress one of the chemical processes whereby the bacillus of leprosy feeds on human tissues.51 But changes, if any, in European diets after the ravages of the Black Death seem totally inadequate to explain the widespread and abrupt decrease in leprosy that occurred.

  A more likely hypothesis looks at changing patterns of disease competition. More specifically, leprosy may have retreated because of a rising incidence of pulmonary tuberculosis among Europeans. The reason for thinking this might explain what happened is as follows: immunity reactions provoked by the bacillus of tuberculosis, at least under some conditions, seem to overlap with immunity reactions provoked by Hansen’s bacillus in such a way that exposure to the one infection increases the host’s resistance to the other. In such a competitive situation, tuberculosis had a clear advantage. Moving from host to host via droplets put into the air by the sneezing and coughing of already infected persons, tuberculosis bacilli were far more mobile than their rivals. Exactly how Hansen’s disease passes from host to host remains unsure even today; but it is clear that the disease is not very contagious. The bacillus seems to establish itself in a new host only after prolonged contact.

  It is easy to imagine, therefore, that if pulmonary tuberculosis did in fact become more prevalent in Europe after 1346, it could have interrupted the infectious chain of Hansen’s disease, provoking a higher level of resistance in European bloodstreams simply by getting there first and calling forth antibodies that made things more difficult for the slower-moving bacillus of leprosy.52

  Such a hypothesis at once raises the question whether and why tuberculosis attained greater frequency in Europe after the plague years. Tuberculosis bacilli are among the oldest and most widespread on earth; and liability to tubercular infection long antedated the emergence of humanity itself. Stone Age and Egyptian Old Kingdom skeletons have been diagnosed as exhibiting signs of tubercular damage, although evidence for pulmonary tuberculosis remains, in the nature of the case, exiguous.53

  Under modern conditions, pulmonary tuberculosis propagates itself best in urban settings, where strangers frequently come into close proximity so that coughing or sneezing may transmit the infection from one person to another.54 Towns had of course become increasingly important in western Europe since about A.D. 1000; but townsmen remained a small minority of the entire population in every part of the Continent until long after the fourteenth century. The rise of medieval towns therefore seems in and of itself entirely inadequate to account for a presumed shift away from Hansen’s disease and toward pulmonary tuberculosis.

  A plausible solution to this puzzle suggests itself if we make a detour to consider another disease change that also may have played a part in emptying Europe’s leprosaria after 1346. Yaws is a disease which medieval doctors would have classed as leprosy. It results from infection by a spirochete which is indistinguishable from the organism that causes syphilis. Entering through the skin as a result of direct contact with an already infected person, the disease manifests itself in the form of deep, open sores. Whether yaws existed at all in medieval Europe and how prevalent it may have been if it did exist, canno
t be known, since its nastier manifestations fell within the range of what was recognized as leprosy. There is, how- ever, some reason to believe that Europeans were not unfamiliar with spirochetic infection before the time of Columbus; and a body of expert opinion holds that such infections were, like tuberculosis, among the oldest known to man, carried to all parts of the earth by hunters and gatherers in the course of their initial dispersal around the globe.55

  If we accept the proposition that yaws was one of the infections classed as leprosy in Europe before 1346, it seems clear that the infection decayed thereafter, for when syphilis broke out so virulently at the end of the fifteenth century, it acted like a new disease among Europeans, exhibiting unusually florid symptoms and meeting minimal systematic resistance from the human bodies it invaded. Yet the spirochete causing yaws and that causing syphilis appear to be the same. The difference, it seems, is in how the infection transfers itself from host to host, and in the paths of infection within the body that result from different ports of entry.

  Not one but two diseases may have thus altered their paths of infection among Europeans in the aftermath of the Black Death. If so, why? Obviously, the extent of skin-to-skin contact depended, among other things, on the adequacy of clothing and fuel available to the population at large, and particularly to the poor. In the absence of warm clothing and of enough fuel to warm living space in winter, the only way to conserve body heat was to huddle close together, especially at night, and in wintertime. In the thirteenth century, when wood became scarce in many parts of western Europe, very likely this was the only ordinary way peasants could survive the rigors of cold winter nights. The die-off of the fourteenth century, however, meant that by 1400 something like 40 per cent fewer persons had to find means of supporting life in the same geographic space as had done so in 1300. On the average this obviously meant more fuel, and more wool, to go around. The further fact that winters became distinctly colder in the fourteenth century as the climate worsened may also have meant that huddling no longer sufficed to maintain body heat without more adequate clothing than had been necessary in the warmer winters of the thirteenth century.