Plagues and Peoples (26 page)

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.
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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.
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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 pestis
^y
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.
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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.
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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.
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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.
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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.
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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.
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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, cannot 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.
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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.

It is, of course, a well-known fact that western Europe expanded woolen textile production markedly between the fourteenth and seventeenth centuries. Export of high-quality cloth to Levantine and Asian markets figures more prominently in available records than does the local, shoddy manufacture of woolen cloth for peasant wear. Yet it would be very surprising if the increasing prevalence of sheep, especially in England and Spain, together with the onset of colder temperatures, had not combined to put more cloth on European backs than ever before. Insofar as wages rose, consequent upon manpower shortages arising from plague losses, a rise of real income allowed wage earners to buy better clothing; and even though a rise of real wages was not a uniform nor uninterrupted phenomenon, the basic fact of fewer human bodies in juxtaposition to an increased number of sheep fleeces in western Europe remains incontrovertible. It therefore seems probable that even the poor were able to cover their bodies more completely than before, and in so doing Europeans may very well have interrupted the older patterns of skin to skin dissemination used by Hansen’s disease and by yaws. If so, the emptying out of Europe’s leprosaria becomes readily understandable.

Increasing supplies of woolen textiles, however, would have benefited lice and bedbugs, and thus facilitated the spread of such a disease as typhus, which seems first to have manifested itself as a notable destroyer of European armies in 1490.
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Still another by-product would be a new notion of decency, requiring everyone to cover most of the body most of the time. As is well known, puritanical drives in both Protestant and Catholic countries in the sixteenth and seventeenth centuries aimed at hiding sex, as well as other bodily functions. This in turn presupposed that enough cloth was available to cover human nakedness, even among the poor. The importance of these movements is indeed powerful, though indirect, evidence for the reality of my initial assumption that
cloth did in fact become more abundant in Europe after 1346.

Cold weather and increasing supplies of woolen textiles in Europe may therefore have confronted the bacillus of Hansen’s disease and the spirochete of yaws with a crisis of survival. The latter eventually hit upon a substitute method of passing from one host to another by infecting the mucous membranes of the sex organs. In doing so, symptomatic expressions of the disease altered and European doctors early in the sixteenth century gave it a new name—syphilis.
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Instead of being (as yaws may have previously been, at least among the poor) a widespread infection, common among children and normally incapable of developing crippling sores except when resistance was somehow reduced, the spirochetes now usually invaded only adult bodies. At least initially, they there provoked far more dramatic symptoms, just as our still familiar childhood diseases, e.g., measles, will provoke far more serious symptoms in a young adult than commonly occur among children.
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