Fleas: Some Scratchy Issues Concerning the Black Death
2008; Wiley; Volume: 8; Issue: 2 Linguagem: Inglês
10.1111/j.1540-5923.2008.00244.x
ISSN1540-5923
Autores Tópico(s)Yersinia bacterium, plague, ectoparasites research
ResumoAdded to the list of scathing historiographical epithets we now have: “plague denier.” The opprobrium arises from a controversy about the biological nature of the pandemic of 1348–1349 commonly known as the Black Death. Was it bubonic plague? My present intention is to review this controversy with attention to fleas, literal and figurative. In a later part of this essay I then will pursue some fleas that infest other areas of current Black Death historiography. The plague controversy pits a majority of traditionalists, who believe that modern clinical descriptions of bubonic plague fit the epidemiology of the Black Death as reconstructed from fourteenth-century evidence, against a minority of rebels who propose that the modern plague and the medieval pandemic were different diseases. The traditionalists bask in certainty. John Aberth writes that “we know exactly” how the Black Death was spread because we know that it was caused by a bacterium that produces bubonic plague; John Kelly concludes: “about one thing we can be certain … the Black Death was an outbreak of plague.”1 And yet as a “denier” I will insist that such assurance is unwarranted. We are fully informed about the nature of modern bubonic plague. During a plague epidemic sweeping India, an officer of the British army compiled detailed hospital data in 1896–97. Then, in 1905, the British government established an “Indian Plague Research Commission” to gather clinical findings toward the aim of fighting the disease. Detailed reports were published regularly in The Journal of Hygiene in the years between 1906 and 1914. Traditionalists and deniers agree that these reports represent a “medical revolution in the understanding and nature of epidemic disease” as well as “models of interdisciplinary and comparative research.”2 This evidence demonstrates beyond dispute that the modern plague is a bacterial disease of rats communicated to humans by fleas. An apothegm to this effect, voiced in 1901 by one of modern science's greatest bacteriologists, Robert Koch, was quoted with approval in the first report of the Indian Plague Research Commission: “plague is a disease of rats in which men participate.”3 Humans, however, do not participate as a result of rat bites. Rather, it is the rat flea, forced to depart from the infected dying rat, which carries the plague bacteria to humans by means of a bite that regurgitates the bacteria into the human bloodstream. Once a human being is infected, the bacilli are carried by the lymphatic system to the lymph node nearest the site of the bite, where they multiply. After three to eight days the colonies of bacteria are large enough to cause swellings known as buboes, and three or four days after that the infection reaches other organs, usually causing death. The bubo, of course, is the most obvious symptom of eponymous bubonic plague. Because fleas find it easiest to bite around the ankles, the preponderance of buboes grow from the lymphatic node nearest the bite, namely the groin. According to the British records, between 55 and 75 percent of plague buboes were located in the groin, followed by 10 to 20 percent in the armpits and some 10 percent forming in other glands. Whether in the groin or elsewhere, in 94 percent of cases the buboes were found in only one location.4 The modern literature on bubonic plague often refers to a sibling, “pneumonic plague,” a disease of the lungs that results in frightful coughing. Here misunderstanding often arises because of the lack of proper distinction between “secondary” and “primary” forms. Secondary pneumonic plague is simply bubonic plague that has reached the lungs. Victims have buboes but also start coughing, and because they frequently cough blood they are likely to die from that. Modern research shows this happening in between 10 to 25 percent of bubonic plague cases. Before such victims die, however, they can infect others with their coughing, and recipients so infected may infect still others in the same manner. In other words, this is the primary form: true pneumonic plague, transmitted by coughing directly from human to human. Primary pneumonic plague is highly lethal, but in fact “too lethal for its own good.” Many of those infected die within a day, before having time to develop any cough at all, and those who do cough usually die within a day after they start coughing. Consequently human-to-human infection by means of coughing is minimal: the most serious incidence of primary pneumonic plague recorded by the British during the Indian bubonic pandemic of the early twentieth century resulted in a death rate of 0.4 percent of the population.5 This leads to one more salient point about the modern plague: contrary to common belief, bubonic plague as known since the nineteenth century is not highly contagious. In this regard it falls well behind other epidemic diseases such as measles, smallpox, or scarlet fever. An initial outbreak of plague in nineteenth-century China traveled extremely slowly, moving at about ten to twenty miles a year; observers in India noted that the disease seldom infected doctors or nurses; malaria there killed ten times as many people as the plague.6 It will already be evident that great discrepancies exist between the clinical evidence regarding modern bubonic plague and the numerous medieval accounts of the mid-fourteenth-century pandemic most familiarly known as the Black Death.7 For these reasons, clear-sighted twentieth-century historians had difficulty reconciling the modern and medieval data. To take one example, the prominent American medievalist David Herlihy conceded in an essay of 1974 that bubonic plague as known from modern observations is not highly contagious, whereas numerous medieval descriptions and the documented rate of spread of the Black Death leave no doubt of extraordinary contagion. To account for this, Herlihy offered the stand-in of the pneumonic form, which could spread directly through the air. In fact Herlihy seems not to have understood that the pneumonic form is too fulminantly lethal to account for high rates of contagion, but he was too honest not to concede a different objection to the pneumonic alibi—that contagion from coughing is most frequent in winter months but the medieval epidemic spread more quickly in Mediterranean regions in the summer. Nevertheless, he left this as a puzzle and did not retreat from his categorical statement that the medieval disease was bubonic plague. Only in a second account, contained in a series of lectures of 1985 published posthumously as a book, did he come around to granting that “the true nature of the great medieval epidemics remains open.”8 A small number of historians did abandon the plague fixation, but it is one of Herlihy's students, Samuel K. Cohn, Jr., who in my estimation has dealt what should be considered its death blow. In a trenchant book of 2002,9 Cohn demolishes every excuse one by one. Yet it can hardly be said that he has won the day. To me this seems puzzling, for we are not talking here about supercharged ideological issues: not Freudianism, not Marxism, not Creationism. Nobody's cherished belief system should be tottering. All that is at stake is an old chestnut of historiography. Nevertheless, I have failed to notice a single traditionalist who has capitulated. (Unless it be myself, for I used “Black Death” and “bubonic plague” as interchangeable terms in one textbook account and termed the Black Death “a combined onslaught of bubonic and pneumonic plague” in another.10) What I find most remarkable are the extraordinary ways in which different traditionalists attempt to talk their way out of abandoning their partis pris, and these are some of the metaphorical fleas I would like to examine here. I will move from literal fleas, to literal fleabites, to rats. If we posit that the fourteenth-century disease was bubonic plague, then it had to have been transmitted by rat fleas because we have seen that pneumonic plague cannot account for widespread contagion, and pneumonic plague in both its secondary and primary forms depends at any rate on infection by the bubonic plague bacillus. But if fleas were the vector of contagion they strangely seem to have flourished in temperatures that were not congenial to them. The lack of correspondence between high season for fleas and incidence of the Black Death applies for both southern and northern Europe. In the Mediterranean regions incidence of the disease peaked during the hottest months, June and July, despite the fact that the rat flea has difficulty enduring the heat as well as the dryness of those summer months. Had the Black Death plague been carried by fleas, its incidence should have increased greatly in Mediterranean areas with the cooling off and increased rainfall of late summer and early fall. But, much to the contrary, Cohn's plentiful statistics (not just for the first onslaught of the Black Death but for later ones) demonstrate that it dropped off dramatically in August, September, and October.11 John Aberth seeks to account for this by invoking the supposed onset of Europe's “little ice age” around this time. Yet this will not work, for as Aberth then concedes in a footnote, “there is some debate about whether the Mediterranean was part of this colder weather pattern.”12“Some debate” may be an understatement, for the climate historian H.H. Lamb has not only maintained that southern Europe probably avoided the “little ice age” observable in the north, but may also have had hotter temperatures in the fourteenth century than when he wrote, circa 1970.13 Moreover, even if one were to grant for the sake of argument that Mediterranean summers were cooler during every Black Death year than in recent times, it would still be impossible to account for the early fall retreat. Aberth's response to the problem of the lack of correspondence between the Black Death and the known prevalence of rat fleas at the other end of the climate continuum, the cold of the north, is equally unconvincing. Rat fleas do not flourish in temperatures that are much below fifty degrees Fahrenheit, any more than they do when the thermometer really rises.14 And yet in parts of England the Black Death peaked in the winter of 1348–1349. A London chronicler reported that the pestilence arrived in his city around All Saints (November 1) and became most deadly between Candlemas (February 2) and Easter. Closely confirming this is the pattern of wills authenticated in a London court: no wills authenticated in December, nineteen in January, and forty-two in February. In Scotland the second onslaught of the Black Death began on Candlemas of 1362.15 Aberth responds that “a cold climate is no barrier to a flea” on the premise that fleas may flourish in warm homes. But although we have no statistics about mean indoor temperatures in medieval England, judging from modern experience it may behoove us to be careful in assuming the coziness of English winter heating. More certainly, fleas that stay by the fire would not be able to cause a pandemic. Most troublesome is the fact that Aberth proceeds to misrepresent evidence. Having argued that Mediterranean areas would have been cooler than we might suppose on the grounds of a questionable incidence of a “little ice age,” he turns around and states that “the winters of 1348 and 1349 were reported to be mild.” For this the only evidence he offers is a noted report of the medical faculty of the University of Paris, which does indeed state that “the past winter was less cold than it ought to have been.” Unfortunately, however, this report was written in October of 1348!16 John Kelly attempts instead to evade the rat flea problem with an epicycle: the vector fleas were not rat fleas but human fleas. At first glance this seems to be a persuasive alternative because medieval people famously did not wash themselves much and human fleas may have been minimally susceptible to temperature cycles. But whereas the rat flea lives in its host's fur and hence moves with the rat, the human flea is a “nest flea.” This flea, that is, does not actually live on humans or even in their clothes, but nests around beds and emerges at night to feed and lay eggs. Accordingly, this flea does not move with humans and cannot be deemed an effective vector of epidemic disease. When plague was discovered after 1920 in Madagascar, records were kept for two decades and revealed that even though human fleas abounded in unsanitary local hovels, not a single case of transmission of plague by the human flea was recorded.17 A second argument against identifying the Black Death as bubonic plague is based on symptomology: the location of buboes. According to modern clinical records, as we have seen, the preponderance of plague buboes is located in the groin. In fewer instances buboes appear in armpits or, still less often, near another lymph node, and almost always the buboes appear only in a single place. In contrast, the medieval evidence yields a different picture. Although chroniclers often mention large tumors in the groin, they rarely locate them only there. Much more often they have them appearing in two places, groin and armpits, and sometimes in three places, groin, armpits, and behind the ears, or on the throat or neck. Given that the groin, armpits, and neck are the major locations of human lymph nodes, it is reasonable to believe that the Black Death was a lymphatic disease. Yet, the customary references to buboes in two or more places is strongly at variance with the modern evidence about a single place, and the frequent references to armpits and neck (sometimes the groin is not even mentioned) make one wonder again about infection by fleabite.18 Fleas, it is true, can jump very high, but why would they want to do so without a motive? The predominant incidence of buboes in the groin in modern plague cases is easily explained by the fact that rat fleas seeking a new host are most likely to bite on legs or ankles. Anyone who tends a garden in the evening knows that mosquitoes are most likely to go for the legs first if the legs are not covered, to say nothing of sand flies. But the medieval incidence of buboes on armpits or neck was so great that it leads Samuel Cohn to ask sarcastically whether medieval people were particularly supine.19 Angus Trumble, striving to dismiss Cohn's evidence in The Times Literary Supplement, has this to say: “I should have thought that among factors to be taken into account are that, for obvious reasons, groins were hardly mentioned in fourteenth-century Catholic Europe.”20 But perhaps Trumble “should have thought” twice before turning medieval writers, who blushed at nothing, into Victorians. Perhaps it will suffice to recall some Dante: “Ed elli avea del cul fatto trombetta” (And he made a trumpet of his ass); or some Chaucer: “But with his mouth he kiste hir naked ers, ful savourly…” From the flea and fleabite challenges to the bubonic plague thesis I come to what appears to me to be the single greatest challenge, that concerning rats, or rather the lack of them. Given the certainty that modern plague is “a disease of rats in which men participate,” and the undisputed premise that the plague bacillus will only spread from fleas to humans upon the death of rats, one should find many references to piles of dead rats in medieval accounts if the medieval pandemic had been plague. But in fact there are none. The question first arises as to whether rats even existed during the late Middle Ages in some of the northernmost climates where the Black Death indubitably decimated the human population. Ole Benedictow insists that they did in Scandinavia on the scantiest of evidence. Benedictow does admit that black rats do not flourish in extreme cold, a concession that inspires him to offer a rather bizarre proof that the disease in Norway was bubonic plague. As he convincingly demonstrates, when the Black Death arrived in Norway in the summer and fall of 1349, its incidence fell off greatly in November and December; moreover, data for thirty successive epidemics up to 1654 reveal the absence of any winter onslaught. Since Benedictow believes that rats existed in Norway but that they somehow were not present in the winter, he concludes that the absence of the Black Death in the winter “constitutes decisive evidence to the effect that plague in Norway was invariably bubonic plague transmitted by rat fleas.”21 The trouble is that this argument implicitly rests on a belief that rats hibernate. Yet, rats do not hibernate. Although Benedictow subtitles his book on the Black Death, with some bravado, The Complete History, he omits Iceland. Technically this is warranted because he intends to cover only the initial incidence of the Black Death, whereas the frigid island was spared from that first onslaught. Yet when he wishes to adduce the evidence of thirty waves of the epidemic in Norway from 1348 until 1654, or discuss the existence of rats in England in the fifteenth century, he feels free to do so. Above all, Benedictow's prefatory discussion regarding the presence of rats in the north cries out for confronting a crucially important article that preceded his book, but he makes no mention of this. I refer to Gunnar Karlsson, “Plague without Rats: The Case of Fifteenth-Century Iceland.” As the title indicates, Karlsson looks in vain for rats in Iceland even though Iceland experienced two fifteenth-century rampages of what was surely the Black Death. No skeletal rats from this period have been found by archeologists, and Icelandic sagas lack mention of rats even though mice abound. Most telling are two further pieces of evidence. One is a description of the island written by a native bishop dating from 1666, which states explicitly that many mice exist in Iceland, but no rats; the other is an extensive naturalistic account published in 1772 that mentions rats at only one juncture, and then to say that they had recently arrived on a ship.22 One may add that Karlsson apparently knew nothing of Dr. Samuel Johnson, or else he could have followed a nice lead. Familiar in the Anglolexic world is Johnson's remark, reported by Boswell, that he could effortlessly repeat the contents of an entire book chapter: “Concerning Snakes in Iceland.” The reason? The chapter only had one sentence: “No snakes of any kind are to be met with throughout the whole island.” Inasmuch as Boswell reported that this chapter belonged to a work on the natural history of Iceland by one “Horrebow,” I have found it possible to pick up the trail and supplement Karlsson. In Niels Horrebow's The Natural History of Iceland, translated into English from the Danish and published in 1758, the author indicates indirectly but sufficiently clearly that there are no fleas in Iceland. According to him, “no country on the globe is less troubled with insects … the only troublesome thing of the kind are gnats … where fish is cured a great many flies will gather about them … no other sorts of insects are met with.” Horrebow also has a chapter “concerning mice” that states: “there are a great many mice in this island; for as all are obliged to lay up a stock of provision in their houses, the mice find sufficient store.” But not a word about rats.23 As Charlie Brown might have responded: “rats.” To my mind, what clinches the argument in favor of “plague denial” is the lack of any reference in the contemporary sources to rat die-offs preceding incidences of the fourteenth-century pandemic. Because rat fleas will only leave their hosts when the rats have become stone cold, there should have been piles of dead rats in mid-fourteenth-century streets and alleys, but no sources support this. The closest we come is a passage from a Byzantine chronicle about the spread of the Black Death on the Greek islands: “The calamity did not destroy men only, but many animals living with and domesticated by men—dogs and horses and all the species of birds, [and] even the rats that happened to live within the walls of the houses.” As can be seen, this is not a reference to rat die-offs preceding the human mortality, or to the sight of large piles of rats any more than of large piles of dogs or birds. At most, the death of rats accompanied the death of humans and all God's fauna. Moreover, if the report is trustworthy, which is uncertain, it hardly rescues the plague thesis, for modern observations have shown that dogs, horses, and birds are resistant to the bubonic plague bacillus, birds in particular being altogether inappropriate hosts for rat fleas.24 Samuel Cohn quotes an acknowledgment by a previous historian of the Black Death, Robert Gottfried, who states that “virtually” none of the contemporary reports connect the medieval disease with a plethora of dead rodents, and reasonably enough inquires “why insert ‘virtually’?” But the practice continues, as with John Kelly, who admits that “references to pre-plague rat die-offs are exceedingly rare [emphasis mine].” John Aberth, on the contrary, wants students using his source reader to accept his word that “a number of medieval chroniclers … noticed rat mortality in connection with the plague.” But of Aberth's three examples, one is the Byzantine chronicle cited above and a second that of the Strassburg chronicler Fritze Closener. Aberth refers to a selection from Closener contained in his reader, which in turn refers to the “Heavenly Letter” read aloud by a flagellant leader. And here we find a comprehensive list of miseries that the Lord had visited on his people: “earthquakes, famine, fever, locusts, rats, mice, vermin, pocks, frost, thunder, lightning, and much disorder.” To seize on this as “rat mortality” connected with the plague is surely wrong, not only because of the formulaic inclusion of rats with locusts, mice, and vermin, but also because nothing in fact is said of rat mortality.25 Aberth's remaining example is from the chronicle of Giovanni Villani. Students can turn to this source too within his reader, and there they will find the chronicler stating, according to Aberth's translation, that in some far-off place called “Sivas” (the original Italian is “Sibastia,” which probably is Sebastopol), “it rained an immeasurable quantity of vermin, some as big as eight hands, all black and with tails, some alive and some dead … and those who fought against the vermin fell victim to their venom.”26 Medievalists will easily recognize this as a typical account of a fabulous supernatural prodigy; snakes also fall from the sky in late-medieval sources, and so too do stones the size of ostrich eggs. Moreover, Villani's account is even more fabulous than Aberth's translation indicates, for the translation is incorrect (one hopes inadvertently): what Villani actually says is that “it rained an immeasurable quantity of vermin as large as a fist, having eight legs [emphasis mine].”27 Discredited by the sources on every front, those who remain unwilling to abandon the bubonic plague thesis now want to wave the magic wand of DNA. In 1998 a team of French paleomicrobiologists published the results of a study based on samples of dental pulp taken from teeth found in human skeletons in southern French construction sites where quarantine hospitals of epidemic victims had been located from the sixteenth through the eighteenth centuries. To considerable publicity they announced that DNA linked to that of the modern plague bacillus was found in seven of their twelve samples and hence stated that “we have confirmed the presence of the disease [bubonic plague] at the end of the sixteenth century in France.” After the report was criticized on methodological grounds, the team entered the lists again in 2000. This time they located a fourteenth-century grave and found positive results from dental pulp taken from one child and two adults, leading them to state “we believe that we can end the controversy: medieval Black Death was plague.”28 Nevertheless, in 2003 another team of researchers, this time from Oxford, engaged in another study, testing 121 teeth from sixty-six skeletons in five fourteenth-century mass graves, and found no trace of the plague bacillus. According to the leader of this team, “we cannot rule out Yersinia [the plague bacillus] as the cause of the Black Death, but right now there is no molecular evidence for it.” One begins to fear that the Napoleonic Wars are being fought again, now over dental pulp, but the fear is allayed by the existence of a multiple-authored study that appeared after the British one, with contributors from research institutions in both England and France, as well as Germany and the United States. Cautiously, this stated: “it is premature to infer an association between modern molecular grouping and a particular pandemic wave that occurred before the twentieth century.” If there are subsequent findings, I have not kept up with them, but it does seem sufficiently clear that DNA samples offer no magic wand.29 So what exactly was the epidemic disease that entailed so much population loss in the fourteenth century? Those who expect critics of the plague assumption to be silent unless they can answer this question appear to me to be demanding the unreasonable. Graham Twigg, a forceful early “denier,” was laughed to scorn when he suggested that the epidemic disease was really anthrax. Almost certainly it was not, but Twigg's suggestion proved particularly unfortunate because those who derided him then felt licensed to dismiss the rest of his argument that the disease was not plague. What call for acknowledgment are the facts that medieval chroniclers were not clinicians and that most had a taste for the extravagant, resulting in the circumstance that their reports often differ in essentials. The medieval evidence allows us only to be confident that the Black Death was extremely contagious, extremely virulent, and unaffected by severe extremes of temperature. Large swellings near locations of lymph nodes appear to have been characteristic but not invariably so, and many other symptoms, preeminently splotches and sores, were also reported. One may go further and say that even if we had consistent clinical data surviving from the Middle Ages, we probably still would not be able to identify the microbe or virus that caused the Black Death, for just as new diseases appear, old ones almost certainly disappear. David Herlihy was surely warranted to say that “it is not at all certain that the diseases we observe today are the same that troubled our ancestors.”30 Recently one of my colleagues doubted the need for such a fuss about whether the Black Death was really plague: all that matters for the historian is that huge numbers of people died. Having made a fuss myself, I should explain why the question matters to me. Although demographic estimates for the Middle Ages are notoriously imprecise, no one challenges the finding that in the mid-fourteenth century Western Europe was greatly overpopulated. Land reclamation and improved agricultural technology had increased the food supply in the twelfth and thirteenth centuries, thereby stimulating population growth, but roughly around 1300 agricultural expansion had reached its limits while the population was increasing geometrically. Various checks such as famine, war, and apparently abortifacient birth control seem to have contained population growth in the first half of the fourteenth century, but these checks surely did not reduce the population to any significant degree. And then came what contemporaries referred to as “the great mortality.” Obviously, then, one needs to wrestle with the question of whether the Black Death was nature's response to overpopulation. If the disease had been bubonic plague, that approach would be ruled out, for such plague would be an exogenous variable. An invasion from the East of infected rats could have happened at any time (assuming some long-distance shipping), and a flea biteth where he listeth. But if the disease had been something else, then malnutrition might more probably help explain the severity of the pandemic. The speculation is by no means unrelated to qualitative and quantitative evidence. The qualitative evidence, to be sure, is hardly decisive. Two northern French chroniclers explicitly deny a correlation between famine and the great epidemic. But a contemporary Parisian physician wrote that “one who was poorly nourished by unsubstantial food fell victim to the merest breath of the disease.” Particularly evocative was a Florentine memoirist, Giovanni Morelli, who, albeit not contemporary (he wrote about half a century after the events), seems to be drawing on collective memory. Morelli wrote that at the time of the plague Florence was “more stuffed with people than it had ever been before.” Then he contradicted the French chroniclers by referring to a terrible famine of the previous year that contributed to the plague by weakening resistance. As he said, “I believe that no more than twenty out of a hundred had bread or any fodder whatsoever, and those who did had little; people lived on grass and the stubble of grass … and the entire countryside was full of people who went around grazing like beasts. Just imagine how their bodies were affected!”31 Regarding discrepancies in incidence between rich and poor, one contemporary observer noted that “nobles and gentry were less affected than the rest of the population” and another that “in every place the poor and common people die first, in great numbers.”32 If such remarks are to be dismissed as impressionistic, Ole Benedictow, an expert demographer, supplies quantifiable data. Records from Savoy on the continent and Somerset in England reveal an excess mortality of the destitute. All told, “the mortality level among the general population was about 7.5 percentage points higher than estimated for [
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