The Great Mortality: An Intimate History of the Black Death, the Most Devastating Plague of All Time
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Echoing Cardinal Gasquet, the Plague Deniers note that no description of the Third Pandemic, whether written by the Indian Plague Commission or by other Western scientists, contains a list of symptoms comparable to that of Friar Michele and Heyligen, and that includes the symptom of contagion, since until it goes pneumonic, modern plague is spread via rat and flea, not from person to person.
Descriptions of the bubo do appear in accounts of both the Third Pandemic and the Black Death. But as Professor Cohn, a leading Plague Denier, notes, medieval and modern accounts of the plague describe the bubo differently. In modern plague, 55 to 75 percent of the time, the bubo develops in the groin, 10 to 20 percent of the time in the neck. Since the ankle is the most flea-accessible part of the body, this pattern makes sense. However, it is not the pattern described by many Black Death chroniclers. Fourteenth-century accounts usually locate the bubo higher up on the body, behind the ears, for instance, or on the throat, regions difficult for an insect to reach, even one that can jump one hundred times its height.
• Rat die-offs. Since the rat flea, X. cheopis, does not jump to humans until the local rat population is nearly obliterated, in theory an outbreak of human plague should be preceded by a large rat die-off. And during the Third Pandemic, practice usually followed theory. Preplague rat die-offs were common. However, references to them are exceedingly rare in the literature of the Black Death. Some scholars have tried to explain away the omission by claiming that dead rats were so common on the medieval street, chroniclers thought them unworthy of mention. To put it charitably, that theory seems improbable in the extreme. If an epidemic on the scale of the Black Death was caused by a rat-borne plague, the streets would have been knee-deep in dead rats and people would have noticed and written about that.
• Incidence of pneumonic plague. The disease described by Friar Michele, Louis Heyligen, and other medieval chroniclers sounds like a variant of pneumonic plague, and, judging from the frequent references to blood spitting and hypercontagiousness in early accounts of the plague, the pneumonic disease seems to have been very common in the first six to twelve months of the Black Death, even in regions where the climate should have been hostile to it, like the Mediterranean south. In contrast, in modern outbreaks of the disease, pneumonic plague is uncommon. Some scholars claim that as many as 15 to 25 percent of modern plague cases “go pneumonic.” But in Vietnam only 2 percent of the reported cases did.
• Climate. The whole issue of climate and plague is perplexing. Plague outbreaks during the Third Pandemic usually reflected the sensitivities of the rat and flea vectors. Outbreaks were rare during the Indian hot season, when the weather was very hot and dry, but common on either side of the hot season, when humidity increased and temperatures moderated—creating conditions favorable to X. cheopis. By contrast, the Black Death seemed to be largely immune to climatic effects. While outbreaks were slightly more common in warm weather, as Plague Deniers Scott and Duncan note, in some regions of Europe the mortality reached its peak in December and January. Indeed, Y. pestis killed almost as many people in frigid Greenland as it did in temperate Siena.
Before turning to the rejoinders of what might be called the Plague Defenders, a group that includes the majority of historians and almost all microbiologists, mention should be made of two recent discoveries by a team of French scientists. Diagnosing a disease from a list of symptoms in a medieval chronicle or medical tract—a favorite strategy of the Plague Deniers—is fraught with difficulties and imprecisions. One doctor’s carbuncle can be another’s plague boil. More fundamentally, written evidence ignores the fact that diseases, like people, often change over time. Measles and syphilis look and behave a lot differently today than they did when they first burst into the European population.
DNA is a far more trustworthy diagnostic tool. With that thought in mind, in the late 1990s a group of French paleomicrobiologists removed dental pulp from corpses buried in two plague pits in southern France and tested it. One pit dated from the Black Death, the other from a later recurrence of the plague. In a series of papers published in the
Proceedings of the National Academy of Sciences, the French investigators reported finding DNA from
Y. pestis in both samples. The French work has yet to be confirmed by researchers in other laboratories—the final step in scientific acceptance—but Didier Raoult, the lead investigator in the DNA study, is confident of his team’s findings. The “medieval Black Death was the plague,” he says without equivocation.
But what kind of plague?
Adopting the Russian view and describing the Black Death as an outbreak of marmot plague would help to explain many of the discrepancies that trouble the Plague Deniers. For example, marmot plague’s tropism for the lungs would account for the seemingly high incidence of pneumonic disease—even in warm climates, where the weather would not have favored its transmission. Moreover, marmot plague is the only form of rodent plague that is contagious; marmots spread the disease the way humans do, via a marmot version of the cough.
Of course, marmot plague is still marmot plague. But if Dr. Wendy Orent is correct, and at some point the marmot disease evolved into a distinctly human form, given its genetic heritage, such a “humanized” plague might well produce symptoms like chest pain, blood spitting, and, as the lungs and throat became gangrenous and corrupted, a fetid body and breath odor. A humanized version of
Y. pestis would also explain the absence of rat die-offs. Such an ailment would spread the way Friar Michele and Louis Heyligen describe the Black Death spreading, directly from person to person by way of the breath, though very likely other modes of transmission would have also developed. Thus, Dr. Orent thinks that
P. irritans, the human flea, would have played an important role in the spread of a “humanized” plague.
Like their Russian counterparts, many American microbiologists reject the arguments of the Plague Deniers, but for different reasons. Most American scientists do not accept the Russian theory of “host” plague strains—that is, that the lethality of a particular strain of
Y. pestis is shaped by its evolutionary history with particular rodent species. The plague bacillus is only fifteen thousand to twenty thousand years old, says Professor Robert Brubaker, dean of American plague researchers. In evolutionary terms, Dr. Brubaker thinks that is not enough time for the bacillus to have evolved very far away from its original form.
In Dr. Brubaker’s view and that of most of his colleagues, the Black Death and the Third Pandemic were classic examples of rat-borne plague. In the American view, differences between the two outbreaks can be explained largely in terms of external factors. One of the most important of these externals is the very different levels of knowledge available to physicians of the fourteenth and late nineteenth centuries. From firsthand observation, medieval Europeans sensed that plague was affected by factors like sanitation, nutrition, and the movement of goods and people, but this practical knowledge was attached to beliefs about the importance of astrology, miasmas, and bodily humors.
“By the late nineteenth century,” says Dr. Brubaker, “physicians and scientists understood the principles of contagion . . . [and] had a good working knowledge of how infectious disease spreads and the measures needed to be taken to safeguard public health.” One by-product of this new understanding was that seven-hundred-year-old insights could now be transformed into effective public health strategies. The municipal health board of Black Death Florence may have had little success with its sanitary measures, but “the Indian Plague Commissioners believed that they were able to prevent catastrophe [by] imposing aggressive controls on public and hospital sanitation,” says historian and physician Ann Carmichael of the University of Indiana.
Effective sanitary measures also played an important role in controlling plague outbreaks in Hong Kong and Canton in the mid-1890s. However, in those localities, physicians cited two other measures with Black Death echoes as also important—adequate nutrition and decent
nursing care.
It is noteworthy that when measures like stringent sanitation collapsed, as happened in Bombay during a disease outbreak in 1897, the plague of the Third Pandemic quickly began to behave like the plague of the Black Death. In a Bombay hospital a plague commissioner characterized as rife with “fatigue, destitution, filth, poverty and overcrowding,” the death rate reached 64.5 percent in the spring of 1897. Professor Cohn may be correct in saying that no outbreak of the Third Pandemic produced mortalities on the scale of the Black Death, but in the terrible months between August 1896 and February 1897, Bombay lost nineteen thousand people to the disease.
A modern understanding of another aspect of sanitation—personal hygiene—may also help explain why, if the Black Death was an outbreak of rat plague, there were so few rat die-offs. Given the unhygienic state of the medieval body, it is highly likely that
P. irritans, which preys on people, not rodents, played a major role in spreading the plague from person to person.
The Plague Deniers have long argued that
P. irritans’s bite, unlike
X. cheopis’s, transmits too few plague bacilli to make it a very efficient disease vector. However, that weakness may not have mattered during the Black Death. Whatever its form, the medieval plague was extraordinarily virulent; the very high concentrations of bacilli in human blood may have turned even normally weak insect vectors into efficient plague carriers. Furthermore, it is not at all clear that the human flea is that weak a disease vector. Observers as diverse as General Ishii (inventor of the Japanese plague bomb), United States Army Intelligence, and Giovanni Boccaccio have all offered testimonials to
P. irritans’s efficiency as a disease carrier. The two pigs Boccaccio describes as dropping dead after mauling a blanket almost certainly were killed by the bite of
P. irritans, which is a pig as well as human flea.
Perhaps the most compelling testimony about the effectiveness of the human flea as a plague vector comes from Dr. Kenneth Gage, chief of the Plague Division at the Centers for Disease Control. From his personal experience fighting the disease in modern Africa, Asia, and South America, Dr. Gage has become convinced that the human flea plays an important but underappreciated role in the spread of plague.
The weakest part of the Black-Death-as-a-purely-rat-borne-plague theory involves the apparently very high incidence of the pneumonic form of the disease. Secondary pneumonic infections occur in bubonic plague, but, at least in modern experience, only infrequently. French scholar Jean-Noël Biraben hypothesizes that the unusually cold weather of the fourteenth century may have been especially “pneumonic-friendly.” The problem with the Biraben theory is that, south of the Alps, the weather was still warm when the Black Death arrived.
One possible explanation for the high rate of “pneumonic” Black Death is that two disease strains were at work in 1348 and l349. The Manchurian outbreak of pneumonic plague in 1911 arose from marmots. Yet the epidemic occurred in the midst of the rat-based bubonic plague of the Third Pandemic. Perhaps something similar occurred during the Black Death? Another possibility is that over the course of the middle years of the fourteenth century,
Y. pestis underwent a fundamental evolutionary change, as Dr. Orent suggests.
Medievalist and physician Ann Carmichael also has a theory about the medieval plague, one that addresses not only the high incidence of pneumonic disease but, more sweepingly, why, on many clinical and epidemiological indexes, it looks so different from the Third Pandemic. “There may have been something fundamentally different about the nature of the premodern world,” says Dr. Carmichael, “something we don’t understand and which cannot be duplicated today even in Third World regions.”
However, about one thing we can be certain.
Microbiologist Didier Raoult is right; the Black Death was an outbreak of plague.
Index
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Aaron of Lincoln, 236–37
Aaron of York, 239
Abbey of Meaux, 225
Abelard, Peter, 246
Abraham of Bristol, 237
Adam de Carelton, 191
Adversus Judaeos, 237
Afghanistan, Soviets in, 75–76
Africa, plague in modern, 83n
Agatha, Saint, 86–87
Agimetus, 254–55
Agnes, Saint, 72
Agnolo di Tura, 26, 80, 114–19, 213, 277, 285
Agobard of Lyon, 238–39, 247
agriculture, 34, 285, 287
14th–century decline in, 56
East Anglian, 217–18
increasing productivity in, 45–46
post-Black Death, 293
technological innovation in, 45
AIDS, xi-xii, 18
Albert, Friar, 17
Alberti, Leon Battista, 276
Albigensians, 142, 242
alebedrep, 55
Alençon, Count of , 175–76
Aleppo, 6, 48, 235
Alexandria, 48
Alfonso, king of Castile, 198, 269
Alfonso of Cordova, xv
Allalin glacier, 57–58
Almeria, 268–69
Amadeus VI, count of Savoy, 253
Aminigina (Genoese woman), 91
Amulo, Archbishop, 239
An Answer to the Jews, 237
anatomy, 166, 288
Ancient Hymn of the Flagellants, 264
Andreas of Hungary, 91–92, 155–57
Andree, Silona and Augeyron, 134
Andronikos, prince of Byzantium, 81
animals, 36, 71, 205
Black Death die-off of, xii-xiii, 111, 112, 196
Anneys, Henry, 221
anthrax, xvi, 113, 280, 296
antidotes, 173
antigens, 35
antirodent remedies, 65
anti-Semitism, xv, 138–39, 151, 152, 176, 232, 240–41, 261
blood-libel accusation in, 242–43
Civitas Dei and modern, 242–43
in England, 239, 243
of Flagellants, 263, 267
Fourth Lateran Council and, 243
in France, 26, 140–41, 239, 241
as fueled by religious rivalry, 238
as personalized by moneylending, 247–48
of Roman Catholic Church, 237–38
see also Jews; pogroms
apothecaries, 167
Aquetus, 254, 255
Arab-Greco medicine, 165
Aristotle, 165, 244
armies, size of, 73–74
Army, Soviet, 75
Army, U.S., 75, 76, 302
Arnauld of Villanova, 168
Asaf-Khan, princess of Punjab, 65
Ashkenazi, 235, 240
Asia
medieval discovery of, 31–32
routes to, 32–33
“Assassins of Iran,” 50
astrology, 165, 166, 168, 169–70
Atomic Energy Commission, U.S., 11, 95
Audoin-Rouzeau, F., 68
Augustine, Saint, 239–40
Auschwitz, 233, 257
Austria, Peire, 137
Austria, xv, 26, 257, 260, 261
authority, 165–66
autopsies, 159, 166
Averroes, 165
Avicenna, 165
Avignon, xv, 12, 24, 81, 92, 121, 141–61, 180, 185, 267–68, 292
anti-Semitism in, 152, 153
change from pneumonic to bubonic plague in, 160
“column of fire” over, 104
mortality rate in, 150, 160–61
plague pattern in, 215, 260
plague’s arrival in, 150
poverty in, 145
protective measures attempted in, 153
social response in, 152
Avignon papacy, 141–46
see also specific popes
Aycart, Jacme, 13
4, 135–36
Baardson, Ivar, 58
Baghdad, 51, 236
Baillie, Michael, 82n
Bakeman, Alice, 221
Balavigny, 80, 232–34, 243, 253, 254, 255
Balkans, xv, 259–60
Bananias, 250
barber surgeons, 68, 69, 167
Barcelona, 252, 268
Basel, 26, 256, 261
Basse, Beatrice, 60
Bath and Wells, 193–94
see also Ralph of Shrewsbury
bathing, 17, 71–72, 172
baths of Diocletian, 71
Bavaria, 261
Bavaria, duke of, 164
beadles, 70–71
becchini, 107–8
Becket, Thomas à, 17
Belasagun, 8
Belieta, 253–54, 255
Benedict, Saint, 72
Benedictow, Ole, 9, 261, 270–71, 274
Benedict XII, pope, 143–44, 149
Benezeit, Andre, 251
Benitio, Antonio de, 25, 91
Benjamin of Tudela, 235
Bergen, 27, 274, 275
Bessa, Uga de, 136–37
Big Optimum, 44n
Big Science, 41
Biology of Plagues, The (Scott), 295
Biraben, Jean-Noël, 35n, 303
Bircheston, Simon de, 216
Birgitta of Sweden, Saint, 146
Bishop, Morris, 145, 147
black bile, 168–69
Black Death, 13, 41, 56, 57
animal deaths in, xii-xiii, 111, 112, 196
areas escaping, 270
arrival in Europe of, 84
birth rates after, 281–82
black rats as vector for, 66–67, 301
chain of infection in, 19
change in Avignon from pneumonic to bubonic of, 160
Chillon conspiracy theories on, 139–40
Church’s impatience in face of, 222–23
deniers of, 295–303
dissemination rates of, 296–97
early history of, 6–8
end of, 276
environmental upheavals as precursor to, 13–14