The Great Mortality: An Intimate History of the Black Death, the Most Devastating Plague of All Time

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The Great Mortality: An Intimate History of the Black Death, the Most Devastating Plague of All Time Page 34

by John Kelly


  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

  The pagination of this electronic edition does not match the edition from which it was created. To locate a specific passage, please use your ebook reader’s search tools.

  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

 

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