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Disease and DiscriminationPoverty and Pestilence in Colonial Atlantic America$

Dale L. Hutchinson

Print publication date: 2016

Print ISBN-13: 9780813062693

Published to Florida Scholarship Online: January 2017

DOI: 10.5744/florida/9780813062693.001.0001

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Of Plagues and Peoples

Of Plagues and Peoples

(p.14) 2 Of Plagues and Peoples
Disease and Discrimination

Dale L. Hutchinson

University Press of Florida

Abstract and Keywords

Two major historical trends in the Old World initiated the development of infectious disease pools and the global spread of pathogens across previously intractable geographic boundaries: new agricultural complexes and increasing migration and trade. In 1491, Europeans were about to inaugurate those same changes in the New World. Agriculture, the production of and increased reliance on domesticated plants and animals, was associated with many changes in behavior and alterations of environment. Agriculture stimulated a trend toward the built environment through landscape alterations such as cleared fields, terraces, raised fields, ridged fields, and irrigation complexes. Fields and irrigation complexes, especially raised fields and wet rice fields, created aquatic habitats for the reproduction of mosquitoes and other insects (arthropod vectors) that transmit germs.

Keywords:   Agriculture, Old World, Migration

And I looked, and beheld a pale horse: and his name that sat on him was Death, and Hell followed with him. And power was given unto them over the fourth part of the earth, to kill with sword, and with hunger, and with death, and with the beasts of the earth.

The Holy Bible, King James Version, Revelation 6:8

One cannot understand the changing disease patterns of America without first understanding the history of health and disease in Eurasia and what factors contributed to the development of disease patterns there. It is the place where at least some of the diseases new to the Americas originated. It probably would be best to start with a short conversation about disease ecology, which is not so much a discipline as it is a way of looking at things, of appreciating the relationships between organisms and landscapes.

Disease ecologists speak of landscapes broadly. Natural environments figure prominently, but so do those modified and created by humans, the so-called built environments. How humans choose the landscapes they use and inhabit, how they modify those landscapes, and how and when they use them all influence the continuity and transmission of infectious diseases, as well as the prevalence of noninfectious diseases. Transmission is essential in disease cycles. The use of landscapes by multiple species figures into those transmission cycles, and the when-where-how of infectious disease transmission cycles extends beyond people to pets, pests, and pathogens. In fact, transmission cycles are affected beyond biological organisms to habitats, climates, and inanimate objects; and so one can define landscapes of disease or epidemiological landscapes (epidemiologists study what causes disease outbreaks with an orientation toward disease prevention) as the (p.15)

Of Plagues and Peoples

Figure 2.1. Disease transmission cycle for the common cold, a directly transmitted disease.

Chart prepared by Dale Hutchinson.

complex overlaps of environments, behaviors, and biological organisms that contribute to disease (Figures 2.1–2.3).

There are many organisms and many ways in which organisms use other organisms. A few terms will facilitate the rest of our discussions. A parasite is any living thing that lives in or on another living thing. A pathogen is a microorganism that parasitizes an animal or plant (a host) and causes host tissue damage (disease)—germ is a common name for a pathogen. Hosts are organisms that provide some life-cycle support for parasites. Vectors are organisms and devices that facilitate the transfer of (p.16)

Of Plagues and Peoples

Figure 2.2. Disease transmission cycle for malaria, a biologically vectored disease.

Chart prepared by Dale Hutchinson.

the pathogen from one host to another. There are biological vectors that are essential to some part of the pathogen’s life cycle (e.g., the Anopheles mosquito), and mechanical vectors, those that simply carry the pathogen from one place to another (e.g., flies). Rivers, ambulances, and hospital workers can all be mechanical vectors as well. Survival and reproduction are necessary for all those organisms (hosts, vectors, pathogens), and there is a fair amount of interdependence involved. A zoonosis is a disease that cycles primarily among nonhuman hosts. Prevalence refers to the number (p.17)

Of Plagues and Peoples

Figure 2.3. Disease transmission cycle for cholera, a directly transmitted and mechanically vectored disease.

Chart prepared by Dale Hutchinson.

of cases (people) affected by a disease. An endemic disease is one that is constantly present, while an epidemic disease occurs at levels beyond those expected. A disease is pandemic when it reaches global spread.

In a contemporary example of a disease ecology approach, edward michelson and his colleagues examined predisposing factors in the contraction of schistosomiasis among several previously studied populations.1 schistosomiasis, also known as bilharzia, is a disease caused by parasitic worms. the worms spend two segments of their life cycle in freshwater (p.18) snails, and it is through water contact that people are exposed to the infectious parasite. more than 200 million people in the world are affected by schistosomiasis, making it second only to malaria in number of people impacted globally by an infectious disease. the free-swimming larval form of the parasite, the cercariae, penetrate the skins of people in the water and then migrate to the liver to mature into adults. there the adults mate, migrate to the bowel and/or rectum, and produce eggs, which are shed back into the water.

The cycle of reproduction thus involves water, temperature, snails, humans, and water contact. Michelson found, in a marvelous unfolding of the factors involved in the disease cycle, that rates of infection differed between men and women, and that the patterns of infection are linked to who spends more time in the water, and when they spend that time. For instance, in the populations in question, there was a marked sexual division of labor. Women tend to do more washing of utensils and clothes, whereas men tend to have water contact through farming, fishing, and basket weaving. Those activities occur at different times of day, which affects how much chance there is for transmission of the parasite. For two species, Schistosoma mansoni and Schistosoma haematobium, the time when the most cercariae are active in the water is between one and three o’clock in the afternoon. For a third, Schistosoma japonicum, it is after sunset. This study noted that women tend to wash clothes in the morning, when the cercarial density is low. Cultural restrictions regarding water contact reduces the chances of infection for women. In particular, in Muslim communities ritual ablutions are required of males several times a day, while bathing opportunities for women are severely restricted. Thus, behavior and ecology are important factors in schistosomiasis infection.

One of the landmark books that explains the history and context of disease change in Eurasia is William H. McNeill’s Plagues and Peoples. Mc-Neill carefully outlines how the major trends in agriculture and increasing migration between state-level societies led to disease epidemics. McNeill’s perspective takes into account not only the germs that cause disease, but the social, economic, political, and ecological settings in which those germs occur, and it is there that we must turn our attention to appreciate the intricate details.

Agriculture, the production of and increased reliance on domesticated (p.19) plants and animals, was associated with many changes in behavior and alterations of environment. Agriculture stimulated a trend toward the built environment through landscape alterations such as cleared fields, terraces, raised fields, ridged fields, and irrigation complexes. Fields and irrigation complexes, especially raised fields and wet rice fields, created aquatic habitats for the reproduction of mosquitoes and other insects (arthropod vectors) that transmit germs.

Agriculture was associated as well with permanent (sedentary) residence, larger and more aggregated urban populations, houses, courtyards, public buildings, and plazas for large community gatherings. Those all necessitated paths and roads. Domesticated animals served as labor and transport, in addition to being sources of food and other by-products. They tended to be kept in close proximity to humans, sometimes in separate outbuildings, sometimes under elevated houses.

Agriculture and sedentary residence brought about the first major transition in human health patterns. Quite simply, moving about the landscape periodically as a forager reduces several problems. For one, short-term use of resources such as plants, animals, and water tends to lessen overuse and contamination. Human wastes tend to be more dispersed. Population size is smaller. Once people stop moving around so much, human wastes pile up, and with more people there are more piles. Bring domestic animals into the landscape, and the piles get even bigger. With piles there are often parasites, especially those of intestinal nature—worms and the like.

Larger populations packed into smaller spaces enable the spread of crowd diseases, diseases that are transmitted directly. Crowd diseases need an adequate population level to ensure continuous transmission, as well as a steady supply of those who are not immune to maintain it. They are often diseases of childhood where the infectious stages are brief, and they spread quickly: influenza, smallpox, mumps, measles, and chicken pox. Those diseases exist entirely by rapid transmission from one host to another. They generally cannot survive in small populations and thus are among the so-called diseases of civilization.

From both archaeological excavations and historic texts, we know that agriculture and urbanism began as early as 10,000 B.C. in the Middle East, and that similar trends occurred by 500 B.C. in China, India/Pakistan, and the Mediterranean region.2 In those four regions agriculture was accompanied (p.20) by the transition from mobile to sedentary populations. Aggregation, combined with agricultural landscape change, enabled the development of what McNeill termed “civilized disease pools.”3 Each civilized disease pool shared the common characteristics described above for agriculture and permanent villages but retained some unique characters as well.

Among the diseases present in early Egypt were tuberculosis, smallpox, malaria, bilharzia, intestinal tapeworms, and chronic growth arrests. Chinese populations in northern China experienced a dramatic decline in community health after 5,000 B.P., as indicated by stature reduction and increased prevalence of anemia indicators. The same increased prevalence of anemia indicators associated with an increased dietary focus on domesticated plants is present for Neolithic Greek populations. Further, indicators of increased workload and trauma are found during the period from 5,000 to 3,200 B.C. in Greece.4

Beginning in the fifth century A.D., those separate civilized disease pools were united through mercantilism, migration, colonial expansion, and warfare. Particularly important was the Silk Road across Asia, which between 100 B.C. and A.D. 1500 transformed previously isolated geographic localities into stepping stones across Eurasia. Running between Jiuquan, China, in the east, and the Roman Empire (Antioch) in the west, the Silk Road brought populations into contact via the caravans that traversed the route. Plague and several other diseases were likely transported beyond their original foci into other areas through the increased traffic that moved hosts, vectors, and pathogens across the vast space of several empires.5

It was during intensification of trade with central Asia along the Silk Road that the first major outbreak of plague occurred in the Mediterranean during the Justinian Wars. Known as the Justinian Plague, it ravaged Mediterranean populations from A.D. 541 to 542, and appeared intermittently until A.D. 750. Procopius describes the epidemic with great care and observation:

Some doctors were at a loss because the symptoms were unfamiliar to them and, believing that the focus of the disease was to be found in the bubos, decided to investigate the bodies of the dead. Cutting into some of the bubos, they found that a kind of malignant carbuncle had developed inside…. In cases where the bubos grew very large and discharged pus, the patients overcame the disease and survived, as it was clear that for them the eruption of the carbuncle found relief (p.21) in this way; for the most part, this was a sign of health. But in cases where the bubos remained in the same condition, these patients had to endure all of the misfortunes that I just described [madness, quick death].6

Procopius also describes the breakdown of normal conditions and the chaos that follows in the wake of epidemic disease:

And when the existing graves were full of dead bodies, at first they dug up all the open sites in the city, one after another, placed the dead in there, each person as he could, and departed. But later those who were digging these ditches could no longer keep up with the number of those dying, and they climbed up the towers of the fortified enclosure, the one in Sykai, tore off the roofs, and tossed the bodies in there in a tangled heap…. All of the customs of burial were overlooked at that time. For the dead were neither escorted by a procession in the customary way nor were they accompanied by chanting, as was usual; rather, it was enough if a person carried one of the dead on his shoulders to a place where the city met the sea and throw him down; and there they were thrown down into barges in a pile and taken to who knows where.7

The Mongol military campaigns further transected immense spaces of Europe and Asia at fast speed and transformed the political and epidemiological landscape of Eurasia between A.D. 1200 and 1370. The best-known of the early Eurasian epidemics, the Black Death, was connected to the Mongols, but it cannot be understood without considering the context of both the pre-plague years and the behavior of humans during the epidemic.

In the mid-thirteenth century, social and climatic changes in western Europe resulted in crop failures and famine.8 During the 1290s Europe was struck by another series of famines. Conditions deteriorated even further between A.D. 1300 and 1347 when a succession of crop failures and food shortages continued; they would not come to an end until after the Black Death. From 1316 until 1322 a series of livestock epidemics decimated what remained of Europe’s cattle population. The pattern of crop failures continued until bubonic plague began to expand throughout Eurasia.

In 1345 Mongol troops led by Janibeg Khan had besieged Genoese trading merchants at their fortified trading post at Caffa on the Black Sea intermittently for two years. Most information about the set of events that (p.22) occurred then and followed comes from an account by the Italian Gabriele de’ Mussi, written sometime around 1348. De’ Mussi’s narrative asserts that in 1345 an epidemic of plague broke out in the Mongol troops. Seeing how many casualties the disease took, the Mongol commander decided to use it as a weapon to bring the siege of the city of Caffa to an end. In what some have interpreted as the first act of biological warfare, he began to catapult the diseased corpses over the city walls and waited for the disease to finish the conquest.9 It did, and from Caffa in 1346 the Black Death spread via Genoese merchants along sea routes to the Mediterranean ports of southern Europe, then north through Spain and France, east into Germany, and across the English Channel to the British Isles. By 1348 most of France and Switzerland was affected by plague, which soon reached the southern coasts of England, Germany, Sweden, Poland, and, later, Russia.

Those affected had black swellings in the armpits and groin that oozed blood and pus, and they died within a few days. The disease has generally been attributed to bubonic plague, and it spread rapidly from village to village, and country to country. The only recourse was flight, especially away from the crowded spaces of urban centers, and that was available only to those of financial means. Reports of fields and streets full of rotting corpses were common.

In the fourteenth century, rats and fleas were not known to be the vehicles of transmission. Earthquakes were blamed instead, as were “foul winds” and the wrath of God. Because so many thought the plague was brought about by the wrath of God, penitents sprang up; they implored mercy, sometimes with ropes around their necks, sometimes beating themselves with whips. Efforts to cope with the plague were many and varied. Smudge pots lined streets and gates into cities—the aromatic substances they effused were thought to purify the air. Bleeding, purgative enemas, compounds of various herbs and powdered minerals were administered, to no avail.

By the time the plague ended in 1352, by one estimate a third of Europe had died: roughly 24 million people.10 No one really knows how many died, but the Black Death left an enduring vision of epidemics as phantom forces sweeping across vast tracts of land, possessing an urgency of time, and imparting utter certainty that once a village was affected, death could come for anyone, at any moment.

The very foundations of the Middle Ages were torn away by the Black (p.23) Death and replaced with new economic and social power for peasants, and loss of power for the church and nobility.11 Peasants, who undoubtedly suffered the greater loss of population numbers, saw an increased sense of their value, both social and financial, as their relative importance was realized and their wages increased. The nobility suffered less mortality, but since the pattern of inheritance was more important to the nobility than to the peasants, the biological crisis was more severe for nobles. Given the high infant mortality rates during the Middle Ages, it was already difficult to produce an heir. The plague only made the situation worse, and the failure of noble families to produce heirs meant a continual shuffling of power, as old families died out and new ones replaced them.

One response to this tremendous fluidity was a renewed emphasis by the older families on the importance of knightly ritual. Great exhibitions, largely attended by people in ceremonial dress, were held among prestigious knightly orders such as the Golden Fleece. Another response, although less common, was a retreat for the lords toward grace and courtesy. Dozens of books were published on grace and etiquette, and the disdain the nobility felt for the manual laborers and merchants was reflected in these texts. It was essential that the disfranchised, in whatever ways possible, remained so in order that the nobility remain firmly entrenched in the control of economic, social, and political power.

The maintenance and transmission of the plague goes far beyond climatic shifts, crop failure, and human migration, to include host, vector, pathogen, and ecological relationships. A Russian medical geographer, Evgeny Pavlovsky, unraveled the marvelous ecology of plague in the 1930s. Pavlovsky discovered that plague bacteria circulated within a complex web of relationships that Pavlovsky termed a “natural nidus.”12

The natural nidus for plague exists as follows. Plague is a rodent zoonosis transmitted by fleas. Yersinia pestis, the bacterial agent of bubonic plague, circulates continually among rodents living in the Central Asian grasslands, as it has done for centuries. The rodents live in deep burrows with a variety of arthropod inhabitants, such as flies, fleas, and roaches. The rodents show no symptoms and are not bothered by the ancient infection.

The landscape of the rodent communities is influential in their survival. The slope of the land affects flooding during rains, and there must be the (p.24) right kinds of vegetation for the rats to eat, and a certain mix of predators and competitors to keep the population regulated. Undoubtedly, human foragers would occasionally wander into the nidus and become accidental hosts for the disease, much in the same way that Lyme disease or hantavirus have been accidental human infections.

The ecology of plague in European cities is as complicated as the ecology of plague in its natural setting. Space in medieval cities was at a premium. The streets were narrow and unpaved. Chamber pots were often emptied from upper-story windows. Water supplies were generally polluted, and other beverages such as beer usually took the place of water. Houses were dark, with dirt floors. Food was often stored in or near houses. Not surprisingly, there were several other household inhabitants besides humans, including huge urban black rat (Rattus rattus) populations.13

Unlike the Russian steppe rodents, black rats are especially susceptible to the bubonic plague, and in plague epidemics they die in great numbers. In fact, rat corpses probably numbered greater than humans, leaving hungry fleas looking for other blood meals. As with many disease vectors, there is a complicated ecology. The vector has to be able not only to move the pathogen from host to host but also in some cases to keep it alive. Any incompatibility results in nontransmission.

Two of the more historically important vectors are the Oriental rat flea, Xenopsylla cheopis, and the human flea Pulex irritans. X. cheopis is an especially efficient vector, because a bend in its feeding tube, or proventriculus, creates a location for growth of the plague pathogen Yersinia pestis, such that the proventriculus becomes blocked, and the flea, unable to swallow a full blood meal, becomes thirsty. Attempting to dislodge the wad of infected material and quench its thirst, the flea desperately infects multiple new mammalian hosts. Other fleas clear the pathogen more quickly. Equally important is vector behavior—both of these flea species will feed on humans, while many other species will not.

Sometime after 1500 a combination of factors brought about a reduction in European plague rates. One factor was that quite simply the rat population changed. The brown rat, Rattus norwegicus, also a migrant from Asia, displaced the black rat. Brown rats preferred to live away from humans and inhabited sewers and other places where they and their fleas avoided people. Other factors helped end plague epidemics. Climate improved, contributing to better crop yields and thus better nutrition, and improved housing lessened crowding.

(p.25) Modern historians and specialists in historical epidemiology have struggled with several inconsistencies in the picture of the Black Death presented in the last few pages. It seemed to spread too quickly for bubonic plague. As a warm-weather disease, its high mortality during the winter months doesn’t fit the normal pattern of the disease. Both of those issues have led some to ask if the principal causative agent was Yersinia pestis or perhaps either a different disease or multiple diseases. The transmission of the Black Death has often been linked to trade routes, but there is considerable variation in the magnitude of mortality, with some trade cities (e.g., Milan) hardly affected. Oscillations in the temporal and geographic pattern suggest there may have been multiple introductions of infectious disease agents. Other conditions, such as climate, may have been more influential than previously perceived.14

Current information suggests a number of revisions to the classic picture of the Black Death of 1346–52. In addition to detailed analysis of historical documents, several medieval cemeteries that are purported to contain victims of the Black Death have been discovered and excavated.15 Molecular studies conducted over the past couple of decades indicate that people buried in medieval grave sites in the Netherlands, Germany, Italy, France, and England have at least two distinct clades of Yersinia pestis.16 Those molecular studies indicate that there was not a single introduction of the plague. A study of climatic fluctuations also indicates that there was not a single introduction of the plague, but that it was introduced multiple times, and that wild rodent populations were likely impacted by climatic fluctuations and involved in the process.17 Multiple issues regarding plague transmission mechanisms, including the vectors involved and whether rats could have been intermediate hosts, indicate that there may have been pneumonic as well as bubonic plague.18 It would seem at the moment that the conditions under which the Black Death of A.D. 1346–52 embraced Europe were extremely varied.

Plague continues to be resident in rodent burrows, where it is maintained through generations of rodents, often as a chronic disease. In fact, the tourist to the southwestern United States often encounters signs warning that rodents in national parks carry the plague. It has broken out several times in epidemics in the past two centuries, always associated with war, deforestation, natural disasters, or other severe ecological disturbances. One recent example, the Vietnam War, serves to remind us that when the cultural–biological interface is disturbed, plague can quickly (p.26) flare into epidemics. When refugees crowded into Saigon, epidemic plague broke out in the city and the countryside of South Vietnam.19 Plague serves to remind us that the maintenance and transmission of infectious diseases include many variables other than the pathogens that cause them. Agriculture and urbanism in the Old World, while they enabled the development of civilization, also gave rise to the crowd infections that periodically winnow populations.

Agriculture and urbanism came much later to the Americas, after A.D. 500, although cultivation of some plants was under way by 2500 B.C.20 Landscape alterations such as raised field complexes (often associated with aquaculture), terraced fields, and deforestation were also made centuries before the arrival of Europeans. Extensive trade networks were present between the Gulf Coast and the interior midwestern United States by at least 300 B.C., as demonstrated by “exotic” items distributed far from their sources, such as whelks from Florida, copper from the Great Lakes, and mica from Georgia. Large urban centers with plazas, public architecture, and aggregated resident populations were present in many regions of the Americas by at least A.D. 1000.

The changes in the New World epidemiological landscape coincident with agriculture and urbanism, however, appear to have been far less dramatic than those that had occurred in Eurasia by A.D. 1500.21 Infectious diseases and other health issues were undoubtedly common, although documenting them is more challenging in the absence of written records. Human skeletal remains have been a major source of information. Populations inhabiting the Americas between A.D. 800 and 1500 show that in numerous regions the onset of agriculture was accompanied by decreased nutrition and health. Skeletal lesions have been crucial for demonstrating the presence of nonvenereal syphilis, tuberculosis, mycotic (fungal) diseases, and other diseases in the precontact Americas.

Recovery of mummified remains in the Americas has facilitated the documentation of specific diseases such as tuberculosis. In addition to tuberculosis, South American mummies indicate that prior to contact with Europeans, those populations also suffered from treponemal infection (see chapter 3), Bartonellosis, Chagas’ disease, and several types of parasites, including hookworms and whipworms, roundworms, pinworms, and fish tapeworms.22 Mummified individuals from Alaska and the Aleutian Islands provide evidence that coronary artery disease was common, as well as intestinal parasites.

(p.27) There is little evidence that any of the diseases and other health conditions present in the precolumbian Americas decimated populations through epidemics. The expansive mercantilism and rapid transport across great distances characteristic of Eurasia were not present until the arrival of Europeans. However, in A.D. 1500 indigenous Americans were about to experience economic, social, and natural landscape reformation on a level they could never have imagined.


(1.) Michelson, “Adam’s Rib Awry? Women and Schistosomiasis.” The article is a review article that reports on the survey of several previously published studies of schistosomiasis in different parts of the world.

(2.) The earliest domesticated plants and animals occurred in the Middle East beginning about 10,500 B.P. in the area known as the Fertile Crescent, and in the Nile Valley of Egypt. Domesticates in the Near East and Egypt included wheat, barley, sheep, and goats. A couple of centuries later, by 10,000–7,000 B.C., farmers raised domesticated plants such as lentils in the Indus Valley of India and Pakistan. About the same time along the Yangtze and Huang Ho (Yellow) river valleys in China, rice (p.189) and millet became more prevalent. Mediterranean populations were engaged in agriculture by 8,500 B.C. and cultivated such crops as asparagus, broccoli, grapes, and olives (McNeill, Plagues and Peoples, 69–132; Smith, Emergence of Agriculture).

(4.) In Egypt the best evidence for smallpox occurs in two sources, ancient mummies and texts. In Egypt at least 31 cases of skeletal and mummy tuberculosis have been dated to 3,700–1000 B.C. (Sandison and Tapp, “Disease in Ancient Egypt”; Roberts and Buikstra, Bioarchaeology of Tuberculosis.) Three mummies show signs of smallpox rashes on the skin. One is Ramses V (died in 1157), another died in 1570, and a third in 1085, demonstrating that the disease affected Egyptians as early as 1570 B.C. (Sandison and Tapp, “Disease in Ancient Egypt”).

(8.) Glacial and pollen evidence suggests that glacial retreat in the Alps caused milder winters and drier summers that facilitated agriculture (Gottfried, Black Death, 24). This milder weather enabled the tremendous political and social change that occurred between A.D. 800 and 1200. However, by the late twelfth century, the Alpine glaciers began to advance, causing colder and wetter weather. The “Little Ice Age” was disastrous for agriculture, because more-northern pasture (p.190) lands had to be abandoned as the glaciers advanced (Gottfried, Black Death, 23). Fodder crops and pasture were turned over to the raising of wheat in an intensive land use pattern. The monocropping of wheat led to other problems, such as low protein levels for many peasants. Living standards stagnated and then began to decline after 1250 (Gottfried, Black Death, 23–30; Hays, Burdens of Disease; Karlen, Man and Microbes).

(9.) Further reading on the history of the Black Death: Karlen, Man and Microbes; Wheelis, “Biological Warfare at the 1346 Siege of Caffa”; Pollitzer, Plague; Gottfried, Black Death; Nikiforuk, Fourth Horseman; Gregg, Plague!; Scott and Duncan, Biology of Plagues; Zinsser, Rats, Lice, and History. Detailed local responses are described in the literature of the time, the most famous pieces being that of the Italian Boccaccio in his Decameron, and of the Englishman Chaucer in his Canterbury Tales. Wheelis, “Biological Warfare at the 1346 Siege of Caffa,” points out that even though de’ Mussi’s narrative is consistent with the known facts of the plague and biological warfare, the importance of Caffa in the overall plague epidemic is “anecdotal at best” (974). Plague was undoubtedly being disseminated through multiple localities.

(12.) Pavlovsky, Natural Foci of Human Infections and Natural Nidality of Transmissible Diseases. “A natural nidus is a micro-scale region constituted of a living community, among the members of which a disease agent continually circulates, and the habitat conditions necessary to maintain that circulation in the disease system” (Meade and Emch, Medical Geography, 100); see also Wills, Yellow Fever, Black Goddess.

(13.) Black rats are often cited as a recent immigrant species to medieval Europe, having come out of the tropics with the Crusaders across the Indian Ocean to the Mediterranean (Meade and Emch, Medical Geography, 115; Wills, Yellow Fever, Black Goddess, 65). However, archaeological evidence (Armitage et al., “New Evidence of the Black Rat in Roman London”; Rackham, “Rattus rattus) demonstrates that black rats lived in Roman-era contexts in Britain during the first centuries A.D.

(14.) Scholars have been puzzled by records of high infection rates during the winter months, because plague is a warm-weather disease (Cohn, Black Death Transformed; Scott and Duncan, Biology of Plagues). The plague’s arrival in Russia was delayed until 1351, good evidence that it was not carried along international trade routes by river transport, or it might have reached Russia from the Crimean Sea much earlier. Other cities located on trade routes, for instance—Milan—seem to have escaped the plague (Nutton, “Introduction,” 8). These and other contradictory factors have been suggested as evidence for an alternate disease presence of anthrax, which is caused by a much hardier organism, is characterized by pustules with a jet-black center, precipitating the voiding of black blood, and has a pulmonary (p.191) form (Pollitzer, Plague). Undoubtedly, other illnesses accompanied the plague. Illnesses such as pneumonia would not have been recognized or described as separate from the plague. Other ancillary diseases might have been typhus, smallpox, and anthrax.

(16.) The current molecular information and interpretation are undoubtedly changing. Molecular studies that have produced positive data for Yersinia pestis DNA from purported plague cemeteries (e.g., Drancourt et al., “Yersinia pestis Orientalis in Remains of Ancient Plague Patients”; Raoult et al., “Molecular Identification by ‘Suicide PCR’ of Yersinia pestis as the Agent of Medieval Black Death”; Wiechmann and Grupe, “Detection of Yersinia pestis DNA in Two Early Medieval Skeletal Finds from Aschheim [Upper Bavaria, 6th Century A.D.]”) have been countered by negative evidence (e.g., Gilbert et al., “Absence of Yersinia pestis-Specific DNA in Human Teeth from Five European Excavations of Putative Plague Victims”). The current interpretations as I write this, again already out of date, are based on finer-grained DNA analyses (e.g., Haensch et al., “Distinct Clones of Yersinia pestis) and protein capsule antigen information (e.g., Pusch et al., “Yersinial F1 antigen and the Cause of Black Death”; Bianucci et al., “Technical Note,” “Plague Immunodetection in Remains of Religious”). A draft genome of the plague pathogen was published in 2011 (Bos et al., “Draft Genome of Yersinia pestis).

(22.) Chagas’ disease (South American trypanosomiasis) is spread by certain types of the “cone-nosed bug,” also known as “assassin bugs,” “kissing bugs,” and the “triatomid bug.” Assassin bugs live in the walls of adobe mud houses, preferably those with thatch roofs, providing the insects ample opportunity to breed in cracks and crevices of the walls and for them to come forth at night and bite their victims. Those particular types of domiciles are the primary epidemiological factor in Chagas’ disease (Coimbra, “Human Settlements, Demographic Pattern”; Forattini, “Chagas’ Disease”).