MARTIN S. PERNICK
Introduction: Germs Don’t Travel Alone
When diseases travel, the results can be catastrophic. The arrival of plague from Asia in 1347–1349 killed close to half of Europe’s population. Smallpox and other newly imported childhood infections slaughtered about 80 percent of the Aztec Empire by the mid-1500s. The reimportation of yellow fever after a two-generation absence literally decimated Philadelphia in 1793. The global spread of the previously “Asiatic” cholera produced a terrifying series of nineteenth-century pandemics. Well into the twentieth century, Arctic Native villages were devastated by the importation of tuberculosis, while the arrival of measles and influenza nearly depopulated previously isolated Pacific Islands. The echoes of such past disasters still reverberate in current fears of the global spread of new or previously geographically isolated microbes (W.H. McNeill 1976; Garrett 1994).1
Recognition that these disasters resulted from transcontinental disease importation played a key role in the evolution of world history as a discipline. Seminal works, such as William McNeill’s Plagues and Peoples, Alfred Crosby’s The Columbian Exchange, and Jared Diamond’s Guns, Germs, and Steel not only established disease as a crucial component of the history of global exchanges, but also used disease to demonstrate the dramatic importance of the new field of world history (McNeill 1976; Crosby 1972; Diamond 1997).2
Many early histories portrayed epidemics as the seemingly inevitable effect of transplanting new germs in “virgin soil.” Mass death seemed to be the horrific but unavoidable result of introducing new microbes among people who had no prior opportunity to develop “natural defenses.” However, such common interpretations of how diseases travel are seriously flawed. First, simply moving a microbe to a new location is rarely sufficient to trigger a catastrophic new disease. Although a few new germs did lead to some of the most devastating disease outbreaks in history, the vast majority of new germs fall on infertile soil (Gladwell 1995). If every novel microbe caused an epidemic, humanity would not have survived the invention of the ocean liner. Second, the same new germ often produced significantly different effects in different physical and cultural environments. Third, diseases travel to new locations by the importation of environmental, social, and cultural changes, along with, or even sometimes without, the introduction of novel germs. In other words, the arrival of new germs does not determine whether a devastating new disease will result. New germs are neither sufficient, nor even necessary, to produce new epidemics. Rather, the importation of a new disease results from the interaction of new germs with new environmental, economic, and cultural changes.3
Early histories of global disease transmission also initially focused on a few of the most dramatic imported disease outbreaks, especially the Black Death and other bubonic plague epidemics in Asia and Europe, and smallpox epidemics among Native Americans. Other devastating transported diseases, including yellow fever, malaria, cholera, and influenza, have been well examined in individual locations, but are only just beginning to receive sustained attention in their global dimensions, as is the global spread of noninfectious diseases.
This chapter will examine a few selected examples – one extensively studied and several other less familiar diseases in motion – to show how specific pathogens interacted with other physical and cultural changes to produce enormous differences in the mortality and the cultural effects of imported diseases.
Imported Epidemics and the Decimation of Native Americans
Five centuries ago, the Americas were first colonized by people who were accompanied by the viruses of smallpox, measles, and other childhood infections common throughout the rest of the world. The ensuing epidemics devastated Native American populations from the Arctic to the Andes, while largely sparing the arriving Europeans and Africans. Measured by the mortality rate, the proportion of the population killed, the result was the biggest medical catastrophe in recorded history.
Most explanations for this disaster emphasize that because these germs were newly imported, Native Americans lacked immunity to them. Immunity results when an individual who has been exposed to a specific germ, and who survives the initial encounter, thereafter produces antibodies and specifically sensitized blood cells that protect against subsequent infection with that germ. Acquiring immunity requires individual personal exposure to a specific antigen; it is not hereditary. The number of generations without infection does not affect the level of immunity; even one generation without exposure will produce a completely non-immune population.
Native Americans prior to 1492 had no exposure to these germs and thus none of them were immune. They lacked exposure because these germs could not have been transported by the slow-moving, small, and isolated groups who initially populated the Americas from Asia. Any childhood disease virus initially present in such a population would have killed some and left the remainder immune. Without a critical mass of newborns to infect, the germs then would have died out and never reached the Americas.
By contrast, among densely populated and more interconnected regions of Europe, Africa, and Asia, enough children were born to provide the germs with a steady supply of new hosts. The germs remained always present, despite the fact that most who survived to adulthood became immune. These were childhood diseases, not because the germs specifically targeted children, but because it was mostly children who were not yet immune.
Childhood diseases were hardly benign in Europe; about a fourth of all newborns died before the age of five (Bideau et al. 1997). Nor were Native Americans living in a disease-free natural paradise prior to 1492; they suffered health problems, from crop failures to dysentery, that produced periodic fluctuations and perhaps an overall decline in pre-Columbian populations (Mann 2006). But for specific childhood infections, Native Americans lacked the immunity that adults elsewhere usually acquired in childhood.
Does this lack of immunity to new germs fully explain the devastation many Native American populations experienced after European contact? Many historians have assumed so. One 1940s book was titled The Effect of Smallpox on the Destiny of the Amerindian(Stearn and Stearn 1945). In an intentionally provocative 1990s college textbook, an eminent historian summarized this interpretation for student debate: “The doom of the Indians was sealed the moment outsiders began to set foot in America. … The people of the Old World had developed immunities to a wide variety of diseases, but the native Americans had not. … [N]othing the newcomers did, apart from simply being there, had anything to do with the demise of the native American” (McDonald 1991).
However, recent scholarship emphasizes that lack of immunity to new germs was only part of the story. Lack of immunity meant that Native Americans were likely to get sick when new germs were introduced, but it did not determine why some died while others recovered, nor did it determine whether or not the survivors rebuilt their population levels or preserved their cultures. Despite the fact that all Native Americans in 1492 lacked immunity, there were enormous differences in the severity and duration of the effects once new germs were introduced. Such differences in outcomes cannot be explained by immunity; they resulted from the interaction of biology, environment, and culture (Kelton 2007; Jones 2004).
Some social conditions promoted the rapid spread of new germs, such as population density, trade, and war. Such environments made it likely that a high proportion of the population would get sick simultaneously, thus increasing the initial deaths from famine, lack of nursing care, panic, and social disintegration. However, these same factors often promoted long-term recovery. After the initial outbreaks, the immune survivors in a large urban society would have enough children to keep the germs in circulation as childhood diseases, with high childhood mortality but few adult epidemics. Complex hierarchical Native American societies also may have had greater resources for cultural adaptation to survive European conquest.
The physical and emotional condition of those infected likewise altered the odds of their recovering. The question is not whether it was “guns or germs” that caused the decimation of Native Americans. Guns and germs interacted synergistically (see Morillo, this volume). Sick Native Americans were easier to shoot; and getting shot made it harder to recover from disease.
For example, in large densely populated urban-centered empires such as the Aztecs of central Mexico or the Incans of the Andes, the initial contact epidemics were especially devastating, but the population levels eventually rebounded and significant elements of Native language and culture survived. In the decades following the first Spanish attack in 1519, epidemics, a siege-induced famine, internal political conflicts, and the enslavement of many Indians combined to reduce the indigenous population of central Mexico by an estimated 80 percent. But by the seventeenth century the Native American population had recovered to pre-Columbian levels in central and southern Mexico, as it did in the Andes a century later (Cahill 2010: esp. 229–231; Cook 1998).4
Conversely, among smaller, more isolated, migratory hunters living in what is today the US Great Plains, initial contact epidemics tended to be limited to single villages or bands. Too distant and poor to attract conquest prior to the nineteenth century, these groups first encountered new germs brought by other Indians fleeing epidemics further east, or by individual European explorers, missionaries, or traders. Outbreaks might decimate the villages in which they struck, but prior to the 1830s, they usually remained localized. Even the Upper Missouri smallpox epidemic of 1837–1838, which devastated whole villages of Blackfoot and Mandan, barely affected neighboring Crow and Gros Ventres (Jones 2004: 105–107). With their less complex division of labor compared to Aztecs or Incans, the Plains Indians also experienced fewer deaths due to epidemic-induced social disruption or loss of vital cultural skills. Furthermore, the introduction of European horses to the Plains actually resulted in a population increase, with improved hunting, mobility, and military abilities more than offsetting the effects of new germs. However, the small size and isolation of Plains Indian villages made it less likely that they could develop the childhood disease pattern in which most adults would grow up immune. As a result, these small, isolated groups were susceptible to repeated adult epidemics as each new generation grew up without immunity.
The indigenous population of the Great Plains only began to decline in the nineteenth century, when better plows, water pumps, and railroads made it possible for white settlers to farm the prairie, and when precious metals were discovered from California to the Black Hills. The resulting increase in outside contact was followed by conquest, elimination of the buffalo, and forced concentration on reservations that often lacked adequate food. These policies produced an increase in disease deaths far greater than the initial effects of the introduction of European germs (Allen 1975).
Recent scholarship provides many other examples of how differences in physical and cultural contexts resulted in vastly different patterns of disease and outcomes when different specific Native American peoples encountered new germs. In the colonial Carolinas, enslavement, not merely the presence of new germs, produced the greatest Native American mortality (Kelton 2007). In the Southwest, new germs decimated the densely concentrated populations of pueblo dwellers. However, that devastation helped make possible a significant increase in population of the geographically more dispersed sheep-herding Navajo. Imported infections only reversed this Navajo population growth in 1864–1869, when thousands were confined to Fort Sumner on the Bosque Redondo Reservation in New Mexico, where disease, deprivation, and despair combined (Barrett 2002; Kunitz 1983: chs 1–2).
New germs thus played a crucial role in the decimation and conquest of Native Americans, but they alone did not determine the outcome. Although all Native Americans in 1492 lacked immunity to European childhood diseases, the effects varied enormously, depending on the interaction of germs, environment, and culture. It is not possible to separately measure the relative contributions of germs and environment, because the two reinforced each other synergistically. War and deprivation made germs more lethal; germs made war and deprivation more deadly.
Comparing the arrival of the Black Death in Europe with the effects of European diseases in the Americas, the historian Alfred Crosby in 2003 revised his earlier emphasis on the role of new germs in determining the outcome of new diseases, writing:
[V]irgin soil epidemics often do produce high mortality rates, but if left alone the population will recover in numbers. Europe, for instance, lost one-third of its population to the Black Death in the fourteenth century and recovered in time.5 [But] if the Black Death had been accompanied by the arrival of Genghis Khan’s hordes … I think it is unlikely that I would be writing this … in an Indo-European language. (2003: xxii)
Moving Environments and Moving Germs: Malaria and Cholera
Malaria, a widespread, deadly and debilitating disease marked by recurring cycles of fever and chills, is now known to be caused by several different species of the parasite Plasmodium, transmitted by the bite of an infected female Anopheles mosquito. For much of medical history, such fevers were associated with specific geographic places, climates, and atmospheric conditions. (See Simmons, this volume.) Such diseases were generally assumed to stay put in particular locations, and many doctors believed they were solely local rather than imported in origin. However, from the classical Hippocratic work on Airs, Waters, and Places, to nineteenth-century American physicians such as the pioneer medical educator Daniel Drake, doctors recognized that changing the environment might spread or reduce the geographic range of malarial fevers.
Recent historians of malaria have built on these premicrobial insights to emphasize that the spread of malaria globally and intraregionally required not just the movement of parasites and mosquitoes, but the movement of environmental conditions that favored the interaction of microbes, insect vectors, and susceptible hosts. For example, while malaria parasites probably crossed the Atlantic with the importation of slaves from Africa, the successful spread of the disease also resulted from the decision to employ slaves in tasks that created environments favorable to mosquito breeding, such as the importation of African rice agriculture. Throughout the history of malaria, its movement from place to place involved not only the transport of germs but the transit of cultural practices and physical environments conducive to human contact with mosquitoes. From the first industrial revolution, which spread the building of mill dams where mosquitoes bred, to the late nineteenth-century global market for beef, which provided nonhuman alternative blood sources for mosquitoes, nineteenth-century global economic trends disseminated a variety of environmental conditions that first spread and then restricted the geographic distribution of human encounters with malaria mosquitoes.6
The global spread of cholera, among the most widely feared pandemic diseases of the nineteenth century, also resulted not just from importation of the germs, but from the global diffusion of conditions favorable for transmitting the germs. However, unlike recent histories of malaria, studies of cholera still focus on specific outbreaks in specific regions, rather than tracing the global dimensions of the disease. The global history of cholera has only just begun to be studied.7
The infectious agent of cholera is the bacterium Vibrio cholerae, transmitted by food or drink contaminated with excrement from an infected person. The disease causes sudden, massive and painful diarrhea, which can produce rapid extreme dehydration, circulatory collapse, and death within a day. Until the nineteenth century, cholera had been largely endemic to a few densely populated river systems in Asia, especially the Ganges Valley in India. Because people harbor the germ only briefly before they eliminate it or it eliminates them, cholera could not move further inland than an infected person could travel in a few days. So long as overland travel required human or animal power and took a day of hard physical effort to move 10 or 15 miles, cholera could not spread much beyond the river.
In the nineteenth century, a combination of changes in the technology and organization of transportation first made it possible for large numbers of cholera-infected people to travel long distances. Railroads, clipper ships, and steamboats provided the technology. In addition to these new machines, cholera’s mobility also depended on a new model of business organization, the invention of cheap mass transit. For the first time, transport companies organized frequent and regularly scheduled trips, supported by recruiting large numbers of travelers, made possible by offering cut-rate no-amenities fares (Chandler 1977). The post-Napoleonic expansion of the British Empire in India utilized these new forms of transport to move troops and commerce between Asia and Europe, while the famines and revolutions of mid nineteenth-century Europe produced waves of refugees who used the new means of transport to cross the Atlantic. (See Ward, this volume.)
Not only did the nineteenth century produce new ways to move the cholera germ, it also disseminated new social conditions in which the germs could cause disease. Untreated cholera can kill up to half the people who develop symptoms. The vast majority of healthy people who ingest vibrios, however, excrete them without any signs of disease. Conditions that increase the chances of disease include repeated high levels of exposure and prior malnutrition. Poor, hungry, crowded people may be unable to avoid contaminated food and water, while those already marginally malnourished can least afford to lose more nutrients to diarrhea. Cholera was thus especially likely to devastate poor crowded cities that had outgrown their previous food, water, and sanitary infrastructures. While nineteenth-century epidemics were not limited to cities, the rapid urbanization of Europe and the Americas in the nineteenth century produced environments and populations especially susceptible to the germ.
As a result, world-wide pandemics of cholera were a distinctly nineteenth-century phenomenon, with at least five transcontinental outbreaks between 1817 and 1892. The most deadly and widespread pandemic, in 1831–1832, killed about 2 percent of the population of many cities across Europe and the Americas.
Although the German physician Robert Koch eventually identified Vibrio as the disease’s infectious agent in 1892, cities around the world began to reduce their cholera rates as early as the 1847–1852 outbreaks, following British physician John Snow’s identification of contaminated water as a source of the disease, and the development of new institutions of city government with the power and resources to improve living conditions for the poor. Thus the global spread of cholera was made possible by the diffusion of early nineteenth-century social conditions, and it was ended by a later nineteenth-century spread of new social responses (Rosenberg 1962).
Diseases That Traveled without New Germs
Sometimes infectious diseases travel to new locations without any importation of new germs, but simply by the introduction of physical and cultural practices that allow previously existing, relatively insignificant, parasites to cause newly widespread human disease. An excellent example is hookworm. This intestinal parasite was identified as the cause of a growing epidemic in the US South, the Mediterranean, Latin America, and Africa in the early twentieth century. With recognition of its global importance, hookworm became the target of the first international disease control campaign, begun by the Rockefeller Foundation in the 1910s. The foundation’s efforts focused on ways to kill the worms inside the body and to prevent their spread. Researchers assumed that the appearance of the disease in a new region meant that infected individuals had imported the parasites.
However, recent work by historian Steven Palmer demonstrates that hookworm disease outbreaks often spread, not by transporting worms, but by transporting the conditions favorable for already existing worms to multiply and to cause infections. The international diffusion of mining technologies and other industrial practices that concentrated large numbers of impoverished, poorly clothed migrant workers in frontier areas with wet soil enabled already present hookworms to start causing massive outbreaks of disease (Palmer 2009). Similarly, global demand for mining products and the introduction of new mining practices also spread outbreaks of tuberculosis (Packard 1989).
Another epidemic that spread across continents without any movement of the causative germ was paralytic poliomyelitis. During World War II, when soldiers from Britain and America landed in North Africa, dozens at a time fell victim to unprecedented polio epidemics. The source of these outbreaks puzzled and alarmed doctors and military planners. While paralytic polio epidemics were increasingly common in the United States and Western Europe, in North Africa polio was a mild and rare disease of infants. Deadly epidemics among adults were unknown there. A US Army Commission, led by Yale virologist John R. Paul, solved the mystery, by showing that the polio virus caused much milder or unapparent infections in infants than in adults. They found that the virus was so widespread in North Africa that in this environment most of the population got a mild infection and thus became immune shortly after birth. Thus, they concluded, the wartime epidemics resulted from importing non-immune European and American soldiers into settings where the virus was already widespread, not by importing the virus (Paul 1971: 348–366).
One key environmental factor in the movement of infections has been famine. Malnutrition lessens resistance to, and slows recovery from, new pathogens; while the physical and emotional impact of an epidemic can undermine the ability and the will to produce food or even eat (Benedictow 2004: 263). Furthermore, famines, like epidemics, spread by the interaction of biological and social causes. The Irish famine of 1848 resulted from both the importation of potato-blight fungus and British land policy. In turn, the famine made the population especially susceptible to cholera, while it spurred a mass diaspora that furthered the global spread of the epidemic.8
Finally, while the best-known and fastest-spreading diseases that travel are usually infections, historians are just beginning to realize that some of the deadliest recent diseases to spread globally are not germ diseases at all. Global industrialization contributes to the spread of modern epidemics from lung diseases induced by air pollution to heavy metal and radiation toxicity. The globalization of high-fat, high-sugar diets seems to be causing a global increase in heart disease, obesity, and diabetes. And the post-1945 export of American cigarettes is clearly producing a global pandemic of heart and lung diseases. Allan Brandt’s recent history of American cigarettes concludes with a section titled “Globalization: exporting an epidemic,” which documents the basis for the World Health Organization projection that by 2030, 70 percent of tobacco-related deaths will be in the developing world (Brandt 2007: section V, see chart on p. 451).
The importation of new diseases has also often spurred the spread of new medical treatments and preventive measures. Plague epidemics, for example, produced a diffusion of government health boards, pest-houses, and quarantines from city to city across Europe and beyond (Cipolla 1981). The arrival in 1721 of epidemic smallpox in Boston prompted the Reverend Cotton Mather to introduce the practice of preventive inoculation, based upon the African experience of his slave Onesimus, and the news of Ottoman practice as disseminated by the Royal Society of London (Hopkins 1983: 248). In the early twentieth century, the Rockefeller Foundation’s international campaign against hookworm disease became a model for subsequent international health agencies – from the Pan American Health Organization to the League of Nations and the World Health Organization (Palmer 2009).
Conclusion
When diseases travel, mass death can result. Some of history’s most deadly new diseases involved the importation of new microbes. The fear of such deadly new microbes remains deeply resonant in mass culture, including popular films like The Andromeda Strain(1971), Outbreak (1995), andContagion (2011). But new germs are rarely either sufficient or necessary to transport new diseases. The most deadly diseases in human history have arrived most often where newly introduced pathogens are accompanied by the spread of new social and cultural disease environments.
Notes
1 Estimating premodern disease rates involves applying sophisticated demographic tools to limited and fragmentary evidence. Diseases have evolved, data are incomplete, and past diagnoses don’t correspond to modern disease categories. There is thus considerable uncertainty and controversy over these numbers (e.g. Benedictow 2004). This chapter focuses on diseases that modern science sees as having been transported. For examples of the history of responses to diseases that people in the past perceived as imported, see Kraut (1994); Markel (2004); Pernick (2002); Wald (2008).
2 These authors differ significantly in the extent to which they see germs alone as sufficient causes, and in their accounts of the role of cultural and environmental factors, but all give primacy to the arrival of new microbes.
3 Histories of world diseases that emphasize social factors include Watts (1998); Hays (1998); Kiple (1993).
4 There is however great debate and uncertainty about the magnitude and timing of these statistical estimates.
5 More recent, detailed estimates place the Black Death mortality at over 50 percent: see Benedictow (2004: ch. 33).
6 For global histories of malaria see Packard (2007); Webb (2009). An important early environmental history was Ackerknecht (1945). Other historians taking this environmental approach include J.R. McNeill (2010); Valencius (2002); Grob (2002: 129–133); Humphreys (2001); Nash (2006). For analysis of Alexis de Tocqueville’s insightful early nineteenth-century comments linking rice and fevers, see Pernick (2012). There are many similarities between malaria and another mosquito-borne disease, yellow fever. A few historians who have studied both malaria and yellow fever do make the connection: Humphreys (1992); J.R. McNeill (2010); Peard (1999).
7 See Hamlin (2009). Important local studies include Rosenberg (1962); Kudlick (1996); Evans (1987); Arnold (1986).
8 Famines can have a complex relation to epidemics. The spread of the Black Death of 1347 followed the Great Famine of 1315, but the specific places most devastated by famine were not necessarily hardest hit by plague (Kelly 2005: 60–64).
References
Ackerknecht, E.H. 1945. Malaria in the Upper Mississippi Valley, 1760–1900. Baltimore: Johns Hopkins University Press.
Allen, V. 1975. The white man’s road: Physical and psychological impact of relocation on the Southern Plains Indians. Journal of History of Medicine and Allied Sciences 30 (2): 148–163.
Arnold, D. 1986. Cholera and colonialism in British India. Past and Present 113: 118–151.
Barrett, E. 2002. The geography of the Rio Grande Pueblos in the seventeenth century. Ethnohistory 49: 123–169.
Benedictow, O.J. 2004. The Black Death, 1346–1353: The Complete History. Woodbridge, UK: Boydell.
Bideau, A., B. Desjardins and H.P. Brignoli. 1997. Infant and Child Mortality in the Past. Oxford: Clarendon Press.
Brandt, A.M. 2007. The Cigarette Century: The Rise, Fall, and Deadly Persistence of the Product That Defined America. New York: Basic Books.
Cahill, D. 2010. Advanced Andeans and backward Europeans: Structure and agency in the collapse of the Inca Empire. In P. McAnany and N. Yoffee, eds, Questioning Collapse: Human Resilience, Ecological Vulnerability, and the Aftermath of Empire, pp. 207–238. Cambridge: Cambridge University Press.
Chandler, A.D. 1977. The Visible Hand: The Managerial Revolution in American Business. Cambridge, MA: Belknap.
Cipolla, C.M. 1981. Fighting the Plague in Seventeenth-Century Italy. Madison: University of Wisconsin Press.
Cook, N.D. 1998. Born to Die: Disease and New World Conquest 1492 to 1650. Cambridge: Cambridge University Press.
Crosby, A.W. 1972. The Columbian Exchange: Biological and Cultural Consequences of 1492. Westport, CT: Greenwood.
Crosby, A. W. 2003. The Columbian Exchange: Biological and Cultural Consequences of 1492. 30th anniversary edn. Westport, CT: Praeger.
Diamond, J. 1997. Guns, Germs, and Steel: The Fates of Human Societies. New York: W.W. Norton.
Evans, R.J. 1987. Death in Hamburg: Society and Politics in the Cholera Years 1830–1910. Oxford: Clarendon.
Garrett, L. 1994. The Coming Plague: Newly Emerging Diseases in a World Out of Balance. New York: Farrar, Straus & Giroux.
Gladwell, M. 1995. The plague year. New Republic, July 17, pp. 38–46.
Grob, G.N. 2002. The Deadly Truth: A History of Disease in America. Cambridge, MA: Harvard University Press.
Hamlin, C. 2009. Cholera: The Biography. Oxford: Oxford University Press.
Hays, J.N. 1998. The Burdens of Disease: Epidemics and Human Response in Western History. New Brunswick, NJ: Rutgers University Press.
Hopkins, D. 1983. Princes and Peasants: Smallpox in History. Chicago: University of Chicago Press.
Humphreys, M. 1992. Yellow Fever and the South. New Brunswick, NJ: Rutgers University Press.
Humphreys, M. 2001. Malaria: Poverty, Race, and Public Health in the United States. Baltimore: Johns Hopkins University Press.
Jones, D. 2004. Rationalizing Epidemics: Meanings and Uses of American Indian Mortality since 1600. Cambridge, MA: Harvard University Press.
Kelly, J. 2005. The Great Mortality: An Intimate History of the Black Death. New York: HarperCollins.
Kelton, P. 2007. Epidemics and Enslavement: Biological Catastrophe in the Native Southeast, 1492 to 1715. Lincoln: University of Nebraska Press.
Kiple, K. ed. 1993. The Cambridge World History of Human Disease. Cambridge: Cambridge University Press.
Kraut, A. 1994. Silent Travelers: Germs, Genes, and the “Immigrant Menace.” New York: Basic Books.
Kudlick, C.J. 1996. Cholera in Revolutionary Paris: A Cultural History. Berkeley: University of California Press.
Kunitz, S. 1983. Disease Change and the Role of Medicine: The Navajo Experience. Berkeley: University of California Press.
Mann, C.C. 2006. 1491: New Revelations of the Americas before Columbus. New York: Vintage.
Markel, H. 2004. When Germs Travel: Six Major Epidemics That Have Invaded America since 1900 and the Fears They Have Unleashed. New York: Pantheon.
McDonald, F. 1991. Debate: Were the Indians victims? In V. Bernhard, D. Burner, and E. Fox-Genovese. Firsthand America: A History of the United States, p. 54. 1st edn, combined. St. James, NY: Brandywine Press.
McNeill, J.R. 2010. Mosquito Empires: Ecology and War in the Greater Caribbean, 1640–1914. New York: Cambridge University Press.
McNeill, W.H. 1976. Plagues and Peoples. Garden City, NY: Anchor/Doubleday.
Nash, L.L. 2006. Inescapable Ecologies: A History of Environment, Disease, and Knowledge. Berkeley: University of California Press.
Packard, R.M. 1989. White Plague, Black Labor: Tuberculosis and the Political Economy of Health and Disease in South Africa. Berkeley: University of California Press.
Packard, R.M. 2007. The Making of a Tropical Disease: A Short History of Malaria. Baltimore: Johns Hopkins University Press.
Palmer, S. 2009. Clinics and hookworm science: Peripheral origins of international health, 1840–1920. Bulletin of the History of Medicine 83: 676–709.
Paul, J.R. 1971. History of Poliomyelitis. New Haven: Yale University Press.
Peard, J.G. 1999. Race, Place, and Medicine: The Idea of the Tropics in Nineteenth-Century Brazilian Medicine. Durham: Duke University Press.
Pernick, M.S. 2002. Contagion and culture. American Literary History 14: 858–865.
Pernick, M.S. Forthcoming 2012. Disease and the racial division of labor in America. The 2011 Garrison Lecture of the American Association for the History of Medicine. Bulletin of the History of Medicine.
Rosenberg, C.E. 1962. The Cholera Years: The United States in 1832, 1849, and 1866. Chicago: University of Chicago Press.
Stearn, E.W., and A.E. Stearn. 1945. The Effect of Smallpox on the Destiny of the Amerindian. Boston: B. Humphries.
Valencius, C.B. 2002. The Health of the Country: How American Settlers Understood Themselves and Their Land. New York: Basic Books.
Wald, P. 2008. Contagious: Cultures, Carriers, and the Outbreak Narrative. Durham: Duke University Press.
Watts, S. 1998. Epidemics and History: Disease, Power and Imperialism. New Haven: Yale University Press.
Webb, J.L.A. 2009. Humanity’s Burden: A Global History of Malaria. Cambridge: Cambridge University Press.