The Columbian Impact

Although evidence of varying quality exists for human penetration of Nearctica prior to the arrival of Columbus in 1492 (Boland 1961), that event and the almost simultaneous arrival of Africans were to be catastrophic in terms of the disease ecology of the continent (Ashburn 1947; Crosby 1972, 1976;' McNeill 1976). Europeans and Africans represented a totally different set of disease foci and introduced pathogens that initially devastated the native Americans. The age of contagious or infectious disease had dawned in America. There were two basic reasons for this, beyond the obvious one of disease importation. The first involved the zoonoses introduced as a result of the transfer of animals previously unknown to the continent; the second related to the colonization that led to communities having threshold populations that could sustain infection.

In the initial period, European diseases spread rapidly into the interior, outdistancing the newcomers who had brought them, while decimating native populations (Dobyns 1983). This fact, in turn, gave rise to the realization that Europeans — and in the south, Africans - entered what Francis Jennings (1975) has called a "widowed" land. This interpretation, in contradistinction to that of the "Black Legend" (Newman 1976), which blamed the decline of native populations on the cruelty and warfare of the invading peoples, views the role of accidentally introduced disease as critical. "Virgin soil" disease ecolo-gists argue that persons having no previous contact with the larger pathogen pool of humanity are immunologically defenseless. And so the Amerindians who had not before encountered Old World bacteria and viruses succumbed in large numbers to ailments that scarcely touched the immune Europeans (Hauptman 1979; Joralemon 1982; Dobyns 1983; Curtin 1985; Hader 1986). M. T. Newman (1976), however, warns:

There is mounting evidence that American Indians were no more susceptible to most of these infectious disease imports than other populations where these diseases had not struck within the lifetime of the people — none of whom therefore had acquired specific immunities.

For this reason Newman quotes W. R. Centerwall (1968), who called for "a réévaluation . . . with respect to the primary susceptibility of the Indian to .. . diseases of civilization, such as pertussis (whooping cough), smallpox, and tuberculosis"; and Centerwall concluded that "during the conquest, cultural disruption should be added to the impacts of the new pathogens, compounded by the force of European arms and the later ill-treatment of slavery."

Numerous other scholars have also implicated psychological, economic, and social factors stemming from introduced disease in the high mortality and even decimation of Amerindian populations (Crosby 1976; Dobyns 1976,1983; Meister 1976; Miller 1976; Trigger 1985). In any event, the indigenes went into decline as their battle with disease resulted generally in high death rates - up to 90 percent has been mentioned in some smallpox outbreaks, with case fatalities of 74 percent in others (see Fenner 1970; Joralemon 1982; Hader 1986).

This kind of die-off, of course, did not occur simultaneously or uniformly across the continent (Meister 1976). Pertussis, smallpox, pulmonary tuberculosis, measles, diphtheria, trachoma, chickenpox, bubonic plague, malaria, typhus, typhoid fever, cholera, scarlet fever, influenza, and a number of intestinal infections arrived with the Europeans at various times over 5 centuries. Of these, smallpox has generally been seen as the most dramatic (Ashburn 1947) and was one of the earliest to arrive. In Española it made

16th and 17th Centuries

'765

18th Century

'765

18th Century

19th Century

Map VII.8.1. Diffusion of smallpox among native Americans. (After Heagerty 1928.)

SCALE

500 1000 1500 2000

its appearance by 1519 (Crosby 1986), and was present in North America prior to the middle of the century, spreading northward from Mexico (Dobyns 1983; Trigger 1985). As a new disease moving without an intermediary vector, from person to person, it hit those of all ages, although the mortality of young males in many populations was especially devastating (Ray 1974).

Most Europeans had experienced smallpox in childhood, and hence were protected, but this was not true for the Amerindians or, for that matter, many of the blacks in America. Repeated introductions along the East Coast and up the St. Lawrence led to further outbreaks from the seventeenth to the nineteenth century, including an outbreak that dramatically influenced the population decline in Hu-ronia in 1639-40 (Trigger 1985), and the 1837 epi demic on the Great Plains, which decimated about half the remaining natives there (Hearne 1782, quoted in Innis 1962; Crosby 1976).

Maps VII.8.1 and VII.8.2, based on J. J. Heagerty (1928) and H. F. Dobyns (1983), respectively, summarize in a stylistic manner the history and geography of these outbreaks and illustrate that full elucidation of these events awaits an in-depth study based on original accounts, documents, and interpretations. Thus the hypothesized lower susceptibility, of those with a dominance of blood group O, noted above, is not borne out by the historical evidence. On the other hand, the anomalous group of the Black-foot Indians, with their A blood group, certainly suffered very severely; over two-thirds or some 6,000 Blackfoot were decimated in the smallpox outbreak of 1837 (Bradley 1900; Ewers 1958).

The Europeans, however, were not all immune to smallpox, as population growth in the colonies increased the number of susceptibles. Thus, in Boston a 10 percent death rate from this scourge was recorded for 1721, and in each of the years 1702, 1730, and 1752 over 6 percent of the population of that city died from this one disease (Dobson 1987).

Measles was also introduced in the seventeenth century from Europe, and as early as 1635 the Jesuits reported an outbreak among the French and Indians (Duffy 1972). The disease was very contagious, and a series of epidemics such as those of 1713-15 spread inland from the seaports. Indeed, in 1772 measles was a leading cause of death in Boston (Duffy 1972) and was claimed to be more often fatal in America than in England as in the former it took the form of a series of introduced epidemics and affected a larger number of adults in the New World. Only late in the colonial period, with population clusters in excess of 500,000, could measles or, for that matter, smallpox become established as endemic in America (Black 1966; Fenner 1970; Cliff et al. 1981). When and where this first occurred is not known, but it was probably not until the nineteenth century (Cartwright 1972). The fact that the pair of diseases was confused in the records does not help in establishing this important turning point.

Unlike the two diseases just discussed (and other purely human diseases such as scarlet fever and diphtheria), vectored diseases and zoonoses required infective agents to become established in the New World. Just two of these - plague and malaria — will be discussed. Plague was one of the earliest diseases to be introduced from Europe (Williams 1909; Posey 1976). Rats infested every ship that crossed the Atlantic, though only occasionally was the rat-human relationship as close as that described by Colonel H. Norwood (n.d.) in the mid-seventeenth century. "The infinite number of rats that all the voyage had been our plague, we now were glad to make our prey to feed on." No doubt, however, those that survived landed and by 1612-19 in Florida and New England, these newcomers and their fleas had given rise to human plague (Dobyns 1983). As D. A. Posey (1976) explains, "Once the rodent carriers were transported to this virgin territory, the plague would have spread as wild native rodent populations became reservoirs of the dreaded disease . . . and few, if any animals, except the louse were more common in Indian and colonial camps."

Thus, the conditions were present for plague long before the first fully documented case was recorded in 1899 as having come from Japan into San Francisco (Link 1953; Schiel and Jameson 1973). Three views of plague in the hemisphere can be sustained on the basis of present knowledge. One view is that it has long existed, even from prehistoric times as a sylvatic cycle disease in rodents. The remaining two, more probable, views entail its introduction from Europe, followed by possible extinction in eastern locations, and the documented transpacific reintroduction in the late nineteenth century. Certainly this third route has given rise to endemic plague from the Mexican border to Alberta primarily among ground squirrels and their fleas (Hubbard 1947). Unfortunately, domestic animals from time to time pick up these fleas and transport them into Western homes where occasional human infections are contracted, the annual incidence rate being 3.4 cases per year, 1927-69 (Canby 1977).

Falciparum malaria, dysentery, smallpox, intestinal worms, yaws, guinea worm, schistosomiasis, and yellow fever were contributed by the African slave (Ashburn 1980; Dunn 1965). Of these African diseases, malaria and yellow fever were the most significant (McNeill 1976), but their impact differed among the major population groups involved (Postell 1951; Duffy 1972; Kiple and Kiple 1977). In the case of malaria, the African slaves usually had been previously exposed, or had blood anomalies to protect them. Malaria among this group was generally a childhood disease in terms of mortality, though recurrence in later years was debilitating. On the other hand, among native Amerindians mortality from malaria could be as high as 75 percent (Dobyns 1983), but malaria was more often a predisposing condition rather than a fatal disease once the milder vivax malaria (introduced from Europe) became established in the Mississippian west. For Europeans (who may have been exposed to the vivax variety in England), falciparum malaria was deadly wherever it had been introduced to the local mosquitoes by slaves along the marshlands of the Atlantic and Gulf coasts (Childs 1940; Savitt 1978).

Although a variety of strains and perhaps even both major species may have been introduced by diverse carriers at a fairly early date, a more probable model, given the flow of immigration and the prevalence of vivax in Europe and falciparum in Africa, would have strains of the former entering during the first half of the [seventeenth] century, followed by the gradual establishment of areas of stable, low-level endemicity. The shattering of this picture would occur as blacks in numbers began arriving from a variety of African areas, bringing with them new strains of. . . falciparum. ... [A] qualitative change occurred sometime in the second half of the century as falciparum entered the colony... . [T]he benign vivax was prevalent in the 1670's but was supplanted by the more virulent falciparum in the 1680's. (Rutman and Rutman 1976)

Further vivax introductions from African sources would be strictly limited because of the absence of the Duffy blood group determinants Fya and Fyb in most individuals of African descent, which prevents them from hosting the disease (Mourant, Kopec, and Domaniewska-Sobczak 1976).

The transmission, of course, depended on the transmission of infection to Anopheles mosquitoes from those suffering with malaria parasites. Unfortunately, Nearctica was already amply provided with potential vectors (Freeborn 1949), and these mosquitoes became instrumental in spreading the infection from the south and east right up the Mississippi Valley as far as Canada, where seasonal transmission took place among the native peoples and settlers locally into the 1940s (Drake 1850/1954; Moul-ton 1941; Ackerknecht 1945). Furthermore, malaria was widespread in the nineteenth century in the Pacific Northwest of the continent (Boyd 1985; see also Map VII.8.3). Indeed, infection and even death from this imported disease still take place in North America, although changed environmental and social conditions led to its retreat to the South. By the 1950s, malaria - "the United States disease of the late 19th century" (Meade, Florin, and Gesler 1988) - had been eradicated. Much of the resurgence of the South and its development as the "Sun Belt" are related to this aspect of disease ecology.

The nineteenth-century social and economic condi

Map VII.8.3. Malarial disease deaths per 1,000 population, 1870. (Based on Ninth U.S. Census; assembled by author.)

tions, together with improved communication and ever increasing flows of immigrants, opened the continent to further invasions of disease. Indeed, immigrants, poverty, and disease were almost synonymous in many circles in this period. Most dramatic of these imported epidemics were those of cholera, with its ability to kill an estimated 40 to 60 percent of its victims within hours (Morris 1976) and an etiology that was unknown until Robert Koch discov ered the microorganism Vibrio cholerae in 1883. In the pandemics of 1831-2, 1848-50, 1853-4, and 1866, North America was not spared. Entering at port cities such as New York, Quebec, and New Orleans, the disease spread with the migrants and created terror but eventually catalyzed the development of meaningful public health reporting and treatment networks (Bilson 1980). This result would perhaps have taken much longer to achieve than it

Deaths per 1,000

Map VII.8.4. "Consumption" deaths per 1,000 population, 1870. (Based on Ninth U.S. Census; assembled by author.)

actually did had not this one condition had such a powerful effect on the population as a whole.

The other great scourge of the nineteenth century was pulmonary tuberculosis, also known as the "white plague." As previously noted, mycobacteria had long been present in the Western Hemisphere, but it was only in the nineteenth century, with urbanization (crowding of masses of people, often in poor-quality housing and lacking good nutrition), that this person-to-person infection assumed epidemic proportions (Ashburn 1947; Cockburn 1963).

It came to "transcend all maladies in the total number of its victims and the cost to society" (Ashburn 1947; see also Map VII.8.4).

That Amerindians had little experience with epidemic tuberculosis prior to contact with Europeans (Clark et al. 1987) is borne out by the dramatic susceptibility of Indians after exposure. For example, R. G. Ferguson (1934) wrote:

A most disastrous epidemic appeared among the tribes settled on the reservations and within a few years [after

1879] the general death rate among them was varying from 90 to 140 deaths per 1,000, two-thirds of these due to tuberculosis.

In 1928 the U.S. Bureau of the Census reported that 11.6 percent of Amerindian deaths were due to tuberculosis, as compared to 5.5 percent of Negro deaths and 5.6 percent of all white deaths (Ashburn 1947).

As far as blacks are concerned, some suggest that tuberculosis was rare among slaves (Postell 1951), though all agree that during Reconstruction it became a major cause of ill health and mortality, as social and economic conditions for most blacks declined markedly (Savitt 1978). As for other mycobacteria, leprosy is said to have been introduced with the slave population (Ashburn 1947) and remained an endemic disease in small numbers into

Map VII.8.5. Leprosy area of New Brunswick, predominantly in the nineteenth century. (From Heagerty 1928.)

modern times. (Among Europeans, it had been introduced [Heagerty 1928] but never became established, except for a brief period in the Florida Keys. Only a handful of persons - for instance, in New Brunswick - are recorded as having had the disease; see Map VII.8.5; Losier and Pinet 1984).

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