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Manitoba History: Review: Paul Hackett, A Very Remarkable Sickness: Epidemics in the Petit Nord, 1670 to 1846

by Sarah Burton
Public History Inc., Winnipeg

Number 46, Autumn/Winter 2003-2004

This article was published originally in Manitoba History by the Manitoba Historical Society on the above date. We make it available here as a free, public service.

Please direct all inquiries to webmaster@mhs.mb.ca.

Paul Hackett, A Very Remarkable Sickness: Epidemics in the Petit Nord, 1670 to 1846.Winnipeg: University of Manitoba Press, 2002. $24.95, 313 pp. Illus. ISBN 0-88755-659-0.

It has been twenty years since anthropologist Henry Dobyns published his controversial book Their Number Become Thinned in which he argued that Old World diseases spread throughout the North American continent from South America, having been brought by Columbus and the Spanish. These diseases wiped out large numbers of the pre-contact population on the rest of the continent and it was these remnants, Dobyns argues, that later European explorers encountered. While Hackett expresses his indebtedness to Dobyns work, and in fact relies on it throughout A Very Remarkable Sickness, his book argues against Dobyns main theory. It serves as both a response to and an elaboration of Dobyns work.

As the title of his book indicates, Hackett explores epidemics in the Petit Nord. Named such by French traders, this region encompassed the area between the north shore of Lake Superior and the east shore of Lake Winnipeg. Its eastern boundary was the divide between the Moose and Albany Rivers’ drainage systems, its northern boundary the Hudson and James Bays.

In particular, Hackett looks at “acute crowd infections” such as smallpox, flue, measles, whooping cough and so on, since it was these diseases that proved so fatal to so much of the population. Acute crowd infections have three main characteristics: they are infectious and can be communicated via contact, air, food, water and so on; they are directly transmitted and do not need an intermediate host; finally they are acute or severe, brief infections that, if they do not kill, will impart at least a partial immunity on the victim. This latter trait means that an acute crowd infection requires a large and dense population with a steady supply of “susceptibles,” those who have never had the disease and therefore have no immunity, in order to survive.

Generally, areas of dense population such as cities contain their own disease pools. Eventually people within these areas grow to tolerate the diseases of the pool and they develop immunity. The disease becomes endemic or constantly present and only seriously affects susceptibles, mainly children. “Critical community size” or CCS is the size of the population required to support a disease, in order for that disease to survive and remain endemic. CCS differs for different diseases: measles requires a population of at least 250 000 to survive while scarlet fever only requires 48000. Once endemic, crowd diseases settle into a pattern of low level incidence, affecting mainly children and supported by births. Every few years the number of susceptibles reaches a ‘critical number’ and an epidemic occurs.

Occasionally disease spreads to other populations. Each disease pool has an “urban disease frontier” which is the range its endemic disease may affect people beyond its limits. ‘Near populations’ are those populations situated close to a city or disease pool that have regular contact with that pool and consequently suffer regular, mild epidemics, affecting mostly children. ‘Peripheral populations’ are too far away to have regular contact with a given disease pool and so the diseases of the pool do not become childhood diseases. There are longer intervals between epidemics and more severe effects, on children and adults alike. Peripheral populations can become near populations withfactors such as increased travel or migration and the development of temporary pools of disease within a disease frontier.

Europe in the 15th century was like a big city and America the surrounding rural area, a peripheral population susceptible to the most severe effects of epidemic disease. Hackett’s book looks at the Petit Nord’s transition from a peripheral to a near population, from the period when epidemic disease was introduced to when it started to become endemic.

Hackett focuses on the time period between 1670 and 1846. 1670 marks the introduction of the Hudson Bay Company into the area and the start of the historical period in the area. 1846 marks the last significant epidemic of acute infectious disease in the Petit Nord before chronic diseases like tuberculosis gained prominence and eclipsed the impact of acute infections.

Chapter One examines the spread of epidemics in Mesoamerica as well as in northeastern America. The first known Old World epidemic hit South America in 1518-1519, twenty years after initial contact. These diseases became more and more common as more migration occurred and large urban centres were established. In densely populated areas these diseases became endemic, affecting children only, and Mesoamerica became a disease pool in its own right. But how far did the influence of this pool extend? While Dobyns theorizes that the disease frontier of Mesoamerica extended throughout the continent, Hackett argues there is no archaeological evidence to support this claim. As well, the Jesuit relations do not indicate the existence of epidemics among the Mohawk or the Huron until the 17th century. Hackett believes the epidemics of the 17th century came from the east rather than the south.

Beginning in the 17th century, the interest in eastern North America was less in exploration and trade than in settlement. Transportation had become faster, making migration easier. More and more communities sprang up and the population grew rapidly. Mass migration occurred in New England in the 1630s bringing lots of children (susceptibles). Although rapidly growing, these communities were still not large enough to become pools of endemic disease. Acute crowd infections remained epidemic, arriving at the major ports and moving back and forth between colonies. Aboriginal people were often the main vehicle of this diffusion, travelling to large communities to trade and carrying disease into the interior. Epidemics increased and became more frequent. While there is no direct evidence that the Petit Nord experienced any of these epidemics at this time, Hackett surmises it is quite likely that at least its margins were affected.

The historical period begins in the Petit Nord in 1670 with the establishment of the Hudson Bay Company and its record-keeping practices. The HBC served as a connection between the Petit Nord and the east and facilitated closer contact between aboriginal people and European traders. HBC competition caused French traders to increase their efforts resulting in further exploration, more direct contact with aboriginal people and more posts. While the first four years of the HBC’s existence remained disease-free, trading posts soon became nodes of disease, centres where disease accumulated and spread throughout the surrounding area via the aboriginal people. 1674 saw an epidemic among the Cree at James Bay cause by intertribal trade. In 1720 the first documented outbreak of smallpox in the Petit Nord occurred at York Factory.

Diffusion of 1779-1783 smallpox epidemic in the Petit Nord. From A Very Remarkable Sickness.

The smallpox epidemic that hit the region in 1737-38 originated in Boston almost adecade earlier, brought from Ireland via ship. In the mid- eighteenth century, the English colonies in eastern North America were quite interdependent. People, goods and information moved freely and easily between them, as did disease. This particular epidemic spread to Albany, New York, a frontier community that carried on an illegal trade with Montreal. From Montreal the epidemic spread into the interior and the pays d’en haut to the Teton Sioux, the Ojibway of Chequamegon (on the south shore of Lake Superior) and finally to the Council of Maurepas that took place March 4-5, 1737. The Cree and Assiniboine who were present at this council subsequently carried the disease to their lands around Lake Winnipeg and eventually to the area around the Lake of the Woods. The 1737 epidemic did not spread throughout the Petit Nord but remained on its western and southwestern margins. However, the effects of the epidemic were felt much further. Migration out of the region left ‘population vacuums’ that other groups moved in to fill. For instance, the Ojibway spread north and west into what had once been Cree territory.

The 1740s was a period of relatively good health in the Petit Nord, however from 1751 on to the 1780s the region saw an increase in acute respiratory disease (described as ‘colds’ in the HBC records). These epidemics were not continuous but tended to ebb and flow, depending on local conditions. Then, in 1779 the Petit Nord was hit by another smallpox epidemic. This was one of the most severe pandemics for the aboriginal people and it spanned a continent. Starting in Mexico, the disease spread as far north as Great Slave Lake, south to South America, east to Lake Superior and west to the Pacific Northwest. While some bands remained untouched, many were decimated. Exogenous disease was no longer a rare occurrence in the Petit Nord.

In the period between 1784 and 1818 competition between the North West Company and the HBC encouraged the latter to move inland, decreasing the distance aboriginal people needed to travel in order to trade. More posts were built, serving as concentrated disease centres, more exploration was undertaken and more contact took place on a more frequent basis, all of which facilitated the spread of infectious disease. South of the border, cities in the northeast United States had finally grown large enough to support disease pools of their own. Roads, stagecoach services, and migration westward into the interior ensured the frequent spread of infections.

Despite its proximity to the new disease pools of the United States, the Petit Nord was not much affected until after 1820. It remained isolated because migration was focused south along the Ohio River and because a buffer zone of aboriginal people, many of whom were hostile to American encroachment, existed between the Petit Nord and the settlement frontier. There were only seven recorded incidents of epidemic disease in the period from 1810 to 1818 and these were not major attacks but merely ‘temporary inconveniences.’

By the nineteenth century, epidemics began to occur so often they overlapped. Compound epidemics resulted in higher rates of mortality. Normally non-fatal diseases were capable of killing victims already weakened from previous epidemics. In 1819 to 1820 the main sickness was measles. Whooping cough was also common as were localized afflictions like influenza.

After 1821 the area experienced an increase in the occurrence of epidemics. Once rare diseases became common and new diseases such as chicken pox and mumps appeared. This increase was not incremental: 1821 marks a clear break in the history of disease in the Petit Nord. The region was no longer a peripheral population but now existed within the limits of the disease pool. Smallpox was the only disease that did not occur more frequently, thanks to the HBC’s program of vaccination.

1846 saw three major epidemics hit the region: flue, measles and dysentery, marking ‘the culmination of all the changes in epidemic distribution since arrival of HBC 1670’ (page 199). A vast number of people died and traditional treatments like sweat lodges and exposure to cold water often exacerbated the effects of the disease. Dependency on the HBC for relief and medicine increased. Indeed, aboriginal groups who lived close to trading posts often faired better being closer to a source of aid.

Perhaps a more lasting legacy than the physical suffering caused by these epidemics was the change in the way aboriginal people related to their world. High rates of mortality had a profound psychological effect on many aboriginal groups. Traditional mourning practices were forsaken and practices once considered unthinkable, such as the abandonment of the dead and dying, were adopted. A passage in a letter from Donald Ross (at Norway House) to George Simpson, written on 19 September 1846, illustrates this change:

I noticed this season, however, what I never perceived before, a marked degree of callousness and indifference among the Indians, to the loss of even their nearest and dearest relations and even death itself seemed to have become so familiar to them as to have lost much of its usual terror (cited on page 235).

Hackett’s thesis is that generalizations about the spread of disease can be useful but need to be qualified by specific examples. Groups and regions differ in the way disease affects them. Timing and penetration of first infection, frequency and severity of an epidemic all varied across the New World. These factors even varied within regions such as the Petit Nord. It is not accurate to assume that what happens in one region (such as post-contact Mesoamerica) happens in all regions, which is Hackett’s main problem with Dobyns’ theory. Many factors beyond infectious period affect a disease’s diffusion potential and its impact is highly dependent on local conditions. Social, political and geographic factors all can affect patterns of disease diffusion.

A scholarly work that is as much a history of the Petit Nord as it is a study of the complex behaviour of infectious disease, Hackett’s book is skilfully written and well researched. Relying, necessarily, on HBC records for much of his data, Hackett recognizes the limits of these sources and makes an effort to include other sides of the story using archaeology, aboriginal oral histories and winter counts (pictorial records of significant events). The work is extensively footnoted and the footnotes themselves contain a good deal of interesting information. Hackett tackles a complicated subject in a way that will make the book accessible to many, including those unfamiliar with either epidemiology or western Canadian history.

Page revised: 19 September 2010

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