A Very Remarkable Sickness: Epidemics in the Petit Nord, 1670 to 1846 0887556590, 0899707127, 9780887553042

Table of contents :
Cover
Contents
List of Diagrams, Tables, Maps, and Illustrations
Preface
Acknowledgements
Introduction
1. Old World Disease Transmission Patterns
2.The Early Historical Period in the Petit Nord: 1670-1837
3.The Smallpox Epidemic of 1737-1738
4. Epidemic Disease in the Petit Nord: 1739-1780
5.The Smallpox Epidemic of 1779-1783
6. Epidemic Disease in the Petit Nord: 1784-1818
7. The Measles and Whooping Cough Epidemics of 1819-1820
8. Epidemic Disease in the Petit Nord, 1821-1845
9. The Epidemics of 1846
Conclusion
Endnotes
Bibliography
Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

Citation preview

Manitoba Studies in Native History Manitoba Studies in Native History publishes new scholarly interpretations of the historical experience of Native peoples in the western interior of North America. The series is under the editorial direction of a board representative of the scholarly and Native communities in Manitoba. I

The New Peoples: Being and Becoming Metis in North America, edited by Jacqueline Peterson and Jennifer S.H. Brown

II

Indian-European Trade Relations in the Lower Saskatchewan River Region to 1840, by Paul Thistle

III

"The Orders of the Dreamed": George Nelson on Cree and Northern Ojibwa Religion and Myth, 1823, by Jennifer S.H. Brown and Robert Brightman

IV

The Plains Cree: Trade, Diplomacy and War, 1790 to 1870, by John S. Milloy

V

The Dakota of the Canadian Northwest: Lessons for Survival, by Peter Douglas Elias

VI

Aboriginal Resource Use in Canada: Historical and Legal Aspects, edited by Kerry Abel and Jean Friesen

VII

Severing the Ties that Bind: Government Repression of Indigenous Religious Ceremonies on the Prairies, by Katherine Pettipas

VIII

The Ojibwa of Western Canada, 1780 to 1870, by Laura Peers

IX

Women of the First Nations: Power, Wisdom, and Strength, edited by Christine Miller and Patricia Chuchryk, with Marie Smallface Marule, Brenda Manyfingers, and Cheryl Deering

X

Night Spirits :The Story of the Relocation of the Sayisi Dene, by Ila Bussidor and Ustiin Bilgen-Reinart

XI

"A National Crime":The Canadian Government and the Residential School System, 1879 to ^6, by John S. Milloy

XII

MuskekowuckAthinuwick: Original People of the Great Swampy Land, by Victor P. Lytwyn

XIII

Preserving the Sacred: Historical Perspectives on the Ojibwa Midewiwin, by Michael Angel

XIV

"A Very Remarkable Sickness": Epidemics in the Petit Nord, 1670-1846, by Paul Hackett

This page intentionally left blank

"A Very Remarkable Sickness" Epidemics in the Petit Nord, 1670-1846

Paul Hackett

UNIVERSITY OF MANITOBA PRESS

© Paul Hackett 2002 University of Manitoba Press Winnipeg, Manitoba R3T 2N2 Canada www.umanitoba.ca/uofmpress Printed in Canada on acid-free paper by Friesens. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, or stored in a database and retrieval system, without the prior written permission of the University of Manitoba Press, or, in the case of photocopying or other reprographic copying, a licence from CANCOPY (Canadian Copyright Licensing Agency), 6 Adelaide Street East, Suite 900,Toronto, Ontario M5C 1H6. Cover Design: Kirk Warren Text Design: Sharon Caseburg Maps: Paul Hackett Cover: "Canada, ou, Nouvelle France" by Pieter van der Aa (1713), from The W.H. Pugsley Collection of Early Canadian Maps, reproduced courtesy of the Rare Book and Special Collections Division, McGill University. Canadian Cataloguing in Publication Data Hackett, EJ. Paul (Frederick John Paul), 1961"A very remarkable sickness": epidemics in the Petit Nord, 1670-1846 / Paul Hackett.

(Manitoba studies in native history ; 14) Includes bibliographical references and index. ISBN 0-88755-659-0 1. Epidemics—Manitoba—History. 2. Indians of North America—Diseases—ManitobaHistory. I.Title. II. Series. RA650.55.C32M3 2002 614.4'.2'0899707127 C2002-911211-7 The University of Manitoba Press gratefully acknowledges the financial support for its publication program provided by the Government of Canada through the Book Publishing Industry Development Program (BPIDP); the Canada Council for the Arts; the Manitoba Arts Council; and the Manitoba Department of Culture, Heritage and Tourism. The Manitoba Studies in Native History series is published with the financial support of the people of Manitoba, through the Department of Culture, Heritage and Tourism, the honourable Eric Robinson, Minister. Manitoba Studies in Native History Board of Directors: I. Bear, M. Bennett, J. Burelle, J. Fontaine, G. Friesen, E. LaRocque, P. Kulchyski, W Moodie, A. Perry, D.Young.

For Mom and MJ

This page intentionally left blank

Contents

List of Diagrams, Tables, Maps, and Illustrations

viii

Preface

xi

Acknowledgements

xv

Introduction

3

1. Old World Disease Transmission Patterns

21

2.The Early Historical Period in the Petit Nord: 1670-1837

37

3.The Smallpox Epidemic of 1737-1738

59

4. Epidemic Disease in the Petit Nord: 1739-1780

75

5.The Smallpox Epidemic of 1779-1783

93

6. Epidemic Disease in the Petit Nord: 1784-1818

119

7. The Measles and Whooping Cough Epidemics of 1819-1820

137

8. Epidemic Disease in the Petit Nord, 1821-1845

155

9. The Epidemics of 1846

199

Conclusion

237

Endnotes

245

Bibliography

303

Index

305

List of Diagrams, Tables, Maps, and Illustrations

Diagrams 1. Epidemiological relationship between urban disease pool and outlying populations / 10 2. Community size and periodicity of measles / 12 3. Epidemic activity at selected posts, 1821-1846 / 196 Tables 1. Crowd diseases and agents / 6 2. Diffusion potential of infectious diseases 715 3. Epidemic disease in eastern North America, 1675-1716 / 53 4. Isham's record of deaths / 83 5. Order of disease introduction / 241 Maps 1. Petit Nord/ 16 2. Freeze-up and break-up / 18 3. Smallpox and measles epidemics in Boston / 30 4. Seventeenth-century trade routes / 35 5. Voyage to Hudson Bay / 39 6. Diffusion of the 1669-1670 smallpox epidemic / 47 7. Petit Nord, 1674-1736 / 51 8. Origins of 1737-1738 smallpox epidemic / 63 9. Petit Nord, 1739-1780 / 76 10. Pre-1805 horse-trading network / 97 11. Approach of the 1779-1783 smallpox epidemic / 98 12. Diffusion of the 1779-1783 smallpox epidemic / 104 13. Petit Nord, 1784-1818 / 120 14. Initial outbreaks of measles, 1818-1819 / 139

15. Diffusion of the 1819-1820 measles and whooping cough epidemics / 142 16. Changing patterns of settlement in the United States, 1800-1840 / 158-159 17. Canal construction / 161 IS.Travel times from New York City, 1800 and 1830 / 164 19. Locations of present-giving ceremonies in the Sault Ste. Marie area / 166 20. Systems of epidemic diffusion / 170 21. Post-merger HBC brigade routes / 173 22. Petit Nord, 1821-1845 / 177 23.The epidemics of 1846 / 201 24. Red River Settlement, 1857 / 208 Illustrations 1. Hudson's Bay post at Sault Ste. Marie, 1853 / 74 2. Sault Ste. Marie, 1870/92 3. Red Lake chief and followers arriving at Red River, 1825 / 154 4. Departure of the second colonist transport from York Fort to Rock Fort, 1821 / 198 Abbreviations ARD

Acute Respiratory Disease

CCS

Critical Community Size

HBC

Hudson's Bay Company

HBCA

Hudson's Bay Company Archives

MHS

Minnesota Historical Society

NWC

Northwest Company

PAM

Provincial Archives of Manitoba

RSV

Respiratory Syncytial Virus

This page intentionally left blank

Preface

IN 1983, AN AMERICAN ANTHROPOLOGIST, HENRY DOBYNS, STIRRED

up the anthropological and ethnohistorical research communities with the publication of his provocative book, Their Number Become Thinned.1 Dobyns argued that Old World diseases introduced among the Aboriginal people of the Americas following the arrival of Columbus took a devastating toll in human life, almost from the outset of renewed contact. Moreover, he concluded, the effects of these earliest epidemics were not confined to the regions of direct contact, but instead spread almost to the limits of the western hemisphere. Consequently, almost all the European intruders who made contact with the Aboriginal people in succeeding centuries did so with but the remnants of once far more numerous groups, whose cultures lay in shambles with the deaths of so many. The effect of this work was galvanizing, the response swift and largely polarized. Many researchers embraced his ideas and incorporated them into their own research and cognitive framework, accepting his heavily revisionist estimates of the precontact population of the hemisphere. Others remained unconvinced, and soon began to question his handling of the meagre evidence and his broad,

xii

PREFACE underlying assumptions concerning events beyond the direct observation of literate observers.Two decades later, his views, and the intellectual schism that arose between his supporters and detractors, have not gone away, but instead continue to shape the way in which we portray pre-contact Aboriginal groups and the nature of the contact process.2 In a very real way, the journey that leads to this book also began with Dobyns's stimulating and controversial research. In 1988,1 began my graduate studies in geography at the University of Manitoba, equipped with a vague sense that I wanted to study the historical evolution of urban communities in Canada. By chance, I took a course offered by Wayne Moodie on the historical geography of Canada's Aboriginal people.The subject matter and Wayne's teaching style quickly captured my imagination and all thoughts of pursuing research in urban morphology were abandoned. As it happened, he had chosen that year (and that year alone) to introduce his students to some aspects of historical demography, and to Their Number Become Thinned in particular. Finding the topic of Aboriginal health intriguing, I turned my attention to the study of epidemic disease in a small part of the Canadian Northwest once called the Petit Nord. As a geographer, I felt it important to focus on the diffusion of these diseases, a quintessentially geographical process that for me was the central issue in Dobyns's book. Thereafter followed a term paper, a thesis, and a dissertation. This book is the extension of that earlier research. What follows is a study of the diffusion, or spread, of Old World epidemic disease in the Petit Nord from 1670, which marked the start of significant White penetration into the region, to 1846, by which time nonAboriginal people threatened to overrun it. As a work of historical geography, both space and time figure prominently. Here, the focus is on the varied patterns of diffusion within the region and also on its place within a continental framework of epidemic disease. This last is critical, for an explanation of the presence of these foreign afflictions can only be gained through the consideration of the external factors that favoured or hindered their diffusion. These patterns did not remain static, though, and so this study is also concerned with the changes that occurred in epidemic diffusion over time, and the key historical factors that precipitated those changes. In writing this book I have drawn heavily upon a vast documentary record left us by the fur traders, explorers, and missionaries who worked within, or travelled through, the region. Of these, the rich body of journals, letters, and reports of the Hudson's Bay Company stand out. Lauded by the noted historical geographer A.J. Ray as "an excellent source of information regarding diseases and the general health of the Indians,"3 these

PREFACE xiii diverse and extensive documents have figured prominently in several historical studies of epidemic disease. At their best, these records provide a relatively dense network of observation points—that is, fur-trading posts— that can enable us to track the progress of an epidemic disease within the region and beyond its borders. Equally valuable, in some ways more so, is the voice of the Aboriginal people of the region. The importance of such testimony in the study of historical epidemiology can be immense,4 as it is only through the study of oral history that we can begin to comprehend the full impact of these diseases. In places I have incorporated some of this body of oral testimony that has been published in written form, either directly or as interpreted by the fur traders and explorers, although much less than I would have liked. The book's approach borrows greatly from the contemporary disciplines of geography and epidemiology, particularly with respect to establishing the timing and location of outbreaks, identifying diseases, and documenting the patterns and mechanisms of diffusion. It employs modern biomedical concepts throughout, both to identify the particular afflictions recorded in the written record and to explore their behaviour.While this approach is not uncommon in the literature, there are difficulties in applying such modern knowledge in an historical study set in a period long before the recent past, and a few caveats must be kept in mind. For instance, there may always be questions about the reliability of the observations that have been left to assist the modern scholar. In this case, the medical knowledge of the day, both that of the profession and that of the observers, leaves much to be desired where present-day epidemiological procedures are concerned.5 We are left with two choices: dismiss the disease descriptions and identifications in the records, or acknowledge the limitations of these data and accept them tentatively where no conflicting interpretation exists. I have chosen to do the latter.6 A more insidious problem with the data, and with the use of presentday disease concepts for epidemiological analysis, is posed by the identity or behaviour of the sicknesses being observed during the study period. There are several potential facets to this. For example, we cannot always be certain that the historic disorder we wish to identify even has a modern counterpart. Occasionally in human history, there have been afflictions that have suddenly emerged from the shadows to wreak havoc on an ill-prepared population, only to disappear again. Even those readily identified today may have behaved differently in the past, having evolved over time. Towards the end of the nineteenth century, smallpox declined considerably in its overall virulence with the appearance of a new, less destructive,

xiv

PREFACE strain, variola minor, while scarlet fever appears to have undergone several changes affecting its severity since the eighteenth century. Finally, we should not necessarily expect these diseases to behave in a familiar way among groups that are almost entirely susceptible, or that are comprised of people who have lowered resistance due to underlying health problems, such as concurrent chronic infections, nutritional disorders, or other stressors. For these populations, diseases that we might weather with relative ease may pose a serious threat to life, may be accompanied by other, opportunistic, infections, or may linger in their effects long after we would expect them to have gone. Still, these concerns need not stop us but only give us pause for thought. With these limitations in mind, we can now begin to consider the epidemic history of the Petit Nord.

Acknowledgements

IN THE COURSE OF RESEARCHING AND WRITING THIS BOOK I accrued debts to many individuals and organizations, debts that, by all rights, I must now acknowledge. In today's academic world, pursuing full-time studies is an expensive proposition. It would have been impossible for me to complete the level of research that went into this book without the financial support of several generous institutions, and in particular the Hannah Society for the History of Medicine (Associated Medical Services Inc.) and the University of Manitoba. As well, the rewriting of this book was completed while I was funded as a Postdoctoral Fellow by the Canadian Institutes of Health Research.These contributions freed me to pursue my topic as far as I felt that it was necessary to go. I must also express my collective thanks to the various archives and libraries where this research was conducted. Foremost of these is the Hudson's Bay Company Archives, housed in the Provincial Archives of Manitoba, which, luckily for me, is located in Winnipeg. It is no exaggeration to say that this work would not have been possible without their cooperation. In addition to allowing me to quote from the records of the HBCA, for which I am grateful, PAM/HBCA's employees have been a joy to work with

xvi

ACKNOWLEDGMENTS over the years, and have always made me feel welcome. In this regard I would like to single out Chris Kotecki, who has offered me a wealth of information and pleasant conversation. Others helped me in my research in other ways. Victor Lytwyn, Mike Angel,Jim Daschuk,Ted Binnema, and Lacey Sanders all provided valuable data collected in their own investigations and insights into Aboriginal history related to their fields of expertise. Victor, in particular, has provided a superb foundation of historical geography on which much of this book rests. Robert Boyd, whose work I admire greatly, generously provided me with a draught copy of one of his key publications, for which I am most appreciative. Within my former (geography) department, Bill Norton and Dick Foster never objected to discussing my research, and they favoured me with information that has made this book far better than it otherwise would have been. I was also lucky enough to have had a formidable PhD review committee, whose help has been just as valuable in the process leading up to this book as that leading to the dissertation. Skip Ray has given me much encouragement and excellent advice about writing, and, like Victor, his groundbreaking work has set the stage for my own. Gerry Friesen, especially in his capacity as head of the Manitoba Studies in Native History Board of Directors, has been instrumental in seeing this book through, and has encouraged me to publish from the start. Barry Kaye, through an early course and many enjoyable discussions over the years, has shaped my ideas about the changing role of the Red River Settlement in epidemic diffusion. Thanks, too, go to Adele Perry, of the Department of History, who offered much helpful advice after reading the original manuscript. Kue Young, my present post-doctoral supervisor in the Department of Community Health Sciences, has provided a wealth of knowledge about Aboriginal health research and writing for publication. I was truly sorry to see him depart for the greener pastures of Toronto. Not all of my debts are to members of the academic community. Friends and family played their own roles in seeing this through or in keeping me grounded enough to write. I owe my good friend Mark Shymanski many thanks for getting me to focus on life beyond the ivory tower, extolling the virtues of the Winnipeg Zoo and canoeing trips. My eldest sister, Laurel Lee Mayo, has always cheered me on while warning me about the pitfalls of academic life. My brother Fred has given me much advice about computers (and goaltending, as if I needed it). Finally, my older brother Chris has been an all-round, and indispensable, help in the world of historical

ACKNOWLEDGEMENTS xvii research and computers, and our far too infrequent discussions, tennis matches, horror movies, etc. have made life much more enjoyable. In writing this book I soon realized that the world of publishing is a foreign place to me, and that I would require much guidance in preparing it for publication. I have been most fortunate to work with the University of Manitoba Press. Managing Director David Carr has been instrumental in getting me to see the value of my research and the need to revise it for the public. Pat Sanders, my editor (if I can presume to call her'my' editor), has been remarkable in her patient help and sagacious editorial advice. In the final tally, two people are most deserving of my outmost thanks. The first is Wayne Moodie, who served as my advisor at the University of Manitoba. Wayne did yeoman's work in helping to shape and polish this research, and a large part of any success that I have had is owing to his help and guidance. I could not have asked for a better mentor, for he has the valuable gift of getting the best out of his students. The other person is my long-suffering wife, Jennifer. Although she had no idea how long it would take when she agreed to my pursuing the PhD, she nonetheless continued to support me throughout, and has been at the fore in getting me to complete the revision of my manuscript. Lastly, I would like to thank my two children, Devon and Colin, who, while doing little to expedite my work, have done much to make my life more enjoyable.

This page intentionally left blank

"A Very Remarkable Sickness"

This page intentionally left blank

Introduction

FOR THE OJIBWAY WHO TRADED AT LAC SEUL, IN WHAT is NOW

northwestern Ontario, the first half of the 1840s was a nightmare from which they could not wake.Year after year they fell ill during epidemics. Year after year they struggled to endure repeated sicknesses, often taxed to the limit simply to gather food to survive. For many, death was the final outcome of a fresh outbreak. Buffeted by an almost endless run of epidemics, survival, either of the individual or the group, was by no means certain. Charles McKenzie, a long-time veteran of the fur trade, played witness to these hardships from his Hudson's Bay Company post, and in his journals recorded with concern the frequent bouts of disease. While he sympathized with these people, he also had his own problems. The many deaths and sickness during this difficult period also struck a blow against his returns, and so his credibility in the company. During the 1840s, life and commerce at Lac Seul were precarious indeed.1 And yet, it had not always been this way. Earlier in McKenzie's career the Aboriginal people of Lac Seul, and of the region west of Lake Superior in general, had enjoyed much better health, their lives generally free of

4

INTRODUCTION epidemic disease except on extremely rare occasions. Some forty years earlier, according to the trader, they had been superior in size and were much more robust, a claim that was supported by the local elders.2 In spite of his inquiries, the reasons for this precipitous decline in health escaped the trader, as did an adequate explanation for the vast increase in the number of epidemics appearing in his district. Had McKenzie been able to cast his gaze even farther into the past, the decline in the fortunes of the Aboriginal people would have seemed even more remarkable.When British fur traders first appeared in the lands to the south and west of Hudson Bay during the late seventeenth century, they encountered a country that, in one way at least, was a revelation. The people whom these traders met suffered from very few diseases, and their lives, on the whole, seemed vigorous and healthy compared to those of the Europeans.3 Indeed, for the visitors, who came from the disease-rich environment of western Europe, the absence of common afflictions such as smallpox and measles, whooping cough and chickenpox, and, apparently, even influenza and colds, among many others, was astounding. While the people of Hudson Bay and the lands that bordered on it were not entirely free of the host of illnesses to which humans may fall prey, for the early traders this was as close to a disease-free paradise as they could imagine. Between the emergence of the fur trade in this area and the last few decades of Charles McKenzie's fur-trading career at Lac Seul, then, this near-paradise had been lost. The decline that McKenzie witnessed among the Lac Seul people was far from unique. Rather, it was part of a much larger process of disease intensification that had begun in the Americas in the early sixteenth century, a by-product of renewed contact between the eastern and western hemispheres. Its roots lay in a period long before the trader had even been born. Moreover, in order to understand the process as it affected his district, he would have had to look for changes occurring far beyond its borders, something that was outside the experiences of a single trader in charge of an isolated trading post. On the other hand, the passage of time provides the modern researcher with opportunities that were not available to the trader, enabling us to understand what he could not: the long process of decline in the fortunes of the Aboriginal people who lived in the broader region surrounding McKenzie's post during this era.

INTRODUCTION New Diseases from the Old World Recent research has dispelled the previous perception that the western hemisphere was disease-free before contact.4 Prior to the late fifteenth century, the Aboriginal people of the Americas suffered from a substantial, though highly variable, disease load. Depending upon the local environment, the complexity of the population, and their location, among other factors, a group might have been exposed to a wide variety of infections and disorders, including several fully capable of taking human life. Nevertheless, it is also clear that a great many afflictions were absent from the Americas prior to the arrival of Columbus. Over the following centuries, many of these began to appear as part of a process of inter-hemispheric biological transfer that the noted ecological historian Alfred Crosby has termed the "Columbian Exchange."5 With this largely one-sided exchange, the people of the Americas suffered devastating epidemic after epidemic, their numbers dwindling in the face of these new diseases from the Old World. The tendency for some scholars to characterize the terrible epidemics that accompanied the Columbian Exchange as part of a unique phase in human history is understandable, for there does not seem to have been another demographic event of its extent and magnitude. However, it is also possible to see them as part of a much older process of epidemic diffusion, stretching back thousands of years to the origins of urban civilizations in the Old Wo rid. The full extent of the diseases introduced from the Old World is not known, but even a partial list is bound to be extensive, encompassing ailments such as bubonic plague, measles, influenza, cholera, and smallpox. Among this overall group of exogenous diseases is a particular class of afflictions that, as a group, was responsible for much of the monumental loss of human life that resulted from the Columbian Exchange. These are the directly transmitted, acute, infectious diseases, otherwise known as the acute crowd infections (Table I).6 These disorders share three basic characteristics: they are infectious; they are directly transmitted; and they are acute. Infectious, or communicable, diseases are caused by a specific agent or organism, such as a virus, protozoan, or bacterium, which is passed directly or indirectly to a susceptible host from another source. There are four basic modes of transmission from an external source of disease: by air, physical contact, food or water, and insect or animal.7 A second common characteristic is that they are directly transmitted. There is no intermediate host or reservoir other than humans during the life cycle of the causative organism. Directly transmitted diseases

6

INTRODUCTION

Table 1: Selected Crowd Diseases and their Agents (After Ramenofsky, Vectors of Death, 140)

are thus dependent on humans for their existence. This is in contrast to vectored diseases, such as typhus, malaria, yellow fever, and bubonic plague, which exist for part of their lives within animals, arthropods such as lice, mosquitoes, or fleas, or even the environment.8 Finally, they are acute.These diseases are of only relatively brief duration, the course of the affliction being measured in days or perhaps a few weeks, after which the victim either recovers or dies. In many cases either total or partial immunity is conferred, meaning that additional susceptibles, people who have never contracted the disease, must be present in order for the disease to survive within a particular population. True crowd infections can survive only in densely populated, urban communities where there is a continuous supply of susceptibles. Consequently, the existence of crowd infections will be temporary in a lightly populated region. This is in contrast to chronic infections, such as tuberculosis or syphilis, which may persist in an infected (and infective) individual for years or even decades, and which are not population-density dependent. The current belief concerning the origin of crowd infections is that they arose from the transfer to humans of diseases that were endemic within animal populations.These crossovers were the product of two fundamental changes in the human way of life. The first was the domestication of herd animals, or of animals that lived in large groups in the wild. As humans came into closer contact with certain animal species, they were exposed to the common diseases of these animals (their zoonoses), which eventually crossed over and became human diseases. Thus, for instance, it is thought that rhinoviruses came from horses, smallpox from cattle or perhaps monkeys, measles from dogs, and influenza from swine and poultry. The first

INTRODUCTION transfers of crowd diseases from animals to humans may have occurred shortly after the beginnings of animal domestication. However, these diseases were probably unstable at first, as the early groups practising animal husbandry lacked sufficient numbers to maintain them. Instead, the affliction might flare up briefly as a severe but localized epidemic, disappearing as soon as the supply of susceptibles was exhausted.This changed only with the development of large urban civilizations, when some zoonoses were permanently transferred to these populations, and thereafter emerged as distinct diseases of human cities. This process of permanent transference is thought to have begun only after the rise of Sumeria about 5000 BP.9 Historian William McNeill has been at the forefront of documenting the role that disease played in the expansion of urban civilizations.10 He described an historical process that began with the development of several densely populated, separate, and epidemiologically distinct, Old World urban disease pools. Over time, the urban dwellers and the crowd afflictions that emerged among them settled into a relationship of mutual toleration wherein these diseases affected only children, and with far less mortality than had earlier been the case. However, diseases that became endemic, or constantly present, within these urban pools tended to spread into the surrounding rural areas occasionally, killing many people and clearing the way for further expansion of urban societies. After 500 BC these pools began to exchange diseases and to expand their epidemic influence through territorial expansion, military excursions, new trading connections, and other modes of contact. As new urban civilizations emerged, and connections among them increased, a new process of disease homogenization began that would eventually span the entire world. This process was well underway in Europe and Asia by the late fifteenth century, when sustained contact between the eastern and western hemispheres was initiated. Following 1492, the Americas began to be included in this homogenization through the transoceanic transfer of Old World diseases, to the great detriment of the Aboriginal people of the western hemisphere. This transfer, then, can be seen as part of a much larger, and much older, process of disease homogenization between urban disease pools. At the same time, it was also part of a long-standing pattern of urban to rural disease diffusion. Epidemiologically, the most significant attribute of these early urban disease pools was their abundant populations that became sufficient to permanently maintain crowd diseases. The large number of people in a major urban community provided a continuous supply of susceptibles for these diseases in the form of children who had been born since an earlier epidemic or those who escaped earlier infection. Researchers have estimated

7

8

INTRODUCTION the threshold population required for the continuous presence of several crowd diseases, a figure that is called the "critical community size" or CCS. It is estimated that a population in the order of 250,000 would be sufficient to maintain measles in an isolated community, providing the estimated 4000 to 4500 new cases per year needed to support the disease.11 Scarlet fever may require a population of 48,000 to support it permanently; the CCS of whooping cough was estimated at 106,000, and that of rubella at 151,000. Influenza is believed to require substantially larger populations than the other diseases, due to the instability of the influenza virus. For this disease the CCS may amount to several millions.12 These figures are estimates based upon circumstances found in modern cities or certain island communities. In practice, many factors can affect the CCS in a given population or region.13 For instance, the number of births required, and thus the base population, could be substantially less for "nonisolated urban areas" due to immigration of susceptibles from surrounding areas.14 Population density could also play a role in determining the threshold value, in that the number needed in a less densely settled area might be far less than in a similarly sized, but more densely populated, settlement. With fewer contacts between individuals in a dispersed community, the opportunities for a single infective person to pass on the disease would be less, slowing down the speed of diffusion and potentially prolonging an epidemic to the point where it failed to die out. More importantly, it is probable that another type of urban endemicity, a shared endemicity, could result from the regular communications between closely settled, smaller cities. The epidemiologist Francis Black concluded that, although measles cannot persist in a single pre-agricultural society, "it can sometimes spread from one community to another and thus extend its stay "15 Given large enough communities with frequent communications among these distinct populations, it is very possible that they could extend that stay indefinitely, acting as a communal disease pool for measles and other crowd diseases that circulate among them, even though no single community exceeds the CCS. Once established as fully endemic afflictions, these crowd diseases settle into a predictable pattern of infection within the urban disease pool. For most of the time they exist at a very low level of incidence, supported by new births and among children who are susceptible. In most cases, adults will have contracted these diseases in their youth and, for this reason, they are also known as diseases of childhood. Every few years, as the number of available susceptibles reaches a critical number, an epidemic will erupt.The period between these epidemics is regular if the population is a stable one,

INTRODUCTION and is dependent on the size of the community.16 The normal age of first exposure is influenced by social and cultural factors, such as the age at which a child enters the school system. Periodically, the diseases within the urban pools will spread outward among other populations. Therefore, it can be said that each pool has an urban disease frontier, a range within which its endemic afflictions may affect people beyond its immediate limits. In this way communities with numbers below the CCS share indirectly in the endemic status of the urban disease pool, or even of multiple disease pools. Depending upon the pool's interactions with the outside world, this frontier can extend to include peoples living on other continents, and can cross oceans or other significant obstacles. The distance of that frontier from the pool can change as conditions change, and is not the same for all diseases. A pool's disease frontier may encompass different groups within its boundaries, but the experiences of those groups with the crowd diseases may be very different. How a crowd disease affects a given group is, in large part, determined by the frequency of that group's contact with that disease. In turn, the frequency of such exposure is primarily a function of the nature of communications between these outlying groups and the disease pool. McNeill presented a basic but useful model describing the epidemiological relationship between an urban centre, which corresponds to the urban disease pool, and two categories of outlying populations: near populations, or what McNeill called the rural peasantry, and the more distant peripheral populations (Diagram I).17 Near populations live immediately beyond the urban centre, and are well connected to it by regular interaction. This provides frequent opportunities for the introduction of the full range of acute infectious diseases, which regularly erupt as mild epidemics affecting only the youngest portion of the population. Although the disease disappears between epidemics, this pattern is very similar to that experienced under endemic conditions. An example of the relationship between near populations and urban disease pools can be seen in the case of smallpox in eighteenth-century Britain. The disease was initially endemic only in London, but, by the mid-eighteenth century, was also constantly present in Glasgow and Edinburgh. In these major communities, smallpox flared up as epidemics every two to three years but was otherwise present in low levels. In the smaller towns smallpox was transient, and was only present in epidemic form. However, these epidemics occurred about every five years, a sufficient frequency to maintain smallpox as a disease of childhood despite the fact that the populations of these smaller towns were insufficient to maintain it

9

Diagram IrEpidemiological Relationship between Urban Disease Pool and Oudying Populations (Adapted from McNeill, "Historical Patterns," 95)

INTRODUCTION endemically.18 In this respect, their experience with smallpox was similar to that of communities with populations exceeding the endemic threshold. In contrast to the near populations are those peripheral to the urban centre (Diagram 1). For these people, communication is too irregular for crowd diseases to return with sufficient regularity to become childhood diseases. Instead, they reappear after longer intervals and are much more severe, affecting adults as well.19 In some cases, the geographical extent of the urban disease frontier could be immense, such that diseases carried from the pool could spread to peripheral peoples living thousands of miles away. For some extremely peripheral groups, several generations might pass before a disease such as smallpox or measles returned.Thus,for example, in Iceland, an island nation whose population fell well below the threshold for measles endemicity, measles outbreaks were extremely rare during the nineteenth century, with several decades passing between them.20 This was also the case for many Aboriginal groups in North America who, during the post-contact period, experienced crowd diseases only infrequently, and who suffered severely for their isolation. The degree of isolation or connection with the pool is not the only factor determining the frequency of epidemics, however.To a lesser extent, the size of the outlying population may also influence the timing of the return of an exogenous crowd disease, and thus its effect on a group. The English mathematician Maurice Bartlett identified three basic patterns of measles periodicity in British urban communities.21 Type I cities are those in which the population is sufficiently large to maintain measles as a disease of childhood (that is, it exceeds the CCS) (Diagram 2). Type II cities have a population less than that required for endemicity, but greater than about 10,000. When the possibility of measles introduction is constantly present, these cities will experience epidemics at regular intervals that match the rate of the larger, endemic, cities, but the disease will be absent during the inter-epidemic periods. Type III communities, or those with fewer than 10,000 people, will suffer periodic measles epidemics, but will miss some, since they may not have built up a sufficient supply of susceptibles to fuel an epidemic by the time the disease is reintroduced from an external source. In such cases the inter-epidemic gap may be significantly greater, with a corresponding rise in the average age of the victims. Nevertheless, even with the smallest of type III populations, it is unlikely that measles and the other crowd diseases would affect significant proportions of the adult population.

11

12

INTRODUCTION

Diagram 2: Relationship between Community Size and Periodicity of Measles Epidemics (After Cliff et al., Spatial Diffusion, 40)

Missing from McNeill's model of the relationships among urban centres and outlying populations, however, was a process component, the key concept that a population's status can be transformed as its situation changes. As changing conditions lessen the isolation between a peripheral population and an urban disease pool, the population may assume a new relationship with that pool, becoming a near population. This shift in status can be thought of as an epidemic transition.22 There are two basic characteristics of this transition. The first is that certain diseases return with increasing frequency and that, overall, crowd diseases become more common than before. If they appear often enough, they cease to be major epidemic diseases, and instead become diseases of childhood.23 The second characteristic is the presence of new afflictions. While isolation persists, the range of diseases is small and limited to those with an enhanced ability to diffuse, such as smallpox. As isolation declines, other sicknesses begin to appear in the community. Once the transition is complete, a wide range of crowd diseases will appear with some regularity. If the transition proceeds to its

INTRODUCTION completion, the result will eventually be a mutual toleration with limited mortalities as these diseases become those of childhood. However, until that balance is achieved, the increased frequency associated with this enhanced disease load will likely lead to a more severe experience with these repeated infections. There are several potential reasons for the decline in isolation that triggers this transition. • There may be greater numbers of people travelling between the pool and the outlying population, enhancing the opportunities for crowd diseases to survive a journey to the peripheral community. This is especially the case if there is a change in the nature of the movement to include greater numbers of children, who are much more likely to be susceptible to the crowd diseases. In the past, this has often occurred due to a shift from exploration to settlement phases of travel, particularly in those areas colonized from Europe. • Patterns of travel or migration may be altered, exposing new populations to exogenous diseases. Throughout history, changing migration patterns have resulted in the sudden appearance of new diseases. Likewise, new transport linkages may place the isolated region within the disease frontier of other pools or of multiple pools. • Faster methods of travel or improvements in communication may be introduced, reducing travel times. In turn, this simplifies the potential chain of infection, reducing the number of susceptibles needed to maintain the disease during the trip. Periodic transport innovations, such as steamships, trains, and jet aircraft, have been instrumental in facilitating the longdistance diffusion of crowd diseases into new areas by increasing the speed, volume, and range of travel.24 • New temporary pools may emerge within the disease frontier. The growth of new population centres that fall below endemic thresholds may have a significant effect on long-distance patterns of diffusion by creating temporary holding bodies for crowd disease, thereby acting as intermediate sources of infection. • A new pool or pools may emerge in closer proximity to the outlying population as other nearby communities grow and achieve endemic status in their own right, thereby creating a closer source of infection. Once again, we can turn to measles in Iceland as an example of this process. Andrew Cliff and his colleagues documented only two full-fledged measles epidemics for the island during the period between 1751 and 1900, and these caused considerable mortality. Between 1900 and 1945, the level of contact between Iceland and the outside world increased continuously, and

13

14

INTRODUCTION there were more epidemics, all of lesser mortality. This decline in the severity of measles in Iceland after the 1882 epidemic was attributed to the increased frequency of the disease. Following 1945, Iceland's relative epidemiological isolation disappeared, as both ship-based and air-based links increased significantly. Thereafter, measles epidemics occurred much more frequently, were less localized, and caused fewer deaths. Increasingly, the pattern of measles in Iceland came to resemble that found in the more densely populated parts of western Europe and eastern North America, although its total population remained below the endemic threshold. Iceland had experienced an epidemic transition and was no longer a peripheral population.25 There is considerable variation in the ability of crowd diseases to spread beyond their urban limits. In general, certain afflictions diffuse earlier, faster, and farther than those only able to travel short distances until circumstances change significantly. Some diseases will appear in an isolated, or peripheral, population that others are unable to reach. As communication between the pool and the periphery intensifies and becomes more regular, and as isolation decreases, new disorders will appear and earlier afflictions will return more frequently. Given sufficient decline in isolation of the population, the result will be the epidemic transition.The order and timing of the introduction of specific crowd diseases reflect a combination of local contact conditions and the ability of those diseases to spread. The measure of this ability to spread is known as diffusion potential. Anthropologist Ann Ramenofsky suggested that the diffusion potential of a particular disease varies with three factors: the length of the infectious period; the population density of the location and the surrounding region; and the contact mechanisms between communities or regions. Using the characteristic infectious period as a measure, she assigned a rank to several of the major epidemic diseases, dividing them into three classes (Table 2). By her classification, smallpox and whooping cough were the most proficient diffiisers, and colds and influenza were the least able. Such a ranking should also, she believed, indicate the order of introduction into a formerly isolated region. Thus, she said, "Parasites with longer periods of communicability were introduced [to the New World] earlier and resulted in extensive spatial waves."26 As conditions change and lessen that isolation, other diseases with lesser potential then appear. The concept of diffusion potential is a valuable one, although, in practice, Ramenofsky's system of classification requires refinement in order to explain fully the order of disease appearance in real-life situations. The infectious period of a disease is but one of many characteristics that would

INTRODUCTION

Table 2: Diffusion Potential of Selected Infectious Diseases (After Ramenofsky, Vectors of Death, 167)

determine its ability to diffuse. Disease attributes such as the individual immune response, incubation period, severity, and infectivity, among others, would also have to be considered in order to develop a system that can be used by researchers to predict the sequence and perhaps even the timing of exogenous disease introduction in a specific historical context. This system would also have to be tested against known disease records that provide data over a lengthy period of time to provide a more precise division. The Geographical Setting The Aboriginal people of the Americas did not all have the same experience with the diseases introduced from the Old World.27 Instead, there were wide variations in the timing and severity of the epidemics, often depending upon the location of the group or the sequence and intensity of contact with the Europeans. Consequently, detailed studies of specific Aboriginal groups or regions need to be undertaken in order to understand their particular disease experiences. This book will examine the epidemic history of one such region, the Petit Nord. The term Petit Nord, or Little North, was an informal regional designation employed first by the French fur traders, and later by the Montrealbased English and Scottish traders, to describe the large and valuable fur-trading country north of Lake Superior and east of Lake Winnipeg (Map 1). Roughly, the area was bordered on the north by Hudson and James bays, on the east by the divide between the Moose and Albany river drainage systems, and on the south by Lake Superior and the Boundary Waters that approximate the current US-Canada boundary between Lake Superior and Lake Winnipeg. The region was bounded on the west by Lake Winnipeg and the Hayes River system.Together with the Grand Nord, whose lands extended to the north and west of Lake Winnipeg, it formed part of the larger regional entity known as the Canadian Northwest.

15

16

INTRODUCTION

Map 1: The Petit Nord

The land once known as the Petit Nord is actually comprised of two very different physiographic regions. The northern third is part of the Hudson Bay lowlands, a large, flat, and swampy plain that is underlain by easily eroded sedimentary strata from the Paleozoic era. Although poorly drained, it is crossed by broad rivers with gentle gradients that flow long distances from the interior of the region to Hudson and James bays, dropping over fall lines as they emerge from the Canadian Shield. Among the most significant are the Albany, Severn, and Hayes rivers, and the Nelson and the Moose rivers flow into the two bays just beyond the region's borders. The dominant vegetation of the lowlands is muskeg and bog, but there is also a narrow strip of tundra running along much of the length of the coast. While researchers have long thought that the historical food resources of the lowlands were marginal and therefore insufficient to support Aboriginal people prior to the fur-trade period, recent archaeological evidence has demonstrated that this was not the case. Instead, people

INTRODUCTION inhabited the region long before contact, subsisting on seasonably available food resources, notably the extensive caribou herds, marine mammals, fish, and migratory birds. Nevertheless, during the historical period, population densities in the lowlands were considerably lower than those to the south.28 The remainder, and by far the greater extent, of the region was part of the Canadian Shield.This is an area of much older, erosion-resistant, igneous and metamorphic Precambrian rock, heavily modified by glacial action, a land broken by lakes, swamps, and rivers, and with low divides between watersheds that provided ready access to the interior of the Petit Nord by water but denied any long-distance overland travel. The dense, largely coniferous tree cover characteristic of the Shield also hindered overland travel during the fur-trade period.29 Instead, population movement throughout the year followed the streams, rivers, and lakes, with snowshoes and sleds replacing canoes during the winter.The major routeways into the interior of the region were via the Nipigon and Albany rivers, which connected with a complex network of interior waterways. The southern and western margins of the region were significant transport corridors that carried traffic beyond the Petit Nord, to the waterways of the Great Lakes in the east and to those of the Grand Nord in the west. The climate of the Petit Nord was, and is, predominantly continental, notable for its long, cold winters and short, relatively warm summers. The seasonal cycles affected all aspects of human life, including the availability of food, and played a role in determining the timing and patterns of epidemic diffusion. During the summer, travel by canoe was comparatively easy and the Aboriginal people tended to congregate in larger numbers along the shores of major lakes and other waterways where food was plentiful. As fall approached, the larger regional bands broke up into much smaller groups and began to leave for their winter quarters. Although deep snow and travel by foot made movement more difficult during the winter months, the camps were shifted to new hunting grounds periodically. Nevertheless, contact between winter bands or hunting groups was limited from the late fall to the early spring, hindering epidemic diffusion during this period. Movement proved impossible for a brief time during the freezeup and break-up periods (Map 2), and diseases introduced at these times would suffer delayed diffusion or might be stopped entirely. During the late spring and summer, the tendency towards agglomeration favoured the spread of infectious disease. The food resources of the Canadian Shield were richer than those of the Hudson Bay lowlands, and this was reflected in the relative densities of the human populations within the region. However, these resources were

17

Map 2: Freeze-up and Break-up in the Petit Nord (After Alwin, "Mode, Pattern, and Pulse," 31, 32)

INTRODUCTION not evenly distributed throughout the Shield—there was a general south to north gradient of decreasing density between the southern margins and Hudson Bay. These differences in population density affected the speed with which an epidemic could spread within the Petit Nord as well as the distance that it could penetrate into the region. For example, the Boundary Waters area provided an abundant selection of seasonably available foods, including big game, smaller animal species, waterfowl, berries, maple sugar, wild rice, and, especially, several varieties of fish. By the early nineteenth century, several groups in the region also planted crops for subsistence and trade purposes. The shores of Lake Superior afforded rich locations for fishing sites, particularly at Sault Ste. Marie, where large numbers of Aboriginal people gathered from all around during the seasonal runs. Gatherings in the Boundary Waters area at Rainy Lake and along the Rainy River were also conspicuous, where the fisheries supported groups of more than 1000. Such large gatherings were ideally suited to the spread of epidemic disease, both because they attracted people from far around, some of whom would be infective, and because they gathered susceptibles in a single location where they interacted socially with those who were infective. In the vast interior of the Petit Nord, however, group sizes were smaller and the people more dispersed than in the south. While big game, smaller species of animals, and waterfowl were available, this was beyond the range of maple sugar and wild rice, and fish were not available in the extraordinarily large runs found to the south. People in the interior spent much of the year in smaller hunting and fishing groups of between ten and thirty people. Even during the seasons when the food resources were most abundant, as in the summer, the concentrations of people were much smaller than in the south, numbering at the most 200 to 300 people. In turn, this meant that it was more difficult for acute infectious diseases to penetrate into the interior of the region, where population densities were much lower, compared to its southern flank. Finally, there were additional layers of complexity to this pattern of human geography in the Petit Nord that helped to favour or hinder the spread of epidemic disease in the region. The likelihood that a disease would be passed between neighbouring Aboriginal peoples within the region was by no means universal, and varied with a number of different factors beyond the season and the ecological environment they inhabited. While familial, political, and economic ties among some groups favoured diffusion in certain directions, there were also buffer zones, and even outright hostilities, between some bands that tended to hinder the progress of epidemics in others. Superimposed on this were the movements of the fur trade and the

19

20

INTRODUCTION less predictable presence of other non-Aboriginal people. Moreover, these complex patterns of human interaction within the region changed regularly throughout the study period, further complicating our attempts to understand and to explain epidemic diffusion within the Petit Nord.

1

Old World Disease Transmission Patterns

THE ISOLATION THAT HAD LONG PROTECTED THE NEW WORLD from the diseases of the Old World shattered with the coming of the Europeans in the late fifteenth century. Within two decades of Columbus's arrival on the island of Hispaniola, crowd diseases began to appear in continental North America.1 The historical period did not begin in the Petit Nord until a century and a half later. In-between lay a long period of uncertainty during which exogenous, or external, influences, including epidemics, may have made their way to the region. Although the fate of the people of the Petit Nord during this obscure era must remain a mystery in the absence of any direct evidence, we can still examine the changing conditions that favoured or, conversely, would have hindered such protohistoric diffusion. In turn, this period set the stage for the centuries that followed. Mesoamerica: A Southern Disease Pool In late 1518 or early 1519, smallpox arrived at Santo Domingo, the administrative centre of New Spain, situated in what is now the Dominican

22

CHAPTER ONE Republic. By 1520 this sickness had made its appearance in Mexico, ushering in a new era of disease in North America. The number of victims taken by this first epidemic is unknown, but undoubtedly the mortalities were staggering.2 It was, however, only the beginning. Thereafter, Old World diseases were an increasingly frequent threat in Mexico, Central America, and the northern part of South America, as large numbers of susceptibles made the trip across the Atlantic. In part, these susceptibles came from the ranks of the Spanish settlers, clerics, and adventurers who sought their future in the bounty of the New World. From an epidemiological perspective, though, more important were the large numbers of slaves who were brought from Africa each year to the Spanish colonies, people who by virtue of their origins were far less likely to have been exposed to the afflictions of large urban civilizations than the adult Europeans. Once this migration began in earnest, such diseases became relatively common in Mesoamerica, despite attempts at quarantine. With the Spanish penchant for establishing urban centres and the growth of communication systems between these settlements, these diseases spread wider and stayed for longer periods of time.3 This pattern of frequent introductions from external sources of disease was repeated wherever the Spanish established bases of operation in the New World. For instance, at least twenty-five localized and eight widespread epidemics occurred in Guatemala between 1519-20 and 1632. Likewise, epidemics appear to have been common in Ecuador during the sixteenth century. In the more densely populated parts of New Spain, some of these afflictions became diseases of childhood. During the sixteenth century, epidemics of smallpox and measles occurred about every ten years in the city of Quito (Ecuador), or slightly less frequently than under endemic conditions, and severe epidemics struck central Mexico repeatedly during that same century, only to emerge as endemic threats, thereafter flaring up as outbreaks affecting mainly the young.4 The repeated reintroduction of afflictions from Europe and elsewhere and their circulation through colonial Spanish territories, combined with the eventual shift to endemicity in some more populous areas, meant that Mesoamerica soon developed into a potent disease pool. Once established, this pool carried the potential to infect the entire hemisphere. What is unclear (and an important question for the study of Old World disease in the northern part of North America) is the spatial extent of this Mesoamerican pool's disease frontier, and the degree to which the early epidemics spread during the sixteenth century. In the controversial view of anthropologist Henry Dobyns, this frontier extended far to the north and south. The initial 1520 smallpox epidemic, he argued, diffused across the

OLD WORLD DISEASE TRANSMISSION present US from its entry point in Mexico, and "through all of the most densely populated portions of the Americas," probably reaching "the no man's land between Indians and Inuit."5 Moreover, he believed that subsequent disease introductions to the south continued to flow far to the north during the following century, as there emerged a system of diffusion that carried epidemic disease from Florida northward to the peoples of New England, before heading inland to the Iroquois tribes of the Great Lakes. In his view, "the entire Atlantic coastal region from Florida to the [Great] lakes and New England ... constituted what may be termed one 'epidemic region.'" Once introduced within this system, any epidemic disease was liable to spread throughout by way of Aboriginal movements and connections, far outstripping the direct influence of the Europeans.6 Given his conviction in the spread of pandemics from Mesoamerica to Florida during the sixteenth century, such a system would have had enormous consequences for the people of the Great Lakes and, therefore, for those of the Petit Nord. Dobyns's argument is derived more from faith than epidemiological principals, however. The northern limit of the 1520 epidemic, so authoritatively stated, is based simply on his rather spurious assumption that the epidemic had to have spread as far north as it did south, a principal of uniformity almost certainly unwarranted. Setting aside the problematic nature of the evidence for the southern extent of diffusion, this assumption ignores any differences in Aboriginal population density or interactions between the area south of Mexico and that to the north, as well as the effect of chance, nor does it account for any buffer zones between tribes that would have stymied the northward diffusion over long distances. According to epidemiologist Stephen Kunitz, this constituted an example of the danger of "inappropriate extrapolation from cases that we understand, to cases about which we know little or nothing."7 The evidence for the "epidemic system" running between Florida, New England, and the Great Lakes is far from conclusive and has been contested by other, more circumspect, researchers. It rests largely upon a tenuous connection within a speculative inventory of protohistoric epidemics among the Aboriginal people of Florida, a statement from the 1630s that the Narragansett people of New England had experienced earlier epidemics in conjunction with a series of earthquakes, and archaeological evidence of settlement shifts by the Seneca, an Iroquoian tribe living in what is now New York State. The Florida epidemic inventory has been questioned by several scholars, especially as it relates to Dobyns's use of evidence,8 but even so, the possibility that early epidemics spread to the New England

23

24

CHAPTER ONE tribes and the Iroquois, groups with whom the Aboriginal peoples of the Petit Nord had either direct or indirect communication, is of considerable importance. Few data support possible sixteenth-century epidemics among the New England and other Atlantic coastal tribes. The strongest is testimony collected by settler Roger Williams in the late 1630s and attributed to the Narragansett. According to Williams's informants, they had been struck by four earthquakes, in about 1568,1574,1584, and 1592, and each was associated with an epidemic. None of these diseases was described or identified. By adjusting the dates, Dobyns suggested that three of these were part of pandemics that spread from Florida. Anthropologists Dean Snow and Kim Lanphear presented evidence suggesting that the Aboriginal people of New England remained numerous until a devastating epidemic struck them early in the seventeenth century. The fact that Dobyns failed to consider the possibility that these epidemics were of diseases that were aboriginal to the Americas is also a significant limitation to his conclusions.9 In the end, although interesting, this testimony does little to clarify the case for the existence of widespread epidemic disease in this area during the sixteenth century. Research conducted on the nations living farther into the interior of North America also fails to lend support to Dobyns s theory. Snow and William Starna, who undertook archaeological work in the Mohawk Valley of New York, concluded that "the Mohawk nation was not significantly affected by epidemics prior to 1633." Likewise, another anthropologist, Bruce Trigger, who has done much to clarify the ethnohistory of the nearby Huron, could find no evidence of epidemics among these people prior to the seventeenth century, despite the penetration of European trade goods into southern Ontario as early as the 1530s.10 The case of the Huron is significant for two reasons. The first is that these people provided much information about themselves to the Jesuit priests and French explorers, but never mentioned that they had been decimated by epidemic disease prior to the 1630s.The other is that the Huron were closely linked by trade to the people of Lake Superior, and so evidence of early epidemics among them might suggest similar afflictions within the Petit Nord. Dobyns s own evidence for sixteenth-century pandemics affecting the Seneca of New York State is far from compelling. He equated signs of village abandonment and subsequent resettlement by the Seneca with the presence of Old World disease. Drawing upon published archaeological studies, he theorized that these relocations were the result of a succession of severe epidemics, and attempted to link them to his pandemic chronology.

OLD WORLD DISEASE TRANSMISSION However, such movements occurred for many other reasons among nearby groups, such as the Mohawk and the Huron, and no precise date can be assigned to these relocations, rendering it impossible to correlate them with supposed epidemics. Moreover, village abandonment occurred prior to the arrival of Columbus, and so cannot simply be assumed to have been a response to the introduction of Old World disease.11 More intriguing is a single description of what appears to have been a more localized outbreak of some unidentified and deadly disease. In the winter of 1535-36, the St. Lawrence, or Laurentian, Iroquois who lived at Stadacona suffered from an unknown but mortal disorder. According to Jacques Carder, "In the month of December we received warning that the pestilence [la mortalite\ had been out among the people of Stadacona to such an extent, that already, by their own confession, more than fifty persons were dead. Upon this we forbade them to come either to the fort or about us. But notwithstanding we had driven them away, the sickness broke out among us accompanied by most marvellous and extraordinary symptoms...."12 Citing this passage, Dobyns claimed that the French had given some sickness to the Stadaconans, even though the original text suggests the opposite.13 Moreover, he tried to connect this episode with the subsequent disappearance of the St. Lawrence Iroquois, who vacated the valley between 1542 and 1603. He stated that "the disappearance of the Laurentian Iroquois implies either that the 1535 epidemic so weakened them that they migrated not long after Cartier sailed for France, or that later sixteenth-century disease so weakened them that they moved from the river valley...."14 Once again,Dobyns ignored many more satisfactory explanations for the disappearance of the St. Lawrence Iroquois, including warfare, land exhaustion, climatic pressure, and cultural practices, to focus on the single interpretation that matched his overriding theory, that of Old World disease, no matter how improbable.15 Had there been massive protohistoric pandemics among the people of northern North America during the sixteenth century, it is likely they would have left some clear indication in the archaeological record. However, the crowd diseases do not generally leave direct paleopathological evidence in the skeletons of their victims, and so researchers have instead had to work with indirect indicators of sudden population decline. Using such indicators, Ann Ramenofsky attempted to verify the presence of protohistoric Old World epidemics among three different Aboriginal populations, including the Iroquois of NewYork State and the village tribes of the upper Missouri River (her "Middle Missouri").16 Her analysis confirmed the impact of the seventeenth-century afflictions among the

25

26

CHAPTER ONE Iroquois, epidemics that are documented in the historical record, but no evidence suggested that such epidemics also occurred during the previous century.The archaeological record among the village tribes was ambiguous regarding sixteenth-century episodes, but indicated population decline during the mid- to late seventeenth century. By that time, Old World diseases had been present in the east for several decades, and by mid-century critical disruptions to the eastern Aboriginal groups caused by the fall of Huronia may have fostered the westward diffusion of epidemic disease. This conclusion is not inconsistent with epidemics spreading from the east, rather than from Mesoamerica. Another anthropologist, Sarah Campbell, also attempted to obtain evidence of early protohistoric epidemics in North America, this time among the people of the Northern Columbia Plateau in the Pacific Northwest.Turning once again to the archaeological record, she concluded that the indirect archaeological indicators she had examined pointed to a massive population decline in 1520, followed by a period of continuous population recovery until the late eighteenth century.17 Although these conclusions seem to lend credence to Dobyns's theory of sixteenth-century continental pandemics, David Henige of the University of Wisconsin has identified several fundamental errors in Campbell's analysis. Not the least of these was the fact that her data showed an even greater population loss between 1375 and 1425, or long before the arrival of Columbus, a loss she didn't address.18 Here, then, as elsewhere in northern North America, there is no clear and reliable archaeological evidence for the extension of hemispheric pandemics from Mesoamerica during the sixteenth century. Finally, although it is by no means definitive, some evidence suggests that Old World diseases did not appear so early among at least one of the peoples living west of Lake Superior. Oral testimony by the Ankara living on the upper Missouri indicates that one crowd disease, smallpox, was a very rare visitor among them up to the late eighteenth century. In 1794-95 the fur trader Jean Baptiste Truteau travelled to the Ankara, who informed him that they had suffered from smallpox epidemics on three occasions prior to that time. One of these was the smallpox epidemic of 1779 to 1783 that devastated many of the plains groups, including the Arikara, and the two others were likely epidemics of smallpox or a smallpox-like disease that struck the Arikara in the 1730s and the early 1750s.19 For these people, at least, there is no reason to suspect that the afflictions that circulated within the disease pool of Mesoamerica from the early sixteenth century were making their way far north prior to the eighteenth century.

OLD WORLD DISEASE TRANSMISSION An Eastern Source: European Settlement on the North Atlantic Coast The situation was far different along the Atlantic coast, in what is now the northeastern United States and eastern Canada, than in Mesoamerica. Here, settlement lagged far behind the rich lands of Spanish America, and the mass migrations that made possible the import of crowd diseases waited until the early seventeenth century. Earlier European activities in the region had been limited to exploration, fishing, and the establishment of a few small settlements of little duration, with a small amount of trading with the Aboriginal people.20 The epidemiological impact of these early activities has sparked a vigorous debate among scholars. Some have concluded that contacts between the Aboriginal people and untold numbers of fishermen, explorers, and traders must have led, at the very least, to repeated localized epidemics of Old World diseases, perhaps as early as the 1480s.21 Others have been more cautious. Citing the logistics of trans-oceanic disease diffusion during that period, Dean Snow concluded that it is unlikely crowd diseases were introduced to New England prior to the seventeenth century.The early crews were too small (and included too few susceptibles), he argued, and the pre-1600 voyages too lengthy, to enable a crowd disease to survive the crossing.22 Both arguments have some validity, and are not necessarily contradictory. The limitations cited by Snow suggest that the situation was very much against the direct importation of childhood diseases, such as smallpox and measles, from Europe to northeastern North America prior to the seventeenth century, diseases that were to emerge as the most destructive to the Aboriginal people. On the other hand, we cannot rule out the possibility that the Europeans introduced chronic or vectored afflictions, or that even acute infections such as influenza or colds arrived in this manner.23 These were by no means mild diseases and some were clearly capable of taking a great toll in human life. Even so, there is almost no direct evidence to suggest that Old World crowd diseases were ravaging the Aboriginal people of northeastern North America prior to the seventeenth century. As we have seen, the archaeological record provides no support for these early epidemics, while the written record is little more forthcoming. One oft-cited statement by a Jesuit missionary, Father Pierre Biard, has been interpreted to suggest that acute infectious diseases were being passed from an early date. In 1616 he noted that the Micmac "are astonished and often complain that, since the French mingle with and carry on trade with them, they are dying fast, and

27

28

CHAPTER ONE the population is thinning out. For they assert that, before this association and intercourse, all their countries were very populous, and they tell how one by one the different coasts, according as they have begun to traffic with us, have been more reduced by disease."24 Dobyns offered this passage in support of the direct introduction of contagious disorders by European sailors and traders during the sixteenth century, disorders, he argued, that subsequently spread to the people of the "Great Lakes-Laurentian cultural area."25 Conversely, Virginia Miller, a student of the early population history of the Micmac, came up with a different interpretation of this passage. In her view, growing reliance on European foodstuffs, which were often spoiled, and overindulgence in alcohol led to severe population decline among the Micmac.26 Indeed, the afflictions reported among these people (dysentery, lung, chest, and intestinal diseases) may have been related to dietary change, chronic infections introduced by the Europeans, or indigenous disease exacerbated by nutritional problems. In any event, the fact that the Micmac suffered such mortality only after experiencing direct and sustained contact with the French argues strongly against the presence of waves of epidemics sweeping into the interior prior to direct contact with the Europeans. Instead, the era of Old World diseases in the northeastern part of North America began in the seventeenth century, an era that was initiated by the coincidence of improved transport technology and changing patterns of settlement. After 1600, the length of a voyage from Europe was shortened from an average of six weeks to four, and this change proved significant to the survival of acute diseases. Moreover, as the century progressed, everincreasing numbers of Europeans began to settle in newly founded colonies along the north Atlantic coast.27 This migration was especially pronounced following the establishment of Plymouth in 1620 as part of the Massachusetts Bay Colony. From a base population of only 900 in 1630, the colony had swollen to over 9000 by 1640.Thus, during the 1630s, there began a mass migration into New England, including large numbers of children, who served ably as a vehicle for the transportation of crowd diseases from the outset.28 Similar growth occurred in New France and New Netherland as well as in the other English colonies, leading to the importation of infectious diseases. By 1663 there were about 25,000 people of European descent in Canada, and 5000 arrived over the next three decades.29 At the same time, slave ships also became a significant factor in the introduction of disease to the English colonies, as they had long been in Mesoamerica. These changes led directly to an era of unprecedented epidemic activity in northeastern North America, which, to the detriment

OLD WORLD DISEASE TRANSMISSION of the Aboriginal people, had become intimately connected with the disease pools of the Old World. Despite their rapid growth, these colonies were nowhere near large enough to emerge as pools in their own right during the seventeenth century. By the end of the century, the two largest, Massachusetts and Virginia, had populations less than 60,000 each, falling far short of the lower limits for endemicity for most crowd diseases. Unlike in Mesoamerica, these afflictions did not become endemic in the northeastern colonies until, at the very least, late in the eighteenth century, perhaps a century and a half after their initial introduction. Rather, each epidemic began with the arrival of a ship carrying disease from an external source, from Europe, Africa, or the West Indies, coming either directly from major disease pools or places in close contact with those pools. Infectious disease was commonplace on these early transatlantic voyages, and while typhus, typhoid, and dysentery were probably the greatest threats, smallpox, measles, and other crowd diseases were also frequently present. Because of the key role played by these ships in the introduction of Old World diseases, main ports including Boston, New York, Quebec, and Charleston were vulnerable to repeated outbreaks of Old World epidemics.30 This situation accelerated during the eighteenth century, as further decreases in sailing times, larger numbers of ships making the crossing, and a greater population density combined to significantly increase the frequency of epidemics (Map 3). Boston and the other ports did not exist as discrete disease centres, however. Instead, the entire region soon emerged as a kind of disease system. From an early date, epidemics raced back and forth between the colonies. For example, in 1634 smallpox passed from the Dutch to the English, and in 1646 an influenza epidemic appeared among the French, Dutch, and English. A smallpox epidemic in Boston in 1666 may have come from Canada. Measles appears to have spread from Quebec to New England in 1687-88. Other diseases spread from the English to Canada, a pattern that seems to have been more common.31 Often, it was the Aboriginal people who served as middlemen in the diffusion between colonies, especially between the French and English. Such inter-colonial diffusion extended the stay of crowd diseases in the broader region, long after they would otherwise have died out. By the end of the seventeenth century, the total population in the American colonies amounted to perhaps 250,000. Another 2000 lived in Quebec and 1500 in Montreal, and 10,000 Canadians lived on farms along the St. Lawrence.32 Although crowd diseases were not endemic in northeastern North America at this time, the region nonetheless served as a temporary pool in which

29

Map 3: Smallpox and Measles Epidemics in Boston, 1640-1800 (After Caufield, "Early Measles Epidemics," 552-553; Duffy, Epidemics in Colonial America, 36; Currie, Historical Account, 36; Lemon, "Colonial America," 122; Mitchell, "Colonial Origins," 104)

OLD WORLD DISEASE TRANSMISSION the diseases of more densely settled communities circulated prior to diffusion to the limits of the disease frontier. Thus, between 1675 and 1775, smallpox disappeared from colonial America for as long as five years only twice, and only once was it absent from the middle colonies (New Jersey, New York, and Pennsylvania) for a ten-year span.33 Critically, this continual circulation also meant these illnesses were carried from communities with strong external (to North America) connections, but where there was less contact with the Aboriginal people, such as Boston, to frontier communities where the interaction between Whites and Aboriginals was routine. This made it more likely they would find a suitable mechanism of transport into the interior. More often than not, during the first half of the seventeenth century, this meant diffusion through Aboriginal movements and contacts. Although missionaries, traders, and soldiers have shouldered much of the blame, more significant as a vehicle for the westward spread of disease was the large number of Aboriginal people who visited places like Quebec, Fort Orange (Albany, New York), Trois Rivieres, and Montreal for trade or political negotiations. Certainly this was the case for the earliest round of epidemics in Canada during the 1630s, when parties from the interior carried smallpox and other crowd diseases from the east towards the upper Great Lakes or died in the vicinity of the French settlements.34 In this way, afflictions endemic in distant pools were carried ever closer to the Petit Nord. The threat posed to the Petit Nord by these eastern settlements was not uniform throughout the seventeenth century. Between 1600 and about 1630, epidemic activity appears to have been limited in northeastern North America.Thereafter, it increased substantially, and epidemics began to spread far into the interior from the coastal colonies, arriving at least on the doorstep of the Petit Nord. For the most part, these contagions followed longestablished lines of communication until 1649. In that year the Iroquois destroyed their Huron rivals. A period of massive disruption and dislocation of Aboriginal populations followed, as well as fundamental shifts in the patterns of their movements. These greatly affected at least the patterns of diffusion into the interior, if not also the frequency of these epidemics. There is very little evidence for epidemics in either the Atlantic coastal area or in the interior between 1600 and about 1630, perhaps due in part to a lack of documentary evidence. It is also probable that Old World diseases were extremely rare in this part of North America at this time. The first widespread epidemic in northeastern North America occurred along the coast of New England between 1616 and approximately 1619, but failed to spread far inland, being limited to parts of present-day Massachusetts,

31

32

CHAPTER ONE Maine, and Rhode Island. This devastating episode caused extremely high levels of mortality. It has never been identified conclusively, but bubonic plague is perhaps most likely.35 Two smaller outbreaks occurred in the interior, not too distant from the Petit Nord. In 1611 many Algonquin perished due to an undifFerentiated fever. At this time the Algonquin lived along the Ottawa and upper St. Lawrence rivers. Twelve years later, many of the Weskerini, an Algonquian-speaking group who lived just below Allumettes Island on the Ottawa River, died of disease and hunger. However, there is nothing to suggest that either outbreak was of an Old World disease.36 A new era of epidemic activity began in the northeastern part of the continent following 1630.Thereafter, Old World diseases routinely appeared in the eastern colonies and often spread among the Aboriginal people. Of particular concern is a series of four epidemics that devastated the east between 1634 and 1639, epidemics that spread at least as far west as Georgian Bay on Lake Huron. In 1634-35 an unidentified rash-producing disease spread westward through the St. Lawrence and Ottawa river valleys, probably by the movement of Aboriginal traders.37 Whether it was smallpox that had been introduced by the English or, perhaps more likely, measles that had been brought by the ships from France, the epidemic reached the Huron during the summer. Two years later, in the fall of 1636, the Huron were again attacked, this time by a much more severe epidemic of influenza that, once again, had spread from the St. Lawrence.38 It was also carried by the Nipissing people into northern Ontario. In the summer of 1637 another unidentified epidemic, possibly scarlet fever, reached the Huron.39This time, the disease seems to have come from the Susquehannock, who lived near the Dutch settlements. It reached the Huron by way of the Wenro, who lived to the south and who traded with the Susquehannock, and it also diffused along the Ottawa River. Finally, in 1639 a virulent smallpox epidemic spread throughout the St. Lawrence valley, killing the people who travelled to Trois Rivieres and Quebec to trade, and devastating the Huron and other eastern groups.40 Its origin is not clear. The epidemic either came to Canada from New England by way of some Algonquin who had gone to visit the Abenaki, or it had been introduced to Quebec by French ships, and had subsequently spread westward along the St. Lawrence. In either case, the disease was brought among the Huron by some of their people returning from Quebec. The presence of these diseases among the Aboriginal people of the Ottawa and St. Lawrence rivers and, especially, the Huron, threatened the people of the Petit Nord. During the first half of the seventeenth century, this region was connected to the east through important, long-standing

OLD WORLD DISEASE TRANSMISSION trading networks. Each year the Huron travelled east to the Canadian settlements with furs from the upper Great Lakes to exchange for European goods. They had obtained these furs (and other commodities) largely by acting as middlemen for the more distant tribes, including those of Lake Superior. The key to this trade was a transportation backbone that ran along the Ottawa and St. Lawrence rivers. In turn, two of the Huron's main trading partners, the Ottawa and the Nipissing, were engaged in a more distant trade of their own. The Ottawa also traded with the groups living on Lake Superior, while the Nipissing made annual trips to James Bay to trade among the northern peoples. At the same time, James Bay was linked to the lower part of the St. Lawrence via other commonly used trading routes that ran between the Saguenay and Rupert rivers.Thus, Aboriginal trading routes connected the eastern part of the Petit Nord to areas that were then experiencing the ravages of epidemic Old World disease. There is a very real possibility that one or more of these epidemics reached the Petit Nord. Historical geographer Conrad Heidenreich concluded that two, the influenza of 1636 and the smallpox of 1639, spread from the Ottawa River to the Moose River area of James Bay, just to the east of the Petit Nord. He also speculated that the same 1639 epidemic and the unidentified illness of 1637 might have diffused into the Lake Superior area, after having reached Georgian Bay on Lake Huron. Trigger believed that at least one of these epidemics spread to the Winnebago, who then resided at Green Bay on Lake Michigan.These would have followed wellestablished pathways of Aboriginal communication, pathways closely connected with lines of movement into the Petit Nord. Thus, the first documented round of epidemics to spread into the interior of the northern part of North America may also have diffused into the Petit Nord.41 Epidemics continued to occur periodically in the east between 1650 and 1669, and some seem to have penetrated at least partly into the interior of the continent.42 By then, however, widespread disruptions had befallen many of the Aboriginal groups of the Great Lakes area, greatly altering potential pathways of diffusion. In 1649 the Huron were attacked and dispersed by the Iroquois, and many of the survivors headed westward. This event set about a sequence of relocations in which many of the eastern groups fled to escape the wrath of the Iroquois, emptying southern Ontario. The nearby Petun were scattered in 1649-50 and retreated, first to Lake Michigan and later to Chequamegon on Lake Superior. The Algonquian-speaking groups of the Upper Country also withdrew, including those of the Georgian Bay area and the Ottawa River. Among them were the Ottawa and the Nipissing, many of whom ended up at

33

34

CHAPTER ONE Chequamegon and Lake Nipigon, respectively. Others fled northward to James Bay. As more and more people travelled into the area to the north and west of Lake Michigan, large refugee villages emerged of mixed affiliation, including key communities along the shores of Lake Superior. These villages proved vulnerable to the ravages of the Old World diseases, and no doubt the flood of people travelling from the east posed a significant risk for the spread of such disease. With the Huron and other eastern groups dispersed, the Iroquois pursued their raids over even greater distances, including into the Petit Nord.43 These raids had a significant impact on the patterns of movement in eastern North America. For many years following the fall of Huronia, the Iroquois made the Ottawa River valley a dangerous route for the people of the upper Great Lakes. Consequently, trade was directed along routes that avoided the Ottawa, particularly along those that were connected to James Bay, for they bypassed the most dangerous areas. In 1657 Father Gabriel Druillettes learned of the existence of five, major, Aboriginal routes of travel leading from the south to James Bay (Map 4).44 One began at the lower St. Lawrence, nearTadoussac, and included the Saguenay River, Lake Mistassini, and the Rupert River. Another ran from near Trois Rivieres along the St. Maurice to the Nottaway River. Three others involved systems far to the west. A traditional route of the Nipissing followed the Ottawa River and Lake Temiscaming to Abitibi Lake. From there, they proceeded by the Abitibi River, which flows into James Bay. A fourth ran between the Spanish River, emptying into Lake Huron at Georgian Bay, and the Matagami River. Finally, Lake Nipigon and the Albany River connected Lake Superior to James Bay.The result was bilateral traffic that enabled furs from the interior to be exchanged for European goods from Canada with far less risk of plunder by the Iroquois. Although the Ottawa RiverSt. Lawrence River route was lightly travelled at this time, if at all, the Petit Nord nonetheless remained well connected to the east, a crucial source of epidemic disease. Consequently, Old World infections that spread from Canada into the interior with Aboriginal traders still stood a good chance of being directed towards James Bay, and the eastern margins of the Petit Nord.

Map 4: Seventeenth-Century Trade Routes in Northeastern North America

36

CHAPTER ONE Exploration into Hudson Bay The potential threat of epidemic disease spreading to the Petit Nord came not only from the east and the south during the protohistoric period. For a few decades at least, there was also the possibility of Old World sicknesses arriving from the north. Between 1610 and 1632, several exploration expeditions originating in Europe entered Hudson and James bays. Henry Hudson is credited with having led the first European expedition to this region, having explored both bodies of water in 1610 before a mutiny on June 22, 1611, in which the famed explorer and a small party were set adrift and left to die. Thomas Button (1612-13) soon followed, as did Jens Munk (1619-20), Luke Foxe (1631), and Thomas James (1631-32).Thereafter, however, such voyages seem to have ceased until the arrival of the Nonsuch in 1668.45 In theory, each ship that sailed to Hudson Bay was an epidemic threat to the Petit Nord. We have already seen, for instance, that the European ships were quite capable of introducing OldWorld disease elsewhere in the hemisphere. We know, too, that the English mariners of the seventeenth century suffered from a wide variety of medical complaints, including some infectious diseases.46 Indeed, some of the exploring crews suffered illnesses at this time, so they might have inadvertently passed on an OldWorld disease to the Aboriginal people of Hudson Bay or James Bay. In practice, however, such cross-oceanic transfers probably didn't occur until much later. The presence of an active host on board a ship, if indeed there were any aboard these few ships, was not enough. It was also necessary that the infected individuals interact with Aboriginal people. Although several of the exploring parties spent the winter at the bay, there was almost no such contact at this time.47 Without contact, obviously, there could be no transfer. Instead, these factors only fell into place after the arrival of the HBC later in the century, which ushered in the historical period in the region.

2 The Early Historical Period in the Petit Nord: 1670-1837

A LACK OF DATA CONSTITUTES A SIGNIFICANT LIMITATION TO THE study of historical epidemiology. Without descriptions of some kind, whether written or oral, it is impossible to know what, if any, epidemics occurred in a region or among a people, or how frequently they arose.This was the case with the Petit Nord for most of the seventeenth century. Despite growing epidemic activity in the east, we cannot know if any of the Old World diseases made their way that far into the interior of the continent. Towards the end of the century, however, non-Aboriginal explorers, traders, and missionaries began to arrive in the Petit Nord in ever-increasing numbers, gradually ushering in the historical period in the region. This began in 1670 as the HBC commenced its long tenure in the Canadian Northwest. With the firm's penchant for maintaining detailed records, and the French penetrating into the region in answer to the English competition, the protohistoric period gradually gave way to the historical. It is only then that we begin to have a glimpse of events that earlier would have gone unrecorded, including direct observations of epidemic activity in the Petit Nord.

38

CHAPTER Two At the same time, the very presence of the HBC in the Petit Nord proved crucial to the region's epidemic history for another reason. The founding of the company set in motion changes to the fur trade that had a profound effect on the patterns of movement of the Aboriginal people and on their connections with the European settlements of the east. In turn, these structural changes enhanced the possibility of disease diffusion into the Petit Nord by increasing the frequency of contact between the Aboriginals and the traders travelling from the eastern settlements, the source of much of the region's later epidemic activity. To a lesser extent, the founding also enhanced the possibility of exposure to afflictions brought directly from Europe, through the company's transport system.With these changes, the Petit Nord became firmly established within the periphery of distant disease pools. The Founding of the HBC: The Historical Period Begins In 1668 an English ship, the Nonsuch, sailed to Rupert River on James Bay, where the men erected Charles Fort. Before their departure for England the following August, they traded furs with approximately 300 Aboriginal people.This successful enterprise led to a royal charter for the HBC in May of 1670, and a second expedition was dispatched in that year. From then on, the company was a near-constant presence in the Hudson Bay drainage basin and beyond, and within fifteen years had settled forts at the mouths of the Rupert, Moose, Severn, Albany, and Nelson rivers. With few exceptions over the next 180 years, supply ships were dispatched annually from England. These events had a considerable impact on the disease load of the Petit Nord. The presence of the HBC men and the annual contact with England did not, as one might anticipate, of itself lead to a wholesale and immediate increase in epidemics in the Petit Nord. Rather, the HBC played only a limited role in introducing Old World diseases into the region prior to 1737, when compared to continental sources of disease. This was owing to the nature of these sicknesses and of the HBC's maritime transport system. Although the trans-oceanic route appeared ideal for the transmission of epidemic disease from the pools of Europe to the periphery of the Petit Nord, significant factors worked against its being the source of most of the major crowd diseases.1 During this era, the HBC ships typically began their passage in London, departing for the port of Stromness in the Orkney Islands some time between mid-May and early June (Map 5). By the time of the founding of the HBC,

Map 5:The Voyage to Hudson Bay (After Catchpole,"Ships'Log-Books")

40

CHAPTER Two London was a cosmopolitan and populous city, and a potent and constant source of infectious disease for surrounding communities. Many diseases were endemic, and those that were not might be introduced from elsewhere by the constant ship traffic. The population of the city on the eve of the HBC's first voyages was almost one-half million, sufficient to maintain most, if not all, crowd diseases endemically. For instance, by this time smallpox had settled down into a "steady prevalence from year to year," although it was not exclusively a disease of childhood.2 It was, however, a prime example of an urban disease pool. After a journey of four to seven days, the HBC ships arrived at Stromness, in the Orkney Islands. The brief layover there of between three and seven days was significant as, in addition to ballast and water, the ships took on new employees bound for Hudson Bay. In theory, these additional men could provide a new reservoir to maintain an acute infectious disease on the journey to Hudson Bay. In practice, this was a very rare occurrence, however. The second phase of the journey, the voyage across the Atlantic, limited the importation of acute infectious diseases to Hudson Bay via the company ships. The journey from Europe was long, crews were small, and no families accompanied them. Acute diseases are of brief duration and many provide the survivor with lasting immunity. As such, the longer the voyage, the less likely that the disease will be passed on at the destination, since at some point the ailment will have run its course among all susceptibles on board. If the transit period is decreased substantially, however, the number of consecutive cases needed to maintain the disease, expressed in generations of the disease,3 will be reduced.This, according to Snow and Lanphear, was the main reason for the sudden emergence of epidemic disease in New England after 1600, when the voyage had been reduced from an average of six weeks to about four. Geographer Peter Haggett offered a similar explanation in examining the introduction of smallpox, measles, influenza, and rubella to Australia, New Zealand, and the southwest Pacific. Again, decreases in the trip length led directly to the introduction of "new" diseases. Compared to the voyages to New England, the journey to Hudson Bay remained of long duration during the entire eighteenth century. An analysis of the travel times from their final departure point in the British Isles to the first landing at the HBC posts during the period from 1719 to 1737 reveals a mean duration of just over sixty-seven days, or of more than seven weeks. Of thirty-two voyages during this period, only two lasted less than fifty days, both in 1731, when the journey was made in forty-six days. Even the most rapid of voyages during this period was significantly

EARLY HISTORICAL PERIOD: 1670-1837 longer than the four-week voyages to the Atlantic seaboard that facilitated the spread of disease to that region in the early seventeenth century.4 The small potential reservoir to support the afflictions during the voyage was also a limiting factor. The HBC ships sailing to Hudson Bay were small and carried few passengers and crew, compared to the large colony ships sailing to the Atlantic coastal colonies or to the Pacific countries studied by Haggett. The crews of the HBC vessels generally numbered less than thirty, and the passengers might consist of a few tens of men sent to serve in the company's posts, especially during this early period. Moreover, the vast majority on board were adult Europeans, and thus less likely to be susceptible to crowd diseases than many of the colonists, since many of the diseases that were most destructive in the New World were, by the time of the founding of the HBC, largely diseases of childhood throughout much of the more populous parts of Europe. On any given voyage, only a very few people, if any, were likely to have been susceptible to the major Old World diseases, excluding influenza and the colds.With such lengthy trips and limited numbers of susceptibles on board, the possibility of HBC ships transporting most of these disorders across the Atlantic was also limited and, in this respect, they were similar to the early fishing ships sailing to eastern North America.5 When compared to conditions found by Haggett for the southwest Pacific, it is evident how unlikely was similar diffusion to Hudson Bay. In the case of measles, for example, Haggett found that among the early immigrant ships to Fiji, requiring about seventy days to complete the journey and carrying some 500 passengers of all ages, none carried the disease on arrival although one third had had active infections aboard when they departed. In this case, the average length of the trip was almost identical to that of the HBC ships during this period, and the number of passengers was far in excess of the company's ships' total of crew and passengers. What is more, the ships bound for Fiji carried a significant percentage of children, unlike the HBC ships, and yet none maintained the crowd infections to be passed on at their destination. As conditions changed, however, the barrier to Old World diseases that protected the southwest Pacific broke down. Once the much faster steamships replaced the sailing vessels, and began carrying still larger numbers of passengers, one half of the ships with active measles cases aboard when they departed for Fiji remained infective when they docked.6 Conversely, there were no corresponding changes in the HBC ships engaged in transport to Hudson Bay prior to 1850, and the epidemiological impact of HBC shipping on the Petit Nord remained limited with respect to the main crowd diseases, although influenza and

41

42

CHAPTER Two respiratory diseases were repeatedly introduced from Europe to the Aboriginal people of Hudson Bay over time. Other changes brought about by the coming of the English traders were of greater consequence to the epidemic history of the region. The arrival of the English fur traders in James Bay coincided with, and contributed to, the beginnings of a shift in spatial relations between the Europeans and the Aboriginal peoples of the Petit Nord. In turn, this shift placed the region more firmly within the periphery of the European urban disease pools, through the medium of the emerging colonies located along the north Atlantic coast of North America. The key to the increased potential for epidemic diffusion into the Petit Nord during the late seventeenth century was an increase in travel from the east, particularly with respect to the movement of Europeans into the interior of the continent. Prior to 1666, very few Europeans had been able to travel any great distance westward from the Atlantic seaboard. In that year, following French military excursions against the Mohawk, a peace was made between the Iroquois Confederacy and the French and their allies. Among other things, this peace freed the way for French traders to penetrate into the interior of the continent, thereby bypassing the Aboriginal middlemen who had once brought the furs to the French settlements located on the St. Lawrence River. The entry of the HBC into direct competition for the prime furs from the area north of Lake Superior, and the subsequent construction of posts at strategic river estuaries along James Bay, outflanking the Aboriginal middlemen trade, stirred the French to further action.7 The French learned of the English presence at Rupert River in September of 1671 when, at Lac St. Jean, Father Charles Albanel met five canoes of Attikamegue and Mistassini people. They brought word that "2 vessels had anchored in Hutson's bay and conducted extensive trading with the Savages, having taken their station there for purposes of traffic. They showed us a hatchet and some tobacco, which they obtained from a Papinachois, who had been on a trading trip to the North sea, that very summer."8 The impact on the French trade was immediate and substantial, forcing them to respond to the English threat by increased exploration and direct contact with the Aboriginal people and by expanding their trading posts to the north and west into the Petit Nord for the first time.9 Within a few years large numbers of coureurs de bois began to enter the Northwest from Montreal each year, where they traded and wintered with the Aboriginal people. By 1688 Sault Ste. Marie was described as "a great Thoroughfare for the Coureurs de Bois that trade with the Northern People,

EARLY HISTORICAL PERIOD: 1670-1837 who usually repair to the banks of that Lake [Superior] in the Summer."10 Shortly after the establishment of the HBC, the Petit Nord experienced rapid, annual, and frequent traffic from Canada, a circumstance conducive to transporting acute infectious disease into the region. The French also began establishing permanent posts at key sites in and around the region as bases of operation in response to the English encroachment. In 1673 they constructed a post on Lake Mistassini to attract people from over a wide area, including the eastern portions of the Petit Nord. In 1678 the Sieur Duluth settled Kaministiquia on Lake Superior and in 1684 his brother, Claude Greysolon de laTourette, established a post at Lake Nipigon. Nepigon, on the Nipigon River north of Lake Superior, was constructed in 1679. By 1685 the French had moved into the Albany River system and established a post at its confluence with the Kenogami. A post at Temiscaming and another at Lake Abitibi were intended to intercept furs intended for Moose Fort. Within a few decades, Detroit and Michilimackinac emerged as major entrepots in the fur trade of the interior. In turn, the penetration of French fur-trading posts had profound effects, not only on English trade, but also on the annual movements of the people who traded directly with the French. Rather than make the long journey to Canada to trade their furs, they could now wait for the Canadians within their own territories, or travel much shorter distances to the French posts.11 This influx ofWhite traders into the Petit Nord carried the potential for the introduction of epidemic disease. The rapidly moving brigades annually penetrating into the Petit Nord from the active disease centres of the eastern seaboard must have carried acute infectious disease with them on occasion. Ships from Europe periodically brought acute infectious diseases to the eastern ports, and the resultant epidemics often diffused widely through the Atlantic colonies and to the eastern Aboriginal groups. The greater numbers of people annually leaving Canada for the lands north of Lake Superior and east of Lake Winnipeg, following the founding of the HBC, meant an increase in the number of potential vectors for transporting these diseases. Likewise, the new trading posts, visited by people from throughout the region, afforded ideal points for disease redistribution, effectively serving as nodes of diffusion by concentrating Aboriginal populations in a single location, one that was directly connected to the eastern colonies. The disease frontier of the distant urban centres in Europe had taken a step closer to the Petit Nord.

43

44

CHAPTER Two Epidemics in the Petit Nord: 1670-1736 The initial era of disease history, from 1670 to 1736, can be further divided into periods separated by the Treaty of Utrecht, signed by France and Great Britain in 1713. Prior to the treaty, control over the bayside posts passed back and forth between the French and English, with the HBC at times limited to the bottom of James Bay, or to York. For instance, York Fort was captured by a French sea force in 1694, lost in 1696, and regained in 1697, thereafter remaining under French control to 1714. Albany was captured by the French in 1686 and recovered by the HBC in 1693. These changes in control over the key bayside forts influenced, and were influenced by, the course of the fur trade in the interior. As long as the French controlled the more economical ship-based approach to Hudson Bay, they diverted their efforts away from the canoe-based, direct approaches to the HBC hinterlands. They could outfit strategic forts and have the Aboriginal people bring their furs to them just as did the HBC. This was especially significant in the case ofYork, as initial southern thrusts to the west of Lake Superior were quickly abandoned. In 1688, with York yet in HBC control, Jacques de Noyon first explored the Boundary Waters on behalf of the French. However, nothing came of this until the eighteenth century, as only a few years later they captured York and its fur-trade hinterland. Only after the treaty did the French resume their expansion of the direct fur trade into the Boundary Waters. Unfortunately, as a result of these disruptions, the documentary record from this period remains a poor one, placing significant limitations on our understanding of the nature of epidemic activity throughout much of the Petit Nord.12 In 1714 York was returned to the English as the French abandoned Hudson Bay by the terms of the treaty and resumed their expansion into the Northwest. Historical evidence becomes increasingly available for the period thereafter, especially on the part of the HBC. Although the company had yet to settle inland from Hudson and James bays, by the 1720s it was reasonably well informed of significant events in the interior, and was routinely identifying individual groups of Aboriginal Uplanders. At the same time, French expansion into the southern part of the region, culminating in LaVerendrye's explorations onto the plains, was enhancing knowledge of events in the south. Thus, the records that stem from these activities during this era provide a clearer view of the epidemic history of the Petit Nord than did those of the period prior to the treaty.

EARLY HISTORICAL PERIOD: 1670-1837 1670-1713 It did not take long for an epidemic to reach at least as far as the margins of the Petit Nord, following the arrival of the HBC. In 1669-70 smallpox spread from New France to Sault Ste. Marie on Lake Superior. Although it is not known if this epidemic continued its path of diffusion into the Petit Nord, it is nonetheless worthwhile to examine its progress for the insights that it might provide into the diffusion of earlier epidemics, its potential impact, and the immunity that the survivors would have acquired.13 Of all of the exogenous diseases introduced to the New World following contact, smallpox (variola) was considered the most destructive.While it was mainly a disease of childhood in the major cities of western Europe, by the late seventeenth century smallpox had already killed untold numbers of Aboriginal people in the Americas. It is an acute, directly transmitted disease caused by the variola virus, capable under some circumstances of producing a very high fatality rate. There are two recognized strains of smallpox, variola major and variola minor, differing only in severity. The latter causes few complications and case-fatality rates are usually, although not always, low. Variola major takes a variety of forms and, depending on the conditions of the victim and the type, is generally fatal fifteen to forty percent of the time, although specific conditions might greatly increase the fatality rate. In cases designated as fulminating smallpox, for instance, death is almost invariably the outcome. An attack of either v. minor or v. major usually grants full and lasting immunity to both strains.14 Smallpox is normally spread by respiratory emissions or by contact with the skin lesions of infected individuals, from which the virus enters the respiratory tract. Other, external, sources such as corpses, clothing, flies, and rags, on which the virus can survive for extended periods, may also spread the disease. Following infection, the victim experiences no symptoms during an incubation period lasting ten to twelve days. Initial symptoms of smallpox then commence and may include headache and often backache, sudden fever, general malaise, and vomiting. Two to four days later, the characteristic rash generally, although not always, appears. It develops first on the face, and thereafter on the body and extremities.15 The infectious period of smallpox can be lengthy, perhaps as many as twenty-one days. Because of this, Ramenofsky placed it in the highest category of diffusion potential. Moreover, the variola virus's ability to remain viable outside the human body also contributes to its success at diffusion. This may explain why it was one of the first of the Old World crowd diseases to cross the Atlantic, reaching the New World in the second decade

45

46

CHAPTER Two of the sixteenth century. It is thus not surprising that it was also the first recorded disease to appear on the margins of the Petit Nord.16 The overall pattern of the 1669-70 smallpox epidemic resembled the general pattern of diffusion that had emerged in northeastern North America during the first half of the seventeenth century, particularly with respect to its source. During this era, Canada and the other European colonies along the east coast of the continent had yet to develop their own endemic disease pool. Instead, they remained within the urban disease frontier of the cities of Europe, and disorders were usually introduced by ship to the major colonial ports, subsequently spreading to other communities as well as to the Aboriginal people. In this case the smallpox virus was likely introduced from Europe by a ship that landed at Quebec in the summer or early fall of 1669 (Map 6).17 This was but the beginning of the epidemic's devastation, however, as it diffused far beyond its local source. Crucial to the further diffusion of the disease was Quebec's long-standing role as an important meeting place for Aboriginal people from far afield. During this era, the town was a seasonal hive of activity with people from as far as the Atlantic coast and the upper Great Lakes visiting for reasons of commerce and diplomacy. The visitors exposed themselves to the disorders that were occasionally introduced to Canada, and they carried the diseases back towards their own lands, thereby spreading sickness far beyond the initial locus of infection. This mode of epidemic diffusion had been common since the first devastating epidemics of the 1630s, and though the increasing movement of Europeans into the interior of the continent would, in time, lessen its significance, it remained the dominant mechanism as of 1669-70. As was common at this time, Quebec hosted many Aboriginal visitors during the summer and fall of 1669, and these people contributed to the wider diffusion of the epidemic. For instance, several of the Onondaga Iroquois travelled to Quebec to attend a peace conference with the Algonquin of the upper country, and they seem to have transmitted the sickness to their people and the other Iroquois.18 There was also a ceremony held to choose a successor to replace the deceased Sillery chief, Captain Noel Tekouerimat, a leader of considerable influence. This convention was attended by representatives from many far-flung groups, including the Algonquin, the Huron, the Montagnais, the Gaspesiens, the Attikamegue, the Abenaki, the Etechemins (the Malecite of New Brunswick), and the Nipissing. Once again, some of the attendees were infected and smallpox began spreading in both directions along the St. Lawrence as a direct consequence of this diverse gathering.19

Map 6: Diffusion of the 1669-1670 Smallpox Epidemic

48

CHAPTER Two From Quebec smallpox moved quickly down the St. Lawrence aboard a French shallop bound forTadoussac, which became a local centre of diffusion. Aboard were Aboriginal visitors who were returning from their trip to Quebec. By the time they reached the lower part of the St. Lawrence, the disease had hit full stride, and one Jesuit described the sick passengers as resembling "monsters rather than human beings, their bodies were so hideous, emaciated, and full of corruption." After the ship landed nearTadoussac, the disease spread rapidly, turning the local mission into a hospital for the smallpox victims. Many did not recover.There were more than 120 casualties among the mission people alone, and the total losses among the nearby Aboriginal people were undoubtedly much higher. In normal years 1000 to 1200 people would have gathered atTadoussac; however, by the spring of 1670, only 100 had been seen. By December smallpox had spread to nearby Isle Verte and into the Gaspe region, also accompanied by heavy losses.20 Thereafter, the epidemic moved up the Saguenay River fromTadoussac, and this placed the northeastern part of the Petit Nord at potential risk through traditional long-distance trading patterns. When the Jesuit Father Charles Albanel visited the Kakouchac (Montagnais) of Lac St. Jean in 1671-72, he noted they had been diminished in numbers recently, "by their latest wars with the Iroquois, and by the smallpox, which is the pest [peste] of the savages."21 This lake had been the "place whither all the Nations between the two Seas, those of the East [the Atlantic] and the North [Hudson Bay], used to repair for purposes of trade,"22 and a significant trading corridor stretched between Tadoussac and James Bay. The potential was there for epidemic diffusion as far north as Hudson Bay. However, Father Albanel noted no evidence of sickness to the north of Lac Ste.Jean. In this case, diffusion may have been partly defeated by the rapidly emerging changes in the spatial structure of the fur trade brought on by the arrival of the HBC on James Bay. With posts at Rupert River and, in 1670, at Moose River, the English had begun attracting the trade that formerly would have gone to Lac St. Jean or to Tadoussac. In response to the nearer opportunity being provided by the HBC, the bands that in previous years went south to trade with the Montagnais, and through them the French, had begun heading north to trade. The real threat to the people of the Petit Nord in 1669-70 lay in the westward diffusion of the disease, from Quebec towards the heart of the continent, and this followed traditional lines of communication, along the St. Lawrence from Quebec to Montreal and from there to the upper Great Lakes. Following the succession ceremony for the Sillery chief held at

EARLY HISTORICAL PERIOD: 1670-1837 Quebec, smallpox devastated the Attikamegue living up the St. Lawrence nearTrois Rivieres, some of whom had been in attendance. This community was almost completely abandoned by the Attikamegue after the epidemic.23 By the spring or early summer of 1670 the disease had broken out at Montreal, the jumping-off point for the upper country. Shortly thereafter, it appeared at Sault Ste. Marie, an Ojibway fishing and trading village on the St. Mary's River between lakes Huron and Superior. In his Relation covering the summer of 1670, the Jesuit Father Gabriel Druillettes noted that upon his arrival at Sault Ste. Marie, "a grievous disease broke out among the greater part" of those resident at the falls. In fact, several diseases appeared to be present, given the wide variety of diverse symptoms described by the Jesuits, including, perhaps, epidemic dysentery.24 Nevertheless, it is also apparent that smallpox reigned as it was recorded that "a young Kilistinon, seized at Montreal with an ailment which, during the past year, swept off many Savages, was in a very feeble condition."25 From this description, the ailment that plagued the young man could only have been smallpox, the disease that had devastated the east in 1669. With smallpox at Montreal, it was almost inevitable that it would appear at Sault Ste. Marie, for the two communities were inextricably linked by the seasonal flow of the fur trade. Each spring large canoe brigades of Aboriginal people from the Upper Country made their way to Montreal to trade their furs. Many passed through the Sault, which was described at this time as "the great resort of most of the savages of these regions,... the almost universal route of all who go down to the French settlements."26 This long-standing pattern of movement eventually gave way to an even larger flood of French traders, moving in the opposite direction, but in 1670 it still remained intact. In that crucial year, more than 900 Ottawa from the upper Great Lakes accompanied the fur trader Perrot to Montreal in order to trade, and the French explorer De Brehant De Galinee observed another party of Kilistinon preparing to depart Sault Ste. Marie for Montreal at the end of May, all potential vectors for the disease.27 Among the latter, no doubt, was the young Kilistinon man who subsequently appeared at Sault Ste. Marie suffering from smallpox. Much suffering and a large number of fatalities accompanied the diseases that struck the people gathered at Sault Ste. Marie, although the Jesuit priests claimed otherwise. As was not uncommon for what was, in large part, a fundraising device, the Relation of the day made glowing reports about the success of Father Gabriel Druillettes, claiming that, owing to his efforts, not a single person died, that 300 people were baptised by the following January, and that there was universal acceptance of Christianity and the elimination

49

50

CHAPTER Two of polygamy at Sault Ste. Marie. However, writing in the eighteenth century, the Jesuit historian Charlevoix described a more likely scenario, stating that "in the first two years [1669-71]... [the Jesuits of the Sault Ste. Marie mission] baptised at least three hundred persons, most of them apparently dying children."28 Among those stricken were several from the Petit Nord. This included members of the Monsoni and Kilistinon, who resided in the country to the north and west of Lake Superior.29 The presence of smallpox at Sault Ste. Marie in 1670 also posed a substantial risk to the people who remained in the Petit Nord, due to the complex interactions and movements of the Aboriginal people of the region. The Sault attracted seasonal gatherings of up to 2000, supported by an abundance of whitefish.The Saulteur, or Pahouitingwach Irini, resided permanently at the rapids of the St. Mary's River, by which the Sault derived its name, but shared their summertime resources with several other nations who came from the upper Great Lakes and the country north of Lake Superior, as far as Hudson Bay.30 During the same seasons, the shores of Lake Superior were visited by "twelve or fifteen distinct nations coming, some from the north, others from the south, and still others from the west," who sought to fish or trade.31 Such gatherings provided excellent opportunities for widespread dissemination of infectious diseases as people congregated along the lake's shores and then dispersed for their homelands. It is thus possible that smallpox could have spread into the Petit Nord. At the very least, Old World diseases had arrived along the eastern margins of the Petit Nord. Despite the presence of these and other acute infectious diseases near the eastern part of the region, the Aboriginal people trading at Hudson Bay appear to have escaped the epidemics for a few years after the arrival of the traders. HBC documents from the first four and one-half years of the company's existence show an abundance of trading but no epidemic disease. It is significant that Thomas Gorst wrote in 1671 that, at Hudson Bay, scurvy "is there the onely disease."32 This ended in 1674, when company servants witnessed the aftermath of a lethal epidemic among some of the Lowland Cree of James Bay. During July and August, Governor Thomas Bayley and several other men explored the western coast of James Bay and Hudson Bay, from Charles Fort as far north as the mouth of the Severn River (Map 7). On July 16, the party sailed by sloop from Moose River. On the 23rd, they met seven "distress'd" Aboriginal people on an unidentified point to the north of Akimiski Island, whom they took on board and transported to the mouth of Ekwan River some 100 leagues south.There, Bayley observed several people dead. By way of explanation, he commented that "there had been a great Mortality among them, and several were starv'd

EARLY HISTORICAL PERIOD: 1670-1837

Map 7: The Petit Nord, 1674-1736

to Death for want of Food; this Country being such a miserable Wilderness, that it affords not sufficient Sustenance for the wretched Inhabitants."33 This was not a case of simple starvation, however. Food resources, including fish, waterfowl, and caribou, would have been plentiful at this season and, indeed, throughout the summer. In particular, the large herds of caribou that summered on nearby Akimiski Island would have provided a reliable resource for the local Cree.34 Instead, it is much more probable that the primary cause was an unknown epidemic disease, although, as was common with other virgin soil epidemics in the New World, starvation was a secondary impact.Whatever it was, the English traders had not introduced the disease. There was no mention of a disorder among the HBC men and, more importantly, there had been no sickness among the Aboriginal people who had traded directly with the English at either Charles Fort or Moose Fort. Instead, the disease appeared among the people summering near Akimiski Island, a group that does not seem to have made

51

52

CHAPTER Two contact with the English before. Rather than coming from the English, the most likely source is diffusion through inter-tribal trade, which flourished in this vicinity.35 Thus, we can point once again to traditional patterns of epidemic diffusion in which Aboriginal people, rather than European traders, played the main role in spreading crowd diseases. The epidemiological impact of the expanding fur trade had yet to be felt within the Petit Nord. This would not last long, however. For four decades following the epidemics at Sault Ste. Marie and the Ekwan River, there were occasional bouts of sickness among both the HBC men and the local Cree at Albany Fort. Most seem to have been isolated illnesses of individuals, but a few may have been part of broader epidemics. As a consequence of this increased sickness, Hudson Bay lost its formerly healthy reputation. In August of 1712, Anthony Beale wrote to the governor and committee of the HBC that "Your country is very much altered to what it was formerly for we have had many sick this winter "36 The following summer brought word to Albany Fort of an epidemic in the interior of the Petit Nord. In July a lone canoe arrived from up the Albany River and Beale was informed that "there was a sickness amongst them which destroyed abundance of ye french...."37 Here was evidence of the new fur trade, with French traders travelling far to the west in search of furs, but more importantly it may have signalled the emerging epidemiological impact of this trade. With devastating epidemics periodically arising in the east, even to the margins of the Petit Nord (Table 3), and everincreasing numbers of traders, soldiers, explorers, and missionaries moving into the interior, the fortunate isolation that the people of the region had once enjoyed was beginning to crumble. 1714-1736 As a result of the return ofYork Factory to the HBC in 1714, evidence of events in the Petit Nord increases substantially for the subsequent period. This evidence reveals a somewhat unexpected contrast between the reports of epidemic activity at the two major HBC posts in the region,York and Albany, and in their hinterlands. At Albany, which was closer to the eastern disease centres, there were few reports of widespread sicknesses, although chronic afflictions and those affecting only a single individual occurred frequently. AtYork, which was more distant from the disease sources, reports of epidemic activity were more common, at least for the first few years. This discrepancy illustrates a fundamental characteristic of the entire

Table 3: Recorded Epidemic Disease in Eastern North America: 1675-1716

54

CHAPTER Two epidemiological history of the Petit Nord: the diversity of the epidemic experience within the region. For the most part, region-wide generalizations about exposure to epidemics, the impact of a disease, and the reactions of the inhabitants tend to conceal the essential epidemiological patterns, rather than to shed light on them. There were few incidents of epidemic disease at Albany and within its hinterland between 1714 and 1736. Early on, colds and "great colds" were an occasional problem among the HBC men, culminating in a major outbreak in the spring of 1720.The latter may not have been the simple respiratory disease, however, since a "great cold" sometimes meant influenza in the English usage of the day.38 There are few clues as to the identity of the other epidemics recorded at Albany during this period. For example, an unknown infectious disease afflicted the Albany River Lowland Cree seven years later, sending them to war the following spring. Thus, on May 25, 1728, Joseph Myatt wrote in his journal that "this morn Eight Curnoes of our home Inds fitted out from here in order to goe to Warr wth the Esquomays, I Endeavored all I could to oppose it, but in vain, for severall of the Home Inds being Disordered the last winter they attribute all those things to the Mallice of their enemies.. ,."39 Myatt s description rings true. According to an English seaman who overwintered at York in 1746-47, when a sickness occurred among the Lowland Cree, they went to war with the Inuit, whose sorcery they blamed for their misfortunes.40 Shortly thereafter, epidemic disease was again among the Albany people, but this time, those of the interior. In May of 1730, thirty-eight canoes of Uplanders arrived at the fort, complaining that "it hath been a very hard year with them, they haveing been very much afflicted wth sickness..." Two weeks later, seven canoes of Sturgeon people arrived from the interior and brought news that it had been a very sickly year in their home country, and that several of their people who normally traded at Albany Fort had died, including a leading man named Weques.41 The identity of the disease and the extent of its spread in the interior are unknown, but in all likelihood it encompassed at least the southeastern part of the Petit Nord, since these Sturgeon almost certainly came from the Lake of the Woods.42 Finally, during November of 1732, reports indicated that there was "a great sickness" among the Albany Lowland Cree, although the illness was not identified. In this case the disease likely came from the interior and may have spread widely; intelligence received at York in the spring of 1733 conveyed the information that "severall [Upland] Indians Dyed last winter with Ailements...."43 It is entirely possible that the disorder was brought into the area through the movements of the fur trade, which was undergoing

EARLY HISTORICAL PERIOD: 1670-1837 a period of further expansion into the eastern part of the Petit Nord. In 1732 it was reported that the French had established two posts somewhere on the Albany River, and that several Canadians had wintered with the Upland people.44 At the same time, some Ojibway were moving north onto the lower reaches of the Albany, to within 250 kilometres of the fort, where they were trading with the Uplanders. Both sets of traders, Canadian and Aboriginal, brought trading connections with the east, the French with their native Canada, and the Ojibway with both Canada and the English at Oswego, and so both were potential vectors of infectious disease.45 At York Factory the situation was somewhat different during this period, with frequent epidemics early on, followed by an extended period with very little disease activity. Almost immediately after Governor James Knight arrived in the fall of 1714 to take over from the French, there were reports of epidemics among nearby groups.The following summer brought news of a fatal illness among some Aboriginal people who had left York for Churchill, while in the summer of 1716 a great many others were sick and died, no doubt due in part to the starvation brought on by the non-arrival of the ship. A "malignant feaver," interpreted by the medical historian William Ewart as influenza, raged among the Cree of the York region during the winter of 1716-17, and among some Chipewyan visitors living at the post and with the Cree.The sickness afflicted the latter "one after the another" and was, according to trader James Knight, "as mortal as if they had the Plague."46 All this was a prelude to the first documented outbreak of smallpox in the Petit Nord, in 1720, the first of three such appearances of the disease at York Factory during the course of the eighteenth century. On March 23rd, 1721, Governor Henry Kelsey recorded in his journal that "2 of the Capt [Captain's] family came here for food and say he and some others are very ill altho most of the Indians that have lain here all winter have had the Small Pox which I never saw amongst the home Indians before."47 Kelsey's observation on the rarity of the disease among the Homeguard Cree is an important one, for his experiences in Hudson Bay covered much of the period of the HBC's existence. For almost forty years, between 1684 and 1722, he was a key figure in the company's employ, and was rarely absent from the bay. He had served in many capacities at several posts, having travelled inland from York on voyages of exploration, served as governor of all the bayside posts, and even captained the Knight in a shipbased Eastmain trade out of Albany. He had a facility with several Aboriginal languages, and a keen and curious mind, and was also no doubt familiar with fur-trade traditions, which would have made note of prior smallpox epidemics. More than anyone in the HBC to that period, Henry Kelsey had

55

56

CHAPTER Two an intimate and long-standing knowledge of the people of the Hudson Bay lowlands. His statement can be considered key testimony regarding the epidemic history of Hudson Bay.48 This epidemic appears to have originated in a true rarity, the transport from Europe of a crowd disease on board an HBC ship. Smallpox was "exceedingly prevalent" in London during the spring of 1720, at the same time that the HBC frigate Hannah was departing the city for Hudson Bay.49 It is probable that the virus was brought on board, either with an infected human or on a fomite, such as the surface of trade goods intended for Hudson Bay. After a trip of eighty-nine days, the ship arrived at York on September 3. No doubt the variola virus's ability to remain viable on an external object preserved the disease during this long voyage. Shortly thereafter, the affliction appeared among the Homeguard Cree. The timing of the outbreak was consistent with a ship-based origin. Initial infection "would have occurred shortly after the ship arrived, and before the Homeguard prepared to disperse to their wintering grounds or the fall goose hunts. Allowing additional time for diffusion among the Homeguard, a prolonged wintertime epidemic, such as was described by Kelsey, would have resulted. The smallpox outbreak of 1720-21 doesn't seem to have spread far beyond the initial point of infection. Instead, it probably was limited to the immediate vicinity ofYork Factory, since there is no mention of the sickness in the records of the two other permanent posts on the Westmain: Churchill and Albany.50 Here, the timing of infection may afford an explanation for the lack of diffusion. By the time the ship arrived at Port Nelson, the Uplanders had already departed, and were therefore spared the effects of the epidemic. The sickness could go nowhere but among the local Cree population. Just as it must have seemed to the traders that epidemic disease was to be a near-constant companion at York Factory and within the post's hinterland, it inexplicably stopped. After eight years of frequent epidemics, from 1714 to 1721, the remaining years until 1736 were comparatively healthy ones. To be sure, there were a very few bouts of sickness among the HBC men and the Aboriginal people, including an unidentified illness that accompanied starvation among a group of Lowland Cree who had been unable to hunt deer in 1722,51 a few colds among the HBC men in June of 1724, and a disease that affected some Uplanders during the winter of 1732-33.52 None of this approached the series of years that culminated with the smallpox outbreak of 1720-21 in terms of either severity or frequency, however.

EARLY HISTORICAL PERIOD: 1670-1837 The arrival of the HBC in the Petit Nord during the late seventeenth century confirmed the region's place within the frontier of the urban disease pools of Europe. As we have seen, epidemic disease was an occasional, although not yet frequent, visitor to the region. The appearance of these traders also brought about spatial changes in the fur trade that enhanced the spread of epidemic disease into the interior of the continent. Initially during this early period, epidemic diffusion through traditional modes of dissemination—long-distance Aboriginal movements—was most common. Over the next century and a half, newer and more efficient mechanisms became increasingly significant. It began during this era with the seasonal relocations of European fur traders, both on land and across the ocean. Nevertheless, the region remained firmly on the periphery of the European pools at this stage, with epidemics appearing only infrequently. The conditions that were to bring the region into a closer relationship with the external pools lay many years in the future.

57

This page intentionally left blank

3 The Smallpox Epidemic of 1737-1738

SMALLPOX RETURNED TO THE PETIT NORD IN 1737, THE THIRD TIME

since the founding of the HBC. Although the historical record from this period does not allow us to draw precise conclusions regarding the frequency of return of all exogenous diseases, it appears nonetheless that, given its repeated appearance and its potential for human destruction, smallpox had emerged as the greatest threat of all the epidemic diseases to the Aboriginal people of the region. Thanks in large part to the westward expansion of the French into the southwestern part of the Petit Nord under La Verendrye, which began only a few years earlier, we are able to track the progress and impact of the 1737-38 smallpox epidemic in far more detail than the earlier visitations. When combined with the records of the HBC, the documents left by this fur trader/explorer provide important insights into an infection that had significant consequences for the people of the Petit Nord.1 There has been some confusion among scholars as to the origin of this epidemic. Some have insisted it came from Hudson Bay, introduced by the HBC traders.This conclusion was based on a statement given to LaVerendrye by the Cree of the Winnipeg River to the effect that smallpox had been

60

CHAPTER THREE passed to another group of Cree "by those who had gone to trade with the English [qui leur a eteporteepar ceux qui ont etc trailer chez lesAnglois]"2 If this interpretation were correct, then this would have paralleled the outbreak of 1720 at York Factory, providing evidence of two such incidents in just over a decade and a half. In turn, this suggests that the HBC ships constituted a potent threat for the introduction of this destructive disease. However, the HBC records provide no support for this interpretation. There is no mention of an epidemic or even of an unusual sickness in the daily journals of the HBC posts of Eastmain, Churchill, York, Albany, and Moose during the year (1736-37) leading up to the eruption in the south. Had smallpox appeared among the people at the post, the traders would have made note of it, for its impact on their work or on their returns would have been considerable. This suggests that the disease had come from a source other than the English. In this case, the problem may be in the modern interpretation rather than in the historical record. LaVerendrye's Aboriginal informant had not claimed that the disease had been contracted from the HBC, nor that it originated at Hudson Bay, but only that it came from those who had traded with the English. Instead, the 1737-38 smallpox epidemic followed a long-standing pattern of diffusion, similar in its essential characteristics to the epidemic of 1669-70. As with the earlier epidemic, its origin lay in the urban disease pools of Europe, transmitted by sea to one of the rapidly expanding European communities along the Atlantic seaboard. Its spread into the interior of the continent also appears to have been largely a result of Aboriginal movements and communication. Despite the overall similarity, there were also differences between the epidemics, differences that reflected changing conditions of European settlement and movement in eastern North America, and that foreshadowed new and efficient patterns of diffusion that emerged later in the century. In the latter part of 1729, a virulent form of smallpox was introduced to Boston. It had arrived aboard a ship from Ireland, despite the city's established practice of quarantining vessels from infected ports. It raged until the fall of 1730, before spreading to other nearby English colonies. At this time Boston was the largest of the colonial urban centres of the northeast, though with a population of only about 12,000.With insufficient numbers to support smallpox endemically, the disease instead made irregular appearances in the community, each time introduced from elsewhere. Its period of return up to the mid-eighteenth century was still fairly lengthy, and it generally reappeared in epidemic form every ten to twenty years. It was not yet a disease of childhood, but instead also took a toll on the adult population.

THE SMALLPOX EPIDEMIC OF 1737-1738 Thus, it was reported in 1746 by one observer that the people of Boston were "more afeared . .. of the Small pox than they are of the Devil."3 The people of Boston were not the only ones who had cause to fear the disease, however. By the mid-eighteenth century, in northeastern North America, an urban system emerged, stretching from New Jersey to Newfoundland, what the cultural geographer D.W. Meinig has referred to as a Greater New England. This was a functional region within which people, goods, and information moved more or less freely between the English-speaking communities. If the colonies of the seventeenth century had been small, selfcontained, and somewhat isolated from each other, the towns and cities of the eighteenth were far more interdependent and interconnected. Consequently, diseases spread more easily between them. With Boston as the commercial and cultural focus of this Greater New England, it is not surprising that smallpox began to diffuse beyond that port to the other major towns and cities of the region. By January of 1731 the disease had surfaced in the provinces of Pennsylvania, New Jersey, and New York. Philadelphia and New York City were especially hard hit, where the disease had a prolonged and destructive stay. An attack rate of greater than fifty percent of the total population in the latter is testament to the infrequency of smallpox's appearance in the city at that time.4 The epidemic's subsequent spread northward from New York City to Albany was crucial for the further diffusion of the disease into the interior. Albany lay on the frontier between the largely settled area along the Atlantic coast, a region of near-contiguous settlement from Norfolk,Virginia, to Bangor, Maine, dominated by people of European origin, and an area of interdependence between the Aboriginals and Europeans, where the interests of both groups were "locked together for their mutual advantage." In part because of its location, it was one of only a few remaining communities in eastern North America of intense intercultural relations between the two worlds, and it was thus a gateway for the spread of epidemic disease to the Aboriginal realm beyond.5 To a great extent, such intercultural relations revolved around the official fur trade as well as around a lucrative, though illegal, trade in smuggled goods and furs between the English colonies and Canada, and these proved deadly for the Aboriginal visitors. For example, a Seneca man introduced smallpox among the Six Nations Iroquois on his return from Albany. As it spread among the Iroquois villages, it left large numbers of dead in its wake. Despite an attempt by Beauharnois, the Governor of New France, to establish a quarantine in 1731, by 1732 it had continued its northward progress

61

62

CHAPTER THREE to Canada. It appears to have done so through the clandestine trade carried on between Montreal and Albany by the Canadian Aboriginal groups, as it appeared first among the middlemen in that trade, the Mohawk of Sault St. Louis (Caughnawaga) and the Nipissing of Lake of the Two Mountains, before breaking out in Montreal during the fall of 1732 (Map 8). Of course, this was nothing new, as the people of the area had long acted as a conduit for the spread of disease back and forth between the valleys of the Hudson and the St. Lawrence.6 The epidemic ravaged the people of Canada, just as it had those of the English colonies to the south. Smallpox spread throughout the French colony during the remainder of 1732 and into the next year. Here again it is apparent that the disease had been absent for a considerable time. By the fall of 1733 it had claimed nearly 2000 Canadian lives, 900 in Montreal alone from a total population in the low thousands, and it was far from over. This was a significant loss for a colony that numbered just over 43,000 in 1739.7 At about this time, the disease began its long journey into the interior. Beauharnois soon learned that the epidemic had "spread among all the [Aboriginal] nations" of the Upper Country, the Pays d'en Haut.This was the vast area lying beyond Lake Ontario, south of the other Great Lakes to the Ohio and west to the Mississippi. Among its victims were the Canadians' allies living in the lands around Lake Michigan and Lake Huron, the Miami, the Potawatomi, the Wea, and the Piankeshaw.8The Miami, in particular, were hard hit, and the epidemic may have lessened the influence of the traditional chiefs, who were unable to protect their people. In turn, this seems to have led to the emergence of alternative chiefs, such as Pied Froid, who was said to have delivered his people from smallpox. There is also evidence of epidemic disease among the Illinois tribe, then living in modern Illinois and the eastern portions of Missouri and Iowa. Once again, smallpox had found its way to the upper Great Lakes and beyond.9 We don't know how the sickness arrived among the people of the Pays d'en Haut at this time, but there are several possibilities. Both Aboriginal and non-Aboriginal people continued to travel between the Great Lakes and the east during this era. During the summer months, people from the region were frequent visitors to Montreal, and the Ottawa, Huron, and Miami also began trading directly at Albany during the first decade of the eighteenth century. For their part, the French were sending troops into the interior while maintaining a series of fortified posts, each with a garrison. And, of course, there were the near-ubiquitous French Canadian voyageurs. Each year about 500 men departed Montreal for the west, and most travelled

Map 8: Origins of the 1737-1738 Smallpox Epidemic

64 CHAPTER THREE through Michilirnackinac, near Sault Ste. Marie. All these people would have provided a ready vehicle for the disease to travel into the interior of the continent in 1732-33. Smallpox was also present at Detroit, but in this the epidemic of the 1730s was unlike earlier epidemics. Detroit had been established as a French and Aboriginal base of settlement in 1701, and it was followed in close succession by French agricultural settlements in the Illinois country at Kaskaskia, on the Mississippi above the Ohio, and at Vincennes, on the lower Wabash near the lands of the Wea and the Piankeshaw.The presence of a non-Aboriginal community this far into the interior was a new dynamic in the spread of disease in the northern part of the continent, and of increasing importance as new temporary pools emerged in the long-distance diffusion of disease, thereby expanding the range of the true urban disease pools. Although by the 1730s there remained few people settled at Detroit and the other towns, limiting their potential epidemiological impact, over the next century the increasing trend toward White settlement in the interior had a drastic impact on the health of the Aboriginal people across the continent. By 1733-34, then, this smallpox epidemic was firmly established among the Aboriginal people living south of Lake Michigan, perhaps as far as the Mississippi. Over the next few years the disease continued its westward diffusion, crossing the Mississippi, but it also began to spread towards the north, entering the vast prairies of the interior plains. This epidemic maintained a surprisingly slow rate of diffusion. Its North American phase had begun with the introduction of the disease to Boston late in 1729, and four or five years later it had reached only as far as the Mississippi, roughly 1600 kilometres distant. However, such lethargic advancement was not uncommon. In his study of epidemic disease in sixteenth-century Mexico, Hans Prem found that smallpox epidemics sometimes travelled only short distances over long periods of time, even in densely settled areas without the pronounced seasonal variations in population density and interaction found in northeastern North America.10 Across much of the northern part of the continent, winter's scarcity required many Aboriginal societies to disperse into smaller and, often, more isolated groups. This seasonal ebb and flow helped determine the timing of trade, social interactions, and even warfare. It also played a considerable role in determining the rate of progress of an epidemic, and delays in diffusion were almost invariable during periods of winter dispersal or isolation. The next evidence of the disease comes from the Teton Sioux, the westernmost division of that feared tribe, who were, by this time, established

THE SMALLPOX EPIDEMIC OF 1737-1738 on the prairies across the Mississippi. Three Teton winter counts depict as the key event for 1734-35 an epidemic of a disease causing cramps and "cutaneous eruptions," both symptoms of smallpox. These counts were collections of annual pictographs, maintained by members of some tribes, with each picture serving as a mnemonic of an important event for that year. They are also a rich source of data on epidemic disease among the tribes that maintained them. Despite close trading contact between the Teton and the other divisions, the epidemic did not sweep through the entire Sioux nation. Another winter count belonging to the Lower Yanktonai, part of the Middle (Wiciyela) division, the John K. Bear count, makes no mention of the disease for this period, making it highly unlikely that they had been visited by this devastating sickness.11 Still, it is possible that the disease spread to the Teton at the Dakota Rendezvous, an annual "pan-Siouan" trade gathering, which also attracted groups living east of the Mississippi River. Donald Lehmer, who made an early study of epidemics among the Aboriginal people of the upper Missouri, identified this assembly as a potential mechanism for the spread of smallpox from the Great Lakes to the prairies.12 Indeed, such was the case at any major trading fair. According to Raymond Wood, "in addition to staples of the trade, most anything could . . . change hands at trading fairs," and "the flow of goods—not to mention of persons and disease organisms—from one area to another was a simple matter and . . . often exceedingly rapid."13 Dobyns also noted the potential for epidemic disaster for Aboriginal groups living at major trading centres, suggesting that the "intimate interpersonal interaction during trading-center fairs favored direct aerosol transmission of viruses."14 It is, therefore, possible that the disease passed from the eastern tribes to the Teton during the Dakota Rendezvous. Shortly after appearing among the Teton Sioux, smallpox spread to their allies, the Ojibway of Chequamegon, on the south shore of Lake Superior. In June 1736, on an island on Lake of the Woods, a large war party attacked and killed a brigade of French voyageurs, with whom were travelling a priest, Father Jean-Pierre Aulneau, and LaVerendrye's son, Jean Baptiste. Many historians thought that the attacking party was comprised exclusively of members of the Sioux nation, but this was not the case. A few outsiders were among them, and it is their motivation for the attack that alerts us to the presence of the disease among the Ojibway. In 1928 the ethnographer John Cooper collected an oral tradition from an Ojibway chief at Lake of the Woods, Jim Eliud, who stated that his ancestors had participated in the massacre: "A certain clergyman ... was a friend of the

65

66

CHAPTER THREE Indians, but they were 'wild' then and tried to kill him, actually succeeding in their design. They believed that he was responsible for an epidemic of measles or smallpox from which many of the Indians had died. Jim mentioned Massacre Island, down the Lake, as the place where the killing had occurred."15 The accusation that a priest brought epidemic disease echoed some Huron claims during the epidemics of the 1630s, and sprang from traditional disease etiologies among some Aboriginal groups, including the Ojibway, which blamed disease on malignant magic by the spiritually powerful. There can be no doubt that this statement referred to the Aulneau massacre, and so it is critical that we verify the precise composition of that war party. An initial report of the day suggested that "a party of Prairie Sioux to the number of one hundred and thirty" was to blame.16 However, further testimony provided by a French trader named Rene Bourassa contradicted the earlier report. In a strange twist of fate, Bourassa had been captured by the same Sioux party on the same day, but had been released prior to the massacre. By his account, "the larger portion of the savage party was composed of the Prairie Sioux, of some Lake Sioux, and some from the post of Monsieur de la Ronde."At this time the French acknowledged two divisions of Sioux: those of the Prairie, who lived to the west of the Mississippi River; and those of the River or the Lake, who lived to the east. Unlike the first two mentioned, the third group was not a Sioux band, but was Ojibway. Louis Denys, Sieur de la Ronde, then had charge of the French trading post at Chequamegon, on Lake Superior, and it was the Southwestern Ojibway who traded at his post.17This particular band was called the Ojibway of the Point—that is, of Chequamegon—and at the time of the massacre they were allied with the Sioux against the Assiniboine, Cree, and Northern Ojibway. Confirmation of the Ojibway presence among the Sioux comes from a letter received in December of 1736 by La Verendrye from Bourassa and his partner, who were then at a post on Vermilion River, just south of nearby Rainy Lake. He was informed that "a great number of Saulteur have sought refuge with them through fear of the Sioux. They questioned [the Saulteur] closely in order to ascertain how the Frenchmen had been killed, but they were unwilling to say, though amongst them there was one Saulteur who had been present at the tragedy."18 The term Saulteur was used by the French to refer to the Ojibway living south of Lake Superior, from Sault Ste. Marie to Chequamegon. Shortly after the massacre, the alliance between the Southwestern Ojibway and the Sioux had failed, and many of the Saulteur were fleeing north to escape their former allies. Ojibway

THE SMALLPOX EPIDEMIC OF 1737-1738 from the south of Lake Superior continued to move into the Boundary Waters, and to Lake of the Woods in particular, during the period following the epidemic.19 In this way, a fragment of oral history that belonged to the Ojibway of Chequamegon found its way to what had once been the stronghold of their enemies. Jim Eliud's oral tradition offers more insights than the fact that the Southwestern Ojibway contracted smallpox during this epidemic. It can also help us to narrow the possible time frame during which their outbreak occurred. Normally, oral traditions do not refer to standard chronology, which makes dating the described events extremely difficult or impossible. In this case we know the date of the event. The Aulneau massacre took place on June 8, 1736, and so the outbreak must have occurred prior to that date for it to serve as a motivation. Assuming that Father Aulneau had to have been present in the west when the disease first struck these Ojibway in order for those people to have cause to blame him, the timing can be pinned down even further. The priest arrived at Fort St. Charles, on Lake of the Woods, only on October 23,1735. This would imply, then, that the epidemic broke out among the Ojibway who participated in the massacre some time between October of 1735 and June of 1736, in all probability after the Sioux had been infected but before the disease was passed to the Cree and, subsequently, the Northern Ojibway. Finally, the epidemic may also have made its way to another of the major trading groups on the prairies, the Arikara. In his discussion of the sociocultural effects of epidemics on the Plains people, John Taylor presented circumstantial archaeological and historical evidence for the same epidemic among the Arikara, one of the agricultural village dwellers living along the upper Missouri.20Their traditional economy revolved around hunting,planting corn, and trading with numerous Plains groups through their role as middlemen in a continent-wide trading network.This last activity put them at risk of participating in the long-distance diffusion of epidemic disease, and one of the their major trading partners was theTeton Sioux.We do not know for sure if they contracted the disease at this time, but, if so, it could explain how the virus diffused between the Sioux and the tribes living towards the Red River, and why there appears to have been a delay. The disease might have passed from the Teton through the Arikara to the Cree, rather than directly from the Sioux.This would have been the final link in the diffusion of smallpox from Europe to Red River. On March 4 and 5, 1737, LaVerendrye held a general meeting at Fort Maurepas, on the Red River, with several Cree and Assiniboine bands. Some of these groups had come from a considerable distance.The impetus

67

68

CHAPTER THREE for the Council of Maurepas was LaVerendrye's desire to prevent retaliatory strikes against the Sioux for the Aulneau massacre, but the discussion included other subjects, notably the construction and relocation of French posts. Some of the people present at the meeting were already infected with smallpox, and the disease began to manifest among two of the attending groups shortly after the talks were concluded.21 On the 26th of May, La Verendrye was visited at Fort St. Charles, on Lake of the Woods, by sixty Cree whose territory lay along the Barrier Falls of the Winnipeg River. They informed the trader that "the Winnipeg Cree [ks Cris du Ouinipigon] whom I had left at fort Maurepas had all died of small-pox."22 These Cree also lived on the Winnipeg River, towards Lake Winnipeg, and they probably contracted the disease while at the Council of Maurepas. Two days later, LaVerendrye's son, Louis-Joseph, arrived after a sojourn with an unnamed band of Cree, who had probably come from the north end of Lake Winnipeg.23 While he had been "with them, the disease had broken out amongst these people. Thereafter: Those who escaped made a stop and threw into the river, according to their custom, all the beaver, pichoux, marten, etc., belonging to the dead as well as their own, so that the shore was lined with them and the portages full, all of which was a loss, as no one among the savages ventured to touch them. In the ten lodges that were with my son there was not one death; this was due to the remedies he gave them and the good care he took of them, which augmented their friendship for him and the French as well as their confidence in them; but they stopped like the others to succour the rest of the afflicted families. Only eighteen men came with him to join the warriors.24

Setting aside the undoubted exaggeration concerning Louis-Joseph's success rate at treating his hosts, this statement makes it clear that there had been a considerable amount of death among these Cree. His account of abandoned pelts describes a traditional act of bereavement that was a widespread practice throughout much of the Canadian Northwest, an almost universal reaction to the death of a close relative.25 This would have had a significant impact on the returns of the French trade for the year, a trade with which LaVerendrye's enterprise was inextricably linked. The disease lingered in the Lake Winnipeg area into the following year, and by the spring of 1738, it had broken out among other Cree groups, and among a key band of the Northern Ojibway. In a letter dated October 1, 1738, Beauharnois wrote that he had received a letter which the son of [La Verendrye] wrote me from the

THE SMALLPOX EPIDEMIC OF 1737-1738 Lake of the Woods on the eleventh of last May, by which he informs me that the Assiniboin to the number of eight hundred had left at the end of April to go and take vengeance on the Sioux for [the massacre], and that the Cree and the Monsoni had also raised war parties, though he does not give the numbers, but the small-pox broken out among them they were obliged to stop with the loss of a considerable number of their people carried off by that disease.26

The delayed presence of smallpox among these people was almost certainly due to their absence from the Council of Maurepas. It had attracted Cree and Assiniboine from long distances, but the Cree and Ojibway from the Lake of the Woods and eastward appear not to have participated.27 The Monsoni, who were the main inhabitants of the country about the Rainy Lake and Rainy River, had not gone to the council, and had thereby escaped infection until the spring of 1738. Thereafter, however, they were devastated. From the records left by LaVerendrye during his sojourn among these people, we can see for the first time the epidemic-induced disruption that had no doubt occurred before among the Aboriginal people of the Petit Nord. A rough indication of the magnitude of the epidemic's impact on the Monsoni can be seen in the decline of their warrior strength, a figure that usually corresponded to the number of adult males. Prior to the smallpox of 1737-38, LaVerendrye's estimates indicated that the Monsoni boasted substantial numbers of warriors. For example, on May 7,1734, nearly 400 Monsoni warriors gathered to go to war against the Sioux. The actual number may have been higher, since this included only those who were assembled at the time. Shortly after the epidemic, the Monsoni claimed only 140 men in three bands in the Rainy Lake area, with a few more residing on the Winnipeg River.28 Given a conservative estimate of four persons per warrior, their population may have declined from perhaps 1600 to just over 560. Faced with the devastating impact of a virgin soil epidemic, Aboriginal groups were often forced to adopt new strategies for survival, and there are hints of some of these strategies in the actions of the Monsoni during the years following 1738. For instance, some found it necessary to replenish their numbers through warfare. Historian Susan Johnston identified a pattern of post-epidemic behaviour in which some groups, such as the Iroquois of the northeast and the Piegan of the Canadian plains, went on military expeditions to capture enemy females and children to replace those lost in the epidemic. During post-epidemic periods of an earlier era, Huron warriors

69

70

CHAPTER THREE captured by the Iroquois were kept alive, to be adopted into their tribe.The same strategy appears to have been attempted by the Monsoni.Three years after the epidemic, the Monsoni, under their prominent chief La Colle, again went to war against the Sioux of the Prairie, and took back large numbers of their enemy as slaves. Never before had LaVerendrye described the acquisition of "slaves" as a motive for their war excursions, and it is likely that the Monsoni, like the Iroquois and the Piegan, were desperately trying to build up their numbers, which had been so reduced in 1738.29 Virgin soil epidemics have also routinely induced survivors to pursue strategies that are more spatial in nature and, once again, there are clues that the Monsoni turned to others to preserve their existence. In discussing Aboriginal responses to epidemic depopulation, Dobyns identified four main behavioural patterns commonly seen in the wake of virgin soil epidemics: abandonment of settlements in marginally productive environments; migration to more productive environments; amalgamation of survivors from abandoned settlements into new or existing settlements in order to maintain an optimum population; and amalgamation of survivors from diverse lineage and ethnic origins.30 All these were in evidence in the Petit Nord, but the last pattern especially stands out in the case of the Monsoni. The coalescence of the remnants of formerly autonomous peoples who had been ravaged by disease into a larger, combined, social group in order to surpass a population threshold, either for defensive or subsistence purposes, was one of the most frequently documented responses to severe mortality among Aboriginal groups in North America. In many cases this involved survivors from the same linguistic and tribal divisions re-forming into new arrangements, but it could also lead to the emergence of "polyethnic" villages. Perhaps the best example is that of the Mandan who, following the smallpox epidemics of 1779 to 1783 and 1837-38, merged with the surviving Arikara to produce new villages.31 This post-epidemic, inter-group amalgamation involving the Monsoni can be seen in two different examples. The first is the movement of a few Monsoni to the Winnipeg River. Prior to 1738, LaVerendrye pictured the Monsoni as an independent people, living in a contiguous territory in the Rainy Lake-Rainy River area. This territorial coherence was reflected in the maps of the period. However, by the early 1740s a small number of Monsoni were living with the Barrier Cree along the Winnipeg River. Previously, as late as 1736, Father Aulneau had identified the Winnipeg River as solely the domain of the Cristinaux, or Cree.32 More important in the long run was the migration of the Southwestern Ojibway into the Monsoni heartland, the Rainy Lake region. Either because

THE SMALLPOX EPIDEMIC OF 1737-1738 the Monsoni were unable to stop the other Ojibway or, more likely, because they sought the security of additional allies, given their low numbers, during the decades following the epidemic the Monsoni were increasingly joined by the Saulteur and other people from Lake Superior. Although the Monsoni did not disappear as individuals, their group supremacy within the region faltered enough that the bear clan joined the moose clan (the Monsoni) as the dominant totems of the people living in the region, and their name fell out of common usage.33 The epidemic also made its way northward to Hudson Bay in 1738. On February 26, 1739, Chief Factor James Isham noted the scourges of this sickness, writing in the journal that "a very Remarkable Sickness and Casualtys is very much [among] our Indn hunters this year wch is ye Chief occasion of ye Inds drawing to ye factory so soon."34 These were the Homeguard Cree, the coastal people who remained near Hudson Bay all year round, and who furnished provisions and other necessaries to the HBC posts during the eighteenth century. The infection may have been passed to them during the previous trading period, which began in May of 1738. In June 1739, the English trader learned that many of the inland people with whom he had traded were dead, in all probability due to smallpox. Isham was told by a group of inland traders that "near 50 canoes yc was here [York Factory] last summr, are [?] Dead + ye rest gone to war against ye poets [Dakota Sioux] ,"35 Thus, some fifty canoes of Aboriginals, perhaps as many as 150 people, perished some time after late May 1738, when the people of the interior first began to arrive at York Factory to trade. In part due to this calamity, the numbers of canoes arriving at York Factory from the interior declined severely in 1739 from the previous year. In 1738, more than 214 canoes arrived at York Factory carrying Upland traders. In 1739 the total was only 134.36 Although smallpox was present in the western part of the Boundary Waters and in the York Factory area, the 1737-38 epidemic does not appear to have spread far into the Petit Nord. Other than Isham s reports, there is no evidence of the disease in either the HBC journals or the French records. The absence of any additional descriptions in the records of Albany Fort is especially significant, since its hinterland included the eastern half of the region at this time. Aboriginal people from the interior, including those who traded with the Canadians, continued to arrive at Albany, without mentioning epidemic disease. Thus, it appears the epidemic spread only along the western and southwestern margins of the Petit Nord. This is not to say that the epidemic did not have an effect on other parts of the region, however. The impact of virgin soil epidemics could extend

71

72

CHAPTER THREE far beyond the immediate area of infection. Although Dobyns's examination of post-epidemic behavioural patterns included an important discussion of the tendency for survivors to migrate away from their traditional lands, he did not deal with an equally important consequence of such migration, the movement into vacated lands by groups who had been left untouched by the epidemic. The massive depopulation and post-epidemic migrations that have been described in detail by researchers such as Dobyns would have opened up lands onto which opportunistic people from more marginal areas would have settled. In short, virgin soil epidemics created population vacuums that other, unaffected, groups migrated to fill. There is reason to believe that a similar spatial dynamic was at play following the mortality among the Cree living at the north end of Lake Winnipeg, triggering population movements and a shift in the territorial boundary between the Cree and Northern Ojibway. In his study of the historical geography of the Lowland Cree, Victor Lytwyn concluded that the Northern Ojibway, under the name "Bungee," did not appear in the York Factory records until 1741, after which date they appeared frequently. Consequently, it would seem that the Northern Ojibway had not traded at York until that date, at least with any regularity or in large numbers. Lytwyn further suggested that this date "may have also indicated their recent arrival in the York Factory hinterland," as they began a northward territorial expansion.37 Given the apparent mortality among the Cree, it is possible that valuable fur-producing territory in the northwestern part of the Petit Nord and along the Saskatchewan River had been opened in the wake of the 1737-38 smallpox epidemic, freeing the way for Ojibway population movements. A similar westward shift by the Ojibway occurred following another smallpox epidemic later in the century. The 1737-38 smallpox epidemic followed a long-standing pattern of diffusion, introduced by ship from the disease pools of Europe to the American colonies of the north Atlantic. From there, the disease moved far into the interior, largely through Aboriginal connections. It progressed generally in a westerly direction, before heading north to Hudson Bay. This had been the trend of epidemic diffusion since the 1630s, and it was considerably reinforced over the next century, even as conditions changed in terms of European settlement and transportation in North America. In contrast, Dobyns implied that it was part of a broader epidemic, a pandemic that stretched from the southeast to Hudson Bay, and to Texas, during the period 1738-39.38 Dobyns's error in describing the date of the epidemic is not in itself a large one, nor, even, is his conclusion regarding the source of the disease; such errors are simply one of the hazards of

THE SMALLPOX EPIDEMIC OF 1737-1738 relying on secondary accounts, 'which is often necessary when attempting to conduct historical epidemiology on a grand scale. Rather, the most serious implication stems from Dobyns's decision to link these events together, based solely on their supposed dates of outbreak. In so doing, he glosses over the actual patterns of epidemic diffusion that emerged following contact, and the tremendous variability that occurred in the epidemic histories of specific peoples and regions, such as the Petit Nord.

73

Illustration 1: Hudson's Bay post at Sault Ste. Marie, 1853. Sault Ste. Marie had emerged by the early nineteenth century as a potent source of disease for the Aboriginal people who visited the HBC post, or who passed through on their way to receive presents from the British government. Sketch by William Armstrong (Algoma Art Gallery, Sault Ste. Marie ON / PAM, HBCA 1987 / 363-S-7/8 [N15269])

4 Epidemic Disease in the Petit Nord: 1739-1780

DURING THE MID- TO LATE EIGHTEENTH CENTURY, EPIDEMICS,

largely of respiratory diseases, increased in the Petit Nord. In part, this may reflect a more complete record, as the HBC began to settle additional posts in the region (Map 9), and their documents expand our view of the interior especially, but also it is evident that, overall, acute infectious diseases were increasingly more common. As well, during this period a new disease—measles—first appeared in the Petit Nord. Together, these suggest that conditions had changed to bring the region somewhat closer to the external disease pools during the period from 1739 to 1780. Despite the overall increase in disease activity, this time was not one of continuous epidemic growth. Rather, there were periods when very few exogenous ailments penetrated the region; during others, such diseases were rampant. There were also regional ebbs and flows. Thus, for stretches of several years, Aboriginal people living in one part of the region suffered from few or no ailments, while those living elsewhere experienced frequent epidemics. Such departures from the overall trend were due to temporary conditions or factors that either favoured or hindered the diffusion of acute infectious diseases.

76

CHAPTER FOUR

Map 9:The Petit Nord, 1739-1780

Despite an overall increase in the frequency of epidemics in the Petit Nord over the entire period, the first dozen or so years were remarkably free of unusual disease activity. None at all was noted at Albany Fort or at Henley House, the HBC's first inland post. Nor was there any in their hinterlands, if the company's records are an accurate indication. Only at York, and the western part of the region, is there meagre evidence of epidemic disease between 1739 and 1750. Initially, there was an outbreak of "violent colds" among the men at the post in the spring of 1744, with perhaps a second later in the year, although this may also have been a continuation of the first. As we have seen, acute respiratory diseases, generally labelled "colds" by the HBC men, had been an occasional problem in the Petit Nord since the early eighteenth century.1 The incidence of such diseases increased considerably during the period from 1739 to 1780, as these early outbreaks were a precursor to the waves of acute respiratory diseases that would sweep into the region later in this era. Still, their impact during 1744 was minimal, and was largely confined to the HBC men.

THE PETIT NORD: 1739-1780 More significant in terms of mortality was an unnamed, but highly lethal, epidemic among the Uplanders who normally traded at York. The main evidence for this is a brief mention in the annual general letter from the York Factory Council to London, dated August 18,1747, which commented that "there has been a sickness amongst the [Upland] Natives y£ [that] has carried of]T| a Great many this Last year... ."2 Curiously, nothing appeared in the post's journal to either confirm the sickness or to provide additional information. It seems likely that it was connected to an unknown illness among the Lower Yanktonai Sioux, who then wintered towards the Missouri River, as the entry for 1746 in the John K. Bear winter count was "They-were-struck-by-an-epidemic."3 Increased Incidence: 1751-1759 The brief period of relative freedom from epidemic disease during the 1740s abruptly gave way to a new period in which sicknesses appeared in the region with greatly increased frequency, beginning in the following decade. This increase was felt unevenly in different parts of the region, however. There were only two incidents recorded in the eastern part, the area served by Albany Fort and Henley House. This was a very modest increase over the previous twelve years. In contrast, the York records describe frequent outbreaks, epidemics, or apparent disease-related mass mortality. Indeed, these were a routine occurrence at York Factory between 1751 and 1759.4 One of the two eastern sicknesses was a minor episode of colds that broke out among the Albany Lowland Cree in September of 1753, shortly after the arrival of the Seahorse from England.5 This was part of a general trend during the eighteenth-century pattern, in "which the HBC ships emerged as a vehicle for the overseas transmission of respiratory diseases. Far more serious was the other eastern outbreak, which had occurred two years earlier. Smallpox returned to the Petit Nord after an absence of only a dozen years, part of a general epidemic in the upper Great Lakes during 1751-52. In 1751 the disease broke out among the Ojibway at Michipicoten along the north shore of Lake Superior, where the French maintained one of their fur-trading posts.6 Consequently, we have evidence of the local impact of the sickness in the "Reports from the Northern Posts" authored by the Governor General of Canada, the marquis de la Jonquiere, dated September 17, 1751. In it, he noted that "out of forty savages at the post of

77

78

CHAPTER FOUR Michipicotton, thirty-four have died and the remaining six have gone in the direction of Hudson's bay."7 This would have been a mortality rate of eighty-five percent. Such devastation is consistent with the human loss experienced by many Aboriginal groups during a virgin soil smallpox epidemic. As well, the subsequent panicked flight noted by la Jonquiere is strongly suggestive of a post-epidemic reaction, which was a general response to epidemic disease among Aboriginal people in the New World. Once again, we can point to a probable eastern origin, this time based on tradition. In 1832, an American physician, Dr. Douglass Houghton, collected oral testimony concerning the occurrence of smallpox among the Southwestern Ojibway of Lake Superior. According to his source, in about 1750, "a war-party of more than one hundred young men having visited Montreal for the purpose of assisting the French in their then existing troubles with the English, became infected with the disease, and but few of the party survived to reach their homes. It does not appear, although they made a precipitate retreat to their own country, that the disease was at this time communicated to any others of the tribe."8 Smallpox was widespread in northeastern North America in 1749-50, and friction between the English and French was indeed drawing Aboriginal people from the Upper Country to Canada.Thus, for instance, in June and July of 1750, la Jonquiere summoned some of the Ottawa and Ojibway of the Upper Country to Montreal to question them regarding trade with the English. However, during the same period, large numbers of the Ottawa and Ojibway from the eastern part of Lake Superior and from Lake Michigan were visiting Oswego, in New York, near eastern sources of disease. The Michipicoten Ojibway may have contracted the disease themselves while travelling to the east or, alternatively, others may have conveyed it to them.9 At about the same time that smallpox broke out in the southeastern part of the Petit Nord, a run of consecutive epidemic years at York began in 1751, lasting until 1754. It began with another crowd disease, measles, which was making its first appearance in the region. On June 13, 1751, Chief Factor James Isham wrote that there were "14 Inds very bad upon the plantation of a sort of mesalls, they are taking at first with violent cold, coughs sore throats swell faces, and very full of spots."Two days later there were more than twenty people ill, and by June 17 "most of home Inds [were] very bad [and] not able to pitch away." On the 24th, however, Isham commented that "most of the Inds [had] recoverd." Despite this optimism, the sickness continued among the Lowland Cree and was not as mild as Isham first thought. On August 26, he noted that "one cannoe came down the River, brought the unwelcome news of 2 Indns Dying, I am sorry to

THE PETIT NORD: 1739-1780 hear of the Death of many Indns since last June, also one cannoe from the Baptist Creek our men has but one Cask of Geese as yet one Indn man Died there." The following day, his subordinate, Samuel Skrimshire, informed Isham of sickness among several of the people tenting about Flamborough House, a dependency ofYork Factory located just over thirty kilometres up the Hayes River. Thereafter, all mention of this disease ceases in the York Factory records.10 This "sort of mesalls" was probably rubeola. Rubeola (ICD-10 B05), or measles, is an acute, highly contagious, crowd disease that provokes a lasting immunity and, consequently, becomes a disease of children in larger urban populations. The measles virus has no non-human reservoir and is spread via droplet emission, through direct contact with nasal or throat secretions, or, less commonly, through indirect contact with objects contaminated with these secretions.The virus enters through the respiratory tract. After infection, there is a seven- to eighteen-day incubation period followed by a brief prodromal period, which produces fever, cough, coryza, and conjunctivitis. There is generally a fourteen-day period between exposure and the appearance of the rash. The macula characteristic of measles are flat, reddish brown, and tend to coalesce to form large blotches. They appear first on the head before spreading down the body and outward to the limbs, and may last four to seven days. Some measles victims will also suffer from periorbital edema (swelling of the tissue covering the eye socket) during the prodromal period, giving the appearance of a swollen face.These symptoms correspond generally to those observed by Isham. Measles can cause exceptionally high case-fatality rates when introduced among virgin soil populations, for a variety of reasons. Nutritional and environmental factors, including malnutrition, lack of adequate, or appropriate, care, and the failure to treat complications, contribute the most, although the geneticist James Neel speculated that perhaps as much as twenty percent of "excess mortality" suffered by virgin soil populations could be attributed to genetic factors.11 Complications and secondary bacterial infection, such as middle ear infections (otitis media), pneumonia, blindness, diarrhoea, and encephalitis, can make the disease especially severe. However, the severity of the disease can be lessened by even basic care, and so no doubt the assistance and sustenance provided to those encamped at the HBC post resulted in fewer mortalities than would otherwise have been the case. By working back from the beginning of the local outbreak, we can identify the immediate source of the measles virus. Initial identification of the disease among the Lowland Cree occurred on June 13. None of these

79

80

CHAPTER FOUR people seems to have been ill prior to that date, and so infection probably occurred about fourteen days earlier, assuming that a positive identification was predicated on the appearance of the characteristic rash. This timing corresponds with the arrival on May 31 of seven canoes of Keskachewan traders, a group ofWestern Cree living on the North Saskatchewan River, far to the west of the Eagle Hills. Among them was a man who was too sick to depart with his countrymen when they began their homeward journey on June 2 and, in all likelihood, it was he who introduced the disease among the local Cree.12 The Keskachewan were not the only Aboriginal group living west of Lake Winnipeg to suffer during this measles epidemic. On July 2, Isham noted in his journal that "38 Cannoes of Misinnipee Inds and Stone Inds came from the North River to trade, informd me a great many cannoes of Sinepoits was obligd to turn back on ace' of Sickness...."13 It's not clear where these Assiniboine lived, but several different bands lived in a relatively narrow country between the forks of the Red and Assiniboine rivers and the North Saskatchewan River at this time. Whether the disease had broken out among out among other groups west of Lake Winnipeg is unknown, but it seems probable. There may be a more remote origin for the disease. Once again, available evidence points to the east. Measles was circulating in eastern colonies over the period from 1747 to 1749 and it may have moved westward from there onto the plains. There is also evidence of measles on the northern plains during the period leading up to the outbreak at York Factory, which, along with smallpox, was said to have ravaged the Pawnee and Witchita, located west of the Missouri in what is now Nebraska. Despite being a western tribe, the Pawnee had connections to the east through their enemies, the Illinois tribes, who lived north of the juncture of the Mississippi and the Ohio rivers. In turn, it has been speculated that the village tribes of the upper Missouri—the Mandan, Hidatsa, and Arikara—all may have suffered from epidemic disease at this time, and perhaps measles passed northward to the Canadian tribes via these agricultural traders.14 Death and disease continued to be frequent visitors to York Factory for three years following the measles epidemic. Between June and July of 1752, the Lowland Cree suffered a widespread, although less severe, epidemic of an unknown disease, which caused coughs, sore throats, and, according to Isham, yellow blood. This disease was probably brought from the interior, since it broke out just after the Uplanders began arriving at the post. It was followed in August by epidemic colds among both the HBC men and the Lowland Cree. This occurred only a week after the Prince Rupert arrived

THE PETIT NORD: 1739-1780 from Europe.Yet another respiratory disease broke out among Isham, most of his men, and all the Aboriginals in July of 1753, once again brought from the interior. This was far more severe than the earlier sicknesses, and was fatal to a great many Aboriginal people, particularly Uplanders. Isham learned that "two Indian woman [are] Dead of the cold aforementiond which has carried a great many Uplanders of[f]." Given its severity, this affliction was more likely influenza than a cold. Finally, the following February brought yet another outbreak of colds among the York Factory men, although no fatalities were noted. This was the fourth respiratory disease at York in three years.15 For two years following the outbreak in February of 1754, no epidemic sickness appeared at York Factory.Then, in 1756, suspicious deaths began to occur among the Aboriginals trading at that post, deaths that appear to have been the result of an unidentified epidemic disease. It is significant that none occurred among the HBC men, who, perhaps, had an acquired immunity. From the fall of 1756 to the summer of 1758, both Uplanders and Lowlanders died at an unusual rate from at least two different sicknesses. The first was less destructive and may have involved only the Lowland Cree. On March 22,1757, two men from the Nelson River arrived at the fort to trade, stating that, since the previous fall, one man and two women had died, another was on the verge of death, and several others were ailing. This was followed a short time later by another suspicious mortality.16 At the end of June, the deaths among the Aboriginal people recommenced. At first, three Homeguards died in short succession, as well as an Uplander who had been left at the fort by his people. Although the cause of these deaths was never explicitly stated, the pattern of mortalities noted in the journal is consistent with a severe epidemic. By August 18, all the Aboriginal people were "in a Sad condition, severall dead." The following day, Isham noted that two more were dead, and he received "sad news Inds Inland dropping off surprizingly." Indeed, something very remarkable was happening. On the 23rd of September, he counted fifteen people dead since August 20. People continued to die into the fall and winter, and on March 2,1758, he wrote, "Nothing material Dead Time of the year, Doubt a good many Inds dead by reason none com'd in, as promised but hope it is otherwise having had too many Died Lately not Less then 2000 Beaver A Year." In June he learned that six men, twelve women, and an unknown number of children had died up the Nelson River since the previous June. The deaths continued to occur into September of 1758, although at a far slower rate.17

81

82

CHAPTER FOUR The mortality among the Lowland Cree and Uplanders during 175758 was exceptional, and must have made a profound impression upon Isham. In response, the trader compiled a table in his journal that identifies by name many of those who died during the peak period of mortality, July 1757 to September 1758.The table also states the numbers of widows and dependants left by the men who succumbed (Table 4). Not only does it record that fifty-four people died, almost certainly an underestimate of the total number of fatalities, but it also shows the impact on the families of the victims in terms of those who died and those who were left unprovided for. Here, then, is an unprecedented glimpse into the human suffering these diseases caused for the people of the Petit Nord. It also shows an important indirect impact of this mortality: the number of widows and orphans who survived.This was a vital consideration for the HBC, which, out of humanitarian and practical motivations, had to provide for these people until other arrangements could be made. For Isham, it must have seemed during this period that the Aboriginal people at York were doomed to die while he could only watch helplessly. With the end of this period of excessive mortality, however, the health status of the local Aboriginals and the Uplanders suddenly improved once again. A Shift in Pattern: 1760-1768 In 1756, France and Great Britain went to war in North America, making official the undeclared hostilities that had been fought through skirmishes and shows of force for several years.The European nations'Aboriginal allies were also involved, including those of the Great Lakes region, and this had a significant impact on the flow of epidemic disease over a vast area. Initially, the massive movements and interactions of the Aboriginal allies favoured the spread of disease into the interior of the continent. Smallpox frequently accompanied the men into battle, and was a tremendous risk for all participants. In fact, these epidemics played a critical role in determining the number of Aboriginal allies that the French could expect from the Upper Country. After the epidemics in 1755 and 1757, the number of warriors arriving from the western nations waned considerably, because of their fears of contracting the disease. Despite this caution, the epidemic of 1757 was carried into the upper Great Lakes region by men returning from the valley of the St. Lawrence.18 The personnel demands made on the French by the war also had an impact on the spread of disease from the east. By the fall of Montreal in

Table 4:James Isham's Record of Deaths at York Factory, July 20,1757, to September 14,1758 (Source: HBCA B.239/a/44:41d-42)

84

CHAPTER FOUR 1760, the French posts in the Northwest had been abandoned, as most of the traders had been called on to defend New France. No longer was there the annual movement of voyageurs from Montreal that had carried disease into the interior. This impact did not end with the Treaty of Paris in 1763, however. For several years the British traders who sought to occupy the void left by the recall of the French were thwarted from entering the Northwest. In part, this was due to the policy of the new British Colonial government in Canada, which reserved the trade of Rupert's Land for the HBC, and in part it resulted from the continued hostility of many of the Aboriginal tribes, who prevented access to the west. Thus, the accidental quarantine that had emerged during the war was prolonged for several years thereafter. Eventually, the British traders and their new Canadian partners regained access to the fur-trading lands of the Northwest, first in the eastern part of the Petit Nord and later in the west. Following Pontiac's Rebellion, trade quickly resumed along the coast of Lake Superior and reports of numerous "French English" trading in the interior began arriving at Albany by 176566. Farther west, the return of the trade was delayed by Ojibway blockades at Rainy Lake until after 1767, when a few traders were finally able to pass through to Lake Winnipeg and also into the interior of the Petit Nord. Thereafter, they arrived in swarms. For instance, in May of 1768, William Tomison informed Andrew Graham at Severn that "the English & French pedlars [were] daily trading what furs the nations catched ... [as they] are nigh hand us and it is a long way to go to your factories."19 Others passed through the southern part in large numbers, on their way to the Grand Nord. With the resumption of these seasonal movements, a familiar vector for the transmission of eastern diseases re-emerged. The disruption to the fur trade that resulted from the Seven Years War and its aftermath coincided with, and no doubt contributed to, significant shifts in the epidemic pattern within the Petit Nord between 1760 and 1768. During this era, no outbreaks were recorded at eitherYork or Severn, and yet they appeared to be frequent at Albany. In a complete reversal of the previous period, the burden of epidemic disease had shifted from the western part of the region to the eastern part. At Albany, however, this period was not uniform, as there were no outbreaks at the post or in its hinterland between 1760 and 1764, the years when the trade was severely constrained, but were annual episodes between 1765 and 1768, when the eastern trade had been reopened. This suggests that the fur trade out of Canada played an important role in the introduction of exogenous diseases to the Petit Nord at this time.

THE PETIT NORD: 1739-1780 The illnesses in the Albany region began with an outbreak of dysentery among the HBC men and many of the Aboriginal people at Albany Fort in January of 1765. HBC trader Humphrey Marten thought first of the quality of the food and possible contamination of the cook's pots. Alternatively, it may have come from the interior. There was an unidentified but mortal affliction at Michilimackinac in 1765, probably the same as the "Great Death" among the inland Aboriginals noted in the Moose Fort journal for the winter of 1764-65. The following autumn, a severe epidemic of colds was at Albany, once again brought from England by the Seahorse, which arrived at Moose Fort on September 4. From there, the cargo and new men were transported to Albany by sloops on September 13 and 14, where they introduced the disease. By October 1, the Homeguards were in very bad health, with severe colds and sore throats, and much the same was occurring among the people at Moose Fort. Although the epidemic was called "colds," this was more likely influenza. A year later, in the fall of 1766, sore throats were common among the Albany men, and during the following April most of the local Aboriginal people suffered from an inflammation of their eyes, perhaps conjunctivitis, as well as another unidentified sickness. Finally, "plurectic [pleuritic] fevers," a non-specific term for inflammation of the lungs, which can be caused by several different disorders, appeared among the Lowland Cree and at least one of the HBC men during the winter of 1767-68. PreRevolutionary Americans employed this and similar terms as "catch-all phrases for all respiratory diseases," and no doubt a similar custom was followed by the HBC men.20 This unprecedented period of frequent outbreaks at Albany Fort continued into the next decade. Return to the Western Petit Nord: 1769-1780 With the way clear after 1768 for travel into the Petit Nord and beyond, the Canadian fur traders flooded the entire region in full force. There was a great influx of Canadian traders in the Albany hinterland in 1769-70, and by 1771 several "Pedlars" were trading at the head of the Severn River. By 1779-80 the HBC's George Sutherland counted no less than seventeen Canadian houses east of Lake Winnipeg, and the country north of Lake Superior was said to be "poisoned" with traders from Canada. Disease accompanied these travellers from the east. The records at all three of the bayside posts, Albany, Severn and York, as well as at Henley House, are replete with references to acute infectious diseases between 1769 and 1780.

85

86

CHAPTER FOUR Overall, such sicknesses were far more common than they had been earlier in the century. This was more of the same at Albany, but represented a significant increase everywhere else, and continental sources were making an important contribution to the increase in the region's disease load. For example, between 1769 and 1780, three outbreaks were noted in the journals at York Factory and two at Severn Fort that either appeared only in their hinterlands or seem to have spread from the interior to the HBC posts. Between 1760 and 1768 there had been none.21 There are several documented instances of epidemic activity inland from the bayside posts during 1769 to 1780, and others undoubtedly went unreported. During the winter of 1768-69, Andrew Graham at Severn noted that there had been "a great sickness" among some of the Upland people, and that two "able providers" died. A suspicious mortality occurred among some of the Aboriginal people living within the York hinterland during 1773-74, and several were also ill of an unidentified complaint at Henley the following March and April, 1774. In 1776-77 an unknown malady, perhaps influenza, appears to have diffused from Henley to Albany. Sickness was common at Henley House following the summer of 1776, and at one time several of the men were ill with fevers. By December of 1776, there was "an epidemic angina & Cough amongst the Europeans & Natives" at Albany Fort, and the chief complaints included fevers, coughs, and pleurisy. In this context, the latter complaint, pleurisy, suggests that pneumonia had developed as a sequel to the original affliction. As before, these symptoms are suggestive of influenza. At one point, several men could only crawl. Though the sickness lasted only into January and no casualties were noted, trader Thomas Hutchins was led to remark that "this year is peculiarly unlucky and unhealthy."22 There were several other outbreaks during this period; their timing indicates that they came from the interior. In April of 1770, John Garbut at Severn was informed by some of the trading Aboriginal people that they had been "very sickly," although whether these people came from the lowlands or beyond is not known. In July of 1773, an epidemic of highly infectious sore throats broke out among the people at Albany Fort. On the 24th of that month, twelve of the men were ill, and two days later several of the Homeguard Cree were also badly off. By the 28th, Humphrey Marten had very few healthy men at his disposal, and the sick included some of the sloopers engaged in the coastal transport between posts. At about this time, violent coughs struck the men of Henley House, and so the disease may have moved back inland from Albany. A few years later, during the winter and ensuing spring of 1775-76, there was a relatively mild outbreak of

THE PETIT NORD: 1739-1780 colds among the Aboriginal and HBC people at York Factory. In the summer of 1777 there was yet another epidemic of nominal colds at York Factory, again among the Aboriginal and HBC people. Symptoms included sore throats, violent coughs, and difficulty breathing, and it is likely that this was no ordinary cold. Geographer Jody Decker speculated that this was a streptococcal infection, but given such vague symptoms it could have been influenza or some other disease. This sickness persisted into the fall and, as before, there is no record of any fatalities. In each of these cases, the timing of the sickness makes it unlikely that the ships were responsible for the initial infection, and so it would appear that the return of the Canadian traders was having a significant effect on the disease load of the Petit Nord.23 One of the most striking features of this period was the great frequency of "colds" of varying descriptions and epidemic sore throats, as diseases of the respiratory tract emerged as by far the most common diseases at this time. Looking back, however, we can see a general tendency towards increased colds during the overall era, 1739 to 1780, and so this was but an elaboration of a long-term trend. In turn, this increase was, in large part, a result of the nature of the disease, or, rather, the diseases. In fact, the colds that the traders noted encompassed a wide body of human sicknesses with roughly similar symptoms, collectively known as Acute Respiratory Diseases (ARDs).The common cold (ICD-10 JOO) encompasses acute sicknesses caused by hundreds of different viruses, notably rhinoviruses and coronaviruses, and respiratory diseases caused by adenoviruses, parainfluenza virus, and respiratory syncytial virus (RSV) would have been indistinguishable to the traders.24 As well, during this early period, English-speaking peoples employed a variety of terms to describe influenza, including "great colds" and "epidemical colds."25 It is almost impossible to differentiate precisely among descriptions of ARDs in the fur-trade records, although the explosive nature and severe symptoms of influenza tend to make it stand out from the others. Nevertheless, there are indications that the behaviour of even the common cold was not always consistent with what we would expect today. These ARDs are not diseases of childhood, even in densely populated communities. In the case of the common cold, universal susceptibility stems largely from the number of different infectious agents. Others induce only a short-lived immune response, while the influenza virus is somewhat unstable, and mutations can render ineffective the antibodies acquired from previous infections. As such, and unlike the true crowd diseases, they often attacked the HBC and Aboriginal people alike. In part, this accounts for the frequency of their arrival in the Petit Nord, as the White employees of the

87

88

CHAPTER FOUR fur trade had little or no immunity and were thus capable of spreading them, regardless of their prior experiences. Influenza (ICD-10 J10,11) is a highly contagious, acute, viral disease of the respiratory tract that is spread from person to person via airborne particles. Its course in humans is brief. Following an incubation period of only one to three days, recovery usually occurs within two to seven days. The infectious period is short compared to many other diseases, lasting only between three and seven days. Common symptoms include a sore throat, cough, a runny nose, fever, chills, weakness, generalized joint and muscle pain, and prostration. Victims may also suffer from severe gastrointestinal problems, such as nausea, vomiting, and diarrhoea. Its complications may also be serious. Sequelae, such as viral and bacterial pneumonia, are responsible for fatalities during epidemics, particularly among the elderly. Subsequent bronchitis may prolong the effects of influenza for weeks or more after the disease has run its course. There is every indication from the historic record that influenza was generally a destructive disease whenever it spread among the Aboriginal people of the Petit Nord. Although it is capable of causing widespread mortality during major epidemics and pandemics, under normal circumstances and where proper medical attention is provided, influenza's case-fatality rate is usually low, generally one percent or less.26 Influenza differs from the crowd infections in that the virus is inherently unstable, and immunity acquired from one episode may not be effective during subsequent outbreaks. Three main types of the disease have been identified, types A, B, and C. All are antigenically distinct and therefore there is no cross-immunity. All three are periodically subject to antigenic drift, a process of genetic mutation that makes a permanent immunity impossible and renders younger adults and children susceptible to the disease. Type A influenza can infect certain species of animals, as well as humans, and is responsible for widespread epidemics and pandemics.27 It is also subject to infrequent antigenic shifts, a more severe mutation that creates an entirely new subtype to which all people are susceptible.Type B is generally associated with regional epidemics, and type C causes sporadic cases and minor localized epidemics.28 Of considerable significance is the rapidity with which influenza can spread and form into epidemics or pandemics, and the great distances this disease can travel. This is largely a function of the instability of the virus, its short incubation period, and its high rate of infectivity. Even before the jet age, "human movement had made the whole civilized world a single epidemiological unit as far as influenza was concerned."29 Periodically, great

THE PETIT NORD: 1739-1780 pandemics of influenza swept across Europe, and on several occasions they reached the Atlantic coast of North America, and beyond. For example, an influenza pandemic that blanketed Europe in 1732-33, beginning with northern Germany, reached North America in the fall of 1733. Similarly, another European pandemic, that of 1761-62, travelled from the West Indies to Halifax and then Boston, before spreading through the settled part of the continent.30There is evidence that Hudson Bay was tied into this worldwide system of diffusion through the HBC ships, and perhaps also through the continental trade. Related to the increased prevalence of ARDs in the Petit Nord was the emergence of the HBC ships as a significant factor in the introduction of acute infectious diseases. Although the company's ships appear to have posed little threat to the health of the Aboriginal people prior to 1739, thereafter the situation changed as, on many occasions between 1739 and 1780, epidemic disease appeared at the HBC's bayside posts shortly after the arrival of the ship from Europe. In addition to the outbreaks of 1752, 1753, and 1765, at least five more followed between 1769 and 1780, a span of only twelve years. Almost all were ARDs.This change in frequency was not the result of a major decline in travel times, nor was it a function of a larger human reservoir aboard the ships. Overall, there was only a modest improvement in the average duration of the journey, compared to the period before 1738, down to about fifty-nine days from about sixty-seven days. Indeed, the ships that transported these sicknesses were not always among the fastest.31 As well, there does not seem to have been an increase in the number of susceptibles aboard the ships to host the disease for longer periods, as the era of major inland expansion by the HBC, during which larger numbers of men were brought from Europe, occurred only after 1780. Instead, it seems likely that something had changed in Great Britain to make these diseases more common or perhaps to increase their range of circulation. The first two diseases introduced by the HBC ships during this period were probably localized around the company's posts. In September 1769 a violent outbreak of some diarrhoea-inducing disease among the York Factory men followed directly upon the arrival of the ship. The next September, moderately severe colds, lasting into October, appeared among the Homeguard Cree and the men of Albany Fort subsequent to the arrival of the sloop with the trading goods from Europe.32 The third such incident, occurring almost two years later, was far more severe and more widespread. On August 25, 1771, the Seahorse dropped anchor near York Factory, after fifty-nine days' sailing from the Orkneys to Hudson Bay. En route it

89

90

CHAPTER FOUR had paused briefly so that the men could trade with the Inuit, but it is likely that the disease it harboured had been brought from Europe. Thereafter, violent colds began to break out among the HBC and Aboriginal people, continuing until the following May. This was an unusually long duration for an epidemic ARD at Hudson Bay, but many of those who at first suffered from this disease later developed bacterial pneumonia, a complication of several cold-like illnesses, even after Andrew Graham reported that the initial sickness was abating. By January of 1772 it had spread to Severn, affecting most of the HBC men during the following month. By the spring, colds, accompanied by sore throats and fevers, had also appeared at Fort Prince ofWales (Churchill), and four Cree and one of the HBC men died there of pneumonia. Although called "colds," it is likely this was influenza. While it did not spread far from its initial locus at York Factory, this is the first documented instance in which an affliction appeared at more than two of the HBC's posts, and it was not typical of the period in this respect.33 The final affliction introduced by the HBC ships during this period occurred a few years later. In 1778 colds and sore throats broke out at both York Factory and Albany Fort after the arrival of the ships. They were widespread at Albany Fort in September, only a week after the sloop brought the goods from the Prince Rupert and brig Charlotte, both of which had sailed from Europe to Moose. Here the disease was universal among young and old, European and Aboriginal.Very likely, the afflictions moved up the Albany River, perhaps with the HBC men who were then travelling upriver as far as Gloucester House, as sickness was common among them and some of the Aboriginal people at Henley House in November and December, including at least one person with a sore throat. It did not spread much beyond Henley, for no illness of this sort appeared at Gloucester, located a short distance upriver. At York Factory, colds were first noted as widely spread among the HBC men at the beginning of October. It is likely that the disease was present immediately after the ship arrived late in the month of August, and that the epidemic built slowly thereafter.34 This pattern of ship-based introduction resembles that experienced by more isolated communities, although on a limited scale. Modern studies of the inhabitants of Antarctic research stations and of the remote islands of Tristan da Cunha and Spitzbergen have found that these populations tend to suffer from extremely severe epidemics of colds when their isolation is broken, generally by supply ships from more populous regions.35 Under these conditions of semi-isolation, the colds behave uncharacteristically. Thus, "any community which is cut off from the rest of the world for periods of a year or more will, on the arrival of visitors, suffer an epidemic

THE PETIT NORD: 1739-1780 of illness of the feverish cold-influenza type...."36 Indeed, the severity of the cold symptoms suffered by an isolated group under such conditions makes it difficult to distinguish the disease from influenza. The same phenomenon has been identified among other isolated populations, at least since the early eighteenth century. Such infections are short-lived, however, and disappear from fully isolated populations a few weeks after the cessation of outside contact. It is noteworthy that they may be transmitted even though the people who bring them appear healthy. Although these outbreaks were nowhere near as regular at Hudson Bay, due to the prolonged length of the journey, they nevertheless resemble those that occurred in the fully isolated communities, particularly with regard to the severity of the disease and the timing of the outbreak immediately following contact with the outside. Therefore, by 1780 the Petit Nord was at risk from another source of disease, albeit one limited to a small range of acute infectious diseases. Overall, during the period of 1739 to 1780, there was a significant increase in the disease load of the Petit Nord over the previous seventy years, suggesting closer connections with the external urban disease pools. This increase was not felt evenly throughout the period, nor throughout the region. As conditions linking different parts of the region to the pools changed, the frequency of epidemics also changed. The HBC ships from Britain and the traders from Canada undoubtedly contributed much to this flow of disease, but they were not the only means by which Old World diseases could reach the Petit Nord.The next major epidemic to appear in the region travelled through Aboriginal movements and connections, and it came from a different source, a disease pool far to the south.

91

Illustration 2: Sault Ste. Marie, Michigan, 1870. By the early nineteenth century, Sault Ste. Marie was a community on the frontier between the traditional world of the Aboriginal people and the expanding world of American civilization. Streamboats such as the one pictured here visited regularly and helped to bring epidemic diseases to the area, which, in turn, were introduced to the Aboriginal people who passed through this growing community. (PAM N5359)

5 The Smallpox Epidemic of 1779-1783

IN THE EARLY 1780S, SMALLPOX ENTERED THE PETIT NORD YET again, this time as part of what has been called "one of the most severe North American pandemics for Native Americans."1 This devastating epidemic originated in Mexico and was perhaps the most widespread in the Americas to that date. The limits to its diffusion can only be guessed at, but it is thought that it spread from Mexico to Great Slave Lake in the north, and from Lake Superior to the Pacific Northwest, blanketing much of the western half of North America. The disease also spread southward into South America, appearing in Guatemala at this time and in Colombia shortly thereafter.2 More than any before it, this epidemic had a profound impact upon the people it struck in the Northwest. In its wake, it left vast numbers of dead and in some cases it almost entirely depopulated individual bands or tribes. Perhaps one half to three quarters of the Ojibway living west of Grand Portage died. It is thought that the Woodland Cree suffered casualties amounting to up to seventy-five percent of their total population. Similar effects were felt among several of the Lowland Cree groups. These deaths caused relocations that reshaped the human landscape throughout the

94

CHAPTER FIVE affected regions. Other repercussions were more subtle, although no less profound, and the terrible mortality of the disease had a great psychological impact upon the survivors. At the same time, it played a major role in shaping the emerging fur trade, facilitating the emergence of a single Canadian competitor to the HBC, the North West Company (NWC). Given its impact on the Aboriginal population and the fur trade, the smallpox epidemic of 1779 to 1783 can arguably be called one of the most significant events in pre-confederation, western Canadian history. Because of the unprecedented severity and extent of this epidemic, many more descriptive accounts have survived for this sickness than for any before in the Canadian Northwest. Its traumatic effects ensured it a prominent place in Aboriginal lore, but it also entered the body of fur-trader oral tradition. In the past, it was customary for the seasoned traders to regale the new recruits with tales gathered from the Aboriginal people and the history of the country, especially during the long winter periods of limited activity. For example, Joseph Robson, who arrived at York Factory in 1744, recorded in his memoirs: The governor who had resided in the country twenty years, was perfect master of the traditional history of it, even from the first settlement of the English; and being a free and communicative man, he used frequently to entertain us with a regular account of all the principal events and discoveries; to which the linguists seldom failed to add the information they got from the natives. By this means I soon obtained a general knowledge of the country, as well inland as upon the coasts.3

The same was true among the Canadian traders. Over the years, these traditions passed from the oral realm to the written, in the memoirs of former traders such as David Thompson, Alexander Henry the Younger, and Alexander Mackenzie. The epidemic of 1779 to 1783 figured prominently in these works. At the same time, the HBC had continued its movement into the interior, and by the time of the epidemic, several of the company's posts were located far from the bay.These, too, provide excellent descriptions of the epidemic. This singular body of evidence is not always helpful, however. Some confusion has surrounded the epidemic's spread. For the most part, the traders were to blame for this confusion, for among them there were as many theories as national interests. This is seen in the words of Ross Cox, an early nineteenth-century fur trader for the Pacific Fur Company and the NWC, who noted in his memoirs: "It is believed in the north-west that this disease was wilfully introduced by the American traders among the

THE SMALLPOX EPIDEMIC OF 1779-1783 Indians of the Missouri... .The Americans throw the blame on the French; while they in turn deny the foul imputation, and broadly charge the Spaniards as the original delinquents."4 Despite these competing claims, it is still possible to identify the epidemic's origin and paths of diffusion. Origins: A 'New' Pool The epidemic had its origin in Mexico City, seemingly signalling the extension of the influence of another disease pool to the Petit Nord. Although it was the "major metropolis of the New World," Mexico was not a true pool in the sense that the disease was endemic within a single community, as was the case in the larger European cities.This is clearly seen in the fear that Spanish officials had for its arrival in the city, and the regulations designed to prevent the disease from reaching it from elsewhere.5 Rather, there was a joint or shared endemicity in New Spain, as the disease circulated constantly within the region. Medical historian S.F. Cook described this relationship: New Spain had been subject to periodic visitations of smallpox since the conquest and during two and a half centuries had become thoroughly saturated with the disease. At intervals epidemics of greater or less intensity would arise, run their course and subside, leaving behind a residuum of infection from which a new epidemic might be generated.6

The same was no doubt true of the other crowd diseases. And so, in August of 1779 a smallpox epidemic broke out in Mexico City, providing the spark that set most of western North America on fire. After starting slowly, it gathered momentum during the ensuing months, and an increase in virulence meant a similar leap in the death toll. The epidemic persisted into the early months of 1780, with perhaps a total of 40,000 fatalities. Thereafter, the city could no longer contain the disease, and it began spreading northward. By late spring, smallpox had reached the larger towns of what is now New Mexico, where it stayed throughout the summer and into autumn.This was followed by a second, deadlier, wave in New Mexico the next year, which travelled up the Rio Grande. With this second wave the disease struck the Aboriginal population with great ferocity, and this proved critical for those living far removed from the area. Smallpox reached Santa Fe, the heart of the continental horse trade, during the first three months of 1781, and thereafter it spread rapidly northward.Within a few more months, it had reached the Canadian plains.7

95

96

CHAPTER FIVE The key to this rapid diffusion was a trading network of vast proportions, a network that by the 1780s blanketed much of North America west of the Mississippi River, carrying trade goods between Mexico and Canada. This extensive system was fuelled by the northward flow of horses from Spanish territory. Once on the northern plains, the horse-trading system met a complementary gun-trading system, which sent firearms of European manufacture in a southward direction. On the eastern part of the plains, European goods that had been obtained from the HBC or the Canadians were taken to the Mandan and traded for other commodities, as the two trading frontiers converged during the mid-eighteenth century. In this way, unmounted people, including the more northern Cree and the Ojibway, were tied into a trading network that began far to the south, and they were, therefore, at risk to any diseases that spread within that system.8 In theory, the arrival of the trading network on the northern plains was an event of fundamental epidemiological importance, as it had the potential to carry epidemic disease vast distances over relatively short periods of time. The use of horses greatly increased the traders' rate of travel and allowed for longer trade expeditions in a single season. According to ethnohistorian Michael Trimble, "an infectious disease with a long incubation period could be transported several hundred miles and introduced into a new host population by trading parties who unknowingly were infected."9 Moreover, even when the traders fell sick, they could travel far greater distances than would have been possible when they moved about on foot. As well, the widespread adoption of the equestrian culture and the attendant horse trade fostered extensive and more frequent tribal contacts among different Plains groups. Such contacts facilitated disease transmission, as did the changing warfare conditions that emerged as a result of the horse. Post-horse alliances were more complex and raids more common than during the pre-horse era, while war parties could travel much greater distances and could be much larger. All of this favoured the spread of acute infections.The horse trade thereby helped to overcome fundamental barriers to the northward diffusion of these diseases, including a paucity of navigable rivers, low population densities, and great distances.10 In 1781, this trading network proved efficient at carrying the smallpox virus on its wide-ranging journey. However, no single group could carry the disease the entire way. Even with horses, it would have died out long before it reached Canada. Rather, far-ranging equestrian nations such as the Comanche, Cheyenne, Crow, and Pawnee carried the virus northward in stages from the southwest to their trading partners throughout most of the northern plains (Map 10). By the summer of 1781, two years after it

THE SMALLPOX EPIDEMIC OF 1779-1783

Map 10: The Pre-1805 Horse-Trading Network of the Central Plains (After Ewers, Horse, 11)

first broke out in Mexico City, but only a few months after it struck Santa Fe, the disease had reached the very margins of the Canadian Northwest. Soon after, it was among the Blackfoot, Cree, and Assiniboine, all of whom were equestrian by this time. Over the next two years, it continued its northward diffusion, long after its spread had carried it beyond the limits of the horse frontier. The epidemic's final movement onto the Canadian plains came not through trade, but through another regular activity: warfare. According to

97

Map 11: Approach of the 1779-1783 Smallpox Epidemic to the Petit Nord

THE SMALLPOX EPIDEMIC OF 1779-1783 Edward Umfreville, a one-time HBC and NWC trader, "it was introduced among them [the Aboriginal peoples of the Northwest] by some of their war parties during the summer of 1781; and by the fall of the year 1782, it had diffused itself to every known part of the country."11 There were two major avenues of diffusion into the Northwest, and they were eerily similar. In one, the virus was carried northward from the Shoshone, or Snake, people into the western Canadian plains. The other derived from the village-dwelling tribes of the upper Missouri and penetrated into the eastern Canadian plains. Both carried the disease into the Petit Nord, although from different directions, and both were brought northward by returning war parties, as Umfreville suggested (Map 11). The Western Thrust In the summer of 1781, a large party of Cree, Assiniboine, Piegan, Sarsi, Blood, and Atsina warriors encountered their Shoshone enemies near the Red Deer River in what is now southern Alberta. The Shoshone, who were sick and dying of smallpox, could offer no resistance. A Cree elder named Saukamappee, who was part of the war party, later told David Thompson that "there was no one to fight with but the dead and the dying, each a mass of corruption. We did not touch them, but left the tents, and held a council on what was to be done. We all thought the Bad Spirit had made himself master of the camp and destroyed them."12 Subsequently, the disease spread to the attackers, and was carried northward by those who fled in terror. In this way the disease reached the North Saskatchewan River. The diffusion process was described by Matthew Cocking at York Factory, who noted that the Cree, Assiniboine, Blackfoot, Piegan, Sarsi, Blood, and GrosVentres (Atsina) met with a Tent of Kenapick Athinewock (i.e.) Snake Indians who were all ill of the Small Pox (and were supposed to have received it from the Spaniards whom tis said those people trade with) killed them all and scalped them to carry away with them. By this means they received the infection and almost all of them died on their return, what few reached their own Country communicated the disorder to their Friends and it spread through the whole Country above here in some parts of which it yet rages.13

Here the disease passed between two, major, Aboriginal economic systems. No longer was it among the wide-ranging and rapidly travelling equestrian tribes of the plains, who had carried it from Santa Fe to the

99

100 CHAPTER FIVE northern plains in the space of, at most, a few months. Instead, it was now spreading through the more northerly Aboriginal people of the parkland and the forests, who travelled more slowly by canoes. In moving from the people of the horse trade to those of the fur trade, the epidemic's velocity declined considerably as it spread farther afield. By October, the HBC men stationed along the North Saskatchewan had become eyewitnesses to the horrors of the epidemic. During the middle of the month, men from Hudson House encountered several victims who were just recovering at the Eagle Hills, survivors of a once larger party who had become too weak to move away from their deceased countrymen. According to one of the men, Mitchell Oman, three-fifths of this group had died and the disease was then widespread among the Aboriginal people of this area. On October 22, a party of infected people arrived at Hudson House. On December 11, 1781, the disease reached the HBC post of Cumberland House, farther down the Saskatchewan. By Christmas Eve, most, if not all, of the Aboriginal people living in the country about Cumberland House were suffering its effects and, shortly thereafter, so too were those of nearby Basquia. About the same time, it began to spread into the Petit Nord.14 As William Tomison, the master of Cumberland House, travelled the Hayes River route to York Factory in June of 1782, most of the Aboriginal people he encountered were either sick or dead of smallpox. Indeed, the epidemic had already spread widely among the people living along the trade routes between Lake Winnipeg and York Factory. On June 10, a brigade of sixteen canoes of Bungee, or Northern Ojibway, from south of the Nelson River arrived at York Factory, the first infected Aboriginal people to reach the HBC fort. They told Chief Factor Matthew Cocking that "a violent disorder has raged among their people which they describe as an eruption on the skin,"15 and that it had caused widespread mortality among those living to the west of Lake Winnipeg. Members of this group had first contracted the disease on a wintertime trip to Cumberland House and it had spread among their people thereafter. By pure chance, they did not pass on the disease to the Homeguard Cree at this time. For a time, the Homeguard Cree of the York Factory area were spared this terrible disease, which was well-entrenched among the Upland traders and which had already spread to some of the other Cree living within the lowlands. This fortunate, but temporary, circumstance was the result of Cocking's desperate attempts to shield the Homeguard and the few remaining Upland people who remained healthy.Thus, on July 8,1782, with two Aboriginal people on the plantation suffering from the disease, Cocking

THE SMALLPOX EPIDEMIC OF 1779-1783 101 directed the men to prevent others from coming to the fort, to preclude contact with the two victims. They were also directed to tell any trading people that he would send men to meet them at a nearby creek, rather than at the fort. On August 6, he confined a brigade of Ojibway to the creek, as some of them were ill with the disease, lest "our Homeguards in the Marshes would most probably catch the disorder either by coming to the Fort or by our peoples cloaths who must have gone over in a boat occasionally to them."16 He also declined to send a packet to Fort Prince ofWales by some Homeguard, fearing that the disease had already appeared among the people there. In this, Cocking showed considerable knowledge concerning the transmission of the virus, both directly and via fomites. Subsequently, he ordered the masters of the HBC's bayside posts to follow his lead. This policy was outlined in a letter to Peter Willdridge at Severn, dated August 12, 1782, in which the Severn master was told to keep a strict look out, that none of the Homeguards come to the factory but keep them at a proper distance so that none of the Pungee's [Bungee or Ojibway] that come for debt may have any Communication with them. Should you find the disorder has attacked any of them, do all in your power for their preservation. If the Englishmen have been handling any person that may have had the small Pox, you must be careful that they shift, wash and air their Cloaths as well as themselves ere they go near one of the homeguards.17

For a considerable time, this policy was successful, for over two months after the arrival of the first smallpox victims atYork Factory, William Falconer could write that "by this prudent precaution the homeguards here are preserved."18 Nevertheless, the York Factory Homeguard Cree would not be protected from infection forever. In this they were the unwitting victims of the American Revolution. In August of 1782, the French navy, under the command of the Comte De Laperouse, attacked Fort Prince ofWales and York Factory. This attack was meant as a blow to British interests during the Revolution and the English men were dispersed to Europe and the HBC posts at the bottom of the bay. However, it was the Aboriginal people who paid a far greater price in the end.The Homeguard, left on their own, eventually contracted smallpox and suffered terribly in the HBC men's absence. When Humphrey Marten reoccupiedYork in 1783, the remaining Nelson River Homeguard gave "a melancholy account of the havoc death hath made in the North River Indians most of whom are cutt off as are

102 CHAPTER FIVE also the Churchill home guard, so that this country for some hundred of miles may too truly be said to be depopulated."19 The disease continued its eastward diffusion, quickly spreading to the Severn Fort hinterland. On April 14,1783, post master John Hodgson was visited by two men who, with their families, had travelled down the Severn River to trade. They informed him that "they have seen but one Indian during the Winter, that they are all dead Inland, these are very deeply marked with the small Pox, one of them has lost all his Children by it except one poor Boy, which is both blind and Lame, and they have been obliged to haul him all the Winter."20 Hodgson also learned that "they are intending to stay here to hunt Geese in the Spring, and as they have all been well of the small Pox since last Fall, there will be no possibility of the homeguards catching it."21 Initial infection of the people of the Severn hinterland had likely occurred during the summer of 1782, just as the disease was spreading around York Factory. It also seems that, as of the spring of 1783, the Severn Fort Homeguard had yet to contract the disease. In all probability, smallpox had entered the Severn hinterland via the Shamattawa River, part of an ancient thoroughfare between the Hayes and Severn river systems. Nicholas Jeremie, who lived at Port Nelson between 1694 and 1714, learned that one could ascend the Shamattawa from the Hayes, cross a portage, and descend the Beaverdam tributary of the Severn (see Map 12).22This crossover between the two drainage systems allowed the Ojibway of the Severn River region to visit and hunt for York Factory. It was also the route by which infected Ojibway carried smallpox from the York Factory region to the Severn hinterland. As HBC trader William Tomison travelled down the Hayes in June of 1782, he encountered several infected parties of Aboriginal people "and several more Sick that are gone up the Shemattaway River."23 Similarly, Mathew Cocking was told by another Ojibway man of the ravages made by this cruel disorder among the Pungees. He says that Himself and the rest of our Deer hunters were on their way to their own parts in Shemattaway River when several of them became ill of the Small Pox most of which died before those who had not yet become ill left him and whom he expects have most of them shared the same fate by this time.24

Contrary to Hodgson's information, the epidemic did not spread throughout the entire Severn hinterland. In the spring of 1784, his successor,William Falconer, wrote that "as to trade I foresee next Summer will produce a small share to us as well as you, the Natives being either gone to the Pedlars

THE SMALLPOX EPIDEMIC OF 1779-1783 103 or out of the world but hope time will bring things to a better bearing."25 Of these two, the Canadians appear to have been a more pressing concern, as in a subsequent letter he claimed that "the trading natives belonging to this place have strolled away to the Pedlars."26 Indeed, despite fears of damage to the trade, Severn was subsequently visited by many canoes of Ojibway and Winisk River people, all with no mention of the disease.27 It may be that only the most western of its Upland people were affected at this time. Smallpox was very slow to strike the Lowland Cree living near Severn. They were probably first exposed to the disease while the post was deserted by the HBC men, between August 20 and October 4 of 1783.There is, however, evidence that they suffered greatly. Donald Gunn, a former HBC employee turned historian, stated that even as late as 1815,"the bleached bones of those who had become the victims of the plague, were to be seen in great quantities at several points on the shores of the Bay,"28 and one of these points was undoubtedly Severn. Few hunters remained alive to attend the goose hunt during the spring of 1784, although there were many widows and orphans about the place. Subsequently, attempts were made to attract replacement hunters to the fort from among those who traded at Albany Fort, by raising the standard of trade.29 In reaching Severn and its hinterland, smallpox had penetrated a considerable distance into the Petit Nord. This was not the full extent of its diffusion, however, and others in the region were also being exposed to its deadly effects via the wave emanating out of the village tribes of the upper Missouri. Before it was done, this epidemic was to have a tremendous impact on the people living far to the south. The Eastern Thrust Coincident with the epidemic's diffusion from the Shoshone to the Saskatchewan River, and then into the Hudson Bay lowlands, a parallel wave spread from the upper Missouri into the Red River area, and from there into the southern portion of the Petit Nord (Map 12). Concerning this phase of the epidemic, David Thompson wrote in his Narrative, "From the best information this disease was caught by the Chipaways (the forest Indians) and the Sieux (of the Plains) about the same time, in the year 1780, by attacking some families of the white people, who had it, and wearing their clothes. They had no idea of the disease and its dreadful nature."30 The statement has an air of authority, and many modern researchers have accepted it, either at face value or with minor alterations. There is only one problem, however: it is almost certainly wrong.

Map 12: Diffusion of the 1779-1783 Smallpox Epidemic in the Petit Nord

THE SMALLPOX EPIDEMIC OF 1779-1783 105 When we look at Thompson's Narrative closely, an interesting pattern emerges. Rather than identifying a single means of diffusion, he noted three, including that the disease was brought from Canada and, as has been noted above, that it spread to the Northwest via the Shoshone.31 This is understandable, if we remember that he was still in Europe at the time of the epidemic and so he had to rely on the memories and speculations of others. In fact, Thompson also had to rely on his own memory, and this may have introduced errors into his interpretations. He began work on his manuscript, which was never completed, during the 1840s, while he was in his seventies and infirm. This was long after he had received the information and it may be that he had become confused over time. Fortunately, eyewitness accounts of the spread of the disease to the Ojibway have survived into the present, and these provide a detailed view of the epidemic's diffusion from the upper Missouri to the Red River area, and beyond. One account is based on testimony gathered from an Ojibway chief of considerable repute, who said the disease was carried back to the Red River area through an attack on another tribe living near the Missouri River, and not from a raid on White families. This would explain the disease's presence in the southern margins of the Petit Nord. William Warren, the Ojibway historian, was given a detailed explanation of this event by Esh-ke-bug-e-coshe, or Flatmouth, the noted leader of the Leech Lake Ojibway. At the time of the epidemic, Flatmouth was a young boy, and as a youth he lived for a time with the Assiniboine and Cree of the Red River area. Flatmouth s age, his earlier life among the Assiniboine and Cree, and his status as an Ojibway spiritual leader, and thus a keeper of tribal history, make him a very credible witness. Moreover, he was probably present when some of these events unfolded.32 According to Flatmouth, shortly before the epidemic, a combined party of Cree, Assiniboine, and Ojibway gathered at a large Cree village located at what is now known as Netley Creek, near the mouth of the Red River.33 They were preparing to go to war against the Gros Ventres or Hidatsa, against whom they periodically fought up to the late 1830s. The Hidatsa comprised one of the village tribes living roughly to the southwest of Lake Winnipeg, along the banks of the Missouri near the Knife River. The warriors proceeded westward and thereafter encountered a village of their foes, near or on the banks of the Missouri River. Upon attacking this village they found that "the resistance made to their attack was feeble. This they soon overcame, and the warriors rushing forward to secure their scalps, discovered the lodges filled with dead bodies, and they could not withstand the stench arising therefrom. The party retreated, after securing the scalps

106 CHAPTER FIVE of those whom they had killed."34 The lack of resistance was due to the effects of smallpox among the Hidatsa, the war party having arrived at the height of their enemy's sickness. Although the allied tribes' military success was total, they also contracted this disease during the raid and, as they made their way homeward, it began to manifest among their ranks, with disastrous consequences. After the first death, they proceeded homeward with quickened speed. Every day, however, their numbers decreased, as they fell sick and died. Out of the party which must have numbered a considerable body of warriors, but four survived to return home to their village at Dead River.35

Thus, in a manner similar to the Shoshone, the Hidatsa had avenged themselves by the very mechanism of their own defeat. While most of the war party mentioned in Flatmouth's account succumbed to smallpox on their precipitous retreat from the Missouri, a few survived to carry the virus back to the Red River region.36 This was probably during the fall of 1781.Their destination was Netley Creek, where the disease was passed to the large camp of people awaiting the return of the war expedition. This was a key location in the Red River Valley and had long served as a major seasonal meeting place for the Cree, Assiniboine, and Ojibway from far afield, as well as a place to leave the elderly and children during the annual trading trip to Hudson Bay. The resulting massive mortality at this place was said by Warren to have given the stream the name of Ne-bo or Death (Dead) River.37 There is further evidence of the impact of this epidemic in the valleys of the Red and the Assiniboine rivers. It was common knowledge among the later fur traders and the Aboriginal people that a large burial mound near the juncture of these two important rivers contained the bodies of those who died during the smallpox epidemic of 1779 to 1783. While he was camped near the mass burial site in 1800, Alexander Henry the Younger was troubled by swarms of water-snakes, which even come into our tents at midday. They appear to lurk and breed in the old graves, of which there are many, this spot having been a place of great resort for the natives in 1781-82; and at the time the smallpox made such havoc many hundreds of men, women, and children were buried here.38

Described by the American fur trader Edwin Denig as "an area of several hundred yards in circumference and ten to twenty feet high, being the cemetery of nearly an entire camp of 230 lodges who died in the infection,"39

THE SMALLPOX EPIDEMIC OF 1779-1783 107 this was actually an ancient mound that was said to predate the Cree occupancy of the Red River Valley, although they used it during the epidemic. Donald Gunn was told by a survivor that "at the commencement of the mortality the Indians, for some time, buried in the mound above described, but did not erect it, and that at a later period of the disease the living did not attempt burying the dead."40 Probably during the initial stages of the epidemic, when there was sufficient manpower, the living could lay the dead to rest. As the epidemic progressed and the dead overwhelmed the living, however, there was no hope of interring the deceased. The grim sight of unburied piles of human remains was seen in the Canadian Northwest in several places for many years after the epidemic, a powerful reminder of the awesome force of the disease.41 From the Red River Valley, the epidemic moved with the fleeing Ojibway in a north and eastward direction.This sort of flight in the face of epidemic disease was a common response among non-sedentary, Aboriginal people in North America, and was often an important factor in its further diffusion. In this case, the disease spread quickly along the major line of communication between Red River and Lake Superior, the southern margins of the Petit Nord, and thereby it passed from the territory of the Cree and Assiniboine to that of the Ojibway and from the plains to the forest. It struck first at Rainy Lake, and this community probably played a key role in the diffusion of the disease. Throughout the historical period, large numbers of people from considerable distances, sometimes numbering in the thousands, gathered there at certain seasons to partake of the rich resources of Rainy Lake and Rainy River, and to engage in social and religious activities. The spring and early summer sturgeon run, and the fall wild rice harvests of this area, were capable of supporting very large populations. This region was almost emptied in the wake of the epidemic. In 1783,Jean-Baptiste Cadotte, a fur trader from Sault Ste. Marie working south of Lake Superior, wrote that there had been many deaths at Rainy Lake, and Flatmouth told William Warren that the location was almost entirely depopulated. On June 22,1782, John Kipling, master of the HBC's Gloucester House, was visited by two canoes of survivors from Rainy Lake and was told that "there is a great Mortality among the Indians and that most of the Indians in and near the raney Lake is dead; and that the assineybols country is almost Depopulated."42 Four and a half decades after smallpox had devastated the Monsoni of the area, the disease had returned to do much the same to those who had settled there following the earlier epidemic. In fact, a similar impact was experienced throughout the Boundary Waters at this time, as the epidemic spread eastward to Lake Superior, entering

108 CHAPTER FIVE new territory, striking people who had been spared during the earlier visitation. In the 1790s, Alexander Mackenzie wrote of Basswood Lake, just to the east of Lac la Croix, that "before the smallpox ravaged this country, and completed what the Nodowasis [the Sioux], in their warfare, had gone far to accomplish, the destruction of its inhabitants, the population was very numerous...," and of Lake of the Woods, "war and small pox had diminished the inhabitants...."43 Finally, the disease was said to have reached Grand Portage on Lake Superior via the Pigeon River route. Overall, in the 1790s, Mackenzie said of the region between the Red River and Lake Superior that it "was formerly very populous, but from the information I received, the aggregate of its inhabitants does not exceed three hundred warriors; and, among the few whom I saw, it appeared to me that the widows were more numerous than the men."44 This was a far cry from the numbers that had been found in the Boundary Waters during LaVerendrye's day. Once it was at Lake Superior, the epidemic curled south and west along the shore before spreading north to the upper Mississippi region, and so it moved along the line of Ojibway settlement. From Grand Portage, smallpox was carried to Fond du Lac, where nearly all of the 300 Ojibway resident there were said to have died.45 From Fond du Lac, fleeing Ojibway carried the disease to Sandy Lake, in the upper Mississippi country, reducing this once-large village to some seven lodges. The trader Jean-Baptiste Cadotte wrote from Sault Ste. Marie on June 16,1783, that "all the Indians from fond du Lac, rainy Lake, Sandy lake, and surrounding places are dead from smallpox."46 The fate of the Sandy Lake Ojibway, like that of the Monsoni before them, gives us rarely seen insights into the changes to the continent s human geography that sometimes occurred in the wake of devastating Old World epidemics. According to Ojibway testimony, in the year 1782, the village of Sandy Lake became nearly depopulated by the dreadful ravages of the smallpox. This band, however, gradually recovered their former strength and numbers, through accessions from the villages of their people located on Lake Superior, who were drawn to the Mississippi country by the richness of the hunting grounds, and facilities of obtaining a plentiful and easy livelihood.47

As was the case with the Monsoni, the band was replenished by the arrival of members of other bands. In this case, however, the arrivals probably did not come from communities that had been devastated by the epidemic, but rather from those that remained unscathed. As such, we can

THE SMALLPOX EPIDEMIC OF 1779-1783 109 add a fifth category to Dobyns's list of common post-epidemic behavioural patterns: the expansion for personal gain of unaffected groups into areas that had been depopulated by earlier epidemics. For some people, massive mortality among their neighbours opened up opportunities for territorial expansion and a better life. Finally, the sickness was carried up the Mississippi River to Leech Lake by some of the Pillager Ojibway, where it "somewhat lessened" their numbers, and to Cass Lake, where the majority of the Ojibway died.48 Arriving at Leech Lake some two years later, a Canadian trader, J.B. Perrault, found a replenished population notwithstanding "que deux ans au paravant il en avoit peri beaucoup par le picotte."49 There the disease was said to have died out. Although widespread, the smallpox epidemic of 1779 to 1783 was not without its limits. Critically, its eastern progress in the Lake Superior area did not carry it among the densely populated Ojibway living south of the lake, nor south to the major Ojibway village at Mille Lacs. According to William Warren, "It did not, luckily, spread generally, over the country occupied by the tribe."50 Instead, the disease halted in its progress in the vicinity of Fond du Lac. Douglass Houghton learned that although "it did not extend easterly on Lake Superior, it is believed that not a single band of Chippewas north or west from Fond du Lac escaped its ravages."51 Similar abrupt transitions between affected and untouched populations were found at many places in western North America as a result of this epidemic, including within the Petit Nord. As smallpox was spreading through the Boundary Waters, or along the southern flank of the Petit Nord, and into the Hudson Bay lowlands along its northern margins, it was also penetrating into the interior of the region from the south (see Map 12). Its probable route lay along the English River to Lac Seul, which, as Edward Umfreville learned in 1784, was the lake by which "all the Indians who trade at Albany Fort pass."52 Although there is no direct documentation of the epidemic from this period, the NWC fur trader Aeneas McDonell referred in 1807 to a sickness at Lac Seul that certainly has the earmarks of this epidemic. In a letter to Roderick McKenzie dated Lac Seul, June 15, 1807, McDonell explained that in that region, "the natives are by no means numerous since the general ravage made amongst them in the year ,"53 (In the copy of the letter in the Masson Collection, no date was supplied, merely an underline.) McDonell also stated that he arrived in the country in the fall of 1803. Since the date was not provided, it may very well be that the event took place before his arrival and he was leaving it to McKenzie to verify the date. If so, and since

110 CHAPTER FIVE there is no record of any catastrophic event among the Lac Seul Ojibway prior to 1803 and after the smallpox epidemic of 1779 to 1783, it would indicate that the Lac Seul people were struck by this epidemic and that population recovery was slow. Another trader, Charles McKenzie, confirmed this over sixty years later in 1845. He noted the death of a woman who may have been the last remaining survivor of this epidemic at Lac Seul: "She was the only one now pocmarked in this quarter—there were a few some thirty years ago—she well remembered when that scourge, the small-pox destroyed the thousands of Indians throughout the country who will never increase to what they were in those days in all probability."54 In recalling the devastation of the smallpox epidemic of 1779 to 1783, the woman was describing events occurring throughout the southwestern Petit Nord. There is more evidence of the epidemic in the records of Gloucester House, in the form of occasional descriptions provided by the Upland people who traded with the English. At the time, Gloucester House was the HBC post located farthest inland within the Petit Nord, and its trading hinterland was extensive. During the 1780s, many of the inland Aboriginal people remained highly mobile, often travelling hundreds of miles to trade, as the peak period of inland expansion by the HBC had yet to occur. As they arrived following the winter of 1781-82, they began to bring word to John Kipling, the trader in charge of Gloucester, of the disaster building to the south and west. On May 27,1782, Kipling "took council with Capt" Abbitywabino and son Concerning the Inland Trade."Abbitywabino, who was from Sturgeon Lake, a small lake lying between Lac Seul and Lake Nipigon, and southwest of Gloucester House, informed the trader that "the Indians Inland was very poor this year that a great Mortality had been among them, [and that] Numbers of the Principal Indians was Dead...."55 The disease had been raging inland from the post for some time, probably since the fall and winter of 1781-82, and it continued to do so well into 1783. Almost a year later, on May 26, 1783, a Lieutenant Metewisito arrived and told Kipling of the deaths due to smallpox of Captain Abbitywabino, another captain from Sturgeon Lake, Macatoppishnew, and many of their followers. The lieutenant claimed that all the Indians on and near Lake Sturgeon are Dead in that Cruel Disorder the small Pox that out of 2 Tribes of Indians that use to resort to this place not more than 2 or 3 children are alive, and amongst them dead is

THE SMALLPOX EPIDEMIC OF 1779-1783 111 2 of the Principal Leaders that belong this (Vizit) Capt.ns Abbitywabino and Macatopishnew.56

Most of Metewisito s people had also died of the disease, and so the location of his country is also significant. It may be that Metewisito was a man named Me,ta,wiss, an Uplander who threatened Gloucester House in 1778. In October of 1778, Kipling was told that Me,ta,wiss and his gang intended to kill the English in the winter of 1778-79 and had "been at Wars with the Natives on Lake St Anns [Lake Nipigon],... and have killed a great Number of that Indian Men,Women and Children.. ,."57 Me,ta,wiss probably belonged to the Wasses, or Ouase (Catfish), a group of Ojibway who lived north of Lake Superior throughout the eighteenth century, and about this time in the Pays Plat region at the mouth of the Nipigon River and at Kaministiquia. It was they who were engaged in conflict with the Aboriginal people of Lake Nipigon at that time, according to both John Long, a trader from Canada, and the HBC men. If Metewisito was Me,ta,wiss, this would suggest that smallpox had also struck the people living east of Grand Portage along the north shore of Lake Superior, perhaps from Grand Portage.58 On May 24,1783, Netauahe and Sheawappennesscome, two other lieutenants, arrived with seven canoes. They could offer the traders little to trade, "having lost some of Their Friends in Winter and they themselves have been sick most of the year so that they are unable to pay their Debts they took up last fall." Unfortunately, it is not known from whence either man came. On June 3, two other leading Uplanders arrived with similarly tragic news. Kipling learned from captains Ca,ca,kes (Caucaukes) and Sheawaquannep (Shewequenap) "that most of their young men is Dead in the Small Pox."The first man may have come from around Sturgeon Lake; the latter was one of two leaders of Pashkokogan Lake, located up the Albany River near Lake St. Joseph. Pashkokogan Lake, like Lac Seul, lay along the route of all the Upland people to Gloucester House and so it is little wonder that the disease appeared there.59 That the mortality among Ca,ca,kes's and Sheawaquannep's men was confined to the young is a significant observation. Given virgin soil conditions and variola major, one would not expect age-selective mortality, especially in a way that singled out young people. It suggests that the older people of these two bands had been exposed to smallpox during a previous epidemic, and were therefore immune in 1782-83. They may have been infected with smallpox at an earlier date, perhaps as part of the movements to Canada during the 1750s.60

112 CHAPTER FIVE The post was unoccupied over the summer and early fall of 1783, and the next notice of smallpox received there was not until June of 1784, when an unidentified individual came to the house, being the first Uplander of the season. He told Kipling "of the Death of a great many of the Gloster Indians." Two weeks later, Captain Caupermertissnewinnekee and Lieutenant Inch arrived at the post, informing the trader that "a great many of their Country men Died of the small pox the last summer."61 Captain Caupermertissnewinnekee came annually to Gloucester House from a great distance inland, and his territory lay towards Lake Winnipeg, probably near the Berens River.The captain also lost his wife and children to the sickness, which, according to Kipling, left him destitute with no one to care for him. His "country men" may have caught smallpox from a number of sources, as the people living along the east coast of Lake Winnipeg travelled widely, and were in contact with Aboriginal people of areas where the disease had already appeared. For instance, the Aboriginal people living east of Lake Winnipeg might go to the lake to await the Canadian traders "and trade with them in there way to Canada," a practice noted by George Sutherland in June of 1778.62 They were also in contact with the York and Severn Aboriginal people, while still others went to the Canadian traders along the Winnipeg River or travelled to the Red River. While any of these may have been the source of the disease, the late date of their sickness suggests that infection from the Severn region was most likely, since the disease had passed through the other areas long before the summer of 1783.63 This was the final reference to this smallpox epidemic in the Gloucester House records. Gloucester House, Henley House, and Brunswick House were all temporarily closed for a time over fears of French attacks. Thus, Gloucester was empty between June 18 and October 24, 1783, a period when further news of the epidemic was filtering down the Albany River. As such, and because the Canadian traders left no record of these epidemic years, the true extent of the epidemic's ravages upland from Gloucester House will likely never be known. It must have been considerable, however, as immediately prior to abandoning Gloucester House, Kipling wrote that "there has hardly been an Indian in but what has lost some part of their family in that Cruel Disorder which I fear will greatly hurt the trade here."64 Nevertheless, all was not total devastation among the Gloucester House Upland people. In June of 1783 an Upland man told Kipling of the Manatie Country, an area lying southwest of Pashkokogan Lake that was inhabited by a great many "Jeppoys," or Ojibway.This was, in fact, the Monontague country, which surrounded Lake Minnitaki, to the southeast of Lac Seul. This description of numerous people hardly seems to fit a post-epidemic

THE SMALLPOX EPIDEMIC OF 1779-1783 113 population, or one in the midst of devastating smallpox. This suggests that, at least as late as June of 1783, the epidemic had yet to reach Lake Minnitaki, although the Aboriginal people living nearby at Sturgeon Lake and Lac Seul were both hit hard by the disease by that time. Unfortunately, this was but a temporary reprieve. A few years later, in 1786-87, a "great sickness" struck the Monontague people, causing an unknown number of deaths.65 In fact, the epidemic managed to penetrate only partway down the Albany River, and its limit in this area lay somewhere upstream from Gloucester House.There is no evidence that the disease ever spread to those who lived in the vicinity of Gloucester House. While Uplanders arrived at the post with news of the epidemic on several occasions between 1781 and 1784, no individual was ever identified as having smallpox when they arrived, nor were the Aboriginal people living in its vicinity ever mentioned as suffering from the disease. Indeed, a letter written by Edward Jarvis at Albany Fort, dated July 5,1783, stated specifically that "small Pox had made its way above Gloucester" [emphasis mine], without suggesting that the disease had progressed to the post.66 As well, while the Upland people were suffering from smallpox during the summer and fall of 1783, and unable to proceed to Gloucester House, Kipling gained his trade chiefly from the home Aboriginals and the "Northward Indians."The latter people were reported to be starving but were never noted as suffering from sickness, and both groups seem to have escaped infection even after the post's temporary closure.67 It appears that the smallpox epidemic of 1779 to 1783 did not spread down the Albany River as far as Gloucester House. Neither did it reach Henley House. Between 1779 and 1784, the post was continuously occupied, except for the summer of 1783 when the men were withdrawn to Albany Fort for fear of French attack. During this period there was no reference either to the epidemic or to sick Aboriginal people, beyond a very few individuals with unidentified ailments. Nor was there any indication given by the local people that anything untoward had happened during the HBC men's absence, unlike the case at some of the bayside posts that were abandoned. If the post records are indicative of the situation, the men at Henley House remained unaware of the epidemic even as it devastated the people living farther up the Albany River and to the northwest, in the Severn hinterland. There is also reason to believe that the disease did not reach Lake Nipigon, then called Lake St.Anns. On the occasions when people from Lake Nipigon visited Gloucester House during the epidemic, they said nothing of the sickness. On July 12, 1782, John Kipling wrote, "Came here a Capt" Antikiskickwescam and Brothers in 2 Canoes, Sons to the Late Capt"

114 CHAPTER FIVE Meetwass (formerly an Albany Leader) from Lake st Anns those is the first Indians that has been here from that Lake, the Distance is not more then 150 Miles from this place...."68 On April 5, 1783, Lieutenant Quesip and another man arrived from that lake and again there was no mention of smallpox. Significantly, of the seven Canadian posts in the Gloucester House area in 1783, Lake Nipigon was one of three that were not abandoned following the epidemic. Perhaps the constant animosity between the Nipigon people and many of their neighbours played a role in preventing the disease from spreading among them. Indeed, in 1784 it was reported that "the Glocr Indians and the St Ann Indians being at variance is afraid to approach so near each others teretorys,"69 and so this buffer area may have helped to limit the diffusion of the epidemic. Victor Lytwyn has suggested that the smallpox epidemic made its way down the Albany River to Albany Fort, arriving there by the spring of 1782, based mainly on the presence of epidemic disease among the people who traded at the fort.70 However, if we consider the epidemic record during the period leading up to the smallpox epidemic, then the presence of such disease was not unusual. Instead, the situation at Albany was complex. Although smallpox did not reach the fort, it came very close, and other diseases, some of them quite virulent, affected the HBC men and the Lowland Cree between 1782 and 1783.This began in May of 1782, when Thomas Hutchins, who had charge at Albany, reported to Edward Jarvis that "there is a great Sickness and Mortality amongst [the Lowland Cree] particularly the Children which quite disheartens the whole."71 By the 24th, seven of the Cree had died and several more were seriously ill. By June 5, five more had died at Albany. At one time, twenty-five Lowland Cree, mainly children, were ill on the plantation.72 Despite the severity of the disease, it was probably not smallpox. Hutchins, a surgeon by training,73 did not identify the disorder as such. Moreover, the mortality among the Albany Lowland Cree was not of a similar magnitude to what was being experienced at York, Severn, or Churchill, and it was concentrated among the children. There is no record of a previous smallpox epidemic in the vicinity of Albany that would have resulted in this pattern. Finally, this outbreak occurred before the disease had even appeared at York Factory, and while it was still confined to the Boundary Waters and the Saskatchewan River. It is highly unlikely that it would have bypassed hundreds of kilometres of intervening territory to strike at James Bay. In short, this was merely a continuation of the truly unhealthy state of affairs that had plagued Albany since the mid-1760s.

THE SMALLPOX EPIDEMIC OF 1779-1783 115 Similarly, another, unnamed, mortal sickness appeared among the Albany people and the HBC men during September of 1782, after Edward Jarvis took over from Hutchins. Within a few days of his arrival, many of the Homeguard were sick and at least three had died, and many of the HBC men were also ailing. Sick people continued to arrive at the fort, seeking medicines, throughout 1782-83, and in November of 1783 an outbreak among the HBC men of an unspecified disease caused sore throats and swelled necks. The latter caused Jarvis to comment that "such a universal sickness is uncommon in the Country."74 It is tempting to take issue with his statement, when we compare the situation then at Albany with that found earlier in the century. The sickness of the fall of 1782 was probably an extension of a widespread and virulent pandemic of influenza that swept through Europe in 1781-82, once again brought to the Hudson Bay lowlands by the HBC ships. The disease had first appeared in Asia in the autumn of 1781 and spread from Siberia to Russia in December. It was in Finland and Germany by February, and reached Denmark, Sweden, and England in April. By early summer of 1782, it had broken out in France, Italy, and most of the rest of Europe. Critically, it appeared in London in mid-May, striking adults in very large numbers.75 At about this time the Seahorse (II), under Captain Joseph Richards, was preparing to sail from London for the Orkneys with fifty-nine men aboard. On June 19 Captain Richards died of "an inflammatory sore throat and fever," almost certainly influenza, while docked at Stromness.Thereafter, the Seahorse took on board nine passengers, and continued on to James Bay, arriving at Moose on August 24. On the 30th, seven of the passengers from the Orkneys were dispatched by sloop for Albany Fort.76 Within two weeks, the disease had assumed epidemic proportions among the HBC men and Aboriginal people at Albany. Such a pattern of ship-based introduction of acute infectious disease to Hudson Bay was by no means rare by the latter part of the eighteenth century, as the Canadian Northwest became more tightly integrated into a worldwide system of disease diffusion. This was not, however, smallpox. Finally, in August of 1784, news of the outbreak of an entirely new disease among the Cree living in the Hudson Bay lowlands near Albany Fort reached Jarvis, some time after the fact. This, finally, was smallpox. On August 9,1784, the trader wrote: In the afternoon Capt" Assup came in so poor that many of his young fellows could not even pay their debts, they tell of numerous deaths among the Indians around them by an epidemical disorder which from their

116 CHAPTER FIVE description should seem to be the small pox, which I fear has made its way from the northward.77

Captain Assup was an influential leader who, along with four other leaders of the Albany Fort Lowland Cree—Questach, Pusquothecot, Saquot, and Archekishick—claimed specific hunting grounds to the north of Albany Fort along the Ekwan and Attawapiskat rivers.78 No doubt the disease had made its ravages among the bands led by these men, but Captain Assup s gang had also suffered severely.79 An oral tradition analyzed by Lytwyn presents a picture of horrendous suffering and mortality among the people gathered along the Ekwan River, and the desperate attempts by the people to stem the progress of the disease.80 This is the only direct indication of smallpox among the Aboriginal people who traded at Albany Fort, and there is no evidence that it spread any farther than among them. As Jarvis suggested, the disease had come from the north, rather than from up the Albany. Its timing was consistent with infection from Severn House, where the disease was late in arriving, and contact between the Severn and Albany Lowland Cree was almost inevitable. There were Severn River Cree at Albany Fort in June of 1783, and the Albany Cree were known to travel in the opposite direction.81 Moreover, 1783 was one of a string of years during which the goose hunts failed and hunger was common in the lowlands around Albany Fort. In response, the Cree turned to the caribou in order to survive, and in the fall of 1783 the goose hunters told Jarvis, "Do not urge us to hunt geese when there are really none to kill, but let us have our debt and get as far as we can from the Factory to the northward where deer are plenty and we can live as we too plainly see should we be distressed you cannot assist us."82Two prime summer hunting grounds for caribou were at Akimiski Island and near Cape Henrietta Maria, to the east of the Severn River. Both destinations were not far from the territory of the "Eastward Home guards" of Severn Fort. Regardless of the means of diffusion, however, this extension to the people of the Attawapiskat and Ekwan rivers remained the northeastern limit of the smallpox epidemic of 1779 to 1783. Once again, there were sharp delimitations on the human landscape between those who had suffered the disease and those who had escaped. The smallpox epidemic of 1779 to 1783 did not spread beyond the areas noted above. In the lowlands, the disease never reached Moose Fort, nor beyond it to the east coast of James Bay. Similarly, there was no mention among the Upland people arriving at Moose from its vast hinterland, as they continued to bring their furs to trade with the English. Indeed, this

THE SMALLPOX EPIDEMIC OF 1779-1783 117 period was a banner era of trade at Moose and its dependencies, with returns rising from just over 9000 Made Beaver (MB) in 1780 and 1781, to greater than 10,000 MB in 1783 and 1784, and then to over 12,000 MB in 1785 and 1786.83There is also no evidence that the disease penetrated into the heavily travelled Moose-Michipicoten corridor between James Bay and Lake Superior. Philip Turner at Brunswick House (or Wapiscogamy) reported an increase in trade in 1782-83 and the Aboriginal people who subsequently arrived at the post had not been exposed to the disease during this epidemic.84 Unfortunately, this was made abundantly clear when smallpox struck the area only a few years later. The varying impact of this epidemic in the Petit Nord and surrounding regions is significant. In addition to the overall limits of the epidemic's diffusion, there were also gaps in its coverage. In many cases, well documented elsewhere in the Northwest but undoubtedly similar in parts of the Petit Nord, entire bands were devastated, losing a significant portion of their population to the disease. Other bands were untouched by this epidemic, particularly those living in the eastern half of the region. Between these extremes were perhaps a few bands whose older members were immune due to prior exposure, but whose young people caught smallpox and died. Similar patterns were seen elsewhere at this time. Ethnohistorian Shepard Krech found evidence that the epidemic had only limited penetration among the Athapaskan tribes of the Arctic drainage lowlands, perhaps striking only the southern groups who traded with the English. Similarly, Cole Harris concluded that there were definite limits to the epidemic's diffusion among the sedentary Aboriginal people living in the coastal region of the Pacific Northwest, with several peoples escaping infection. Despite dense populations made possible by rich marine resources, their "geographically circumscribed lives" led to significant levels of isolation between groups, thwarting the disease's spread. George Lovell, a geographer, found a wide variation in mortality rates experienced by the people of the Cuchumatan Highlands of Guatemala, who became infected during this epidemic. Even on the interior plains, where the transport advantages provided by the horse helped to make the disease almost universally destructive, at least one group, a large band of Crow, providentially escaped infection.85 Over time, these variations in the epidemic experiences of groups living within the Petit Nord, and between them and the people of other regions, became critical factors in bringing about territorial and cultural changes. It is to be expected, for instance, that sudden shifts in relative population

118 CHAPTER FIVE levels would have implications for military balances of power between rivals. As well, population losses would lead to the amalgamation of survivors from different bands, extending even to people of different tribal affiliations, and might result in the relaxation of taboos concerning marriage partners. In the context of the epidemic of 1779 to 1783, however, perhaps the most fundamental change deriving from differential impact was the movement of Ojibway people into the Red River Valley. Evidence suggests that the Ojibway, and to a lesser extent the Ottawa, began to move onto the plains permanently and in larger numbers after the epidemic decimated the Cree and Assiniboine living in the valley. While some of these immigrants may have come from the Petit Nord, it is likely that most came from those areas untouched by the epidemic, to the south and northeast of Lake Superior, as had the Ojibway who moved into Sandy Lake, in the upper Mississippi. This epidemic signalled the end of an era. During the decades that followed, exogenous diseases began to strike the Petit Nord with ever-increasing frequency, if not the same virulence. Gone were the days when epidemics were a rare occurrence. For this, we can point to the emergence of an urban disease pool in the cities of the newly formed United States and the movement of large numbers ofWhites into the interior of North America. At the same time, however, few of the sicknesses that followed achieved the same penetration into the region as this devastating epidemic. As a result, their effects tended to be more localized, and, over time, the epidemic histories of particular groups diverged considerably. Parts of the Petit Nord were subject to frequent bouts of epidemic disease, while others were visited only infrequently. This new era of increasing epidemiological fragmentation began during the last two decades of the eighteenth century, but reached its peak only in the nineteenth.

6

Epidemic Disease in the Petit Nord: 1784-1818

THE LATE EIGHTEENTH AND EARLY NINETEENTH CENTURIES witnessed changes within the Petit Nord and elsewhere that had a significant and lasting impact on the presence, spread, and reporting of epidemic disease in the region. Among the most important were fundamental changes to the spatial structure of the Canadian fur trade. During the initial period of its tenure in the Petit Nord, the HBC remained tied to Hudson and James bays, content to have the Aboriginal people carry their furs to the coastal factories. Although the company was criticized by contemporary observers and modern historians as being "asleep by the Bay," this was a cost-effective way of pursuing the fur trade. As its Canadian rivals increasingly intercepted its supply of furs, however, the company was forced to move inland, beginning in earnest in the 1780s. Thus, between 1784 and 1818, there was a period of unprecedented expansion by the English company within the Petit Nord. The widespread construction of inland posts by both the HBC and the NWC meant shorter distances that many Aboriginal people were required to travel each year to trade, it being no longer necessary to make the long, tedious, and sometimes dangerous, trip to the HBC posts on Hudson and James bays.

120 CHAPTER Six At first, this thrust was modest. Between 1786 and 1795, Albany was the only company bayside post to expand into the Petit Nord. By 1795 it controlled a loose network of establishments stretching from James Bay westward to Lake Winnipeg, and from the Boundary Waters north to the Bloodvein River, flowing into the east side of Lake Winnipeg (Map 13). There was no similar inland expansion within the Petit Nord from York or Severn, and Albany's hinterland quickly grew to envelope the entire southern half of the region, parts of which it once had shared with York Factory.1 The people living in what was then Albany's hinterland were most at risk to being exposed to exogenous diseases in the Petit Nord, not only because posts were established among them, but also because they lived close to the trade routes of the plains and to the heavily travelled canoe routes from the east, which became corridors for the diffusion of disease. In some cases, the traders contracted these ailments as they journeyed to and from their posts in the interior. Consequently, not only were the Albany men

Map 13:The Petit Nord, 1784-1818

DISEASE IN THE PETIT NORD: 1784-1818 121 learning first-hand of the diseases striking the interior following 1784 but, by travelling far inland, they also began to transport these diseases over long distances. After 1795, and until the early nineteenth century, competition between the Canadians and the HBC intensified, spurring greater exploration of the region and additional post construction by both groups of traders.2 During this period, the number of posts in operation within the Petit Nord reached its peak. At the time of the epidemic of 1779 to 1783, there had been only two HBC posts in the interior of the Petit Nord: Henley House and Gloucester House. By the turn of the century, there were over twenty-five. Most were smaller outposts and, in some cases, men were also sent to winter with the trappers, trading the furs as they were taken. Consequently, contact between the traders and Aboriginal people increased and, equally importantly, it occurred throughout much of the year, rather than in a constrained trading season. This greatly extended the potential period for disease transmission, from a few weeks to several months, and therefore also the opportunities for transmission of infectious diseases to the Aboriginal people in the Petit Nord and the likelihood that such afflictions were reported in the HBC records. It was also during this period that York Factory began to establish a presence within the Petit Nord. By the turn of the centuryYork Factory's trading area extended farther south than it had since the beginning of inland expansion, although it was still limited to the northwestern corner of the region. It would be another decade before the York men again traded for the furs of the western part of the Boundary Waters region.3 The fur trade of the Petit Nord changed fundamentally after 1810, particularly that of the HBC. As the NWC scaled back its operations within parts of the region, the HBC radically reorganized its fur trade in the entire Northwest in 1810, as part of the "New System" or the "Retrenching System," in order to reduce costs and to compete more effectively with the Canadians. Fundamental to this system was the creation of two, massive, fur-trading departments: the Northern, controlled and outfitted from York Factory; and the Southern, controlled and outfitted from Moose Factory. No longer was Albany a key administrative centre. In fact, Albany was stripped of many of its inland posts. A district that had once stretched as far as the Assiniboine River was reduced to only Osnaburgh, Gloucester House, Martin's Falls, and Henley House. In contrast, the trade at York Factory derived from a huge territory that covered large parts of the Petit Nord, including most of the western part of the region and much of the Boundary Waters. This reversed the situation that was in place before 1810, as it

122 CHAPTER Six was York Factory whose hinterland now included the more southern lands, while Albany's was severely cut back.4 At the same time as structural changes occurred in the fur trade of the Petit Nord, other changes to the south increased the potential flow of disease to the region. In the period following 1790, there was a significant increase in the presence of non-Aboriginals on the upper Missouri, including fur traders and explorers who visited the village tribes from the south. Most operated out of Spanish-controlled St. Louis, which was then a small but growing community with ties to Louisiana. Men such as Jacques D'Eglise, Jean Baptiste Truteau, and Manuel Lisa were potential disease vectors by virtue of their interaction with both the Aboriginal and nonAboriginal spheres.Thereafter, according to Trimble, "a regularized mechanism existed for the diffusion of epidemic diseases to the villages."5 The Spanish traders were not alone, however, for both the HBC men and their opponents had been conducting their own annual visits to the village tribes since at least the 1780s, arriving from the Red River-Assiniboine River area.These British and Canadian traders completed the cycle whereby epidemic disease could flow from the settled areas to the south through the Mandan and other tribes of the upper Missouri, to Canadian territory.6 Finally, a fundamental change to the east of the region proved far more significant in the long term: the emergence of a domestic urban disease pool in the northeastern United States. During the American colonial period, the urban population of the northeast was such that the crowd diseases had to be reintroduced each time from external disease pools. This occurred in varying frequency and was a limiting factor in the periodicity of epidemics both in the colonies and beyond.Toward the end of the eighteenth century, however, the American urban communities located along the Atlantic coast had grown sufficiently large to permanently host the crowd diseases. Consequently, the disease load of the larger cities and their surrounding hinterlands was substantial, and included afflictions such as colds, erysipelas, hepatitis, smallpox, measles, whooping cough, and mumps, among many others.7 A new urban disease pool had been born, situated in uncomfortably close proximity to the Petit Nord. Initially, these diseases appear to have been endemic within the northeastern United States as a whole, rather than in individual cities.8 This was a shared form of endemicity with multiple urban hosts, and the epidemic pattern that emerged over time in these communities would not have differed greatly from that seen in a major city of the day, such as London. During the eighteenth century, the American colonies had grown tremendously, from perhaps a total population of about 250,000 in 1700 to nearly

DISEASE IN THE PETIT NORD: 1784-1818 123 four million by 1790, most of it along the eastern seaboard. By the census of 1800, the total had risen to 5,305,937.9This tremendous growth came as a result of high birth rates coupled with declining infant mortality and increased immigration. At the same time, the birth of the United States created inter-community transport linkages in the form of roads and turnpikes, along which regularly scheduled stagecoaches connected the coastal cities. From New York City, Philadelphia was but one day by road, while Baltimore was two days away and Washington three to four.10 In turn, this facilitated the circulation of infections. There was as yet no single, dominant city. Instead, the three major cities, Philadelphia, New York, and Boston, all had similar populations, none of which exceeded the endemic threshold of the major crowd diseases until much later.11 Nevertheless, the crowd diseases that appeared in these cities exhibited an endemic pattern. For instance, as of 1792, measles was common, although not yet truly endemic, in Philadelphia, while smallpox was said to be endemic.12 At that time, its population was only 42,400, or far less than the population threshold for measles endemicity that has been calculated by modern theoreticians. After about 1795, measles, too, was endemic in the city, with occasional epidemics, possibly on a seven-year cycle.13 A similar pattern appeared in Boston at about the same time. The emergence of this new American pool contributed greatly to new patterns of disease diffusion beyond coastal North America. For a century and a half, the European colonies along the Atlantic coast of the continent had served only as extensions of distant disease pools. On occasion, ships from Europe or the West Indies introduced Old World diseases into the major port cities, and these afflictions sometimes flowed through the colonies to other, non-Aboriginal communities, and, less often, to the Aboriginal people of the continent. Between epidemics, these diseases disappeared and several years or even decades could pass before their return, depending on the timing of the arrival of another infected ship.14 With the creation of a local disease pool, however, these sicknesses became a constant threat to spread beyond the limits of non-Aboriginal settlement. As new means to carry disease from the new pool also emerged, the frequency of epidemics within the interior of North America increased significantly. Once again, changing patterns of human settlement and travel played a role in extending the influence, and the disease frontier, of an urban disease pool. Following the Revolution, the American people began to move into the interior in increasing numbers, freed of the former constraints that had been set by the British Crown. These migrations and the resulting settlements were key factors in the westward diffusion of infections from the

124 CHAPTER Six new urban disease pool. In a sense, their role paralleled that of the European migrations to the Atlantic coastal settlements during the seventeenth century. Rather than colony ships from Europe, there were stagecoaches, keelboats, and flatboats from the east, carrying thousands of men, women, and children, and rather than colony towns such as Boston, Philadelphia, and New York, there were burgeoning frontier communities such as Pittsburgh, Louisville, and Nashville.15 The consequence, in terms of disease diffusion, was the same. With large-scale, sustained migration came epidemic disease. It took perhaps half a century for the full impact of this expansion to be felt in the Petit Nord, however, largely because this settlement expansion was initially directed southward along the Ohio River. With somewhat of a buffer between the Petit Nord and the settlement frontier provided by other Aboriginal peoples, many of whom remained hostile to the American encroachment on their lands, neither settlement nor the full range of diseases was able to penetrate to the region's margins. Only during the era after 1820 did this migrant flow begin to reach the border on the upper Great Lakes, and with it all manner of epidemic disease. The changes taking place in northeastern North America in terms of epidemic and endemic disease were not isolated. Rather, they were part of new, more extensive, patterns of disease diffusion emerging at this time. According to historian Alfred Crosby, the circulation of many afflictions on a global scale was enhanced during the late eighteenth century by accelerated population growth, urbanization, and improved transportation.16Thus, at the same time that a new pool was increasing the availability of acute infectious diseases in North America, other changes were carrying them throughout the world. Albany Expands Inland: 1784-1795 Acute infectious diseases were regular visitors to the Petit Nord between 1784 and 1795, with at least one outbreak or epidemic in the region almost every year. This was a continuation of the general trend towards increasing sickness that was seen during the period leading up to the smallpox epidemic of 1779 to 1783. Many, even most, of these reports of sickness occurred in the interior of the region, and, of these, all but one occurred in the southern half of the region. This was the portion closest to the main routes of travel along the southern flank of the region, those that connected the Petit Nord with the urban east and the trading routes of the plains.

DISEASE IN THE PETIT NORD: 1784-1818 125 There was a similar disparity within the Hudson Bay lowlands, as sicknesses broke out more often at Albany Fort than at Severn and York. At least seven outbreaks were recorded at Albany between 1784 and 1795, most of them of cold-like diseases.17 This was essentially the same pattern as during the period from 1770 to 1780. Unlike the earlier period, such sicknesses were much less common in the western part of the lowlands, with only three minor illnesses at Severn and two at York.18 This may have been due to a change in the source of disease. During this period, HBC ships introduced acute infectious diseases to the Petit Nord in only two instances.19 Instead, most of these afflictions appear to have come from continental sources. Consequently, Albany, whose trading hinterland encompassed most of the southern half of the Petit Nord, was more exposed to the spread of acute infectious disease than either Severn orYork, through the movements of its inland men, who travelled down the Albany River from the interior each summer. This was an unfortunate and unforeseen consequence of an increasingly complex transport system and the expansion of the fur trade into the region. Most of the sicknesses during the first few years after 1784 were of only momentary impact. As was common during the previous era, many were mild respiratory complaints that did little more than cause a brief inconvenience. There were, however, a few exceptions. In 1785, an unconfirmed report was circulated at Gloucester House that smallpox raged again, somewhere to the west of the post. This was followed soon after by a severe epidemic among the Aboriginal people living to the southwest of Gloucester House, in the Monontague country. During the fall and winter of 178687, an unknown disease raged among the people living immediately to the south of Lac Seul, one of the areas that had been untouched by the smallpox epidemic of 1779 to 1783. In this instance, however, the disease did not spread to the Albany River area.20 A few years later, in 1788-89, smallpox returned to the Petit Nord.This time the disease was limited to the eastern part of the region, another area that had been unaffected during the earlier visitation. Only five years had elapsed since that previous smallpox epidemic had run its course, and this decline in the inter-epidemic period is further evidence that the region's epidemic isolation was breaking down. This was not due to growing connections with the southern disease pools, however. Rather, the disease came from the east, and its path of diffusion was a very early indicator of what was to become a dangerous epidemiological trend for the people living in the upper Great Lakes region and beyond: the growth of non-Aboriginal settlement in the interior of North America and its increasing role in the

126 CHAPTER Six spread of disease. As the trickle of American settlers who headed westward into the interior during the late eighteenth century became a flood during the nineteenth, epidemic diseases returned again and again with staggering frequency. During the late 1780s, this flow of immigrants was directed along the Ohio River. Between October 10, 1786, and December 9, 1787, nearly 6000 American settlers travelled along the Ohio from the settled parts of the United States. Some of these people were probably infected with smallpox, because in 1787 the disease broke out among the tribes living near the southern end of Lake Huron and the western part of Lake Erie, or north of the emerging settlement corridor.The Wyandot and the Munsee, who lived near the southwestern shore of Lake Erie and at Detroit, were exposed, and the smallpox may also have spread to the Piankeshaw (Miami) living on the Wabash.There is good reason to believe that the settlers had introduced the disease, as the Wyandot singled out the White people as the cause of their suffering.21 By the following year it had made its way to Lake Superior. Smallpox reached Michipicoten, on the north shore of Lake Superior, during the spring or summer of 1788, and subsequently spread into the interior.This was a key location in terms of both the fur trade and Aboriginal transportation, as it lay at the crossroads of major transportation corridors linking Lake Superior with Hudson Bay and Montreal. There had been a Canadian post at Michipicoten since 1725, and the Aboriginal people living along the well-travelled river route leading to James Bay routinely visited it. News of mortality reached the nearest HBC post, New Brunswick (or Micabanish) House, late in the summer. On August 28, 1788, Captain Nimica arrived at the post and informed the post master, William Bolland, that" Cap'Mumim both his wives, and several of his Children, died a few days ago, on their return from Mishipicoote."22 Early in September, Captain Sackawabish, who had been scouting out the situation of other Aboriginal people for Bolland, returned from Michipicoten and explained that "a great mortality prevails there."23 He too fell ill a short time later, and remained so throughout the winter. By this time, however, smallpox had already spread to the New Brunswick House area. The following day came news that Captain Nimica and his wife were dead of the same disease, and several more in their family were sick, having taken ill only a few days after they departed the post late in August.24 Throughout the fall and into the following spring, people in the New Brunswick House area continued to fall ill and many perished, including several who had

DISEASE IN THE PETIT NORD: 1784-1818 127 gone to Michipicoten.25 On June 3, Bolland, anticipating a disastrous year for trade, learned that three more of the Indians (belonging the family) that was here in Winter (vide 22nd Jan) died very suddenly this spring and that several others, which I expected in here, to Trade, died in ye Winter, so that there is not now above one fifth, of the Natives, living that I had been inform'd would be in here, which makes me much afraid the Trade will be but very small.26

Bolland's fears proved true, as even those who survived trapped very few furs. Fortunately for the rest of the people in the Petit Nord, this smallpox epidemic penetrated only a short distance into the region. Its direct effects seem to have been felt only in the area between Michipicoten and New Brunswick House.This limited extent, consistent with every epidemic that struck the Petit Nord, once again had broader spatial consequences, both temporary and permanent. For instance, at least one trapper avoided New Brunswick House for fear of catching the disease. On August 12, 1789, Bolland wrote that "O'tash'a'way'kee'shick' came in with a few Furrs, he informs me he would have been in early in the spring, but hearing such a mortality prevail'd about here, he was afraid to come, he therefore went with his Furrs to the Sowe'way'minica Settlemt."27 The Suweawamenica Settlement, or Langue de Terre, was located on the west branch of the Montreal River, to the north of Lake Huron. Avoidance behaviour could also be of longer duration. A year after the epidemic, one of the survivors came calling on the HBC post at Osnaburgh House, far to the northwest of Michipicoten. On June 11, 1790, post master Robert Goodwin wrote in his journal that "at Noon a strange Captain from the Utchepoy [Ojibway] Country came in to see the place & know the track he says all the indians in his Country are dying with the small pox & he intends to leave it and come here to trade ye next year if I use him well."28 This may be an isolated incident, but it may also show part of the motivation for a general westward Ojibway migration that was taking place at this time, one that has been linked to the epidemic of 1779 to 1783. Acute infectious diseases continued to appear in the Petit Nord at the same steady rate between 1789 and 1795.29 Several are noteworthy for their severity or for the broader disease patterns they reflect. For instance, there was widespread sickness among the local Gloucester House Aboriginal people and the HBC men in the winter and spring of 1789-90, followed by an outbreak at Henley House that spring.These were probably the same

128 CHAPTER Six disease. During the following fall and winter, an outbreak of sore throats and colds occurred among the Aboriginal people and some of the HBC men at Henley House, accompanied by pneumonia in some. At least four of the Aboriginal people died during this episode.These symptoms suggest influenza.There had been a massive European influenza pandemic in 178889, and the disease had appeared in New York City in September of 1789. From there the disease spread widely in the east and crossed over to the West Indies.30 It may be that this disease had spread into the interior of the continent as well, reaching at least as far as the Albany River. Also during this period were the first reports of sickness and diseaseinduced mortality in the southwestern part of the Petit Nord, the first such written accounts by non-Aboriginal people from that quarter since the days of LaVerendrye. As the HBC men settled posts throughout more and more of the Petit Nord, they began to observe for themselves the effects of epidemics that before would have been known to them only by (often vague) report. Still, not all were eyewitness accounts, especially during the initial years. In September of 1793, some Escabitchewan people told James Sutherland that there had been a "great death" among those at Lac la Pluie and Portage de 1'Isle.31 Sutherland suspected that this was merely a ploy designed to keep him from travelling beyond Escabitchewan. More certain is a "great mortality" documented among the people of the Lac la Pluie area in the winter of 1795-96. Eleven of diverse ages died, including several prominent men.32 This was the first of many reports of sickness and mortality that would strike the people living within the southwestern part of the Petit Nord over the next two decades. Finally, there was a severe and unusual sickness among the Albany Fort Cree in April of 1795. This latter affliction, which caused a "great and Uncommon Mortality" among the Albany Cree, was unknown to the HBC surgeon, "either by Observation or Tradition."33 There were said to have been six fatalities between April 1 and 21 alone. The symptoms included a swollen and inflamed tongue that made breathing difficult, and a painful swelling that extended from the lower jaw, towards the ears, and down to the sternum, or breastbone. Curiously, it seems to have bypassed the HBC men, despite the presence of several sick Cree people at the post. This suggests perhaps that this was a disease the Europeans had had in childhood and that behaved atypically when among the Aboriginal people. Of the many sicknesses that broke out at Albany between 1784 and 1795, this was

DISEASE IN THE PETIT NORD: 1784-1818 129 the only one that was responsible for deaths among the Aboriginal people or traders. Competition Peaks: 1796-1809 After 1795, both English and Canadian traders entered the Petit Nord in larger numbers than ever before. While the escalation in competition for furs had a fundamental impact on the fur trade in the region, it seems to have had little effect on the importation of disease.The overall frequency of acute infectious diseases in the region remained relatively constant, compared to the previous period. Outbreaks remained a regular occurrence at Albany, with at least ten at the post or in its vicinity between 1796 and 1809. As before, most were ARDs that broke out in the summer or fall.34 Epidemics continued to be rare at the other bayside posts in the Petit Nord, with only three at York Factory and none at Severn. In contrast, there were many reports of sickness of varying extent in the interior of the region, all within the southern half.This was consistent with the pattern of epidemic activity from 1784 to 1795. Even though there is no evidence that the rapid augmentation in the number of fur traders in the Petit Nord between 1796 and 1809 led to an increase in the number of epidemics, it is clear that these men sometimes participated in the diffusion of these diseases within the region. For instance, all three of the outbreaks at York Factory occurred in June or July, the months when the inland crews arrived at the post.35 While this post had a very limited hinterland within the Petit Nord at this time, its trading network extended far into the Grand Nord, along both branches of the Saskatchewan River, and each summer the furs of its inland trading posts were carried to York Factory. As such, it was vulnerable to diseases from the plains and parkland to the southwest, carried by the returning brigades. On several occasions, HBC vessels appear to have introduced sicknesses to Albany. In 1805 and again in 1806, epidemic colds broke out at the Factory in September shortly after the arrival of the Prince of Wales from the British Isles. In two other instances, in August of 1796 and of 1807, the sloop brought respiratory disease to Albany from Moose.36 HBC employees also helped spread acute infectious diseases within the interior of the Petit Nord during this period. For example, outbreaks occurred at Martin's Falls in July of 1801 and July of 1804, just as the men of the Albany Inland District brought their furs to this post to be sent to Albany. In both cases, the diseases subsequently appeared at Albany after men returned from Martin's Falls.37 Afflictions also flowed in the other

130 CHAPTER Six direction, as in 1796, when a virulent respiratory disease spread from Moose to Albany and was also carried up the Albany River by HBC men, perhaps as far as Lac la Pluie. Remarkably, while it is probable that the Montreal-based traders also participated in the introduction of diseases into the Petit Nord and in their spread within the region, there is only one instance during this period, in 1797, when they were implicated in the HBC records. Most likely, this was due to the limitations of the HBC documents and the paucity of the Canadian records, rather than to their lack of participation in such diffusion.38 As during the previous period, there were many disease episodes in the Petit Nord during 1796 to 1809, though few were severe.The first came in 1796 and was among the most widespread of epidemics to that date. During the summer of that year a particularly severe respiratory disease appeared at Moose, and subsequently spread to the Petit Nord. Given its symptoms and severity, it was probably influenza. It had not come from Europe, however, as it was well entrenched among the HBC men and the Aboriginal people at Moose by August 19, the day before the ship arrived from England. On that day, trader John Thomas noted in his journal, "We have now and for some time past, had several Natives under the Surgeon's care with severe colds +c which is afflicting several in the Factory."39 Here the disease proved fatal to many of the Cree, as well as one HBC man. Shortly after, it spread to Albany Fort. On August 25, 1796, the Moose sloop arrived at Albany, bringing several new men, as well as this virulent disease. By the 5th of September, an "epidemical catarrh" raged among the HBC men and some 200 Albany Cree who were tenting around the post. Within a few days, several of the Aboriginal people were dead, while others were dangerously ill, and the sickness was almost universal. By the 24th, many of them had succumbed, and the fate of others was doubtful. It also spread among the people living to the northwest of the post. The disease lingered at Albany long into the winter, preventing the Homeguard Cree from participating in the goose hunt. It also kept many from departing for their winter quarters. These factors would have exacerbated the mortality caused by the epidemic. In the end, more than twenty of the Albany Cree died during the epidemic, and so this disease took a significant toll on the Aboriginal people at Albany as well as at Moose.40 Coming, as it did, on the heels of the mortality of 1795 among the Albany Cree, it must have been especially distressing to these people. The disorder moved inland from Albany during the fall, as several infected HBC men travelled up the Albany River to the posts of the interior. Two men who were bound for Osnaburgh battled the disease from Albany

DISEASE IN THE PETIT NORD: 1784-1818 131 at least as far as Henley House. Others continued farther upriver, despite being ill. On September 10, Peter Laughlin arrived at Martin's Falls while still sick. Donald McKay and his men reached the post from Albany, having been much delayed by sickness. Shortly after these arrivals, most of the Martin's Falls men fell ill of the same disease. Martin's Falls was the main transhipment post of the Albany inland brigades, where furs from the interior were exchanged for goods from Hudson Bay. Thus, this situation was potentially disastrous for the people living up the Albany River, because the men returning to the upstream posts were all potential vectors for diffusion.41 Additional evidence suggests that this influenza epidemic continued to spread to the southwest of Martin's Falls, perhaps reaching as far as the Boundary Waters.Three of the chiefs living in the Escabitchewan area died in the period from September 1796 to May 1797, most likely of the prevailing pestilence. There is also evidence of a severe ARD at Lac la Pluie about this time. In April of 1797, John McKay noted that "the Indians here are all of them very bad with a Cold," as was one of his men.42 If these were indeed linked to the epidemic at Albany, then this disease had travelled farther than any other during this period, having spread across the Petit Nord from James Bay almost to Lake Winnipeg. In this case, the longdistance diffusion was aided by the inland movement of the HBC men during the fall, which was itself a product of the expanding fur trade of the latter part of the eighteenth century. It is thus significant that this disease was an acute respiratory disease, a class of ailments to which most of the HBC men would have been susceptible, rather than a crowd disease that would have found far fewer potential victims among the company's ranks. Thereafter followed an outbreak of yet another severe respiratory disease near Escabitchewan during the summer and early fall of 1797, one that was responsible for a few deaths. Described as a cold accompanied by a sore throat and headache, it also disabled the HBC men at the post. This disease was said by the Aboriginal people to have been introduced by the "Frenchmen," or the Canadians. Early in August an Aboriginal trading captain arrived at the post and brought word of the death of a prominent man (One Arm) and his wife, of "a distemper that the Frenchmen has brought among them."43 The next significant disease episode occurred in the fall of 1798, when an especially deadly, febrile disease broke out at Sandy Lake, near the headwaters of the Albany River. Numerous fatalities were reported among the people trading at the HBC post, while many others were incapacitated by this affliction. It also struck at Lac Seul, and one of the NWC men and three Ojibway died there about the same time, although it did not travel farther east into the Petit Nord.44

132 CHAPTER Six Several additional acute infectious diseases appeared in the upper part of the Albany River and in the western part of the Boundary Waters during the first few years of the nineteenth century. In 1801, HBC fur traders carried a severe diarrhoeal disorder that first broke out at Martin's Falls. From there, it was transported down to Albany, and upstream at least as far as Osnaburgh House. At Albany, it struck with great force.45 This "epidemical disorder" persisted at Albany Fort from mid-July at least until September, and incapacitated most of the people, causing at least one death. It was also carried up the Albany River from Martin's Falls, beyond Osnaburgh, by some of the HBC men bound for Brandon House. That same year, or possibly in 1802, smallpox struck the Aboriginal people of Rainy Lake and Lake of the Woods. Its impact is unknown, but it was part of a much larger smallpox epidemic that ravaged Aboriginal people in the upper Great Lakes and upper Mississippi regions, and was perhaps connected to a smallpox epidemic that struck the plains at about the same time.46 There is no evidence that it penetrated any farther into the Petit Nord, however, nor is it known how great was its extent in the Lake of the Woods area. In 1804, another severe ARD diffused from the interior to Albany. Again, it appeared at Martin's Falls in July, at the same time that the inland men arrived. Thereafter, it spread widely among the post's men. By the end of the month, several of the men from the upland posts had been left behind, being too sick to return to their assigned stations. There was also great difficulty in dispatching boats for Albany Fort, due to sickness among the crews. Nevertheless, John Hodgson, the master of Albany, and several of his men were able to make their return from Martin's Falls at this time, despite being infected with this disease. Following their arrival at Albany on July 25th, he and two other men were incapacitated due to the affliction, which subsequently became almost universal at the post. The timing of the outbreak at Martin's Falls suggests it had been brought by the inland crews. As well, Tanner's map of epidemics in the Great Lakes region indicates that an unidentified epidemic struck the people of the Lake of the Woods area in 1804, possibly the same one.47 The disease may have come from somewhere in the southern part of the Petit Nord and beyond. Two years later, in 1806, some of the Aboriginal people living within the extreme southwestern part of the Petit Nord were exposed to an especially mortal disorder that had never before been recorded in this region, a virgin soil whooping cough epidemic.The only evidence for this outbreak occurs in a brief entry in the journal of George Nelson, a NWC trader who traded at Lac du Bonnet, on the Winnipeg River. On January 15, 1806, Nelson received news from Dominique Ducharme, a fellow NWC trader

DISEASE IN THE PETIT NORD: 1784-1818 133 who was at nearby Portage de 1'Isle, informing him that there the "indians [were] almost continually dying/&/ as if a contagious sickness prevailed in that quarter his only child now about 1 year old is very bad with it." Although the disease was not identified by Ducharme, this outbreak was almost certainly part of a whooping cough epidemic that was active at this time a short distance to the west of the Petit Nord.48 In 1806-07 whooping cough spread at least as far as from the Red River to the Columbia, and from the Missouri River to the Saskatchewan. According to the NWC s Alexander Henry the Younger, the affliction "appeared all along the Red and Assiniboine rivers, on the Saskatchewan even to Fort des Prairies [at the site of present-day Edmonton, Alberta], and in several other parts of the North-west, carrying off many people."49 The sickness was also among the Mandan late in the spring of 1806, and both Alexander Henry and Charles McKenzie witnessed its effects. There, according to the latter trader, the disease killed 130 people in less than a month.50 The epidemic was also noted in at least one Sioux winter count. Finally, it spread almost to the Pacific Ocean as, in September of 1807, David Thompson, another NWC trader, learned that this disease was devastating the Kutenai who were then located near Fort Kutenai, north of the Columbia River in the Pacific Northwest.51 Given the prevalence of whooping cough on the Red River and its wide geographic spread, it is very likely that the outbreak on the Winnipeg River was of the same disease. Whooping cough, or pertussis (ICD-10 A37.0), is an acute, directly transmitted, bacterial disease that primarily affects the respiratory tract. It is highly infective, and survivors gain a lasting immunity, although not to parapertussis (ICD-10 A37.1), a clinically similar disease. Following infection, there is a relatively lengthy incubation period of six to twenty days, leading to a brief catarrhal period, during which the victim experiences minor respiratory symptoms, including a runny nose, a persistent cough, and a slight fever. The victim subsequently develops an irritating cough that may become paroxysmal within a few weeks, and is characterized by a series of violent coughs followed by high-pitched "whoops" or crowing upon inhalation. Adults, adolescents, and infants under six months of age may not present with the paroxysmal cough. The infectious period lasts approximately twenty-eight days, and some symptoms may persist for up to two months or longer, distinguishing whooping cough from many other ARDs. In larger communities, it is a disease of childhood and capable of causing significant mortalities in virgin soil populations, particularly due to a sequel of pneumonia. Convalescence is prolonged, and may require four months to two years for complete recovery.52

134 CHAPTER Six There is a tendency to consider whooping cough an innocuous disease. To a great extent, this is a modern bias. With modern medicine and reasonable levels of nutrition, deaths due to whooping cough are extremely rare. Indeed, with modern vaccines, many people do not contract the disease at all. However, during the early nineteenth century, and especially for the Aboriginal people who lived in the forests of Canada, whooping cough was fully capable of causing great ravages. With limited availability to appropriate health care during widespread epidemics and a subsistence system that could easily be interrupted by sickness, frequently the results were starvation, severe complications, and death.Whooping cough brought special risks for these people by interfering with the food quest—the severity of the cough could make hunting game impossible. Thus, during an epidemic in 1819-20, whooping cough was for the Chipewyan of the Athabaska country "a disease particularly distressing among the Indians as well for its long continuance as its depriving them of the means of subsistence the whole of their caution in approaching an animal being rendered abortive by a single cough."53 The same would have been true wherever the people gained their livelihood from the hunt. This was the first time that whooping cough was noted in the Petit Nord.This is significant in that, unlike many other crowd diseases, whooping cough can be readily identified by its characteristic whoop and by its prolonged duration. Also called chincough, it was rare in colonial America until the middle of the eighteenth century. As well, it was a disease of childhood in England by the mid-eighteenth century, and so there would have been few aboard the HBC ships who were susceptible to the disease. This would partly explain why the disease does not seem to have penetrated to the Petit Nord until the nineteenth century. By the 1790s, whooping cough was apparently a relatively common disease in the US.54 Whether because of the increased presence of the disease in the east, or because of some other factor that assisted its diffusion to the Northwest, the epidemic in 1806 signalled a new era in the disease history of the Petit Nord during which whooping cough appeared repeatedly, following progressively shorter inter-epidemic intervals.This suggests that the disease frontier of the urban pools had moved closer to the Petit Nord. This was the final exogenous disease of any significance to appear in the Petit Nord before the reorganisation of the HBC in 1810.

DISEASE IN THE PETIT NORD: 1784-1818 135 The Fur Trade Reorganized: 1810-1818 After 1810, the fur trade of the Petit Nord underwent considerable change as the NWC withdrew many of its men from the region and the HBC restructured its operations. Coinciding with these changes was a period of limited epidemic activity.There were only seven recorded incidents during the nine years from 1810 to 1818, a considerable decline over the previous two periods. There is no obvious explanation for this decline, although it may have been due in part to the limited number of journals that have survived from this period. Nevertheless, even at some posts with complete (or near complete) journal records, such as Albany and Osnaburgh, there is a dearth of comments regarding disease outbreaks. None was noted at Albany, while there was only one brief period of suspicious sickness at Osnaburgh House over the winter and spring of 1814-15.55 This remarkable turnaround at Albany contrasts with the situation at York, where there were four outbreaks in this nine-year span. During the previous nineteen years, there had been only three. This may be explained partly by the structural changes made to the HBC's operations in 1810. With the loss of its interior posts beyond Osnaburgh House, Albany's men were no longer travelling through or trading in the southernmost part of region, and therefore were not exposed to the diseases that circulated along the main travelling routes. Conversely, the posts in this area were now settled and supplied from York, which may then have been exposed to more diseases through the movements of its own people. None of the sicknesses that broke out during this period was more than a temporary inconvenience to the HBC men or the Aboriginal people. One, "obstinant dysentery" among the employees at York Factory during the fall and winter of 1811, is noteworthy as it was introduced by the European ships. This sickness was still widespread as of mid-December, with a few cases even as late as the following July.56 Unlike the previous two periods, there was no major epidemic in the Petit Nord during these nine years. Thus, the years between 1810 and 1818 were relatively uneventful ones in terms of disease outbreaks. Along with the closure of numerous posts and the reorganization of the fur-trading districts, a third component of the HBC's "Retrenching System" was enacted after 1810. This was the establishment of the Selkirk Colony on the Red River in 1812. Its part in the diffusion of acute infections into the Northwest, including the Petit Nord, was to prove critical, and it helped to usher in a period of rapid increase in the disease load. Over the ensuing decades, the steady but slow growth in the frequency of epidemic

136 CHAPTER Six disease in the Petit Nord that had characterized most of the eighteenth century gave way to a veritable flood of disease. However, the colony's epidemiological impact was not felt immediately. Rather, its part in the import and redistribution of epidemic disease was first experienced in 181920, with a pair of concurrent epidemics that ravaged the Petit Nord.

7 The Measles and Whooping Cough Epidemics of 1819-1820

DURING THE EIGHTEENTH CENTURY, THE PERIODIC APPEARANCE

of new diseases and the marked increase in the frequency of epidemics were signs that the Petit Nord, once an outlying region at a great distance from endemic sources of disease, had taken an incremental step closer to the urban disease pools. As the relationship between the region and the pools continued to build, it was inevitable that at some point such epidemics would come so frequently as to overlap each other in time and space. The result was compound epidemics, major outbreaks of sickness that contain two or more diseases, and these took a heavier toll on the victims. In a single epidemic of all but the most virulent diseases, recovery would usually mean a chance for long-term survival for the victims, although perhaps with some lingering symptoms. In a compound epidemic, even a mild affliction could so weaken the victims that their life was threatened by other diseases they could otherwise have survived.This began to happen in the Petit Nord in 1819-20 with concurrent epidemics of measles and whooping cough.

138 CHAPTER SEVEN The main sickness was measles, which had been absent for almost seventy years, and had never before been observed among many of the people of the region. In this case, the disease struck not only the people of the Petit Nord, but many throughout the Northwest, extending from the western shores of Lake Superior westward to the Rockies, and from the upper Missouri north to Great Slave Lake.1 Less extensive was whooping cough, which had been present in the Petit Nord in 1806. At that time it was limited to a minor outbreak on the Winnipeg River, and so in 1819-20 both diseases found virgin soil. Finally, there were also other, comparatively localized, afflictions of varying severity that appeared in the region, including influenza. Measles While it may not have had quite the virulence of the smallpox epidemic of 1779 to 1783, the 1819-20 measles epidemic rivalled the former in its northward extent on the continent and, in different parts of its range, was accompanied by very heavy mortalities. For instance, an anthropologist, John Taylor, estimated that ten to twenty-five percent of the Sioux and over a quarter of the Assiniboine, Blackfoot, Cree, and Gros Ventres succumbed to this epidemic. In contrast, Arthur Ray, in his seminal study of the historical geography of the Aboriginal people of the western interior, suggested mortality rates approaching forty to fifty percent. These estimates are consistent with losses experienced by other peoples during virgin soil measles epidemics where medical or subsistence aid was not provided. In 1875, thirty percent of the Fijian people died in a single measles epidemic, and about twenty-seven percent of the population of the Faeroe Islands succumbed in an 1846 epidemic. There was a case-fatality rate of twenty-seven percent among those who did not receive aid during an epidemic in Brazil in 1954. Within the Petit Nord, accurate estimates are lacking, but in one case the mortality due to measles exceeded two-thirds of the local population.2 The first evidence of the measles epidemic comes from August 1818, on the north shore of Lake Superior (Map 14). On August 17 two canoes of free traders from Sault Ste. Marie arrived at the HBC post at Michipicoten. Some of these freemen were infected with measles, no doubt carrying the disease with them from Sault Ste. Marie, so it had probably originated in the east. After a week's delay, several of these men and a few of the HBC employees headed north, towards Matagami. That same day two of the

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 139

Map 14: Initial Outbreaks of Measles, 1818-1819 (After Hackett," 1819-20 Measles Epidemic";Warren, History of the Ojibways, 335;Tanner, Atlas, Plate 32)

men who stayed behind were noted in the HBC journal as being "unwell at present with the measles," while others among the canoe bound for Matagami also fell ill. On September 3, post master Andrew Stewart wrote that "Mr. Monin and party that departed from here for Mataugumie on the 24th ULT were still at the first portage about two hours walk from here.... They had not even got their canoe over the portage owing as they say to two of the men being unwell."3 Fortunately, the delay of the brigade near Michipicoten meant that this particular outbreak did not spread any farther into the Petit Nord. However, the following year the disease spread into the region along two distinct pathways. The first of these led directly into the Petit Nord from Lake Superior. The second followed a more circuitous route, spreading south of the lake to the upper Missouri, and from

140 CHAPTER SEVEN there north and east into the Petit Nord. This time, the people of the region did not escape its wrath. According to HBC trader Peter Fidler, measles was "brought up last Summer [1819] by the NW [i.e. the NWC brigades] from Canada."The following August, Fidler commented that measles (together with whooping cough) had been introduced into the Northwest by the NWC traders at Fort William, their major administrative post on the northwestern shore of Lake Superior. Fidler noted "the deficiency of trade all thro' the Northern Department I am sorry to inform you—principally by the Measles + Chincough being introduced last spring 12 month from the Grand Depot of theirs [the NWC's Fort William] on Lake Superior...."4 While there are no records from Fort William for this period, there is evidence of the measles at the nearby HBC post, Point Meuron, in late May. At that time, an employee named Antoine Pacquette began presenting visible symptoms of the disease, no doubt having contracted the disease on one of his visits to Fort William.5 The appearance of measles at Fort William was crucial, for it enabled the disease to reach deep into the Petit Nord. Following the abandonment of Grand Portage early in the nineteenth century in favour of Fort William, each June and July the population of this post swelled greatly with fur traders. As the winterers arrived with their furs from the interior, and voyageurs arrived from Montreal with the following year's trade goods, the NWC's headquarters in the Northwest became more a town than a post, hosting over 3000 people within and just beyond its pickets. Within were a large house, the council house, the doctor's residence, storehouses, a prison, apartments for mechanics, and several other buildings. Outside the pickets were the temporary quarters of the voyageurs, Aboriginal people, and others.6 This made it an ideal temporary host for the virus, as each arriving brigade added new fuel for the epidemic fire. Having obtained their trade goods, the winterers left Fort William for their winter posts, and they carried the disease with them, spreading it as they went. Once measles was entrenched within Fort William, it was only a matter of time before it spread to the local Ojibway.The only extant evidence of its presence among these people comes from two years later. In July 1821, Nicholas Garry arrived at Fort William in order to supervise the rationalization of the newly merged HBC and NWC. He observed a traditional ceremony involving the chiefs of the post, and recorded: We had today the Ceremony ofTwo Chiefs offering their presents in the great Hall "and Receiving a return. The Chiefs preceeded by an English

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 141 Flag marched into the Hall accompanied by all the tribe.... One of the Chiefs then rose and really in a very graceful manner made a speech— He said his Tribe had been afflicted with the Measles and this would a little account for the few People he had brought with him.7

The NWC brigades carried the disease north and westward from Fort William into the Petit Nord. Many of those brigades travelled through the Boundary Waters during the summer of 1819, the main thoroughfare for those bound for the Grand Nord. By early September, the disease was well established among the Aboriginal people at Portage de ITsle. At Garden Island, on Lake of the Woods, measles and whooping cough were proving fatal to the Ojibway by late August.8 At Sabaskong Bay, at the southeastern corner of Lake of the Woods, the HBC trader sent from Lac la Pluie was forced to pay a premium for wild rice as "the Indians ... were violently enraged against us, the NW [the NWC] having circulated a Report among the Indians that the measles which has been so prevalent among them + of which many of them died had been brought into the country by us."9 Ironically, the NWC men, who had brought the disease to the area, were laying the blame at the feet of their English rivals. Measles must have spread quickly among the Ojibway living on Lake of the Woods and along the Winnipeg River, since it was introduced at about the time of the wild rice harvest, when there was considerable interaction among people from far afield. Not everyone in this vicinity suffered during the epidemic, however. At the HBC's Whitefish Lake outpost on Lake of the Woods, returns for 1819-20 exceeded previous years, suggesting that at least the Ojibway who wintered there remained free of sickness (Map 15).10 We don't know precisely when measles reached Lac la Pluie. The HBC post record paused between June 19 and mid-September, as Roderick McKenzie, the new trader, was late in assuming charge of his assigned post. We do know, however, that it was in full force among the people of this area by the fall of 1819. The first mention of the disease in the post journal is not until early October, by which date it seems to have spread widely. On October 3, McKenzie noted that he "endeavoured to get the Indians to Seine but they had all refused Saying how could I expect them to Seine when they are all dying of the measles." Later in the month he was informed that "all the Indians towards Vermilion + Sturgeon lake were Starving + many of them dicing of Sickness which we suppose to be the measles which is among them all over this part of the country."11 Throughout the winter of 1819-20, sickness and starvation went hand in hand among the Aboriginal people of this area, exacerbating the effects of the epidemic,

Map 15: Diffusion of the 1819-1820 Measles and Whooping Cough Epidemics in the Petit Nord

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 143 and on many occasions ill and starving people arrived at the posts in need of sustenance. Only by the spring did the health of the Ojibway of the Lac la Pluie district return. Other NWC canoes carried measles northward into the interior of the Petit Nord. In mid-August of 1819, George Atkinson, an HBC trader stationed at Osnaburgh House, learned of the tragic events then unfolding in the country to the south of his post. At the nearby Pedlar's Path, on the NWC s route to the interior of the Petit Nord, he met a Canadian clerk whose men laboured under sickness. Atkinson grew uneasy when he saw the servants of the N.W. Mr McKinzey (chief clerk) with 10 men in two Large Canoes who informed me of a Distemper raging amoungst the Indians to the Southward, and have destroyed numbers of them—and I much fear that great numbers of these Indians in this quarter will feel the Horror of this malady as they are already numbers of People in a most distressing situation belonging to the NW Servants who are now proceeding to the Northward. He informed me that two of his men were [prevented] from walking and that six more were ill of the same disorder.12

The clerk, Charles McKenzie, was headed first to Crow's Nest Lake and, thereafter, to Lac Seul. By the "southward," Atkinson probably meant the region near Fort William, and possibly the Lake Nipigon area, through which this brigade had travelled. Ironically, despite Atkinson's fears and the passing of these infected men, measles did not appear among the Ojibway of the Osnaburgh House area, nor did it ever spread to Sturgeon Lake, where McKenzie had yet another post. From Osnaburgh, McKenzie proceeded to Crow's Nest Lake and Cat Lake, where he obtained new men, three of his brigade being in no condition to continue. Each time he did so, he reset the chain of infection for his brigade, enabling the disease to penetrate ever farther into the Petit Nord. With no records from the NWC posts of that area, and no HBC posts in the vicinity, we cannot know whether the Aboriginal people trading at the Cat Lake and Crow's Nest Lake posts contracted measles from the infected men who had been left there, although this seems likely. After outfitting his replenished brigade, McKenzie headed for Lac Seul. McKenzie arrived at Lac Seul on September 4 with two canoes and ten men, some infected with measles. According to the few Lac Seul Ojibway who survived the epidemic, it was "the Canadians at Lac Sail [who] had brought the Mesals to that place...."13 The disease attacked the Lac Seul people with a ferocity perhaps unequalled in the Northwest. It is rare that we are left reliable estimates of epidemic losses experienced by Aboriginal

144 CHAPTER SEVEN people during this era. In this case we have statements from a variety of individuals, including the traders and the Lac Seul survivors. These paint a picture of terrible devastation, with perhaps two-thirds of the people dying from the disease. Within four months of Charles McKenzie's appearance, most of the Lac Seul people were dead. On Christmas Day of 1819, Roderick McKenzie at Lac la Pluie was visited by some of the surviving Lac Seul Ojibway, who informed him that "there were no less than Sixty Indians Men, Women, + Children, dead of the Measles +c at Lake Saul since the Fall set in, all that were in that Department excepting three."14 As James Slater passed through the area in June of 1820, he was told by some of the survivors that twenty-three hunters and a total of seventy men, women, and children had died. In his district report he added that there were only five young hunters still alive at Lac Seul who were capable of hunting anything, whereas the previous year there had been thirty hunters attached to the NWC's Lac Seul post.15 In later years, Charles McKenzie stated that two thirds of the Lac Seul Ojibway died during this epidemic, for a total of seventy-six. Thus, it is evident that a tremendous death rate had occurred among those at Lac Seul. In the words of one HBC trader, they "were almost intirely swept away."16 Within a few years of the epidemic, the number of Aboriginal people trading at the Lac Seul post rebounded considerably, exceeding the preepidemic figure. In 1826-27, sixty hunters were attached to Lac Seul and the much smaller Cedar Lake outpost. In 1827-28, there were fifty-one hunters, about one tenth of whom were youths. A more complete description of the population attached to Lac Seul and outposts was provided in the Albany District Report for 1828-29, and included fifty men, fortyeight women, fifty boys, fifty girls, and seventeen widows and orphans. By 1837, Charles McKenzie counted 339 Aboriginal people trading at Lac Seul.17 Seemingly, then, the number of people trading at Lac Seul had increased remarkably over the space of seven years, an increase that continued to at least 1837. Ethnohistorian Charles Bishop emphasized the rapid growth of the Lac Seul population during this era, and suggested an overall gradual population increase during the century, although he also acknowledged the "levelling" impact of the 1819-20 epidemic and other epidemics.18 His implication was that the survivors had managed to quickly recoup their numbers to a point where they exceeded those of the pre-epidemic period.This is a critical issue, for if Bishop was correct, the myriad of epidemics that were to strike Lac Seul and other parts of the Petit Nord over the next twenty-five years were temporary setbacks, rather than significant factors

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 145 in inducing long-term cultural, demographic, and territorial changes.This would have broader consequences for those studying the effects of Old World disease on the Aboriginal people of the Americas. Given a closer look, this argument against a significant and lasting impact falls apart. Clearly, if both the post-epidemic population estimates and the later tallies are correct, then the level of fertility at Lac Seul would have been unbelievably high during this period. Moreover, given the apparent rise in the numbers of hunters, generally adult males, from perhaps five to approximately fifty, recruitment from the sub-adult male cohort would have exceeded the total reported surviving population. Something was incorrect with these estimates or, more accurately, with the way in which they are used. The answer lies in the fact that none of these are truly censuses. The early figures are estimates of the mortality effects of the epidemic, and of the number of survivors. These provide reasonably accurate indications of the post-epidemic population of the Lac Seul people. The later counts, however, are enumerations of those Aboriginal people trading at the Lac Seul post, and include many more than the local people. Following the merger of 1821, many of the posts in the Petit Nord were closed, and by 1825-26, far fewer were operating in the area under the HBC banner and none was settled by the NWC. For instance, Red Lake was not settled after 1821, and some of the hunters thereafter traded at Lac Seul, as did those of Escabitchewan, closed in 1824. Cat Lake closed about the same time, and some of the people went to live or trade at Lac Seul. The Kingfishers, a group of Ojibway who had traded in the Berens River area during the epidemic, also began to frequent the Lac Seul post at this time. Several Lac la Pluie people also traded at Lac Seul following 1821. Moreover, we have already noted the tendency for devastating epidemics to induce postepidemic migrations, and it is apparent that a similar dynamic was at work in Lac Seul. By 1833, the Sturgeon Lake group had overrun the lands of the Lac Seul people, forced there by a fear of the Lake Nipigon group who had in turn encroached on their lands. In 1819-20 the Sturgeon Lake people would have traded at the NWC's Sturgeon Lake post or at the HBC's Osnaburgh House. Following the merger, then, the Lac Seul post attracted hunters from a large territory, including many who traded at other posts in 1819-20. All were being included in McKenzie's post-merger "censuses" of the Lac Seul people.Thus, comparison of these early and later post-epidemic estimates does not provide evidence of a significant rebound of the Lac Seul population following the 1819-20 measles epidemic, nor does it support the hypothesis that there was continuity of population levels in the

146 CHAPTER SEVEN area, other than through migration from other areas.19 Clearly, care must be taken when using such post-based estimates as indicators of demographic trends. In 1819, McKenzie settled two more outposts to the west of Lac Seul, at Red Lake and at Bad Lake, and his men brought measles to the Aboriginal people trading at both those posts. As the NWC began to give advances to the Ojibway of the Red Lake area in September, they also spread the disease. Thereafter, and until the spring, measles circulated among these people and among the HBC men. Four of the five HBC hunters died, for a total of twelve of all ages, male and female, and the number of total casualties would have been higher had not the HBC's Marcus Calder fed the ill who remained at the house.20 How many of the NWC's hunters died is not known. The NWC did not go to Escabitchewan in 1819-20, and so measles arrived later in this area than at Lac Seul or Red Lake. Instead, it came from Lac Seul, introduced early in October by way of some Ojibway who had earlier traded with Charles McKenzie. Others at Escabitchewan soon contracted this sickness, as did the HBC trader's children, and thereafter it spread widely among the local population.Within two weeks, it had broken out at nearby Cut Lake. Most of the twenty-four Aboriginal people attached to the Escabitchewan post contracted measles, and thirteen died. There was no NWC post opposition to the HBC at nearby Big Lake, a two-day walk from Portage de 1'Isle on the Winnipeg River. Once again the disease was late in arriving. Despite being in the vicinity of the Winnipeg River and close to Lake of the Woods, where measles and whooping cough broke out during the summer, measles appeared at Big Lake only at the time of the fall freeze-up, or in mid- to late October. Given its late arrival, most likely it had come from the north, towards Escabitchewan.21 Charles McKenzie s men were not finished spreading measles in the Petit Nord.They also introduced the sickness into the East Winnipeg Country from Bad Lake, sixteen days' travel by canoe from Lac Seul. William Harris, who had been left at Lac Seul during the summer, departed with four men for the Bad Lake outpost on the Bloodvein River shortly after McKenzie's arrival. Here again they infected the Ojibway during the fall trading, who began dying shortly thereafter. According to Donald Sutherland of the HBC, the Bad Lake area was inhabited by the Kingfishers, and during this epidemic they lost their chief, his eldest daughter, and five other men.22 Despite this, the level of mortality was low among those trading with the NWC at Bad Lake, at least compared to that among the Lac Seul people.

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 147 On January 1,1847, Charles McKenzie recalled in his Lac Seul journal that he had passed many new year days at this place [Lac Seul] and never seen our store so very empty of furs as at present on such a day, save in 1819, when the Measles passed before and carried off 76 souls from this post alone— and left us but seven hunters—with plenty widows and orphans—But I had then another post at Bad Lake where the Measles made less havoc.23

Still, its impact must have been substantial for, after spreading widely through the area to the east of Lake Winnipeg, measles resulted in what HBC trader Donald Sutherland called "the Dreadful Death." The people who traded at Sutherland's Big Fall House on Berens River were exposed either directly or indirectly from Bad Lake only after they had traded with the HBC. Others in the East Winnipeg Country were infected elsewhere. Those who lived upstream along the Berens River at Sandy Point Lake received debt at the HBC's Red Lake House, where they contracted the disease.24 With this, the wave of the 1819-20 measles epidemic out of Fort William had completed its diffusion. It had swept through the southern portion of the Petit Nord, leaving the northern half largely intact. Most probably, this was due to the limitations to diffusion imposed by the great distances to be travelled from Fort William to the northern NWC posts. The disease was not quite finished with the region, however, as it subsequently surfaced again to the north of Lake Winnipeg. This time its presence in the northwestern part of the region was part of a second wave, one that came from the southwest. Diffusion from the Upper Missouri Even as measles made its way into the Petit Nord from Fort William, it was also moving westward to the upper Missouri, and from there north to the Red River Settlement (see Map 15).Writing in the summer of 1820, HBC Governor William Williams observed that "the diseases [whooping cough and measles] has been introduced from some of the American out Posts on the River Missouri, and first shewed themselves at the Mandan villages and have from them spread all over the Country like contagions with a rapidity almost beyond belief."25 As noted in the previous chapter, the emergence of a St. Louis-based fur trade on the upper Missouri, beginning in the 1790s, significantly enhanced the potential for the flow of disease to the village tribes.The trips by the traders from the south greatly increased after

148 CHAPTER SEVEN the transfer of Louisiana to the Americans in 1804. These visits had ceased for a time, due to the outbreak of the War of 1812, and, as late as the summer of 1817, Manuel Lisa was still proposing to settle a fort among the village tribes of the upper Missouri, the Arikara, Mandan, and Hidatsa.The American trading expeditions to the upper Missouri began to resume about the time of this epidemic. In December of 1818 a large party of HBC men travelled from Brandon House to trade with the Mandan. They saw no signs of measles or of Americans, and "they learned from the Mandan that the nearest American was 300 miles below but that the next spring they were intended to go up [the Missouri River] and settle at the Mandan villages."26 In doing so the traders from the south brought disease among their hosts. While the HBC men who visited the Mandan missed the arrival of whooping cough and measles, the people who followed them did not. In June 1819, a large party of Assiniboine travelled south to make war on the Mandan, where they contracted measles. Upon the return of the few survivors in late August, Peter Fidler observed,"Only 7 returned, all died by the way, on their return supposed by the Indians to be Smallpox."27 However, it was another party, one that had gone south to trade with the Mandan, that was responsible for introducing the disease to the valley of the Assiniboine River. On October 7, 1818, Fidler noted the arrival of four Ojibway at Brandon House, who traded for dry provisions, and who intended to go to the Mandan villages to purchase horses, "as they are friend."The following April these men left for the Mandan, part of a group of sixteen Ojibway traders under the leadership of a man named Captain Grant, also called Oo ke mow es cume. Within a month they had returned in a desperate state, heavily burdened by their sickness.28 With the return of Captain Grant's ill-fated trading party, both whooping cough and measles soon made their appearance at the HBC's Brandon House and among the Aboriginal people of the area. In late June, Fidler, who was now at Fort Douglas near the juncture of the Red and the Assiniboine rivers, was alerted of the epidemics' ravages at his former post. In the daily entry in his post journal he wrote that "the colony men came from Brandon Ho. where they were left by Mr. Laidlaw enclosing the Ground—most of our people at Brandon badly with the Whooping Cough + Measles—as also the Indians—5 Crees + 4 Stone [Assiniboine] Indians already dead of it."29 What Fidler did not record was that some of these "colony men" were also infected with measles, and as they reported on the tragedy at Brandon House, they introduced the disease among the people of the Red River Settlement.

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 149 By late June, both measles and whooping cough had travelled down the Assiniboine to the Red, with drastic consequences. Just to the west of the Red River Settlement, the newly formed village of Birsay was struck by both measles and whooping cough and was subsequently abandoned. The impact in the Red River Settlement was less dramatic, but significant, nonetheless. By late June, whooping cough was beginning to manifest among the colonists' children, and by the tenth of July, many were labouring under measles, including four of Fidler s own children. At least two people had succumbed.30 Throughout the remainder of the summer, the colonists'children and the Aboriginal population suffered greatly from both measles and whooping cough. On July 27 the Roman Catholic Father J.-N. Provencher wrote that "La cocqueluche [whooping cough] et la rougeole [measles] ont regne cet ete parid et ont fait mourir beaucoup d'enfants^ In October of 1819, Midshipman Robert Hood, of the Franklin Expedition then at Norway House, noted that "the inhabitants [of the Red River Settlement] were swept away by the measles and hooping cough."32 Although it was an exaggeration, it nonetheless indicated the disarray into which the colony had been thrown by these diseases. Once measles appeared on the Assiniboine River, it spread widely and rapidly through much of the Grand Nord, reaching as far as Lake Athabasca by the fall of 1819. In spite of this, it merely touched the northwestern margin of the Petit Nord, where it appeared only at Norway House, and only in mid-November. None of the members of the Franklin Expedition observed either measles or whooping cough at the post when they passed through on October 6. On the 13th of November, however, two Aboriginal men from Swan River, to the west of Lake Winnipeg, arrived at the post and reported that measles and whooping cough were "carrying off a great number of [the] Indians" in their home territory.33 Unfortunately for the HBC traders and their families, these two men were also infected, and introduced both sicknesses to Norway House. A week later, several of the children at the post fell ill of measles, and within weeks, both whooping cough and measles were spreading among the people at Norway House, some of whom were very ill. The references to these diseases cease after November, and neither appears to have broken out among the Aboriginal people of the area, no doubt because they appeared only after the people had dispersed to their winter quarters. As at Michipicoten, the outbreak at Norway House did not lead to further diffusion in the Petit Nord.

150 CHAPTER SEVEN Whooping Cough Whooping cough, like measles, came from the east, following a long-standing pattern of slow diffusion from the upper Great Lakes to the eastern part of the Canadian plains. It was prevalent in Detroit during the fall of 181734 and, over the next year and a half, slowly made its way westward to the Red River Settlement. As we have seen, it spread in concert with measles from the Mandan villages on the upper Missouri to Brandon House on the Assiniboine.35 By late June, it was at Red River, and it soon began to surface to the north and east of the settlement. On July 12, Roderick McKenzie met a band of Aboriginal people suffering from whooping cough at the mouth of the Red River. During the early part of the fall, the disease was observed among the Ottawa and Ojibway at Garden Island, on Lake of the Woods, as well as among the people at Rapid River, near Lac la Pluie.36 No doubt it was present in other communities in this area. It also seems to have hit the Ojibway who lived along the eastern shore of Lake Winnipeg. When Donald Sutherland, the master of the HBC s Berens River post, sought out the people he expected to meet at his post in August, he learned that they were "at Pigeon River all lying badly and near to death." Likewise, he later learned that the people of Little Bloodvein River "were all very badly the Course of the Summer."37 This was prior to the arrival of measles in the area, and so it was probably whooping cough. This disease was also carried directly from the Red River Settlement to the area north of Lake Winnipeg, as far as York Factory. At Island Lake and within its hinterland, the people suffered from whooping cough during the summer and fall of 1819, "brought from Red River ... by some of the half breeds in the Service."38 Although the number of fatalities was not great, the epidemic was nonetheless disruptive of the trade of this area. The Island Lake District report for 1819-20 noted that the trade would have been much better had not the Indians been severely afflicted with a disorder which prevailed among them last summer in all parts of the country. It proved mortal to a few at this place and brought whole families to the verge of distraction for want of food, as it was not an uncommon sight to see a good hunter with three wives (as many of them have) and a number of children reduced to a state of perfect misery all from his being in a condition so as to be unable to give assistance either to himself or his family—at this place two Indian Men who were both good hunters and a woman died of the distemper, many of them were never perfectly recovered during the most part of the winter, consequently could not exert themselves....39

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 151 The sickness was carried to York Factory during the early part of the summer of 1819, again directly from the Red River area. On July 7, James Swain noted in the journal that there were "a number of the Natives and Children afflicted with the Hooping Cough. It has been brought from Red River + seems highly contagious."40 It remained active among the Aboriginal people and the HBC men's families into August, and for a considerable time after, disrupting the fall goose hunt. Among those who suffered was the Arctic explorer Sir John Franklin, who contracted the disease while at the fort. Along the Hayes River, Midshipman Robert Hood wrote that "since our departure from York, Mr. Franklin had been afflicted so severely with the hooping cough, that it threatened strangulation."41 Victims of the disease continued to arrive at the post as late as March of the following year, and Swain's replacement, Adam Snodie, was made aware of the recent deaths of two more people in February of 1820. The trade at York Factory suffered as the prevailing disease carried off several of the best trappers.42 Whooping cough was later arriving elsewhere to the north and east of Lake Winnipeg than at York Factory and Island Lake, including at places closer to the source of the disease. Oxford House, which was settled along the main canoe route to York Factory, was spared until the end of the summer or early in the fall, when the disease appeared among the local people. When the Franklin Expedition passed through in late September, they found several tents of sick people camped by the lake, who were lamenting their deceased relatives.43 With no indication of whooping cough among the HBC men, perhaps it came from the north, through contact with York Factory, or from nearby Island Lake, to the southeast. We have already seen that it appeared at Norway House, to the south and west of York Factory, only after the winter had set in. Clearly, these diseases did not always follow a simple contagious pattern, one in which the populations nearest to the source of disease are infected first. Rather, where the fur trade was involved, the rapid-moving brigades facilitated relocation diffusion, in which disease travels considerable distances before being passed on. In this case, whooping cough bypassed some communities during the initial thrust of diffusion, only to break out at a later date. Other communities were bypassed entirely, as the epidemic did not progress eastward of Island Lake.44 In fact, when we consider the overall pattern of diffusion of both measles and whooping cough in 1819-20, it is apparent how limited that diffusion was. Although the people of the Petit Nord provided virgin soil for both sicknesses, neither could penetrate to anywhere near the limits of human settlement. Instead, measles was

152 CHAPTER SEVEN constrained to the southwestern quarter of the region and along its eastern margins, while whooping cough struck only along a thin band from Rainy Lake to York Factory (see Map 15). Of course, this was typical of all the epidemics within the region, each of which left a variegated pattern upon the human landscape. However, the presence of two such mortal epidemics—in some places overlapping, in other places only one, and throughout the rest of the region, neither disease—produced a more complex pattern than had yet been seen. Other Sicknesses This regional variation was reinforced by the presence of other diseases of varying severity but lesser extent in different parts of the region. For example, dysentery was identified at Norway House and at Lac la Pluie, though there is no indication they were connected. Several of the men of the HBC's Long Lake post, to the north of Lake Superior, suffered from an unidentified disease during the fall of 1819, possibly brought with them on their trip from Albany. Conversely, the 1819-20 outfit year was relatively uneventful with regard to sickness at Michipicoten and at Albany45 Elsewhere in the Petit Nord, a frequently mentioned combination of vague symptoms involved pain of the "breast" or "belly," and often of the head as well.46 If a single disease was causing these symptoms, it may have been epidemic within the region, for the HBC men at three different posts experienced a similar complaint, possibly in sequence. It began during the winter of 1819-20 with Robert Cock, who died at Attawapiscat of a sickness with those symptoms. At Martin's Falls, many of the men developed a similar illness following the renewal of contact with Attawapiscat, and one man, James Graham, did not recover. In addition, some of the HBC men at Osnaburgh also began complaining of pain in the breast shortly after the arrival ofWilliam McKay from Martin's Falls in December of 1819.47 Finally, the eastern part of the Petit Nord was exposed once again to influenza, which was then prevalent in the Great Lakes basin. In the New Brunswick House area, to the east of the Albany River, there were reports of an epidemic respiratory disease. In late May of 1819, Charles McCormick noted in his journal that "there is an epidemical catarrh at present prevailing which affects almost everyone in this quarter."48 The foil owing January, Jacob Truthwaite at Capoonacagami, an outpost to the north and west of Michipicoten, wrote to McCormick s successor, John Murphy, that he and the Aboriginal people had had a "terrible hard cough all the fall and are not

MEASLES AND WHOOPING COUGH EPIDEMICS OF 1819-1820 153 quite clear of it." Murphy responded a few days later, saying that "there are few parts of the Indian Country in which it [the cough] has not been felt this year."49 Bouts of influenza and other respiratory afflictions were still novel in 1819-20, but within a few years became common among some populations within the Petit Nord. This new era of epidemic disease in the Petit Nord, in which influenza rose to the forefront, also meant a rapid increase in the number and frequency of epidemics in the region. After 1821, the convergence of many different factors, both old and new, drew the Petit Nord closer to the external disease pools. Many of these factors had been at play during the epidemics of 1819-20. Established mechanisms of diffusion, such as Aboriginal movements in quest of trade and warfare, and commercially motivated travel by Canadian and English fur traders, took on new meaning with the vastly increased disease load of the post-merger era. More recent developments, such as the movement of southern fur traders to the village tribes of the upper Missouri and the emergence of the Red River Settlement, reached their epidemiological potential only after 1821. Still other crucial changes came only in the decades that followed the first compound epidemic in the region's history. Thus, with respect to the nature of epidemic diffusion in the Petit Nord, the era that followed the 1819-20 measles and whooping cough epidemics represented both continuity and change. In terms of the region's epidemic history, however, this period was distinct from all that came before it, as it underwent a form of epidemiological transition.

Illustration 3: Red Lake chief and followers arriving at Red River, 1825. Continual visits to the Red River Settlement by Aboriginal groups and fur traders helped to spread infectious diseases over long distances during the first half of the nineteenth century, many of which sicknesses subsequently appeared in the Petit Nord. (PAM CN12)

8 Epidemic Disease in the Petit Nord, 1821-1845

THERE WAS AN UNPRECEDENTED INCREASE IN THE FREQUENCY OF

epidemics in the Petit Nord after 1821, and by the early 1830s, comments about the deteriorating health in the country began to appear in the letters, journals, and reports of veteran fur traders throughout the region. In 1833 George Keith observed that "pestilent . . . colds . . . often appear at" Michipicoten,1 and three years later, Charles McKenzie noted with concern that "this country certainly is getting very unhealthy of late years . . . yet some 30, or 20 years ago there were none of these Coughs or Colds in the country either among the natives or the whites."2 By the end of the decade, Mackenzie reported that the Ojibway people at Lac Seul were frequently visited by epidemic disease.3 The situation worsened during the following decade, and in 1843 Donald Ross noted that "every breeze from that quarter [the country to the south of Norway House] ... blows some foul disease or other amongst us."4 Two years later Ross wrote to Governor Simpson, advising him that "as to the propriety, or I may add, in the unhealthy state of the country for some years back, the necessity of having a medical man stationed at this place (Norway House), a Doctor at York Factory is simply useful for that Establishment alone...."5 By then, even

156 CHAPTER EIGHT casual visitors were aware of the situation. Thus, even as Ross was pleading for medical help at Norway House, two British army officers, lieutenants Henry Warre and Mervyn Vavasour, were passing through the southern part of the Petit Nord, later pointing out the effects of sickness on the Ojibway in their report. Having travelled along the north shore of Lake Superior and through the Boundary Waters, they concluded that "the Indians on the route by which we have lately passed, are so reduced in numbers by their intercourse with the white traders, by sickness and other causes, that they may be considered as perfectly harmless."6 By the 1830s and 1840s, diseases that had been described a century before as "very remarkable" for their infrequency had become almost routine. Several new diseases arrived in the Petit Nord in this period, with the frequent return of others that had only recently arrived or had been very rare. Among the new afflictions were two crowd diseases, chickenpox and mumps, the latter breaking out on at least three occasions in a five-year span towards the end of this era. Whooping cough, which had been unknown in the Petit Nord prior to the nineteenth century, appeared three times during this period, and the earliest of these epidemics came on the heels of that of 1819-20. Influenza, once only a very infrequent visitor to the region, began to manifest often as small, localized outbreaks and epidemics, and as spatially extensive epidemics. Other illnesses, particularly respiratory complaints, also began to reappear after increasingly shorter intervals, and compound epidemics became common in parts of the region. On the whole, the people of the Petit Nord suffered from far more frequent and more varied diseases between 1821 and 1845 than ever before. Of course, these changes were not without precedent, as they followed the general trend during the eighteenth century and the early part of the nineteenth. Nevertheless, there was a clear break between the region's epidemic history prior to 1821 and that which came afterward. This was not an incremental increase in disease, as had been the case earlier. Rather, it marked a kind of transition, a change in status in which the region moved from the periphery of several urban disease pools to being within the immediate hinterland of the eastern pool.7 By the early 1830s, the eruption of a virulent epidemic in the eastern cities could strike anticipatory terror in the hearts of people located far into the interior of North America. When cholera broke out in the east in 1832 as part of a worldwide pandemic, Donald Ross wrote with certainty that "that awful calamity the Cholera is it seems raging with deadly violence in Canada & the States—it will reach us of course next Summer if not sooner—God help us all...."8 While circumstances eventually proved Ross wrong, his comments illustrate the degree

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 157 to which the Petit Nord was integrated into the external urban disease pools by the early 1830s. Only one disease ran counter to the overall trend and went into decline. Having appeared in the region several times during the eighteenth century, smallpox did not return to the Petit Nord between 1821 and 1845. Despite being almost constantly present to the south and east of the region,9 its entry was prevented by the HBC. The most feared of the Old World diseases, smallpox was also the only one at this time for which a simple and safe procedure, vaccination, could effectively prevent the spread of the disease. Following Edward Jenner's demonstration in 1796 that infection with cowpox, or what he termed vaccinia (ICD-10 B08.0), a comparatively mild disease, had the beneficial side effect of providing immunity to the far more deadly smallpox, the HBC was quick to adopt this novel preventative. By 1813 company men were vaccinating the Aboriginal people on an ad hoc basis,10 and in 1819 they carried out the first systematic vaccination program in the Red River area.11 Then, in the wake of a devastating epidemic in 1837-38, the company began a far more ambitious program, attempting to vaccinate every Aboriginal person within range of its posts in the region from James Bay to the Pacific, and from the Red River Settlement north to the Arctic.12 By the end of 1839, it is likely that the company vaccinated most of the people of the Petit Nord, removing the fuel for future epidemics, at least until a sufficient non-immune population had been built up.13 Thereafter, the traders needed only to remain vigilant for the disease at critical locations and to administer the vaccine in order to prevent the spread of smallpox into the region. However, the HBC could do nothing to prevent the appearance of every other disease. The main reason for the tremendous increase in the disease load of the Petit Nord was the movement of massive numbers of non-Aboriginal people into the interior of the continent, which in turn pushed the settlement frontier towards, but not beyond, the margins of the Petit Nord.14 With these settlers inevitably came disease, which spread beyond the previous limits of non-Aboriginal settlement. Just as the Europeans who settled along the Atlantic coast during the seventeenth century brought epidemics among the people of the Northeast, the settlers who moved into the interior en masse during the 1820s, 1830s, and 1840s brought sickness with them from the east.This was not lost on the Aboriginal people, who saw their destruction in these intruders. When Henry Yule Hind and his "Red River Exploring Expedition" reached Lake of the Woods in 1857, they did so as the

Map 16: Changing Patterns of Settlement in the United States, 1800-1840 (After Davis, Frontier America]

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 159

Map 16 (continued)

advance guard ofWhite settlement, and the Ojibway were not cooperative. Asked to provide a guide for the route to Red River, they refused, stating bluntly, "We do not want the white man; when the white man comes he brings disease, and our people perish; we do not wish to die. Many white men would bring death to us, and our people would pass away."15 Nevertheless, while they might seek to stem the tide of disease by preventing the movement of settlers through their own territory, they were already suffering the epidemiological effects of the migrations occurring to the south and east of them. These they were powerless to prevent.

160 CHAPTER EIGHT In fact, the Ojibway of Lake of the Woods had much to fear. The settlement frontier, that fabled threshold immortalized by the historian Frederick Jackson Turner as the birthplace of American democracy, was a potent source of disease and death for Aboriginal people across North America. Describing the impact of American westward migration in the early 1830s, artist-traveller George Catlin referred to it as the "blasting frontier," which, as it moved westward, destroyed all over whom it passed.16 This was an especially apt description, as the frontier communities acted as conduits through which many of the diseases of urban life, brought by the thousands of immigrants who departed the east each year for the interior, spread to more remote peoples. On the frontier, according to Peter Harstad, "Common diseases of childhood, such as measles, scarlet fever, whooping cough, chicken pox, and mumps, came as a matter of course "17 Once these diseases were introduced among those who lacked significant group immunity, especially those who had lived their lives beyond the frontier, their impact was anything but "common."18 It took some time before the full epidemiological impact of the settlement frontier began to be felt in the Petit Nord, as it was not until well into the nineteenth century that non-Aboriginal settlement began to encroach on the lands surrounding the region. The movement beyond the Appalachians by significant numbers of Americans began shortly after the American Revolution. Modest in volume at first, it accelerated as the decades passed. As late as 1800, the United States remained primarily a coastal nation with but a few pockets of settlement west of the coastal plains (Map 16). Thereafter, westward expansion increased, particularly after the War of 1812. Initially, these settlers took advantage of the natural waterways and moved along the Ohio and St. Lawrence rivers, and towards the lower two Great Lakes, Erie and Ontario. By 1820 the American settlement frontier extended in a thin ribbon south of Lake Erie and along the Ohio River to the Mississippi. At the same time, Canadian settlers began to move into Upper Canada in greater numbers, settling along the north shore of lakes Erie and Ontario. There remained little in the way of migration into the upper Great Lakes until later in the decade, when both the Americans and Canadians finally began to penetrate to the south and east of the Petit Nord. Accompanying this change of direction was a shift in the flow of epidemic disease from the eastern pool.19 The year 1825 witnessed the completion of the Erie Canal, a watershed event for western settlement. In connecting New York City with Lake Erie and beyond, bypassing Niagara Falls, this canal prompted an immediate and massive increase in migration into the interior, including, for the first time,

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 161 a rapid influx of immigrants from the eastern states into the lands bordering the upper Great Lakes. By 1826, as many as 1200 people arrived at Buffalo, the terminus of the canal system, in a single day, bound for the west.20 Over the following decades, the number of people moving westward along the Erie Canal exploded, in large part fuelled by a considerable growth in migration to the US.The Welland Canal, which connected Lake Ontario with Lake Erie and also bypassed Niagara Falls, was built as a Canadian alternative shortly thereafter, and was also heavily used. By 1830, vessels had a through communication from New York City and Montreal as far as Sault Ste. Marie, and beyond into Lake Michigan (Map 17). Other canals soon followed, creating a network of internal waterways that carried goods and people between the east and the interior. A second improvement in transportation reinforced this westward flow of settlers during the 1830s and 1840s.This was the era of the steamboat on

Map 17: Canal Construction in Northeastern North America

162 CHAPTER EIGHT the Ohio-Mississippi-Missouri river system and on the Great Lakes, and, concluded geographer J.R. Borchert, the appearance of large numbers of these vessels "created major transportation corridors on the western rivers and the Great Lakes and resulted in enlargement of the hinterlands of ports on both the inland waterways and the Atlantic."21 The most important of these ports was New York, and steamboats on the Great Lakes and on the Erie Canal helped to extend both its economic and epidemic hinterlands far into the interior. As these hinterlands were extended westward, the Aboriginal people were either pushed back or perished as the frontier enveloped them.22 By the 1840s the settlement frontier in both Canada and the US seemed ready to engulf the Petit Nord.As of 1837, the settled area of the province of Upper Canada stretched as far north and west as Penetanguishene, on the southeastern end of Georgian Bay, and Amherstburg, opposite the Detroit shore of the St. Clair River. As the population of Upper Canada continued to grow apace, expansion along the north shore of Lake Superior must have seemed imminent.23 For its part, the American settlement frontier had pushed far to the west of the Mississippi River by 1840, reaching the western border of the state of Missouri.There had also been significant infilling of the area to the east of the Mississippi since 1820, including within the southern parts of Michigan and Wisconsin.24 At the same time, communication between the frontier and the villages at Sault Ste. Marie, the gateway to the Petit Nord, was also reaching new and—for the Aboriginal people—dangerous levels of intensity. During the summer months they received regular boat traffic from Penetanguishene as well as large numbers of American vessels from the cities of the east, the latter bound for the frontier communities of Lake Michigan.25 As part of this overall process of settlement expansion, there was considerable growth in many of the American and Canadian towns and cities in the interior of the continent. In particular, several cities of considerable size emerged in the Great Lakes region. Between 1830 and 1850, Detroit grew from only 2222 people to 21,019, Buffalo from 8653 to 42,261, and Chicago from 4470 to 29,963.Toronto, the largest city in Upper Canada, had a population of about 30,000 in 1851. Countless other towns sprang up along the Ohio and the Mississippi, fuelled by the widespread adoption of the steamboat, and certain communities that occupied fortunate sites or situations experienced phenomenal growth. Cincinnati grew from 24,831 to 115,435 people between 1830 and 1850. St. Louis, a gateway to both the upper Missouri and the upper Mississippi, experienced a ten-fold increase, from 6694 to 77,860, during the same period.26 In combination with the

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 163 developing transport technologies, this expansion helped to create a new urban system in North America, one centred not only on the Atlantic coast but also on the burgeoning interior. In turn, this new urban system helped epidemics to penetrate far into the interior by lessening the effects of spatial friction. Although none of these cities in the interior was large enough to serve as a permanent source of disease, they were well suited to act as a temporary pool, a place where, once introduced, an affliction might linger for an extended period of time before continuing its diffusion. By "resetting the clock" for these acute infectious diseases, the cities of the interior greatly extended their range, overcoming a key barrier to diffusion that had long limited the movement of all but a few afflictions. With the urban expansion of the 1830s and 1840s, even the most fleeting of ailments stood a chance of reaching the Petit Nord. Finally, the same canals and steamboats that helped to push the frontier westward also created conditions that enabled disease to flow ever farther from the urban east, by increasing the speed and volume of passenger travel. Improvements in transport conditions have been identified as being crucial in the appearance of infectious diseases in contexts as diverse as Fiji during the nineteenth century and northeastern North America during the seventeenth,27 and there can be no doubt that they did the same for the Petit Nord at this time. The trip from New York City to Sault Ste. Marie that took six weeks in 1800 took only three in 1830, and the journey from Montreal could be done in even less time (Map 18). On at least one occasion, travel from Montreal to Sault Ste. Marie was accomplished in as little as ten days.28 This greatly shortened the chain of infection required to maintain these afflictions from the eastern cities, and placed the eastern flank of the Petit Nord in a perilous position. Given the incubation and infective periods of some diseases, an individual who was exposed to the disease in the east could now be infective even after completing the journey to the threshold of the Petit Nord. At the same time, steamboats offered improvements in size over most sailing vessels plying the interior waterways, and were often packed with immigrant families, many of whom carried communicable sicknesses. Larger numbers of passengers (and especially of susceptibles) meant that, in general, these diseases would remain viable over longer journeys. Over the second quarter of the nineteenth century, the main waterways leading into the interior, such as the St. Lawrence, the Erie Canal, the Great Lakes, and the Ohio, became corridors through which epidemic diseases passed halfway into the continent, and beyond.29

Map 18: Travel Times from New York City, 1800 and 1830 (After Paullin and Wright, A tlas, Plate 138)

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 165 When we look at the spread of epidemics to the Petit Nord from 1821 to 1845, two basic patterns stand out for their frequency, corresponding to two basic systems of diffusion. Repeatedly, sicknesses entered the region from the east and from the southwest, both tied to the expanding settlement frontier.The first pattern was relatively simple: epidemics were brought to the region from the east, via Lake Huron and Sault Ste. Marie. Here, there were several potent threats to the public health, including the growing communities of the nearby American and Canadian frontiers, and the ships that arrived at Sault Ste. Marie or passed frequently through Mackinac Strait during the summertime. At least by the late 1820s, the country between Georgian Bay and Sault Ste. Marie had become a seasonal focus for acute infectious disease, even as it held great inducements for the Aboriginal people of Lake Superior to visit. Indeed, in 1830 George Keith, the HBC's post manager at Michipicoten, called Sault Ste. Marie "a hot-bed which often sends its pestilential effluvia hither,"30 and the country to the east was equally disease-ridden. As people moved back and forth between Lake Huron and Lake Superior, they unwittingly served as vehicles for the introduction to the Petit Nord of the settlement frontier's diseases. The main inducement for the Aboriginal people of Lake Superior to visit Lake Huron during this period was an annual meeting with the agents of the British Crown, a ceremonial gathering that was a crucial factor in the introduction of epidemic diseases in the Petit Nord prior to 1846. Each summer the British government distributed what were termed "presents" to the Aboriginal people of the upper Great Lakes and beyond. Before 1829, the gathering took place at Drummond's Islandjust east of Sault Ste. Marie in Lake Huron. In 1829, the British ceded the island to the Americans and the event moved for one year to nearby St. Joseph's Island (Map 19).Between 1830 and 1835, it was held at Penetanguishene and, after that, at Manitowaning on Manitoulin Island. Participants arrived from far afield, and in large numbers, including, until 1844, many from American territory. Typically, these people came from the upper Great Lakes, the upper Mississippi, and even farther west, as well as, on at least one occasion, Hudson Bay. In 1842, for instance, nearly 6000 people journeyed to Manitoulin Island from as far away as Lake of the Woods and Red River, and in 1837 there were 3700 Ottawa, Ojibway, Potawatomi,Winnebago, and Menominee people present.31 In 1820,4000 people gathered at Drummond's Island.32 Frequently, the unintended result of these gatherings was the dissemination of some infectious disease. In fact, these gatherings were a considerable health threat to the people of Lake Superior. In attracting participants from long distances, including

Map 19: Locations of Present-Giving Ceremonies in the Sault Ste. Marie Area

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 167 White officials and adjuncts such as petty traders from the settled areas, the meeting both introduced sickness to this part of Lake Huron, and encouraged its diffusion, as participants carried the infections back to their homes. Moreover, even the journey to the ceremony was fraught with peril for western Aboriginal people, since it required them to travel through Sault Ste. Marie on their way to Lake Huron.The relationship between travel to Lake Huron, along which lay the settlement frontier, and the introduction of epidemic disease was recognized early by both the HBC traders and American government officials. For example, in 1828 George Keith, the HBC trader in charge of Michipicoten, dissuaded an Ojibway family from going to Lake Huron to receive government presents, in part because in making the trip they would "expose themselves and families to some infectious disease.. ,."33 That same year, the American Indian Agent at Sault Ste. Marie, Henry Schoolcraft, advised an Ojibway named Red Devil (Miscomonetoes) not to travel to Drummond's Island for presents as "such visits were very injurious," for, among other reasons, there they would contract diseases.34The annual migrations continued, despite these strong warnings. In 1844, the HBC trader at Sault Ste. Marie, John Ballenden, informed George Simpson that the Ojibway of Lake Superior "almost always on their return . . . carry with them the seeds of some of the maladies which are prevalent here and along Lake Huron during summer."35 The situation seems to have worsened by the 1840s with the approach ofWhite settlement, and the following year Ballenden added that "on every occasion [they bring] with them some of the diseases more prevalent in the civilized world."36 A second system of diffusion carried disease into the Petit Nord from a southwestern direction, via the Red River Valley. The key to this pattern was the Red River Settlement, which emerged during this period as a nexus for disease diffusion between the US and the Canadian Northwest. This was largely due to its growth, the result of fundamental changes in the fur trade of the Northwest brought about by the merger of the NWC and HBC in 1821. From its inception in 1812 to the merger, the settlement had been a small, relatively insular, and slowly growing colony, whose population was almost entirely European in origin. However, the merger led to a substantial surplus population that was predominantly Metis in origin. Many of these people and their families settled in the Red River Settlement and found employment as seasonal labourers on the fur-transport brigades or through trading ventures with the Aboriginal people or the Americans. After 1821 Red River was thereby transformed into a rapidly expanding, dynamic, regional community that encompassed long stretches of land along the banks of the Red and Assiniboine rivers, and it was increasingly

168 CHAPTER EIGHT comprised of people born in the Northwest. Following 1821, epidemic disease began to appear with alarming frequency. The settlement played several roles during these epidemics. Often it served as a temporary disease pool, hosting an affliction for months on end. With its population numbering in the thousands, it provided a ready supply of susceptibles for the epidemics that passed through, and its decentralized social geography also tended to prolong their stay.37 In acting as a temporary pool, Red River overcame what had been a serious hindrance to disease diffusion, the seasonal nature of communications in the north. Prior to its establishment, acute infections that appeared during the parts of the year when contact between groups was limited might be thwarted in their spread and achieve only limited penetration into the Northwest.With a longer-term local source of disease, the opportunities for further diffusion were much greater. The fur trade was a significant opportunity following the merger, for the local Metis men who left each spring with the HBC transport brigades often carried the seeds of epidemic disease.The similar spread of whooping cough to York Factory and Island Lake in 1819 paled in comparison with what was to follow. Time and again, the transport canoes and boats left death and disease in their wake. Even when the men could no longer continue their journey or had almost ceased to be infective, they passed their sickness on to other brigades. In this way, afflictions that had appeared in the Red River Settlement spread far beyond its limits. The most important role played by the Red River Settlement during these epidemics, however, was that of gateway to the Northwest, because of its far-reaching connections. Many of the major epidemics that spread through the region between 1821 and 1845 first came through Red River. This was a significant departure from the pre-merger period. During the first few years of the settlement's existence, its inhabitants' external connections were limited, and epidemic disease appeared there only once, in 181920. By the late 1820s, however, the situation had changed completely, and all manner of diseases began to appear. Its non-fur-trade connections became far more complex, and its people's interests and economic activities took many of them far away from the forks of the Red and the Assiniboine rivers. For instance, commercial ties between its agricultural citizens and the American frontier communities had grown far closer, and the Metis people were making regular trading ventures to Pembina, the upper Missouri, St. Paul, and nearby Mendota. At the same time, Red River was also a significant crossroads for Aboriginal people from near and far. As a source of seasonal employment for

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 169 the groups of the Winnipeg, Swan River, and Cumberland districts, it attracted a steady flow of people who sought trade or to settle permanently. The large Cree and Ojibway population that resided in the Red River area regularly travelled to Pembina, Turtle Mountain, or the upper Missouri to trade furs with the Americans as part of their seasonal cycle. Others from Red Lake (Minnesota), Lake of the Woods, and Rainy Lake periodically arrived to visit their relatives and renew ties, as did more local people from Lake Manitoba and Pembina. The Assiniboine, who by this time were living in southern Saskatchewan and the northern US, traded with other Aboriginal people and the American fur traders on the upper Missouri, but continued to visit Red River.38 With increased connections between the settlement and the outside world, especially with the south, came increased exposure to disease. Among these many connections, those that linked Red River with the fur-trading posts of the upper Missouri were especially important for spreading disease. Beginning in the mid- to late 1820s, there was a flurry of American post construction along the upper Missouri after a temporary absence of a few years. These new posts increased contact between the Aboriginal people of the region and the Americans, facilitating the transmission of epidemic disease to the northern plains. They also tied the upper Missouri into a trading system that reached downriver to St. Louis, to New York, and on to Europe. As "outliers of the Euro-American settlement frontier,"39 they were sources of disease from the settled area with which they were in communication. Indeed, ethnohistorian Michael Trimble identified Fort Clark, a post built by the American Fur Company (AFC) among the Mandan,"as a repository for epidemic-disease hazards" that the traders carried up the Missouri River.40 Because many of these posts attracted people from HBC territory, the risk of infection was not limited to those living to the south of the 49th parallel, but included the people of the Red River Settlement through its developing connections to the south. Although the trading posts had probably been a source of disease on the upper Missouri since the 1790s, they became far more dangerous during the 1830s. Once again, changes in transport technology were a driving force in the increased disease load. After 1831, steam-powered vessels replaced the much slower keelboats for transporting goods and men up the Missouri River from St. Louis. From an epidemiological perspective, this was a shift of considerable significance, as it brought more people into the area from the settlement frontier, and carried them there in much less time than "was previously possible. In John Sunder's words, "Steam unsealed the upper river: unsealed its isolation, kept the seal broken...."41 In doing so,

170 CHAPTER EIGHT the steamboat greatly lessened the time of the journey from St. Louis to the upper posts; in effect, compressing "time-distance."42 This limited the spatial friction for diseases travelling upriver, increasing their potential range from the settlement frontier. Not all the diseases that reached the Petit Nord from Red River came up the Missouri River, however. In fact, the two major systems of diffusion into the region were connected. Many epidemics broke out first in the upper Great Lakes and later surfaced in the Red River Settlement, having spread westward through American territory (Map 20).This crossover pattern again reflected the strong east-west connections that had developed to the south of the Boundary Waters. For instance, the fur trade of the upper Mississippi region, and even that of Pembina for a time, was supplied from Mackinac, and, every fall, brigades from the Lake Superior-Lake Huron area entered the country southwest of the Red River Settlement. More importantly, the highly mobile Aboriginal people living in American territory also helped to spread disease from Lake Superior to the Red River. Seasonal ceremonies in Lake Superior and Lake Huron routinely attracted people from the upper Mississippi, some of whom also included Red River and the plains in their seasonal cycle.43 In 1842-43, the American missionary

Map 20: Major Systems of Epidemic Diffusion into the Petit Nord

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 171 Frederick Ayer described the patterns of movement of the Red Lake (Minnesota) Ojibway, who numbered perhaps 700 people. When the rivers open in the Spring, the men generally leave, and descend the Red River to the Colony. They are absent about 20 or 25 days.The principal object of this visit to the Colony, is to traffick sugar with the half-breeds and others, for which they receive clothing and goods. Again in the first part of June, a considerable number start out to hunt buffalo in the plains to the West. A few also visit La Pointe and the Sault Ste Marie during the summer. With these exceptions, they spend the spring and summer at Red Lake.The men only go to the Colony and on their hunts in summer. And in their winter hunts, the men do not usually take their families with them. As a general thing the women and children remain here both summer and winter.44

Once the epidemics were within the Petit Nord, the broader pattern of their diffusion usually reflected the transport system of the HBC during this era. In general, the company's men were responsible for spreading these sicknesses over long distances, while Aboriginal movements tended to spread disease locally. In 1841 Dr. Thomas Hodgkin, a noted English physician and a strong social critic, took aim at the company in a letter to Governor George Simpson, charging that parts of the country [the HBC territory] so traversed [by traders] must, at some seasons of the year, produce disease + thus occasion [epidemics] of a more or less destructive character. The diseases of the whites, + more especially small-pox + measles will at times be introduced, + the havoc which they almost inevitably make amongst the people unprepared to meet or treat them, is awfully great.45

Hodgkin's charge was justified, for the HBC men were now transporting disease along with their goods and furs with great frequency. By the 1830s, the Aboriginal people knew to get away from the main transport routes, along which the brigades travelled, when epidemics were abroad. For example, in May 1838, a large group of Aboriginal people collected near Cumberland House, preparing to leave the post. They were off to pass the Summer in the thick woods a considerable distance from hence, so that they may not come in contact with the Saskatchewan Brigade on its way downwards. They are one + all dreadfully alarmed at the idea of catching the small Pox which has induced them to leave off

172 CHAPTER EIGHT hunting rather earlier than usual so as to give them time to get out of the way before the People of the infected part of the Country pass.46

During the decades following 1821, then, the HBC emerged as a potent force in the long-distance diffusion of disease within the Northwest. Although company men had been transporting acute infections within the region since the eighteenth century, it happened rarely, the distances the diseases were carried tended to be short, and, with only a very few exceptions, the afflictions had not included the crowd diseases. After 1821, however, HBC employees became routine participants in the diffusion of ah1 manner of sicknesses, including crowd diseases, and they carried them throughout the Canadian Northwest. In large part this was due to a shift in employment strategy, whereby the company began to favour men of Aboriginal and mixed descent over men from the British Isles, who had once dominated the ranks, especially on the swiftly moving transport brigades. These new employees often lacked acquired immunity to the diseases that had long been endemic in the larger cities of Europe, making them ideal for propagating spatially extensive epidemics. For this reason, many of the post-merger epidemics reflected the movements of the HBC brigades, both in their timing and in their routes of diffusion. Following the merger, three, basic, HBC transport systems covered the Petit Nord, and each played a distinct role in the diffusion of epidemic disease. The western portion of the Petit Nord was part of the Northern Department and of a far-flung transport system that, at its height, ran from just to the east of Rainy Lake to the western Arctic. Each summer, canoe and boat brigades from throughout the department arrived at either Norway House or York Factory, exchanging the returns of the previous outfit for trading goods for the following year, and there was a strong tendency for epidemics to spread in a hierarchical fashion from these posts.Year after year, infectious diseases broke out at these two posts, coinciding with the arrival of the inland brigades. Brigades from the Rainy Lake, Winnipeg, and Island districts reached these posts in June or July, arriving at about the same time as those from the Red River Settlement, making this a crucial period for the dissemination of disease-causing organisms (Map 21). As well, Norway House outfitted the Berens River outpost, andYork Factory supplied Severn and its sometime outpost of Trout Lake. Another brigade from the Red River Settlement, which supplied much of the voyaging labour, went to Rainy Lake during the spring. As a result, the posts of the western Petit Nord were tied into a vast, interconnected, transport system that was readily suited to spreading epidemic disease.47

Map 21: Post-Merger HBC Brigade Routes in the Petit Nord

174 CHAPTER EIGHT A separate transport system served the southeastern part of the Petit Nord, including the Lake Superior District. Following 1821, the HBC established a supply route connecting the posts on the north side of Lake Superior: Sault Ste. Marie, Bachawana, Michipicoten, Pic, Long Lake, Nipigon, and Fort William (see Map 21). Michipicoten was the entrepot, and, during the spring, each post sent its returns there to be shipped to England, at the same time receiving trade goods and supplies for the coming year. Other goods travelled from Canada and the United States to Michipicoten via Sault Ste. Marie. After 1837 a schooner, the Whitefish, was used to outfit the posts of the district. Another set of boats and canoes worked in conjunction with the Lake Superior brigades to transport goods and furs between Lake Superior and James Bay. Each June, brigades were dispatched from Michipicoten via the Michipicoten and New Brunswick rivers to a transfer point at Long Portage, although some canoes continued on to Moose Factory. Other crews headed southward from Moose with the ensuing year's trade goods, and the brigades exchanged cargoes at Long Portage before returning.48 In this case, connections with Sault Ste. Marie and the eastern settlement frontier, as well as its hierarchical structure, made this transport system another potent vehicle for spreading disease. The remainder of the Petit Nord was part of Albany Inland District, stretching from Albany to Lac Seul, and included the posts of Martin's Falls, Osnaburgh House, and Lac Seul, and a few outposts.This transport system was detached from that of the Lake Superior-Moose Factory system, with the only connection being the limited coastal contact between Albany and Moose.This part of the Petit Nord was thus somewhat of a backwater, with only limited HBC traffic moving up and down the Albany River. Each June a few canoes left Lac Seul for Fort Albany. At Osnaburgh House this brigade picked up more men and furs, and continued to Albany before returning to Lac Seul by mid- to late August. Perhaps because of the greater distance between posts, its regional isolation, and the small numbers of men needed for the transport, the company spread fewer diseases through this system than through the other two. Finally, there was also a limited amount of travel by HBC employees between these systems. For example, sloops were used to connect the HBC's coastal factories, including Albany and Moose. As well, a few express and transport canoes still ran occasionally between Canada and the Northwest, passing through Sault Ste. Marie, Lake Superior, and the Boundary Waters. In general, however, contact between the posts within the different systems was rare. Instead, the transmission of disease between them was more often the result of the movements of the Aboriginal people, if it occurred at all.

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 175 1821-1830 The people of the Petit Nord were granted something of a reprieve from epidemics during the first few years following the merger of the HBC and the NWC. Although, in each year except 1821, there were isolated outbreaks, usually of colds or some other respiratory complaint, nothing appeared of any great significance, or indeed of any great extent, until the midpoint of the decade. Perhaps this brief respite was due to the decline of the Montreal-Fort William canoe route in favour of ship-based access from London to York Factory. In the 1830s, long-time NWC trader Charles McKenzie hinted that the traditional voyageur brigades from Canada occasionally introduced disease,49 and their cessation following 1821 may have temporarily slowed the flow of sickness from the east. However, this was but the calm before the storm, as other influences soon combined to more than compensate for the decline in fur-trade traffic along this route. Epidemic disease was much more common in the Petit Nord during the second half of the 1820s than it had been during the first, and it occurred throughout the region. Colds were by far the most common affliction, although dysentery flared up on two occasions, including an epidemic that swept throughout Lake Superior District in 1828.50 A spatially limited outbreak of measles was said to have spread from the Red River Settlement to the Lac Seul region in 1828-29.51 This was only eight years after the previous measles epidemic. Still, with perhaps two exceptions, none of the sicknesses during the 1820s was particularly severe. One of these exceptions was an unidentified complaint that appears to have caused several deaths among the Aboriginal people of the Lac Seul region in the fall of 1829.52 The other was the return of a now-familiar disease. The most extensive epidemic to strike the Petit Nord between 1821 and 1830 "was whooping cough, which attacked both the eastern and western margins of the region. It first appeared early in the summer of 1825 at Drummond's Island during the annual present-giving ceremony, and the participants carried the disease back to their homes. It may have made its way to Lake Superior, given Schoolcraft's and Keith's condemnation of the trips to Drummond's Island just three years later, but with no extant journals, we cannot be sure. We do know it spread towards James Bay. By the fall of 1825, some of the visitors to Drummond's Island had carried the disease northward to the fur-trading area near Flying Post and Matagami (Map 22). In short order, whooping cough was introduced at Albany and Moose. This was virgin territory for the disease, the first time ever that it had been seen at either post, and its effects lingered at Albany into the following

176 CHAPTER EIGHT January.53 The young suffered most of all, typical of a disease that tends to be especially lethal for infants and young children in non-immunized populations. Following its appearance in the upper Great Lakes and at Albany, the epidemic resurfaced in the records in 1827, in the western part of the Petit Nord. Here, whooping cough was revisiting territory it had covered only a short time before. Essentially, this was the same pattern of delayed diffusion as during the 1819-20 epidemics, and it proved common during the years leading up to 1846. The disease broke out to the north of Lake Winnipeg during the fall, appearing among some of the crews manning the outbound boats from York Factory, who subsequently introduced the disease at Cumberland House and He a la Crosse. It also spread to Norway House and to the men, women, and children of Oxford House. It did not, however, extend to the local Aboriginal and Metis populations, probably due to the immunity provided in 1819. Especially hard hit were the children of the HBC men, some of whom bled from their ears and mouth, and choked to the extent that they turned "black and senseless."That same fall, whooping cough travelled from Norway House to the Red River Settlement, where it was confined largely to the children, among whom there were several deaths. Although this loathsome disease was brought back to Lake Manitoba by Aboriginal people who had visited Red River during the winter, it failed to diffuse eastward into the Petit Nord. Despite spanning a considerable distance over a period of two years, the single major epidemic to strike the Petit Nord between 1821 and 1830 only skirted the region, its effects felt only on the eastern and northwestern margins.54 1831-1840 As the changes to the patterns of settlement and transport outside the region accelerated, the epidemic history of the Petit Nord entered a new and much deadlier era. No longer would the Aboriginal people have several years, or even decades, to recover from the diseases that passed through. Instead, as repeated waves of closely spaced—for some, annual—epidemics began to sweep the region, recovery, in terms of either numbers or morale, became difficult.55 While we cannot assign a definitive date for the beginning of the epidemic transition in the Petit Nord, it is clear that as of the 1830s it was well underway. Still, the vast majority of disease episodes during this period were, yet again, little more than temporary annoyances on their own.56 Colds, often

Map 22:The Petit Nord, 1821-1845

178 CHAPTER EIGHT epidemic but rarely fatal, were the order of the day, breaking out frequently during this decade.57 Interestingly, these epidemic colds exhibited no apparent seasonality, but instead could appear during any part of the year. Bowel complaints, including those referred to by the traders as dysentery, were also common, with an outbreak somewhere in the region almost every year. Although colds and bowel complaints were generally mild, they could lead to more serious complications, by weakening the victims for other opportunistic infections, notably pneumonia, or by activating latent infections of tuberculosis. For some people, the parade of minor complaints proved as fatal as if they had been smallpox. One of the hallmarks of the epidemic transition in the Petit Nord was the frequent reappearance of particular afflictions. Should that transition continue to completion, then the affliction would reappear often enough to become a disease of childhood, usually accompanied by a decline in severity. In parts of the region, whooping cough appears to have been on its way to achieving such status, breaking out perhaps twice during the 1830s. In fact, its increased prevalence can be dated to the 1820s. Unknown in the Petit Nord before 1806, it subsequently appeared in 1819-20 and from 1825 to 1827. It returned a scant five years later. In the summer of 1832, Charles Mackenzie recorded in the Lac Seul journal that "the Indians & their Children have a very bad Hooping Cough this summer and some children fell a victim to this cough already and there is every fear that many more will be carried away by it." Within ten days the disease was universal among the people at the post.58 There is, however, no evidence of its path of diffusion beyond the Lac Seul area. Two years later, whooping cough was back, and this time it spread much farther afield. We cannot be certain whether this second outbreak was independent of that of 1832.59 We do know that it came from the AFC's Fort Clark, on the upper Missouri, where it killed many Mandan children during the winter of 1833-34. By the spring or early part of the following summer, both it and a bowel complaint spread to the Red River Settlement from the upper Missouri. Here again, whooping cough was especially fatal to the children.60 As it would so many times during this era, Red River served as the point of departure for the epidemic in its further diffusion. As the boat brigades left the Red River Settlement for the north that summer, they carried the disease. By August it was widespread among the children of Norway House, although not exceedingly fatal. In fact, whooping cough prevailed throughout this part of the country, spreading to the Aboriginal people who traded at Norway House, Oxford House, and Nelson

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 179 River, although not to those who traded at York Factory, or who lived eastward in the interior of the Petit Nord.61 The timing of the sickness proved a significant setback, as it greatly affected the fall hunts and the HBC transport for that year. Nevertheless, this whooping cough epidemic does not appear to have had an overly severe course. The epidemic's depredations were much greater as it spread from Red River to the Boundary Waters. It attacked the Ojibway of the Rainy Lake area by mid-September, and soon spread to the people in the trading post. Here, whooping cough seems to have been joined by influenza, which spread eastward to Fort William by way of several HBC men. Ultimately, this potent mix of diseases was responsible for twenty-nine deaths among the Aboriginal people, including fifteen adults.62 Apparently, the whooping cough epidemic of 1819-20 had done little to protect them in 1834. The Rainy Lake Ojibway spread sickness to their neighbours to the north. Initially they carried whooping cough to the people of Sturgeon Lake and Wabigoon Lake (known as Lac la Glaize), among whom a few mortalities were reported. Later still they brought sickness to Lac Seul, although it is not certain if this was whooping cough or influenza. Early in 1835, Charles McKenzie and the HBC men, women, and children at Lac Seul fell ill with a "dreadful cough," brought from Rainy Lake. Given the prevailing symptoms of the strain of influenza then at large, this might have been either disease.63 This was the second of two diseases to strike the HBC in rapid succession at Lac Seul, the other causing sore eyes, sore throats, and breaking out at the mouth and tongue. Even in an era when epidemics were becoming commonplace in many parts of the Petit Nord, Lac Seul was one of a few posts that stood out for the frequency and variety of disease episodes. There was also some sickness among the Aboriginal people at Cat Lake, located to the northwest of Osnaburgh and north of Lac Seul. However, once again identification of the disease is impossible. As frequently as whooping cough returned to the Petit Nord during this era, it did not compare to influenza. In fact, it would not be unwarranted to conclude that, given its high rate of recurrence, its tendency to spread widely when it did appear, and its potential for human suffering, influenza had emerged as the most significant epidemic threat in the Petit Nord. Although it made occasional appearances in the region during the eighteenth and early nineteenth centuries, only in the early 1830s did it began to appear with regularity.Thereafter, influenza broke out somewhere in the region almost every year.64 This is not unexpected, given the epidemiological characteristics peculiar to this disease. Unlike the true crowd diseases, which could become endemic in single, densely populated, urban

180 CHAPTER EIGHT communities, influenza would never become a disease of childhood. The immunity induced by a case of influenza provided little protection from infections resulting from new strains caused by antigenic shifts or drifts. Of the many influenza outbreaks and epidemics that struck the Petit Nord between 1831 and 1840, two stand out for their extensive diffusion. These were part of a series of widespread, often devastating, influenza epidemics that swept through the western interior of Canada between 1835 and 1850. The first occurred in 1835, and was undoubtedly the most destructive influenza epidemic to strike the Petit Nord to the midpoint of the nineteenth century. Although its source is unknown, once again, the Red River Settlement suffered first. The epidemic quickly became the talk of Red River, which provides evidence of the nature and course of the disease. On June 12, the Reverend David Jones wrote that "there is an influenza becoming very prevalent, + which I fear will prove very fatal to infants + aged invalids; it exceeds in malignity any epidemic I have witnessed in the country"65 No age group was safe from the disease; entire families were incapacitated at the same time. Its symptoms, and those of its sequelae, were consistent and cruel. These included: sore throats, excruciating pain in the chest, weakness and pain in the limbs, violent headache and earache, discharge of pus from the ears, deafness, delirium, inflammation of the eyes, intermittent fever, severe cough, and, in some cases, expectoration of blood. This was a far cry from the vast majority of past influenza epidemics in the region and, as Jones predicted, the disease left many dead in its wake, subsiding only with the arrival of winter.66 As was becoming common in the post-merger Northwest, the Red River Settlement served as a nexus for diffusion through the agency of the HBC boat brigades. Once within the transport system, this epidemic spread immense distances, reaching as far as Fort Simpson on the Mackenzie River. Before that, however, it broke north of Lake Winnipeg. By June 22, or not long after it had achieved epidemic status at Red River, it had emerged among the men of Norway House. Two days later the trader Donald Ross wrote that "there are now 120 individuals, young and old, including Indians labouring under it, at and about the Establishment." This was almost inevitable. Norway House was a depot for the brigades of the remote posts of Athabasca and Mackenzie River, and virtually all the boats and canoes bound for York Factory passed through on the way and on their return, including those from Red River. This placed the post in an especially vulnerable position with regard to epidemics. In fact, there were only two years between 1830 and 1840 in which an infectious disease did not break out at Norway House. The year 1835, then, was typical of this era. After

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 181 breaking out among the post's men, influenza spread to the local Aboriginal people and the brigades that passed through on their way to York Factory. Interestingly, a second and more severe wave swept through the post in October, perhaps reintroduced as new infected brigades arrived. This helped to prolong the stay of the disease at Norway House long after it would otherwise have died out among the small, local population.67 No journal survives for this year from Oxford House, located on the Hayes River route to York Factory. Nevertheless, other evidence indicates that the 1835 influenza epidemic reached this area, and with severe consequences. For instance, the disease was reported at nearby Knee Lake, and the Swan River and English River brigades were forced to stop near the post due to the effects of the disease among their crews. As well, some of the Oxford Cree arrived at Severn in August and, when asked why they had abandoned their post, replied that "their friends and relations had died this Summer and that they would no more return thither on that account." Richard King, an Arctic explorer who was at Cumberland House late in the summer, learned that thirteen people had died at this post. These were not inconsiderable numbers of fatalities when taken from the small groups who lived in these areas.68 Influenza arrived at York Factory on June 19 with five Red River boats. As at Norway House, the disease had been quick to make its way from the south, although here it had been preceded during the spring by outbreaks of bowel and lung complaints and other sicknesses. This was the main depot of the HBC's Northern Department, the point of departure for the furs bound for Europe and the destination of many a brigade from the interior. Consequently, the presence of the disease was no less inevitable here than at Norway House. The scene at York was undoubtedly the same as at the other posts, with large numbers of victims unable to fend for themselves and the resources of the HBC stretched to the breaking point. Here again, the 1835 influenza epidemic exhibited the same explosive contagiousness characteristic of the disease, as well as the high degree of virulence that was demonstrated everywhere by this particular strain. Once introduced, it spread quickly among the men, women, and children of the fort, followed closely by the brigades and the Cree people of the area, who were not clear of it until mid-August. At least sixteen people at York, and fourteen of the people of nearby Nelson River, died during the epidemic.69 The mortality had a negative impact on the gathering of provisions, which was critical for the long winter ahead, and on the transport of goods and furs, which in this era always operated on a tight schedule.

182 CHAPTER EIGHT Although the epidemic was explosive in its diffusion between the Red River Settlement and York Factory, it made slower progress elsewhere. Reports indicate that there was much sickness in the Berens River area during the fall and winter, due to influenza, but few deaths. Perhaps more significantly, the disease failed to spread much to the east ofYork Factory, towards the Severn River area, but instead was largely confined to the corridors leading from Lake Winnipeg to York Factory. The 1835 influenza epidemic was also carried eastward from the Red River Settlement into the southern part of the Petit Nord. The disease appeared at Lac Seul during Charles McKenzie's absence, between June 11 and August 10. During that period all "the natives were labouring under that cruel disease the Influenza...,"including those to the west.The effects of the sickness stayed with them to the fall, and in some cases, they were unable to harvest their wild rice owing to sickness. The lack of food contributed to their infirmity. None of the Ojibway people died at Lac Seul, but several of the neighbouring people did succumb to the sickness.When McKenzie and his brigade returned from Albany, they too contracted the disease and remained in bed for several days, but began improving after three or four. As in the north, diffusion was incomplete, and the disease did not spread eastward to Osnaburgh and Sturgeon Lake. Unfortunately, the loss of the Rainy Lake journal from this period makes it impossible to know of the impact on the people of the Boundary Waters.70 Finally, there was also influenza in the Lake Superior District, although it is not clear that the epidemics were related. Following on the earlier, and seemingly unconnected, outbreak of the disease in the winter of 1834-35, influenza was epidemic at Fort William in September 1835. Similarly, the brigades arriving at Nipigon in August had been suffering from an unidentified disease, while later news arrived at the Pic post that the Ojibway had been sick of an unknown disease during the winter of 1835-36.71 Given influenza's penchant for pervasive and explosive diffusion, it is not unreasonable to conclude that the disease was present from the western to the eastern borders of the Petit Nord in 1835. If the 1835 influenza epidemic was exceptional in its severity, the second widespread influenza epidemic of the 1830s was more typical of the course of this disease.This occurred just two years later, in 1837. Although generally less severe than that of 1835, this disease also proved mortal in some cases and was met with universal susceptibility, indicating that it was of a different subtype than that of 1835. The symptoms this time were less complex, and included respiratory congestion, diarrhoea, and vomiting.Yet again it centred on the Red River Settlement, and this time more is known

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 183 of its earlier history. The Reverend William Cockran, an Anglican missionary stationed in Red River, noted in his journal that the disease had "passed through the Indians of the Plains from the United States.. ,."72 In all probability it was brought back from a trip to one of the American posts, part of an influenza pandemic that prevailed generally in Canada in 1836-37, having come from Europe.73 From Red River, there was a clear progression to York Factory. Initially, the HBC brigades carried the disease northward to Norway House, where it broke out early in July. In turn, the Norway House brigade arrived at Oxford House on July 12, suffering from influenza. By the 15th, several of the Aboriginal women and children about Oxford House were ailing, as were the HBC men, but, unlike the 1835 epidemic, no deaths occurred. That was not the case at York Factory, however, where four of the Lowland Cree had died by August 9 and many others were very sick.74 While we do not know if this epidemic spread towards Severn and its hinterland, it is clear that, unlike the influenza of 1835, it did not diffuse eastward into the Boundary Waters, nor did it penetrate to the Albany River system. The 1830s also brought new diseases to the Petit Nord. One was chickenpox, now considered an obnoxious but minor infection of childhood in larger urban centres.This disease broke out at Lac Seul between December of 1835 and January of 1836, and appeared first among the women and children of the post, thereafter spreading among some of the men. Its source is unknown, but it may have arrived there from the south. HBC trader Charles McKenzie described it as a mild ailment that produced small pustules from the soles of the feet to the top of the head, but no deaths, even of a baby that was born with the disease.75 Chickenpox, or varicella (ICD-10 B01), is an acute, highly contagious disease caused by the varicella zoster virus. It spreads through droplet emission or through contact with fluid from the blisters, and subclinical, or inapparent, infections are common. As McKenzie documented, congenital infections with chickenpox can also occur. A two- to three-week incubation period is usually followed by a slight fever and a widespread skin eruption that may extend to the entire body.The communicable period lasts about two weeks.The morbidity rate of chickenpox is very high, but mortality rates tend to be quite low.76 The presence of chickenpox at Lac Seul is further evidence of the changing relationship between the Petit Nord and the external pools. It is not among the first rank in terms of diffusion ability, and so appears to have been a comparative latecomer wherever it was introduced. In the Pacific Northwest, for instance, the first recorded instance of the disease occurred in 1840, long after smallpox, whooping cough, and possibly measles had

184 CHAPTER EIGHT appeared.77 It is significant that McKenzie felt it necessary to ask,"But what would bring such a disease to this out of the way place?" even though he had seen epidemics of childhood diseases such as measles and whooping cough.78 The other new disease to appear during the 1830s was rubella (ICD-10 B06), commonly known as German measles. It first broke out at Fort William in June of 1837 and came from towards the south shore of Lake Superior, having already been in the Fond du Lac and Grand Portage regions. As with chickenpox in 1835, it appeared first among the women and children, and subsequently spread to some of the men. Described as "something similar to the Meazles, but not so dangerous,"79 its major symptoms included a rash that broke out on the entire body and swelled faces. Although this may have been another outbreak of measles, it was more likely German measles. Rubella is, in general, a relatively mild viral disease that produces a rash very similar to that of measles, although its potential for causing congenital complications, including deafness and blindness due to maternal infection, is well established. It spreads by nasal secretions through droplets or by direct contact with an infective person. The incubation period is lengthy, lasting between fourteen and twenty-three days, and there is usually a very good chance of recovery if the health of the victim is not already compromised. Recovery from rubella generally yields a lasting immunity to subsequent reinfection, and so it becomes a disease of childhood in more densely populated areas.80 There is no evidence that this disease had appeared before in the Petit Nord and so, as was the case with chickenpox, the presence of German measles illustrates the growing decline in the isolation of the Petit Nord. 1841-1845 Countless diseases swept through the Petit Nord during the period from 1841 to 1845, carried there by the closer connections with the urban east. Records of such afflictions from these few short years far exceed those from any earlier era, despite the fact that many of the post journals from this period have disappeared. During this period, all the general characteristics of the advancing transition were evident, including the appearance of new diseases, the repeated return of some familiar afflictions, and a declining inter-epidemic period for many of the region s Aboriginal people. One new arrival was mumps (ICD-10 B26), a directly transmitted, acute, viral disease whose sole reservoir is humans. It is communicated through

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 185 aerosol droplets and direct contact with infected saliva, and results in a lasting immunity. It was a common childhood affliction in densely populated urban areas, before the recent development of an effective vaccine. The incubation period is a relatively lengthy twelve to twenty-five days, commonly eighteen, and the victim is infectious from six to nine days before swelling begins in the glands to about nine days after. Prevalent symptoms include fever and swelling of the salivary glands. It is considerably less infectious than measles, however, and under endemic conditions the mumps victim therefore tends to be of a much higher median age than victims of measles.81 Despite being a relatively easily identified disease with a lengthy infectious period, it was not until 1841 that mumps finally appeared in the Petit Nord, on a rather peculiar mode of arrival. On the 18th of August, the HBC ships Prince Rupert and Prince Albert arrived at York Factory from Great Britain, with mumps prevailing generally among their crews. Herein lies a bit of historical mystery for which there is no obvious answer: why was mumps, a disease of childhood in the larger centres of Europe, prevalent among the European crews when other diseases of childhood seem to have been blocked from reaching the Petit Nord via the HBC ships? In any event, it appeared at York in August, and subsequently spread to some of the post's men and to several of the Aboriginal people. In no case was the disease fatal, but it did linger in the area at least into January of 1842.82 This outbreak ushered in a period when mumps became an occasional, if not frequent, visitor to the Petit Nord and the surrounding country. Over the next four years, mumps broke out three more times, in 1843-44 (in the Red River Settlement and at He a la Crosse), in 1845-46 (in the Lake Superior country and the upper Mississippi), and in 1847-48 (at Fort Union on the upper Missouri). During these latter episodes the disease arrived by land, and there is evidence that it had become more common in the interior. For instance, fragmentary reports of the treatment of the sick at Manitoulin Island between 1840 and 1846 mention the disease at least three different times: in 1840-41,1844, and 1846.83Yet another disease had been added to the expanding disease load of the Petit Nord. Compound epidemics were another characteristic of this period. They had occurred periodically before 1841, but never with the same frequency, nor with as many concurrent diseases. In the Petit Nord, the simultaneous appearance of multiple sicknesses became almost common during the first half of the 1840s. Even so, few years could compare with 1843, during which an unprecedented number of diseases struck the region in overlapping waves. In August of that year, Donald Ross at Norway House noted in

186 CHAPTER EIGHT a letter that "this has been a very sickly season in the interior, Hooping Cough, Influenza, Scarlet Fever and a very troublesome complaint resembling common cholera, are raging with less or more violence amongst us."84 Other diseases were also present in the region, although more limited in their diffusion, making this a year of great suffering. The first to appear in 1843 was whooping cough, which can be traced to an outbreak on Lake Huron in 1842. Once again, it surfaced, along with a virulent diarrhoeal disease, among the 6000 Aboriginal people gathered at the present-giving ceremony on Manitoulin Island. This time, whooping cough seems to have done little damage. In enumerating the diseases among the people on Manitoulin Island, Dr. W. Winder wrote of this sickness, "No note of these cases, as they are generally mild, seldom requiring more than an occasional emetic, and a flannel shirt, if one can be obtained."85 This was a far cry from the devastation that accompanied earlier whooping cough epidemics, and seems to reflect the kind of tolerance that develops in a population frequently exposed to a crowd disease. At the very least, whooping cough was present on the island in 1842,1844, and 1845, during the period from 1840 to 1846, easily often enough for it to become a disease of childhood.86 In short order, whooping cough had spread to the Lake Superior District, where it had a much greater impact. It appeared at Fort William during the latter part of the summer, immediately following the arrival of the post's trading goods for the following year, and persisted well into the winter. Here, the disease struck with considerable force, probably in conjunction with the same diarrhoeal disease that had accompanied it at Manitoulin Island. The resulting mortality of these combined epidemics was, according to John Ballenden, very great. At the same time, whooping cough also spread throughout the Lake Nipigon area, to the north of Lake Superior, and here again there were several deaths among the Aboriginal people.87 Whooping cough continued westward by unknown means, travelling through American territory to reach the plains the following year. By February 1843 the disease was widespread in the Red River Settlement, one of several epidemics to pass through that year. Overall, 1843-44 was a particularly unhealthy period in the Red River Settlement, as indeed it was generally in the North west. There, whooping cough was followed by outbreaks of scarlet fever, mumps, "bilious fever," influenza, and other ailments. Whooping cough persisted for several months but, in the end, this epidemic seems to have had little impact on the settlement, and was overshadowed by the scarlet fever that broke out shortly after.88

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 187 The subsequent progress of the whooping cough is unclear. There is no evidence that it was among the crews of the brigades leaving the Red River Settlement during the spring of 1843, but it did resurface north of Lake Winnipeg the following year. In this case it appears to have spread through the country lying west of that lake, before turning east along the Saskatchewan River.The Reverend James Hunter found the disease prevalent among the Aboriginal people at Cumberland Station in the fall of 1844. At about the same time, it broke out among the children of Norway House and in the nearby Methodist Aboriginal village of Rossville, having come from the Saskatchewan, and was still active as of December 16. In this case, the presence of the disease during the previous decade meant it found fewer potential victims.There was also an unidentified sickness among the Berens River Ojibway during the winter, perhaps whooping cough as well, as it was common for some of these people to spend their summers at Norway House, and to work on the freight boats of that place.89 If so, this marked the furthest extent of the epidemic in the Petit Nord. In the end, this sickness was unable to penetrate into the region, unlike many of the major epidemics from this era, but instead was confined to its margins. The second, and most deadly, of the epidemics that appeared in the Northwest in 1843 was scarlet fever. Scarlet fever (ICD-10 A38), or scarlatina, is one of several bacterial diseases caused by streptococcus pyogenes. It is characterized by fever and a bright red skin rash that does not often appear on the face, but instead erupts on other parts of the body, such as the neck, chest, groin, and elbow. Symptoms may vary widely, but there can also be nausea, vomiting, sore throat, swelling in the neck, and discharge from the tonsils, among others. It is now considered a relatively mild childhood disease. It is usually transmitted directly by droplet infection, and may occasionally cause widespread outbreaks due to contaminated milk or food. The incubation period is short, usually two to three days, and the period of communicability is lengthy, between ten and twenty-one days. Humans are its only reservoir and it is an acute disease. However, there can be longterm carriers. Scarlet fever causes a permanent immunity to the toxin that produces the rash and to the particular strain (of which there are three), and so it rarely attacks an individual twice.90 Although this was the first time that scarlet fever appeared in the records of the Petit Nord, it is quite possible that it or other related streptococcal infections were present before. For instance, some of the many epidemics of sore throats from the eighteenth century may have been due to a streptococcal infection. An outbreak of sore throats at Albany Fort in the summer of 1773 was accompanied by at least one case of erysipelas, an acute

188 CHAPTER EIGHT cellulitis caused by infection with Group A streptococci. For its part, scarlet fever was present in epidemic form in the American colonies as early as 1735, but was irregular in its appearance thereafter. At one time it was a fairly mild affliction, and is considered to be such now, but a much more virulent form appeared in the 1820s and 1830s. This change in virulence was reflected in the high degree of suffering experienced during the 1843 epidemic, but was not universal. For instance, a widespread epidemic of scarlatina on Manitoulin Island in 1844 was described by a medical observer as "very mild." Nevertheless, the disease was anything but mild as it spread through the Canadian Northwest in 1843.91 Scarlet fever broke out in the Red River Settlement in July of that year, possibly introduced by Ojibway from Lake Superior. The people of Red Lake maintained a seasonal round that incorporated trips to both Red River and Lake Superior, and other Aboriginal people from the Red River area undoubtedly headed east to the upper Great Lakes periodically, and vice versa. The American Indian Agent at Sault Ste. Marie, James Ord, wrote in his report for 1842-43 that the people of Ance Keewenaw had been struck by sickness during the winter, probably scarlet fever. Of perhaps 300 people wintering there, seventeen had died. A missionary, John Pitezel, at the mission on the Keewenaw peninsula, recorded in his memoirs that "in the early part of November, the scarlet fever broke out in the settlement. Several of our nearest neighbours were attacked—some were quite sick, but it did not prove fatal in any case."92 Most probably, those who died had been located away from Pitezel's mission. By July scarlet fever reached the Red River Settlement, breaking out first in the lower, or northern, part. It soon spread throughout Red River, persisting well into 1844. All who lay in its path were vulnerable. In all, it is estimated that well over 100 people in Red River died during this epidemic, most of them children. The Roman Catholic parishes were especially hard hit. Trader Duncan Finlayson observed that the poorer people who lived in crowded and unhealthy conditions and without proper diet had a much worse experience with the disease than the more affluent.93 However, in breaking out in the Red River Settlement in July, rather than in June or before, the epidemic fortuitously missed the departure of the brigades, and so its northward progress was limited. Otherwise, the disease would undoubtedly have continued its ravages among the people living to the north of Lake Winnipeg, just as so many other epidemics had done before. Even so, the Berens River Ojibway contracted this sickness in the beginning of October, when they travelled to Lake Winnipeg for their winter supplies. It spread quickly among them, arid those who survived

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 189 fled while still ill, some no doubt carrying it towards the interior of the Petit Nord. In December Donald Ross reported that the people of Berens River were "dying by the half scores," and he rightfully feared that the disease would soon be at Norway House.The trader proposed isolating his post from the southern posts in order to prevent the northward spread of the disease, and perhaps his quarantine was successful, for all evidence indicates that the north of Lake Winnipeg escaped scarlet fever at this time.94 Those who lived to the south and east of Lake Winnipeg were not so fortunate. Scarlet fever spread east from the Red River Settlement, attacking the people of Fort Alexander and Rat Portage, on Lake of the Woods. Ten of the children at Fort Alexander died of scarlet fever and one man succumbed to influenza, which had joined it by then. By early September, scarlet fever had extended from the Boundary Waters to Lac Seul. There, Charles McKenzie noted on the 7th that of the HBC people, two of his men, all the children, and most of the women had scarlet fever, and some of the Ojibway had the blotchy skin and sore throats indicative of the disease. The Lac Seul people generally passed their summers on the Winnipeg River or at Rainy Lake, and in the summer of 1843 some were reportedly trading at Fort Alexander and at Fort Frances, bringing this disease back with them. Also, an unidentified illness that was probably scarlet fever affected most of the people at Osnaburgh in December.95 The whooping cough and scarlet fever epidemics of 1843 are evidence of a vast system of diffusion that involved much more than the Petit Nord. This was a continental system stretching from the cities of the east through the upper Great Lakes and across the interior of North America to the Pacific. Having passed through the Red River Settlement, both these epidemics later surfaced in the Pacific Northwest. Scarlet fever appeared on the Columbia River early in September of 1843. Although anthropologist Robert Boyd has suggested that it might have arrived via the HBC brigades, this is unlikely since, as we have seen, the disease appeared in the Red River Settlement only after the men had departed. Instead, it was probably introduced by settlers moving along the Oregon Trail, which had itself emerged as a potent source of disease transmission during the 1840s.96 Whooping cough appeared slightly later, having come from the east through slower Aboriginal connections. It reached the Columbia in January 1844. Moreover, regular wintertime ARDs began to appear on the Columbia River during the 1820s and 1830s, introduced by fur traders from Red River and the plains.97 This new phenomenon coincided with the emergence of ARDs as a frequent visitor to the Petit Nord.

190 CHAPTER EIGHT The third major epidemic disease of 1843 was influenza, by now a frequent visitor to the Northwest. Its status as the dominant epidemic disease of the 1820s and 1830s was reinforced during the 1840s. Influenza was epidemic somewhere in the Petit Nord at least in 1843,1844,1845,1846, 1847, and 1850. In fact, it is quite possible that the disease was epidemic in each year of the decade. The appearance of influenza in 1843, then, was part of an overall trend of reoccurrence characteristic of the post-merger period. The rapid and extensive diffusion of influenza in 1843 makes it difficult to trace its broader spatial patterns. Likewise, the large numbers of diseases prevalent during this period and the tendency for some traders not to identify or describe the diseases make it difficult to establish the epidemic's coverage. Most likely, the disease followed the familiar pattern of east-towest migration characteristic of the other two epidemics of 1843, travelling from the upper Great Lakes to Lake Winnipeg and the Red River area. It was widespread on Lake Superior at about the same time that it broke out in the vicinity of Lake Winnipeg, and also in the upper Mississippi area. Two other diseases, mild colds and deadly dysentery, accompanied influenza on its tour of Lake Superior. All three moved west along the north shore of Lake Superior. Influenza appeared first among the HBC men at Sault Ste. Marie in July, and it disappeared shortly after the 17th. It then surfaced at Michipicoten with the colds, either late in July or early in August, and there the HBC men, their families, and the Aboriginal people all contracted the disease. It then spread among the Ojibway along the shore of Lake Superior, claiming five lives in the span of a single day, and seven in all. Following in the path of influenza was dysentery, which arrived at Michipicoten some time before September 12, and lasted less than a week. This was the third epidemic sickness to reach this post in less than two months. Only the relatively mild colds reached Pic and Fort William, and no deaths were reported at these posts. On the other hand, dysentery alone appeared at Nipigon, conveyed there directly by a man returned from the ceremonies at Manitowaning in August. There, the disease was extremely virulent, carrying off large numbers of children and a few adults.98 Even as it was erupting at Sault Ste. Marie, influenza appeared in the western part of the Petit Nord. Seemingly, the disease emerged first in the York Factory-Norway House area and extended to the south, east, and west. The York Factory journal noted frequent unidentified illness, predominantly bowel complaints, among the HBC men and a few Aboriginal people from about July 4 to late August. Among the arrivals at York, leading up to the outbreak of the disease, were two Montreal canoes, which would

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 191 have come through the Sault Ste. Marie area and Lake Superior. By August there was a general state of infirmity among the men, including the sloopers, and work came to a standstill. By the end of September, however, the sickness had abated. The Norway House journal contains few references to disease, but it is evident from the correspondence that there had been much sickness there, and that it prevailed at least until December. The dominant symptoms were sore throats and a disorder of the bowels, both of which may be symptomatic of influenza, and Donald Ross concluded that it had a serious impact on the hunts. The Cree around Oxford House suffered severely from the same sickness during the late summer and into the winter. The children were especially hard hit, three of whom died." From Oxford House, influenza spread eastward, into the Severn area. During the fall and winter of 1843-44, the people who lived in the country around the HBC's Island Lake post suffered from the same disease as prevailed at Norway House and Oxford House. A report written in February stated that eight Aboriginal people, young and old, had died in the vicinity of the post. A severe cold and other disorders, likely influenza, broke out among the HBC men at Severn in January and February of 1844. By spring, reports came in that the Cree also had been sick during the winter. Apparently, this epidemic was remarkable: post master John Cromartie considered wintertime sickness at Severn to be very uncommon. In all probability, they were accustomed to infections arriving during the summer and fall, the period when both the HBC men and people from the Severn area would have had contact with people from the Hayes River area.100 Influenza also appeared in the south, in the Red River Settlement, some time after scarlet fever, which had first appeared in July. By that time the disease was already circulating in the Norway House andYork Factory areas.101 There were also reports of unnamed sickness in the interior of the Petit Nord during the fall and winter of 1843. With whooping cough, scarlet fever, and influenza circulating within the region at this time, not to mention several more localized afflictions, it is impossible to determine (or even to guess, for that matter) what they were. In December an unidentified illness affected most of the people at Osnaburgh. There was also a report from Red Lake of sickness among the Ojibway during the autumn of 1843, and similar comments from those who hunted near Escabitchewan. And yet, no sickness appeared at Martin's Falls, a short distance down the Albany River.102 In fact, this was not unusual for this period, and it may be that an epidemic "divide," a zone of limited contact that tended to defeat diffusion, had emerged.

192 CHAPTER EIGHT While 1843 was a year of major epidemics that affected large parts of the Petit Nord, the record of acute infectious disease from 1844 is one of several minor outbreaks, but no identifiable widespread epidemic, excluding the tail end of the whooping cough at Norway House. However, this may have been more a reflection of the lack of journals for this period, rather than its being a relatively healthy year. The situation at Lac Seul in 1844 is worthy of a closer look, though, for the frequency of epidemic disease if not the severity of the afflictions. There, multiple sicknesses occurred in succession during the fall and winter. It began with Charles McKenzie's return from Albany late in the summer, during which the crews of the boats fell sick of unidentified maladies on their journey to Lac Seul.103 Nothing in either the Albany or Martin's Falls journals identifies the source of these afflictions, however. The problems really started after McKenzie's arrival at Lac Seul. The sicknesses that plagued the HBC men on their return trip from Albany were followed closely by an outbreak at the post of what appears to have been influenza in early September.This spread among the Ojibway and the company's employees alike. On September 2, McKenzie commented that "almost all of the men, women, and children and Indians, have their heads tied up in Handkfs—and can scarce sleep a wink, with a most violent cough & so[re] throats."104 This was not the end of their misery, however, as other diseases were abroad at this time. With everyone ill a week later, the trader noted that "every different band of Indians bring us a fresh Cough." Indeed, sickness lingered among the men into December, long past the time when they would be expected to have been over their initial illness. Not only the Lac Seul people fell victim. McKenzie was informed of sickness among the Red Lake Ojibway and those living to the north, as well as among many others who came to trade. Consequently, he commented that "sick Indians coming in with nothing are no novalties here this year," and that "from whatever quarter we hear, Sickness is the Coy [company?]." In this case, neither the cold of winter nor the New Year brought relief, and epidemics continued among the Lac Seul Ojibway into the spring of 1845, as the next wave of diseases struck the area.105 Incredibly, the pattern of non-stop epidemic activity at Lac Seul in 1844 continued in the following year.106 Once again the Lac Seul region was attacked by what seem to have been several distinct diseases appearing over a short period of time. The first new illness of the year appeared in June, though some of the Ojibway people were still ill in April from the previous year's afflictions. On June 1, Charles McKenzie noted that the Aboriginal people were "some + all laboring under a most violent cough

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 193 + otherwise sick besides." In all probability, this was influenza, which McKenzie called the "Red River disease," introduced by some of the people who had gone to the Winnipeg River earlier in the year. Another source of infection was a party accompanying the Methodist missionary, Peter Jacobs, to Lac Seul. Jacobs, his family, a Canadian servant, and six Aboriginal people arrived at Lac Seul from Rainy Lake on June 13. The Aboriginals and the Canadian servant were ill upon their arrival, and they were responsible for introducing influenza to the post, apparently independently of the Lac Seul people.107 At the time, McKenzie and his men were away on their annual expedition to Albany. As in 1844, the brigade was beset by sickness on its return from Hudson Bay, making travel difficult. One half of the crews remained sick when they reached the post on August 17, and they arrived to find most of the people sick with violent coughs, and some already dead. The situation had taken a remarkably familiar turn. Once again influenza was not alone, as McKenzie discerned that "there is some other disease accompanying the cough." Similar fates befell the Ojibway people throughout the Lac Seul District. During the summer, fall, and winter, people from every quarter brought news of their affliction. Altogether, there were as many as 100 sick at the post at this time, leading McKenzie to exclaim, "This house is more a Hospital than a kitchen."108 To his dismay, it was nowhere near over. In fact, the run of epidemics at Lac Seul stretched on for much longer. After appearing at the post during June 1845, influenza lasted until the fall, then was replaced by other afflictions. According to McKenzie, some form of sickness remained at Lac Seul until June of 1846.109 However, yet another influenza epidemic broke out that June, followed by measles and dysentery. Probably not more than a month or two between the spring of 1844 and the spring of 1847 passed when the Lac Seul Ojibway and HBC people were completely free of epidemic disease.The situation at Lac Seul during the mid-1840s was no doubt an extreme for the Petit Nord, but it was certainly illustrative of the profound suffering that some of the Aboriginal people of the region experienced at this time due to the proliferation of acute infectious diseases. The tremendous increase in epidemics within the Petit Nord during the 1840s created an important disease dynamic that the HBC could not have foreseen. Once again, Lac Seul stands out as a prime example. As the Ojibway of the district fell ill in the summer of 1845, and went to the post for assistance, they brought other diseases with them and, when added to those already at the Lac Seul post, this made it more dangerous than the

194 CHAPTER EIGHT place from whence they had come. According to McKenzie, sickness was the rule throughout the district, but "no where so fatal as this place because as soon as they fell sick they congregated here from all quarters each bringing a different branch of the disorder that it joined him in one Body— which formed nothing short of a real pest... ."no Very quickly that summer, the post gained a reputation for sickness and death, and the Ojibway began to leave in large numbers for the ricing areas in a desperate bid to escape these sicknesses.The majority, who were unable to proceed on their own, were carried to their canoes "as from a Pesthouse." Once a safe haven from disease and starvation, the post had become associated with the transfer of disease, rather than with commercial activity or even refuge.111 The influenza that struck Lac Seul in 1845 was part of yet another widespread influenza epidemic, which swept the western part of the Petit Nord in a familiar pattern. It broke out initially in May at the Red River Settlement, having come from the upper Red River, and was characterized by "frequent coughing, much expectoration, strong fever and great debility."112 The Red River boats carried the virus with them as they departed in June, and introduced it at Norway House, where the disease was "very prevalent + very severe" by July 21.113 It was not the only affliction in the area, as Donald Ross explained: "The season is very unhealthy with a most severe Influenza and other complaints which prevail generally throughout the country."114 In turn, influenza was passed to the Aboriginal people and to the crews of the freight boats that ran between Norway House and York Factory, disrupting the shipment of goods between the posts. At this time, it extended to the Nelson River outpost and to Oxford House.115 By mid-July, influenza had moved down the Hayes River to York Factory, arriving on the heels of outbreaks of colds and dysentery, which had disappeared prior to the arrival of influenza. As late as July 10, none of the York Factory men had been on the sick list, but one week later Chief Factor James Hargrave noted that the crews of the four Oxford House boats then at his post were sick with influenza, "a disease prevalent this summer among the natives and servants in the low country." Within a few days, several of the York men were off sick with the "prevailing disease," and it was circulating among the crews of the York Factory boats. By July 25, it was universal. About this time, the disease must have spread to the Severn area through Aboriginal connections, since there is no indication that it had infected the Severn brigade. On August 30, John Cromartie noted that "The Indians is starving and many of them still very sick. Some of them have had a hard trial of sickness this summer but none of them has died...." The Severn Cree had probably brought the disease back from the west, as

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 195 some were known to associate with those from the York hinterland. At Trout Lake, the epidemic disrupted the summer business among the Aboriginal people, and many of the sick sought assistance at the post.There, the disease persisted until the onset of cold weather.116 Once again, influenza spread from Red River through the Boundary Waters and into the southern part of the Petit Nord.The people of the Fort Alexander area, on the Winnipeg River, contracted a very severe sickness, likely influenza, which had been brought from the Red River Settlement. By early June, it was at Rainy Lake. At about the same time, it spread from the Winnipeg River to the Lac Seul area, where, as we have seen, it joined other diseases that together made the lives of the people there a complete misery. Influenza, and perhaps one of these other diseases, was introduced into the upper reaches of the Albany River system at Osnaburgh House. Here, there were two distinct, but brief, outbreaks of sickness. The first appeared in mid-August of 1845, affecting most of the HBC people. This was only days after Charles McKenzie's brigade passed by and, despite George McPherson's suggestion that all were "well and safe" on these boats, it is probable that the Lac Seul men had passed their sickness to the Osnaburgh men.The second outbreak, again unidentified, occurred during the month of December, and nearly all the people at the post were ill.117 Most likely, this was influenza from Lac Seul. Neither outbreak seems to have spread far down the Albany River. As before, the Martin's Falls and Albany areas remained free of epidemic disease while it raged around the headwaters of the river. It is important to remember, then, that although the region as a whole was undergoing an epidemic transition, there was tremendous variability in the epidemic experiences (Diagram 3). Just as there were spatial variations in the impact of every epidemic that struck the Petit Nord, there were variations in the long-term pattern of epidemic activity for different populations within the area. This was the case along the northern margins of the region. There was a great deal of severe epidemic activity at York Factory and Norway House, introduced by the HBC's Northern Department transport network and its connections with the Red River Settlement. Conversely, the Severn area remained isolated from most of the sicknesses that routinely travelled along the Red River-York Factory corridor. With the exception of whooping cough in 1827, none of the more serious epidemics in the Petit Nord reached Albany during 1821 to 1845, due perhaps to the post's limited transport contact with southern sources of disease. Nevertheless, ARDs, generally referred to

Diagram 3: Epidemic Activity at Selected Posts, 1821-1846

EPIDEMIC DISEASE IN THE PETIT NORD, 1821-1845 197

as colds, were often present at Albany. This was much the same pattern as during the period from 1784 to 1818. Similar long-term variability in epidemic activity occurred in the interior of the region.The rarity of sicknesses at Martin's Falls during this era is noteworthy, and understandable due to its relative isolation. There, the annual fur-trade connections with the south were limited, involving only a small number of men in the spring brigade, and a few widely spread posts. As well, the local Aboriginal people were isolated from those to the south. At least by 1839, the people who traded at this post were mostly from the Sucker clan of the Ojibway, people who had moved northward into Cree territory. Their relationship with other groups in the Petit Nord was complex. They maintained ties to the Severn and Albany Cree, intermarrying with them, but regarded their Ojibway relatives to the south and west with fear and suspicion. In particular, they did not cross the highland between Lake Nipigon and the Albany River drainage basin when they were hunting. Although motivated by a fear of warfare, their behaviour helped to preserve them from the devastating diseases that frequently spread to Lake Superior, the Boundary Waters, and the headwaters of the Albany River.118 By contrast, epidemics routinely ravaged the Aboriginal people living around Osnaburgh House and Lac Seul, only a short distance upstream from Martin's Falls. Almost invariably, it was the Aboriginal people who introduced these diseases at Lac Seul, which then spread to Osnaburgh House.Travel between Lac Seul and the Boundary Waters by the HBC men was relatively rare during this period, but was part of the seasonal rounds of the Lac Seul Ojibway who often visited the Boundary Waters. This placed them in direct line of the diseases funnelled through the Red River Settlement.Thus, in contrast to Martin's Falls, where isolation from the southern people protected them from disease, at Lac Seul routine contacts with other groups led to many epidemics among the Aboriginal people.

Illustration 4: Departure of the second colonist transport from York Fort to Rock Fort, Sept. 6, 1821, by Peter Rindisbacher, watercolour on pencil with pen and ink outline. As a key hub in the HBC's transportation network, York Factory emerged as a central place for the distribution of disease, as well as of furs and trade goods, throughout the Canadian Northwest. (PAQY.F.3.0-1)

9 The Epidemics of 1846

FOR THE PEOPLE OF THE PETIT NORD, THE NIGHTMARE CONTINUED in 1846. Indeed, for many, it marked the nadir of their health fortunes to that time. During this year, three major epidemics—influenza, measles, and dysentery—swept through much of the region, causing considerable sickness and an untold number of deaths. Several other, more localized, diseases also appeared among different groups. The result could hardly have been worse. HBC Governor George Simpson, who had first arrived in the Canadian Northwest on the heels of the measles and whooping cough of 181920, and was well acquainted with the influenza of 1835 and the smallpox of 1837-38, stated that the sickness in 1846 "led to a greater mortality than at any former period within my recollection."1 This year, then, was the culmination of all the changes in epidemic distribution that had been building since the coming of the HBC in the seventeenth century. Influenza By the mid-1840s, epidemic influenza was virtually an annual event in the Petit Nord. Frequent local outbreaks and smaller epidemics were punctuated

200 CHAPTER NINE by continent-spanning pandemics. The influenza epidemic of 1846 spread widely through the Canadian Northwest, and it followed a pattern of diffusion similar to that in 1845, making its way through the region from the Red River Settlement. It was first noted in January. The Church Missionary Society (CMS) missionary, John Smithurst, described its effects in his journal in February. On the 22nd he wrote that at his colony churches, "the congregations were very small and there was so much coughing that very little of what I said could be heard. Within the last few days nearly the whole of the Indians have fallen sick with a disease similar to the influenza. It is attended with a constant coughing and expectoration."2 The following day, "On going to the School this morning I found not 1/4 of the children present and so much coughing that nothing could be heard." The next Sunday he preached at Grand Rapids (St. Andrew's Parish), where "the Influenza is raging here as well as at the Indian settlement." On the 1st of March another CMS minister in the settlement, William Cockran, wrote, "The influenza has made its appearance among us and many are dangerously ill." However, by the end of March, it appears to have passed from Red River with little or no mortality there.3 It did, though, spread far afield from Red River, first to the Boundary Waters and from there to the northern end of Lake Winnipeg and beyond (Map 23). Although there are no extant journals for the HBC posts at Fort Alexander, Rat Portage, and Lac la Pluie for this period, there is evidence of influenza among the Ojibway of this region. Charles McKenzie, still stationed at nearby Lac Seul, learned on March 25 that "the people of that place [Rat Portage] and quarter are all laid up with the Influenza of a malignant nature which of course will soon find its way here by the intercourse of Indians of that quarter with our own." On May 19 he learned by letter from Lac la Pluie that "they surfer in that quarter much from Influenza." McKenzie's fears proved well founded. As he predicted, influenza spread to his own fort only days later. On June 1, he noted in the journal, "Our men are entirely laid up with that Confounded Influenza which the Indians brought from the River Winipic."4 For McKenzie, this was yet another damaging blow to the Aboriginal people and to the trade at Lac Seul, and his comments concerning the health of his district illustrate his frustration at a seemingly endless string of sickness. Six days later McKenzie and his men departed for Albany Fort, most of them, including himself, suffering from influenza. It was only with great difficulty that they reached Albany. As the trader observed: Some of the young Indian voyageurs were Spitting Blood among other

Map 23:The Epidemics of 1846

202 CHAPTER NINE Corrupt Matter—those who were well yesterday are the worse to day— this cough did not allow myself an hour of comfortable sleep last night— and they tell me that I am only at the beginning—nevertheless—God willing! We must make a start to morrow morning—and surely never a more miserable crew faced the Albany River with so valuable a cargo.5

As they passed Osnaburgh House on the llth, post master George McPherson penned a letter to Thomas Corcoran at Albany: Mr McKenzie of Lac Seul arrived here in the 11th + went off again yesterday in company with our boat + returns, c. Mr McKenzie and his men arrived here all sick, the most miserable brigade that I ever witnessed, and I do not know how they will reach Albany if they Continue in that state of Health—they [were] obliged to leave two men here not able to go further, say Tom Tait + an Indian and taking two fresh Indians in their places.6

Despite the movement of the infected brigade down the Albany, the disease didn't spread farther east than Lac Seul. Although two men were left at Osnaburgh, there is no evidence that influenza spread to any there. The two quickly recovered and so did the "miserable brigade," before it reached its destination. At the same time, however, influenza spread northward from the Boundary Waters to Norway House and westward from there. By that time the disease's diffusion had merged with that of the next major epidemic of 1846—measles. Measles As we have seen, measles was an infrequent visitor to the Petit Nord. Other than the limited outbreak in the spring of 1829 near Lac Seul, the last significant appearance of the disease had been in 1819-20. During this time a generation had been born and reached adulthood, a generation that lacked acquired immunity to this disease. Many others had been spared during the earlier epidemic, or had had no recorded exposure. Indeed, it is probable that, as late as 1846, some Aboriginal groups were being struck by this disease for the first time in their history; they were true virgin soil populations even as late as the mid-nineteenth century.Thus, measles found no shortage of victims in 1846. Its early diffusion echoed that of 1819-20. As before, we can trace the epidemic back to the upper Great Lakes, to an outbreak that occurred during the previous year. Measles first appeared at Sault Ste. Marie in the spring of 1845.7 By mid-July it prevailed on both the Canadian andAmerican

THE EPIDEMICS OF 1846 203 sides of the river, in some cases proving fatal. It remained active there towards the end of September. As late as October 6, measles was still rampant among the Aboriginal people of nearby Garden River.8 It was exactly this situation, epidemic infectious disease present at Sault Ste. Marie late in the summer, that had long worried the HBC traders of Lake Superior. The people who traded furs at their posts would be going east to participate in the British government's annual distribution of presents on Manitoulin Island, and in so doing would be heading into the very heart of an epidemic at Sault Ste. Marie. To make matters far worse, just as thousands of people were gathering at the village of Manitowaning on Manitoulin Island from all over the upper Great Lakes, the disease was spreading through not only that community but also the Roman Catholic village ofWikwemikong and the nearby mainland. In 1845, according to the artist Paul Kane, who was present that year, this included people "from all parts of the shores of Lake Huron, Nipissing, and Superior, as well as from all the neighbouring islands,"9 and they had carried measles to Manitoulin in the first place. Most likely, the disease was also present among the 2600 Aboriginal people on the US side who were gathered at Mackinac from all over the territory south of the border.10 The chances of avoiding the disease were almost none. In July the Lake Superior people began to make their way to Manitowaning. On July 14 Chief Trader John Ballenden wrote to Governor Simpson that he had met some Ojibway people heading eastward and had attempted to keep them from continuing on to Sault Ste. Marie. On my way to Michipicoton this season, I met a party of Indians from Fort William, who were on there way to Manatowaning to receive a portion of the presents distributed there annually by the British Government among the Indians. Previous to my departure from Sault de Ste Marie, the measels were prevalent among the Inhabitants on both side of the river, + in some cases had proved fatal. Fearing that these Indians might be infected by that disease, + on the return introduce it among the natives in the Interior, I urged them to return to Fort William, representing to them the risk they incurred, + the consequences to themselves and families should they be infected with the malady, but they persisted in proceeding on their Journey.11

Prior experience may have given Ballenden the ability to predict what would happen, but he was unable to prevent it. After the proceedings, people began to head off to their homelands. Late in August, those returning to Lake Superior visited Ballenden at Sault Ste.

204 CHAPTER NINE Marie. As he had predicted, "the Lake Superior Indians who went to Manatowaning have caught the infection, and one of their Children died at Missassague. They passed here about a week ago, several of the children still unwell."12 Once again Ballenden tried desperately to prevent the spread of the epidemic to the Aboriginal people of Lake Superior, this time recommending that these people remain near Sault Ste. Marie, rather than continue to their home territories. He was unable to persuade them to stop, but nonetheless they failed to reach their destination. They were still at Sault Ste. Marie as of September 9, barely surviving. This group had departed Sault Ste. Marie, attempting to continue to Fort William, but the illness of most of their group had forced them to return. By that date, four had perished, an old woman, two boys, and a child, and others were so low as to raise doubts about their recovery. Even before they reached Sault Ste. Marie, they had begun to suffer from that common sequel of measles, bronchopneumonia. Ironically, because of the severity of the disease, they were unable to travel and in this instance measles was prevented from diffusing along the north shore of Lake Superior.13 The HBC men stationed farther west and north of Lake Superior also worried about the possibility that such a terrible disease might spread among the Aboriginal people near them. Thus, at Michipicoten John Swanston wrote in July that: The measles which were said to have made their appearance at the Sault Sl Marys in the early part of the present month, have not I am happy to state, got this far, and I trust through the merciful interposition of a kind providence that we shall be permitted to escape this dreadful scourge, as it would make sad havoc amongst the natives should it unfortunately get amongst them.14

The disease had still not progressed as far as Michipicoten by September 16, although another "eastern" disease had. Swanston informed Simpson that he, his family, and all the servants had been plagued by a severe cold, "brought hither from St Mary's, by some of the Indians on their return from the presents." He also noted that measles had not arrived and the chances of it arriving there were decreasing as the season progressed and communication with Sault Ste. Marie drew to a close. At Nipigon, James Anderson expressed similar concerns on December 26, although everyone's health there was excellent.15 In the end, the delays caused by the severity of the disease were enough, and none of the Ojibway between Sault Ste. Marie and Lake Nipigon was exposed to measles at this time.

THE EPIDEMICS OF 1846 205 Instead, the virus spread south of Lake Superior, accompanied by mumps, which had also been at Sault Ste. Marie during the spring and summer. Like measles, mumps was epidemic in 1845-46 and crossed into the Petit Nord, although most of its diffusion occurred in American territory. At the HBC's post of Lac D'Orignal (or Moose Lake), an outpost of Fort William near Grand Portage on the Pigeon River route, 1846 began with an outbreak of mumps that proved life-threatening to several people. This disease had been brought from La Pointe, in US territory and south of Lake Superior, by some Ojibway who had travelled there to receive annuities from the Americans.16 Once again the large, temporary gatherings of Aboriginal people created by government policy had inadvertently enabled the diffusion of infectious disease. La Pointe was the location of the payments of annuities to those bands who signed the 1842 treaty, and this included those living along the upper Mississippi and the south shore of Lake Superior. Mumps persisted in the Grand Portage area throughout the winter of 1846, and soon progressed as far north as Lake Nipigon. Thus, as James Anderson informed George Simpson, "The Indians and the people of the Establishment enjoyed excellent health till the month of February, when two hands were attacked with the Mumps, some of whom are still unwell, fortunately with one exception, they are indifferent hunters."17 The mumps also continued its westward diffusion, and became epidemic at Red Lake, Minnesota, during the winter of 1845-46. There was also an outbreak of the same disease at Fort Union on the upper Missouri in the winter of 1847-48, witnessed by John Palliser.18 It is not clear, however, if the outbreaks were connected or were separate and thus symptomatic of the growing frequency of acute infectious disease west of the Great Lakes. Measles, too, moved westward, travelling south of Lake Superior. According to James Anderson at Lake Nipigon, both measles "and a kind of putrid sore throat" were prevalent at Fort William by Christmas.19 It continued spreading to the west, into the upper Mississippi country. During the winter it was rampant at Red Lake and few escaped its ravages. No doubt, it had come with the mumps from the annuity payments at La Pointe. Between fifteen and twenty people were thought to have died at Red Lake at this time, about half of them very old people. This suggests that the Ojibway of Red Lake (Minnesota) had not been exposed to measles in 1820, unlike the nearby Sandy Lake and St. Croix Ojibway, who had suffered severely.20 Winter counts kept by the LowerYanktonai Sioux confirm the presence of measles in the Red River-upper Mississippi area at this time, although by coincidence it also appears that the disease had passed through this area in 1844-45 as well.21

206 CHAPTER NINE Measles soon reached the plains. Most of the Teton winter counts describe epidemic disease that may be interpreted as measles in 1846. In contrast to the Lower Yanktonai, though, the Teton bands appear to have escaped with no or few casualties, suggesting that they had been exposed relatively recently, perhaps during the 1819-20 epidemic.22 It was also present on the upper Missouri. Winter counts belonging to both the Mandan and the Hidatsa who lived with them identify measles or a measles-like disease for this period.23 At this time they resided just to the north of Like-aFishhook, which was situated on the same site as Fort Berthold, built in 1845.The disease also appeared among the Arikara villages located near the Mandan and Hidatsa, some time in 1846. The Indian Agent for the upper Missouri,Thomas P. Moore, visited these villages shortly after the epidemic had subsided, and left an account of the effects of the epidemic. After a leisurely journey from St. Louis aboard the AFC's General Brooke, Moore reached Fort Clark injuly/'contiguous to which reside the entire Arickaree nation.They had been recently visited by the measles; and, in consequence of their ignorance of the disease, and its appropriate remedies, it destroyed a large number of them. 24 Thus, what remained of all three of the village tribes of the upper Missouri had contracted measles in 1846. Once on the plains, measles spread like wildfire. We don't know the full extent of its diffusion, but it must have rivalled, or even surpassed, the most far-flung epidemics preceding it, including the smallpox of 1779 to 1783. According to A.J. Ray, measles touched most of the area lying between Lake Winnipeg and the Rockies, eventually reaching as far north as Great Slave Lake through the HBC's boat brigades.25 Moreover, the epidemic also crossed over the Rocky Mountains to California and the Pacific Northwest, thereafter spreading northward through much of present-day British Columbia through a combination ofWhite settlers, HBC transport, and Aboriginal trade networks. It even reached into Alaska in its furthest northward extent. Eventually, the disease was carried across the Pacific to Hawaii aboard an American warship. Influenza dogged the measles epidemic much of the way, sometimes accompanying it, sometimes preceding it.26 Prior to this, however, measles diffused northward to the Red River Settlement from the Missouri, and from there into the Petit Nord, where it first caught up with influenza. Measles arrived at the Red River Settlement during the first quarter of 1846. The nature and path of its diffusion to Red River may be pieced together from statements made by three men who were well acquainted with goings-on in the settlement. According to Anglican missionary William Cockran, the disease had "marched towards the west, from the United States, into the plains and the vagrant hunters brought it to the Settlement." A

THE EPIDEMICS OF 1846 207 letter written by Father J.-N. Provencher, the Roman Catholic bishop at St. Boniface, confirmed that the disease had been brought back from the upper Missouri.27 In a letter written to Governor Simpson from Fort Garry, dated May 25, Chief Factor Alexander Christie of the HBC also commented, "We are all here much in the usual way, with the exception that from the continual intercourse between the Settlement and the Assiniboins during the last Winter, the Measles were brought amongst us, and are now going over the Settlement."28 This makes sense. By 1846 the Assiniboine were living much farther west of the Red River than they had in La Verendrye's time, and had long since begun trading with the American traders, primarily at Fort Union at the confluence of the Missouri and Yellowstone rivers. Even before the Americans settled these posts, traders annually went south to trade with the Mandan, a pattern witnessed as early as 1738 by LaVerendrye, and one which may have dated to the seventeenth century. When the Americans opened posts on the Missouri River, they, too, were included in this trading system. An unfortunate consequence of these trips was the diffusion of disease from the American part of the plains into the Canadian Northwest. In 1837-38 this trading connection proved costly, as smallpox caught at the fort reduced the Assiniboine numbers greatly, just as the Canadian tribes contracted smallpox in 1781 and measles in 1819 while raiding or trading with the village tribes of the upper Missouri. In the winter of 1846, the pattern was repeated and measles was carried to the Red River Settlement, yet again the conduit for epidemic disease into the Canadian Northwest. Once introduced, the disease spread completely through the settlement. Within parishes this diffusion was rapid. The churches probably played a central role in facilitating local diffusion through the services and the schools they organized for the children. Other gatherings, such as the bison hunt, would have had a similar impact. Nevertheless, it still took time for the disease to spread throughout Red River, and we can see a steady, if not spectacular, progression in its movement over the spring of 1846. Measles probably entered the Red River Settlement through the western parishes located along the Assiniboine River, those that were served by the Roman Catholic priests. This would have happened during the latter part of the winter, if Alexander Christie is to be believed. Nothing is known of the early stages of the epidemic in these parishes, but by the 16th of June, when Bishop Provencher wrote to Bishop Bourget of Montreal, all the Aboriginal people of Father Belcourt's Baie St. Paul community had the measles, as did almost everybody in this part of Red River.29 By this time dysentery was beginning to make its appearance on the Assiniboine.

208 CHAPTER NINE By late May, measles was on the Red. On the 24th, Reverend William Cockran noted in his journal that the disease had already made significant inroads among the congregation of the Anglican church in St. John's parish (Map 24).That day he rode to the Upper Church [St. John s] and performed the divine service. A very thin Congregation. Whole families are confined to their houses and bed by measles. This disease having never visited the settlement before, it finds numerous victims. Many persons have suffered severely from it, but thank God it has not yet ended fatally in any case.30

That same day, Cockran performed a service for a large congregation at St. Paul's (Middle Church), lower down the Red River, as the epidemic had yet to become general in this parish.Two weeks later, however, a minimal assembly greeted Cockran at St. Paul's, "owing to the measles being now prevalent in this quarter."

Map 24: The Red River Settlement in 1857 (After Ens, Homeland to Hinterland, 11)

THE EPIDEMICS OF 1846 209 It was also slow to appear in the parish of St. Peter's, located still farther north along the banks of the Red. On June 4 Reverend John Smithurst of the CMS first noted of the disease at the "Indian school" at St. Peter's when an employee of the school, a Mrs. Cook, came to work while exhibiting symptoms. Mortified, Smithurst recounted the events in his journal:"On going to the school this morning to proceed with the clothing of the children I was surprised to see Mrs. Cook with the measles. I at once sent her home sorry she had been among the children."Whether the woman's rash actions had precipitated the introduction of measles to St. Peter's is unknown, but in short order it had spread widely among the people of that parish. Ten days later, on June 14, when Smithurst attended the school, most of the pupils were absent, kept away by the measles. He also observed that "the disease is making its way with great rapidity among the Indians at present however in a mild form." By June 16, nearly half the Ojibway of St. Peters were suffering with measles, and the Anglican missionary was forced to tend the bodies rather than the souls of his flock. It was, according to Smithurst, "by far the heaviest visitation our little community has ever experienced."31 Dysentery With measles firmly established throughout the Red River Settlement, a third affliction, far deadlier than either influenza or measles, joined it in June, attacking the now-weakened population. This was dysentery, and it was extremely virulent. Indeed, some knowledgeable observers likened it to the earlier devastation of cholera in the east and in Europe. Clearly, this was unlike the dysentery that had broken out periodically among some individuals in the past and which was rarely more than a minor inconvenience. In fact, this was a different disease. The name "dysentery," or bloody flux, has long been used for several disorders, all with similar symptoms. Although sharing the same name, these diseases have markedly different causative agents and characteristics, and can vary greatly in outcome. In this case, given the severity of the outbreak, the rapid and wide spread of the disease, and the lengthy duration of patient confinement, it was likely bacilliary dysentery. Bacilliary dysentery, or shigellosis (ICD-10 A03), is a self-limiting, potentially lethal disease with known case-fatality rates as high as twenty percent under hospital conditions. The infectious agent, shigella bacteria, is transmitted through faecal-oral contact, either directly or indirectly, such as by contaminated food, water, or milk, and thrives under poor sanitary conditions and where personal

210 CHAPTER NINE hygiene is inadequate. Such conditions were no doubt found throughout the Northwest.The disease is communicable for up to about four weeks, and has an incubation period of between twelve hours and one week, depending on serotype. Illness lasts between four and seven days on average, and major symptoms include diarrhoea, bloody stools, fever, nausea, vomiting, cramps, tenesmus, and even convulsions. Unlike some other forms of dysentery, shigellosis is a significant epidemic threat and may result in many deaths.32 There is no direct evidence of the origin of this dysentery epidemic. Possibly, it had arrived from the east, like so many diseases before it. Dysentery, in both chronic and epidemic forms, had been a significant health problem on the Atlantic coast since at least the first decade of the seventeenth century. More intriguing, though, is a possible connection with the Pacific. Robert Boyd documented a violent epidemic in the Pacific Northwest of what appears to have been bacilliary dysentery during the second half of 1844. He surmised it had been brought by ship from somewhere in the Pacific, possibly Hawaii or Polynesia, where the disease had been raging since 1843, probably introduced to the Cook Islands by whaling ships.The disease may have continued its diffusion into the interior of the continent, reaching Red River in June of 1846. As in the Pacific Northwest, this was a form of dysentery that doesn't seem to have been present before, and its effects felt along the Columbia River were almost indistinguishable from those experienced along the Red. If indeed this was the source of the dysentery at Red River, then it is the first epidemic that we know of to reach the settlement from the Pacific coast rather than from the Atlantic, further evidence of the expanding and increasingly complex systems of epidemic diffusion in North America, and beyond.33 In the end, dysentery devastated the people of Red River. One prominent citizen, Alexander Ross, provided a sobering vision of the impact of the plague in his book, The Red River Settlement. According to Ross: In no country, either of Europe or America, in modern times—not under the severest visitation of cholera—has there been so great a mortality as in Red River on the present occasion. Not a smiling face in a summer's day. Hardly anything to be seen but the dead on their way to their last home; nothing to be heard but the tolling of bells, and nothing talked of but the sick, the dying, and the dead. In other more populous places such things might be more common and less horrifying, but in a country hitherto so healthy, and a population so scant, it was a new and awful sight. From the 18th of June to the 2nd of August, the deaths averaged seven a day, or 321 in all; being one out of every sixteen of our population. Of these one-sixth were Indians, two-thirds half-breeds, and the

THE EPIDEMICS OF 1846 211 remainder whites. On one occasion thirteen burials were proceeding at once. Many houses were closed altogether; not one of the family, old or young, being left in them.34

Governor George Simpson drew a similar comparison in a letter written on August 20, stating that "at Red River the mortality principally among the children, was for about six weeks greater, for the extent of the population, than that occasioned by cholera in any part of Europe or America during the years 1831 and 1832."35 Given the ravages that had accompanied the cholera pandemic in Europe and North America, this was an extraordinary statement.36 It is important that we understand that the vast majority of disease-related mortality in 1846 was due to dysentery, and not measles.37 Once one of the most devastating of the crowd diseases to appear in the Canadian Northwest, measles had been relegated in 1846 to the status of secondary nuisance, as the level of herd immunity rose due to repeated epidemics. Several reliable observers reported few fatalities owing to measles at this time, and most of these could be attributed to inappropriate health care. The record at Partridge Crop, on Lake Manitoba, where measles preceded dysentery, provides an excellent case in point. There, the CMS missionary Abraham Cowley noted the effects of measles, which had come with him from Red River, and then of dysentery. On July 11, he wrote in his journal: My home correspondence will occupy me a long time I fear, as the measles are rapidly spreading among our people and I attend them there being no one here so well acquainted with such diseases as myself. The present appearances are all favourable though some are suffering acutely. I fear lest the Indians who are still here should follow their own conceits rather than my directions and thus unnecessarily expose themselves. Some have left the place lately for I am told the following reason, viz., that their medicines might act the better and that they may be under no restraint in beating the drum &c. nearly all the School children are under it but are doing well.38

On December 17, Cowley followed up with information about the ensuing epidemic of dysentery, which proved far more fatal. He informed the secretaries of the CMS: When I last wrote the Measles were raging amongst us, few, if any who heretofore had not had them escaped.They were followed by the dysentery which also prevailed as an epidemic.This last carried off as far as I am at present informed some of the Indians left here while suffering under it and I do not know if any more have died since we last heard from them

212 CHAPTER NINE since the death of Hewaytinnoos eight Indians of whom three were adults, one a young woman and the other four children.39

As the summer of 1846 passed into fall and winter, similar scenarios of death unfolded across the Canadian Northwest. Dysentery first appeared in early June among the Metis people of the White Horse Plain, also called St. Francois-Xavier, but it soon spread throughout the Red River Settlement. This Roman Catholic parish was located along the shores of the Assiniboine River, about twenty-five kilometres upstream from the Red.40 On July 9 the Anglican missionary at St. Peter's, John Smithurst, received a visit from two Roman Catholic priests, Father Tache and Father Lafleche, who informed him of a large number of deaths at White Horse Plain due to disease, which he correctly deduced were the result of dysentery.41 He noted in his journal: The Priests informed me that the mortality among the Catholic population during the prevalence of measles has been very great. At White Horse Plain out of a population of about 400 there have been about 70 deaths amounting to above 1 /6 of the whole. It appears to me, however, from their description, as if the measles were followed by another disease distinct from it and far more dangerous. It is a sort of dysentery or bloody flux.42

Here was the epidemic at its worst. Those who left for the open plains on the annual summer bison hunt in mid-June paid perhaps the greatest price. The hunt, an integral part of the colony's resource economy, was an ideal mechanism for the spread of both measles and dysentery, and ensured as complete diffusion as possible among many of the mixed blood and Aboriginal inhabitants of Red River. Generally, two distinct groups from the settlement pursued the bison herds during the summer, those of Red River,43 and those of the White Horse Plain, while a third left from Pembina, south of the American border. In 1846, Roman Catholic priest George-Antoine Belcourt accompanied the people ofWhite Horse Plain and Baie St. Paul on the summer hunt.44 Soon after dysentery broke out among the people living along the Assiniboine, the hunters departed for the south with death in their midst. On June 22 Father Belcourt left his station to join them. The priest was almost constantly employed at tending the sick and dying, and very quickly the "good supply of medicine" that he had brought proved insufficient. Often, three or four died in a day; on the worst he buried eight victims. By the 5th of July, when he wrote to his superior Father J.-N. Provencher,

THE EPIDEMICS OF 1846 213 twenty-five people had perished. The ersatz doctor led a delegation of six of the remaining hunters to Fort Berthold, on the upper Missouri, in quest of assistance.There, a M. Bruguier welcomed the men, and provided Father Belcourt with medicine for the sick. On July 29 he left Fort Berthold for the encampment of the bison hunters, and thereafter returned to Red River. By early August he was back, where the epidemic was now on the wane after having spread throughout the Roman Catholic parts of the settlement.45 Much had gone on while Father Belcourt had been absent.The sickness continued to spread, and day after day, the death toll mounted. Governor Simpson learned that there had been eight deaths on July 27, and another five the next day. On the 29th there were eight deaths in the vicinity of Upper Fort Garry alone, six on the 30th, and five more the following day.46 By mid-July, dysentery spread as far north in the Red River Settlement as the "Indian Settlement" at St. Peter's, where it raged until near the end of September. In his annual report for 1845-46, dated August 1, 1846, CMS missionary John Smithurst described the mortality in the Protestant parishes. The number of deaths in the Upper Church [St. John's] and Rapids District [St. Andrew's] have been great beyond whatever before occurred in the same space of time. The deaths in the Rapids district last week amounted to eleven out of a population of about six hundred.The deaths of the Indian Settlement within the last ten days amount to nine out of a population of about five hundred.47

By the end of September, dysentery was on the decline in his parishes and Smithurst could then tally the fatalities, which amounted to a total of thirtythree at St. Peter's alone.48 In the end, the summer of 1846 was, as Alexander Ross suggested, one of sickness and death throughout the Red River Settlement. The daily and weekly death tallies can only say so much, for, as much as anything, it was the terror and the tragedy that set this year apart from all others, for Aboriginal people and White people alike. News of families losing almost all their members, or of bands of Aboriginal people dying en masse, brought fear and anxiety to all.49 Perhaps the best indication of the effect that dysentery had on the minds of all came in July. With the epidemic at its height late in the month, HBC Governor George Simpson made the extraordinary request to Reverend Smithurst "that the prayer appointed by the Church in times of sickness should be read."50 At that point it seemed that only divine intervention could preserve the lives of those who had as yet escaped the disease. Almost as suddenly as they had arrived, though, the two sicknesses subsided. By early August the tide was beginning to turn. According to Adam

214 CHAPTER NINE Thorn at Lower Fort Garry on the 7th, "within these last ten days the dysentery seems to have taken a favorable turn. The new cases are less virulent as well as less numerous; and perhaps there is also something in this, the people have been so thoroughly frightened that they resort to remedies at an earlier stage of the maladie."51 Thorn's conclusion was echoed by several others who saw an end to what had become a summer of misery.52 By then, however, both measles and dysentery had long since been carried from Red River and had begun a long journey of diffusion to the north and the east of Lake Winnipeg. Diffusion to the North As they had so many times before, the HBC transport brigades spread sickness during the summer of 1846. For experienced fur traders this was easy to predict. As early as May 25, Chief Factor Alexander Christie had expressed concern about infection aboard the brigades, not for the safety of those who lay in their path, but for the delays that such sickness would cause the company's summer transport. It was his task to arrange the crews and departures of the brigades from the Red River Settlement, and measles threatened to hinder his plans. He wrote to George Simpson, "I am most apprehensive of the malady breaking out amongst the trip men, thereby retarding the summer transport very materially—because when the men are exposed to wet in the Voyage, the danger will be infinitely greater." By this period the HBC's boat-based transport scheme was so complex and demanded such precision that any long delays would have meant a significant setback, to the point where distant regions such as the Athabasca might not get their supplies during the assigned season, and their furs might sit at the posts for an additional year. This would have tied up the company's profits, which, in turn, would be unacceptable to the stockholders. In 1846 this was aggravated by the need to transport several hundred of the 6th Royal Regiment of Foot from York Factory to the settlement towards the close of the transport season. They had come by ship from Britain and it was impossible for the factory to support such a large number of extra people during the winter. Failure to transport them prior to freeze-up would have had disastrous consequences. Consequently, Christie made the fateful decision to dispatch the first brigades from Lower Fort Garry "without delay."53 The first boats left Red River shortly after Christie wrote this letter, too early for dysentery, which only entered the settlement in June, but still harbouring the measles virus among their crews. On June 1 Reverend

THE EPIDEMICS OF 1846 215 Abraham Cowley met the first brigade on Lake Winnipeg, just to the south of Berens River.54 That day he "passed several boats on their way from Red River to York Factory and learned from them that the Measles were in the Settlement, indeed members of the Crews were suffering from it." By June 7 the boats were at Norway House. That morning, according to the interim manager, Wemyss Simpson, "4 Boats of Mr Mowet's + 4 ofTho8 Sinclairs arrived with cargoes for York Factory + as they had the measles among the crew, I sent them off after taking fresh bills of lading...—Mr Campbell + family were passengers in Sinclairs Boat + remained here."55 After a quarter of a century, measles had returned to Norway House. This was a rare example of the HBC's failing to follow a preventative policy with respect to the health of the Aboriginal people of the Northwest, a policy it had followed at almost every step during the course of its history. This divergence began with Alexander Christie's decision to dispatch the boats from the Red River Settlement without delay. It continued with Wemyss Simpson's decision to pass on the boats at Norway House without taking appropriate precautions. No concern was shown for the possibility of spreading disease among the Aboriginal people. Financial interests took precedence over public health. Instead of being isolated from the local population, or quarantined on their journey to York Factory, precautions similar to those taken by the HBC during earlier epidemics, the diseased boats were simply sent on. In advancing on their journey, these and subsequent brigades spread disease from Norway House to York Factory and west along the Saskatchewan River and beyond, as far as the Athabasca country. These decisions were to have dire consequences for many of the people living to the north, northeast, and west of Lake Winnipeg. As if on schedule, ten days after the first boats from Red River arrived, the first local cases of measles appeared among several of the new men at Norway House. By the 19th there had been at least one death and the disease had become widespread among the post's men. It soon spread to the Aboriginal people, who had not been exposed to the disease in 181920. On June 28 Donald Ross observed that "the native population are with very few exceptions laid prostrate with the measles," and the trader could foresee the disastrous impact the disease would have on the Aboriginal people and on his returns for the year to come.56 With sickness rampant among the local people, he was finding it impossible to find able-bodied men to work on the brigades, a serious blow to the HBC's transport operations. By early July other sicknesses had joined measles at Norway House. On July 9 a beleaguered Ross informed Simpson that:

216 CHAPTER NINE Since then [he had written to Simpson a few days earlier] I am sorry to say the sickness has become even more prevalent than before, Influenza and severe bowel complaints have become universal as well as the measles, and the poor Indians are in a truly pitiable condition—many of the Company's Servants are also quite incapable of doing their duty.—by the last account their evil had not yet extended much to the low country [i.e. towards York Factory], but there is no question that at a later period of the season, they will extend over the whole of the land.57

The presence of dysentery was inevitable. Although the first boats departed Red River too early for this disease, subsequent vessels were dispatched from Lower Fort Garry after this epidemic had broken out. All were directed to Norway House. The presence of influenza, however, is unexpected, since it had died out in Red River long before the brigades began to depart for Norway House. Most likely the boats had brought it from the Boundary Waters. Described on July 3 as a very bad cold, the disease was thereafter identified as influenza, and Ross himself fell ill later in the month. By July 16 there were "8 men laid up with the Influenza."That same day the Athabasca brigades departed for home, carrying both influenza and measles to He a la Crosse in the English River department. By the fall, it was at forts Chipewyan and Resolution, again almost certainly carried by the brigades.58 Things quickly worsened for the people around Norway House. Reports began to reach Ross of mounting casualties. On July 20 he heard of several deaths at nearby Rossville, an agricultural village of between 300 and 400 people that was run by Methodist missionaries. Early in August other reports started to arrive of deaths among the Nelson River Cree, who were generally ill by this time. There the sickness would become "rather severe" before it ended. Towards the end of August, the "Wood Indians," Ross's term for those who did not live in the Rossville settlement, began to arrive for debt, exposing themselves to disease.59 If that was not enough, a fourth disease struck the Norway House region after the others had run their course. On December 27 Ross wrote to Simpson that: The Measles and Dysentery seem to have passed away, but I am grieved to say a new pestilence has lately appeared in this quarter apparently of a still more deadly nature. I cannot say what the disease really is, but it seems to possess the chief characteristics of a malignant putrid fever very infectious, and with this melancholy particularity, that no one has yet recovered from its attacks, all those who have caught the disease have either died or are still hopelessly lingering under it.60

THE EPIDEMICS OF 1846 217 While we cannot identify this sickness, it seems likely it was the same as the "troublesome fever" that was then inflicting casualties in the Red River Settlement. It may also have been active in the vicinity of Moose Lake, to the west of Lake Winnipeg, for late in January word arrived at Norway House of continued mortality among the Aboriginal people there.61 No estimates are available of the number of casualties among the Norway House people, but they must have been numerous. According to Chief Factor W McTavish, deaths were "very great" as of December of 1846, and Donald Ross believed the sicknesses equally mortal around his Norway House post as they were at Red River. This was unavoidable, not only because of the virulence of the diseases, but also because they struck in quick succession, at a critical time of year when the Aboriginal people needed to prepare for the winter. Because of this, a feeling of despair prevailed among those who traded at Norway House, despair that was, no doubt, common throughout the Northwest that year. Helpless to prevent the ravages of these diseases, in July Ross ordered the distribution of alcohol to improve the outlook of the Aboriginal people and to treat their diseases.62 In an era when the company was trying to curb the trade of liquor, this was a very unusual command, indeed. Perhaps the hardest hit in 1846 were those who worked on the brigades. Just as Alexander Christie had predicted in May, the rigours of travel combined with the crew's sickness usually proved too much.There are frequent references in the HBC records to sickness and death on the brigades between Norway House andYork Factory for the period between the passing of the first infected boats and the last boats of the season, which left Norway House on October 3. The fate of the Oxford House freight boats was by no means unusual. On July 14, Laurence Robertson recorded in the Oxford journal that "the 4 Fret [freight] Boats of this place arrived from YF. On the voyage the [they] got Sick with the Measles and has brought up the Boats with only 3 of the men able to work.—and at present almost all the crew is sick. The Guide is at the point of Death."63 The men of the Norway House freight brigade fared worse still. On the 25th of July, Robertson observed, "The 4 boats from Norway House in charge of wm Ballantyne Guide arrived froniYF after a trip of great suffering from the Sickness of the Crews.—one Indian from Berens River and 2 Indians from this place has died on the passage." Another brigade that arrived at Norway House on August 4 lost five crew members to measles and dysentery.64 For the company, these sicknesses among the brigades during the summer of 1846 "materially deranged" the summer transport, and left cargo for

218 CHAPTER NINE the following outfit in a state of disarray. In most cases the crews generally had to cease travel and attempt to weather the sickness where the men fell ill or, in many cases, died. As the brigades were forced to delay or cut short their journeys, the HBC was unable to fulfil its transportation needs. The result was chaos, as Chief Factor Hargrave said in a letter from York Factory: It is with deep pain I have to report that the sickness which I then [his previous letter of July 12] noticed as prevailing here among our indian Freight Brigades, has proved more fatal to the poor natives than our worst apprehensions had then anticipated. The Norway House, Oxford House and York Brigades, have been swept by it for the season, almost aU the Outfits for the Northern Districts next year (which are absolutely required to be rendered at Norway House this Autumn) are still in our stores; likewise the whole of the Oxford House and part of the Norway House Outfits for the current season. Four of these Boats, (the last of them from the Interior) reached us on the 6th Ultim0, the crews of which were generally affected with Measles, which malady, in a few days, was communicated both to the Indians around us and to the many of our native servants in the Factory.The latter have now nearly recovered without loss of life, but these boats are still on the beach, many of the crews are dead, and such as remain are either in the last stages of disease or are so enfeebled as to be totally incapable of even the slightest labour this season.65

These losses hindered the transport the following year as well, as the labour force had been depleted and there was a much smaller population of able-bodied boatmen. Even among the survivors, employment on the brigades had come to be associated, by the Aboriginal people, with suffering, which made it difficult for some posts to hire men.66 With so many infected brigades travelling down the Hayes River route to York Factory, it was not long before the sickness arrived at Oxford House, although here diffusion unfolded more slowly. The first diseased brigades passed on June 21, and by the 7th ofjuly the Cree of this area were infected with measles through contact with the voyagers. On that date, post master Laurence Robertson noted in the journal, "The Indian Peter was brought here from the Island Dead with the Measles, owing to the Indians being constant with the Brigades in their way as they pass." By July 16 Robertson could not find a healthy Aboriginal person to send to Norway House with a message, and on July 21 he lamented that "this sickness is prevalent all around the Fort, Consequently a great demand for Store Provisions ."Two days later it was apparent that all the Cree residing near Oxford House

THE EPIDEMICS OF 1846 219 were in a bad way with the measles.67 At this point the nature of the sickness in and around this post seems to have changed. Prior to the fourth week in July, the HBC men appear to have escaped infection, with the exception of those employed on the brigades. Moreover, although it was debilitating for the local people, measles does not seem to have led to much loss of life. By the 20th, this began to change. On July 22, Robertson himself fell ill and was confined to bed for several days, while at the same time the men were "very low with this Sickness." By that time, dysentery had reached Norway House and was now at Oxford House. Its stay was prolonged, and even as late as mid-October, it was still common among the people there. The Reverend Robert James passed through in late September of 1846 and observed the disease among the Cree at nearby Knee Lake. The few survivors were in a miserable condition, all of them belonging to Oxford house. He noted that "a fatal dysentery had left but fraction of their number alive." The missionary also commented on the fatalistic reaction of the local people to sickness: "If they have the least ailment they lie down, regardless of all efforts for recovery, and sorrowfully await their death believing that they are so fated."68 No doubt the continued, and indeed increasingly destructive, sickness was taking its psychological toll, not unlike at Norway House, particularly with so many years of epidemics preceding 1846.The loss of hope would have contributed greatly to the suffering experienced by these people. The same boats that brought measles and dysentery to Norway and Oxford houses carried these diseases to York Factory, infecting both the Lowland Cree and the HBC men early in July. By July 12, according to James Hargrave, sickness was "almost universal among our Indians both around this place and in the Brigades."69 In a letter to George Simpson, he painted a telling picture of an epidemic well advanced among the Cree of the York area: The routine here moves slowly . . . but more from the despondency and fear that have crept into the minds of both men and indians.—The House and the Factory and the indian tents -are rilled with the sick,—two natives were buried at the old Factory yesterday and the previous day— more of them are not expected to live,—and the disease is found to be far more lingering and fatal than at first it was expected to be.—The Whites are not [illegible] affected @ yet but both the indians and half caste [word?] are at this time widely under its influence—(more than half of them being presently more or less indisposed) and I fear that scarcely any of them will ultimately escape being attacked.70

220 CHAPTER NINE Little had improved by August 5, as the trader wrote: "The greatest distress and suffering presently prevail among the natives from measles and other diseases. The loss of life has been considerable and the survivors are greatly reduced in strength and energy." Hudson's Bay employee Francis Ermatinger wrote his brother Edward from York Factory on the 8th that "the poor natives around us have been dying by wholesale."71 Two days later, Hargrave noted that the mortality during the previous month had been severe: The distress and mortality among the natives throughout the past month have been very heavy. The number of deaths around this Factory, up to this date, reaches 31; but this applies only to those in our immediate vicinity and buried by the Company Servants: many no doubt have sunk elsewhere who were beyond reach of our assistance; while, as I have said, many more of our most valuable Indians are in so low a state that their lives are also despaired of.72

As many as six had died in a single day at the fort, and, as Hargrave noted, many more had succumbed away from the fort. Overall, the Lowland Cree of the York Factory region suffered greatly during this epidemic, although we do not know how many died.73 A letter penned by Letitia Hargrave, wife of Chief Factor Hargrave, offers an important insight into the recent history of the local Cree with measles, however, and thus into that disease's role in the mortality. She noted that measles had "raged all over the country, & been fatal among the Indians, old, young & middle aged."74 There was, then, no age selectivity. This would confirm that the Cree ofYork Factory had escaped the 1819-20 epidemic and so their experience with the disease in 1846 was as a virgin soil population. Consequently, mortalities were liable to be higher, even without the concurrent appearance of dysentery or influenza. Still other HBC boats carried measles eastward from York Factory into the Hudson Bay lowlands, to the Severn River region.The diffusion process began on June 19 when Severn trader John Cromartie departed the post forYork with Cree men in a canoe. Initially, the men travelled towards the interior, and away from Hudson Bay, employing the BeaverdamShamattawa River route to the Hayes, which they paddled down to the coast.75 En route they met up with William McKay and his men from the Trout Lake outpost and proceeded as a group. On June 29, on the Steel River part of the Hayes River route, they observed other boats bound for York "with most of their Crews all sick."The brigade arrived at York Factory in good health, but then, according to James Hargrave, "in the course

THE EPIDEMICS OF 1846 221 of a few days .. . they were also added to the sum of invalids at this place. Two of their best hands sank under disease [i.e. died] and it was not until the 31st Ult° [July] that I was enabled to get them off again, many of the crew being still in a weak and sickly condition."76 Once again, the decision to dispatch an infected brigade was to have dire consequences for the Aboriginal people. Although the crews harboured dysentery and measles and some of the men had already died, the Severn and Trout men departed for their posts together, their return journey being along the coast to Severn and from thence inland to Trout Lake.There was, it would seem, no time for further delay. This was a voyage as ill-starred as any other in the Northwest. According to Cromartie, they left York Factory with only two able hands in each boat, and along the way, four men died. Others had to be left with relatives along the Hudson Bay coast, in turn infecting them.77 McKay's account of the journey corresponds to Cromartie's and provides greater detail in the rough English of a working fur trader. This morrining [September 19] I arrived with the Boat + outfit of this plase [Trout Lake] after a long and harresting voyage, from york factory to this. I left the above place upon the 1st Augf and ever since being on the voyage—I left york with three boats, two for Severin, one for this, when we started all the Crews were all sick the Company's Servants excepted, all the others bein hired Indians for the voyage, not one of the latter that was not sick when we started the Boats were obliged to be loded by the people of the Factory and we started off with only two in each Boat that could work. Having bad weather along the Cost [coast] we were 19 days along the cost, in that time 4 of the Indians died, and we were obliged to leave the most of them with their friends at Goose River in passing. The cargo of the three Boats were all weate, and would not effect it to be othere ways, with such weather we had, and all along the Cost only two to three all the way in each Boat to work them.78

The men were still sick when they reached Severn on August 19 and so brought sickness among the people of this area. As the boats arrived, they were greeted by people who were anxious to trade before they left for their wintering grounds.79 By August 28 two Aboriginal people were ill at Severn House. Within a few days the sickness was far more widespread. On the 2nd of September, Cromartie noted,"! am afraid that the Indians will not be able to hunt as most of them is sick and no appearance of them getting getting [sic] better as yet." A day later, he received word of the death of the eighth hunter

222 CHAPTER NINE belonging to the post. The timing could hardly have been worse, as the sickness disrupted the important fall goose hunt, ironically during a year when there were plenty to be had. Reports of starvation were received throughout the fall and winter. Part of the problem was that when poor health prevented the hunters from walking, they could not circulate through their resource areas, which limited their opportunities to obtain sustenance. Normally, they would have moved often during the winter in search of food. This could be a huge problem for most big-game hunters in the subarctic who contracted debilitating disease. Although neither mortality figures nor the extent of the sickness in the Severn House area can be pinned down, it is evident that this epidemic spread east of the Severn River, although probably not as far as the Winisk, and that there were considerable casualties among the Cree of this region. Indicative of the degree of disruption and mortality seen during this epidemic, Cromartie wrote on March 28, "Serene + mild for this time of the year but no Indians being sumething very Strange this season above all others they Cannot be all Dead sume of them must be in the land of the living yet."80 William McKay's men continued ill after they departed Severn for Trout Lake, but did not bring their sickness to the post. After a journey of about forty-nine days, they probably would not have harboured active cases of either measles or dysentery. Instead, measles alone appeared, brought back from Oxford House during the summer by some of the Trout Lake Cree who had gone to visit their friends.Very little is known about the epidemic's extent in this part of the country. McKay learned that those people hunting towards Severn Lake, to the west, had contracted measles during the fall and by early winter were doing poorly. Other reports indicated that some of the people wintering at Island Lake, between Oxford House and Sandy Lake, had been confined with sickness for most of the winter. And yet, not all the people in this area were exposed to one of the epidemic diseases circulating in 1846, for a large party of Sandy Lake people arrived the following June 19 and made no mention of disease. If indeed they had escaped sickness during this year, while those around them suffered, it was undoubtedly a stroke of great luck.81 Overall, the mortality at Trout Lake was significant, although perhaps not exceptionally so when compared to other parts of the Northwest. Certainly, it would have been far worse had dysentery accompanied measles. In summing up the outfit year on May 31,1847, McKay wrote, "The returns would have been better had the Indians been all in good health.— But a great number of them were under the measels the first part of the winter. 14 Deaths of men, women + children ammong the whole of the

THE EPIDEMICS OF 1846 223 natives belonging to this post, which has been greatly against the returns."82 This was a devastating loss in what was undoubtedly a small population. Equally important, in a period when epidemics were occurring at relatively frequent intervals, even small losses could accumulate and play a significant role in shaping the lives of Aboriginal people. Diffusion to the East At some point, probably early in the summer of 1846, measles and dysentery followed influenza from the Red River Settlement into the Boundary Waters area.83 Charles McKenzie at Lac Seul noted in his journal that "many deaths occurred among our Indians who pass the Summer on the River Winipic where the Measles was raging since last spring accompanied by a Bloody Flux and Billious Complaints which made a havoc among the Natives."84 Here, it was not the HBC boats that transported these diseases, for the Lac la Pluie brigades did not return until after they had broken out, nor was a brigade from Red River dispatched until late July. Instead, a likely source was the party of the Roman Catholic missionary, Pierre Aubert, who left Red River for Wabassimong on June 20, just as the epidemics were hitting their stride.85 There is some evidence that the people of the Winnipeg River placed the blame for the epidemic on the Roman Catholic mission, which had to be abandoned the following year because of threats to its personnel. Conversely, the Methodist mission at Lac la Pluie was not similarly threatened.86 The twin scourges quickly spread among the Aboriginal people who spent their summers on the Winnipeg River. On August 3 Chief Factor Nicol Finlayson, who was on his downward journey from York Factory to Rainy Lake, wrote to Governor Simpson from Fort Alexander, stating "sickness has made such a ravage among the natives this summer, and the last which has broken out in Red River and the vicinity, which has more the appearance of a pestilence than an epidemic."87 On August 27, an Ojibway man, Quisance's third son, brought news to Charles McKenzie at Lac Seul from Father Aubert's mission on the Winnipeg River. "Our Indians in that quarter," Mackenzie recorded in his journal, "are sick and dying and cannot make Rice altho' Rice is plenty on that River—The accounts these bring us of the Starve of the Measles + Dysentery are dreadful."88 The inability to obtain provisions and the resultant starvation in the face of widespread and severe illness were common complaints whenever Aboriginal populations were exposed to acute infectious diseases with which

224 CHAPTER NINE they had little or no experience. As it often did during virgin soil epidemics, starvation played a major role in the death of these people. Very soon, the same was to happen among the people who traded at Mackenzie's Lac Seul post. Both diseases spread eastward to Rainy Lake, the exact timing unknown. There is some evidence in a letter from the Methodist missionary, Peter Jacobs. Jacobs, who was stationed at Fort Frances, had been at Red River earlier in the year and had left the settlement with measles in full force. Indeed, he had feared that his men would contract the disease. Back at Fort Frances on July 7, he wrote a letter to George Simpson. Evidently, the Ojibway of the area had yet to contract either measles or dysentery, as Jacob's only comment was that "this present year is going to be a great year for wild rice at this place, and that the Indians of this District are preparing for a great rice harvest."89 However, early in the fall, Nicol Finlayson, by now also at Fort Frances, wrote that "rice had been most abundant every where upon this quarter, but unfortunately, measles and other epidemics laid up the natives at the time of the harvest.. .."90 Between Jacob's prediction and the harvest, the diseases had spread to, and disabled, the Ojibway of Rainy Lake. In fact, the harvest itself may have helped to introduce the afflictions. In most years wild rice was collected in late August or early September. Generally, the people began to gather together then in larger numbers, in preparation for the harvest, after having been dispersed through the summer, conditions that were conducive to widespread diffusion. Perhaps, then, the rice harvest had attracted some who were infected, and from whom the diseases passed to all the people of Rainy Lake.91 Here, as elsewhere, the suffering among the Aboriginal people was considerable, the deaths many. As Nicol Finlayson explained to Simpson on January 26, 1847, "My prospects of trade are not flattering; many of my hunters are gone to follow the chase with their Fathers, and all the survivors have lost so many of their children and relations, that but little can be expected from them this season."The returns for the 1846-47 outfit showed the Lac la Pluie district had experienced a reduction of about ^300 over the previous year.92 The story was similar to the north, as both measles and dysentery diffused into the interior of the Petit Nord, to Lac Seul and beyond. Once again it is the hapless Charles Mackenzie who provides us with the most complete version of events. Upon his return to "Bonny Point" on August 13, he was welcomed by first measles and then dysentery. When the boats were landed the men found measles already rampant, as most of the Lac Seul Indians are here on this point waiting the arrival of

THE EPIDEMICS OF 1846 225 the craft [i.e. the Lac Seul boat from Albany] and labouring under the Measles which was brought here from Red River early in July by the men's wives who went there to see their friends in May last.93 Every soul within this fort has had the disease but they are all now convalescence of a death appearance, but no deaths took place so far on the point, except one young woman a few days ago.94

At least influenza had disappeared. The relatively mild nature of the sickness at this time was in direct contrast to the situation on the Winnipeg River, as dysentery had yet to reach Lac Seul. Indeed, with measles having passed through in 1819, there were bound to have been a few survivors. However, throughout the remainder of August, reports came in of death and sickness due to dysentery in the Lac Seul region. By the end of the month, it had reached the post, having broken out among the HBC men and their families. As the Aboriginal people arrived at the post for medical assistance, Mackenzie and his men proved of little help, for by this time they were dealing with their own serious health problems.95 No entries appear in the Lac Seul journal between the 15th and the 24th of September, when McKenzie fell victim to dysentery and was incapacitated. His melancholy description is testament to the total breakdown of conditions at Lac Seul: I have been attacked by the most violent Flux, or Dysentery, that ever attacked man (short of destroying life) on the 15th Instant, and this is the first time I was able to take the pen—what I suffered, and still suffer, I will not attempt to describe—my case was light to that of those who died and are dying about me—no less than 5 died on this point during my sickness Bloody Flux and Bilious Complaint. Robert Gill is laid up with Measles of a very oppressive nature accompanied with a violent cough and sore throat—George Moor and his large family are lying side by side—without a single exception—or one able to assist the other to a drink of water. There cannot be less than from 70 to 80 Souls on this point and not 20 of these are able to go about to get a fish or a Rabbit for the sick—how they exist I cannot say.96

McKenzie was confined to the house for a total of twelve days, during which, he later noted, there were seven fatalities among the Ojibway at the post. Of the HBC people and their families, only McKenzie's wife and Patrick Adhemar escaped dysentery during this epidemic.William Sabiston and Robert Gill died, the latter succumbing to "Measles, and an accumulation disorders—Bloody Flux—Billious, Cough, and Sore Throat." As of

226 CHAPTER NINE September 29, McKenzie had only three men capable of leaving their beds. The effects of so many ill with dysentery at the post were revolting, and were certainly conducive to all manner of disease transmission. Early in October McKenzie commented that "there has been a pestilential infection on this point from first to last and now—no one can out about the place without his stomach being turned and his foot being sunk in human excrement—! "97 Although traditionally the HBC post had served as hospital and commissary during many earlier epidemics, in 1846 neither McKenzie nor his men could offer assistance to anyone, due to their own sickness.The Aboriginal people were almost completely unable to provide for themselves. Like the people ofTrout Lake, who could only watch as the plentiful geese flew on, and those of Rainy Lake, who had not even the meagre strength necessary to harvest a bumper crop of wild rice, the people of Lac Seul were unable even to bring in the rice, to fish, or to trap rabbits. Mass starvation seemed only a matter of time unless a miracle occurred. Then, on September 27, a food source finally appeared that was within their minimal abilities to exploit. On that day, the trader sent three people to the post's garden to dig potatoes. Soon, these few were followed by most of the sick Aboriginal people, who formed a ghastly procession. Unable to walk, the ill were forced to crawl up the hill to the field. Still, they finally had the food they needed to weather their sickness. No doubt, many lives were spared at Lac Seul by this humble crop.98 Having finally gained access to a supply of food, for those at the HBC post, at least, the slow process of recovery began. Given the tremendous increase in the frequency of epidemic disease among the people at Lac Seul over the 1820s, 1830s, and 1840s, the odds of surviving to old age had probably declined precipitously in the nearly fifty years since the start of the century, along with the Aboriginal peoples' general state of health. Immunity to one disease meant very little when several others appeared the following year. The fate of Nigonice, who died in 1846, may not have been that uncommon among the Lac Seul Ojibway for this era. Nigonice was one of the few survivors of the 1819-20 measles epidemic in the region. On September 23,1822, Charles McKenzie wrote that "Neconise took Debts with a good deal of reluctance, he having contracted a large one the year that dreadful disease past in this quarter which almost carried him to his grave." In 1846 he was, of course, immune to measles, but he nevertheless succumbed to dysentery. On October 15 he had helped wash Robert Gill's body in preparation for interment. By the 3rd of November he was dead.99 No doubt, a similar

THE EPIDEMICS OF 1846 227 fate was shared by many others who were granted only a temporary stay of execution during one of the many epidemics in the southern part of the Petit Nord. Although they might survive one epidemic, others were sure to follow. Measles and dysentery spread widely in the country surrounding Lac Seul, even into the more remote areas, as isolation proved no safeguard from sickness. According to McKenzie, the diseases spread throughout,"scattered as the Indians were over the country, the Measles found them out the deep forest was no safety." Often the reason for this was all too familiar. Upon hearing of the ravages of the diseases, or seeing its effects, they fled in panic, hoping to remove themselves from the chance of infection. In many cases it was too late, and they had already been infected. On August 17, it was reported that the people of Eagle Lake, on the Wabigoon River system to the southwest of Lac Seul, were "in the heat of the Measles," which they had brought from Lac la Pluie. Five days later, McKenzie learned that the people to the west of his post were suffering from both measles and dysentery. By that time two hunters had died, as well as an old woman and "many children."Their sickness had yet to peak, however, and McKenzie pessimistically predicted that "more will die of the Bloody Flux than of Measles." On August 31 the old trader was visited by John Moose and his family, returning from nearby Rice Lake,100 and was told that "the Measles and Dysentery reign there as well as here. John reports several deaths to the southward—chiefly that of children." Moose, an Osnaburgh man, died on the afternoon of September 26. Rice Lake was a major ricing area, attracting people from Lac Seul, Osnaburgh, and elsewhere, and thus it became a local centre for the dissemination of disease. By mid-September measles had broken out at Sturgeon Lake, to the southeast of Lac Seul, accounting for many deaths by mid-November.101 Throughout the fall and early winter, reports of sickness and mortality continued to arrive at the Lac Seul post. On November 15 McKenzie, inundated with bad news, wrote,"From whatever quarter we hear, we are sure of fresh reports of deaths!" Indeed, by December his information suggested to him that sickness reigned not only at Lac Seul, "but over all the country on this side Lake Winnipeg."102 Both diseases were somewhat slow to arrive at Osnaburgh. By September 26, however, measles had become so widespread there that post master George McPherson could count only two men still healthy. A week later the men remained ill with measles, and dysentery had appeared. These sicknesses seem to have been introduced from Rice Lake, where many of the Osnaburgh Ojibway had been in search of rice earlier in August. Indeed, towards the end of the month, some had appeared at Lac Seul while

228 CHAPTER NINE suffering from measles, while others never made it back to their lands. Charles McKenzie learned on November 14 of the death of many of the Osnaburgh people. McPherson, however, remained unaware of the extent of the destruction among the Aboriginal people at Osnaburgh House. As late as January 2, he informed his superior, Thomas Corcoran at Albany, that "the returns of present outfit has a poor appearance at present, the Measles + Bloody Flux that came among the Indians in the Fall of the year did a great deal of injury.... I have seen only two Indians since the Winter set in, as far as the rest of them, I do not know whether they are alive or not."103 As the month progressed, however, he began to grasp the extent of the devastation. More than just a few had died. The full scope of the impact of the epidemics of 1846 among the Ojibway in the Lac Seul-Osnaburgh area is unknown, but it must have caused considerable losses. Charles Bishop estimated that the number of fatalities was perhaps forty, and suggested that the epidemics of this era were simply a "levelling factor," by which populations were kept stable in a period of otherwise continuous growth. In fact, the number of deaths was much greater. In December of 1846, for instance, McKenzie stated that he knew of at least thirty-six fatalities among the Lac Seul people alone. He wrote, "I cannot say how many deaths among the natives at this date. I knew of 6 men but of women and children the number cannot be short of 30 souls, in short I scarcely know a family who has not lost a member, some from two to three and this Fort is now surrounded with Widows and orphans."104 Indeed, he would not know the full extent of the mortality until spring, if then. At Osnaburgh, McPherson noted the death of eighteen Aboriginal people in just two families in January, as well as several others.105 Here again, it was some time before he would know the exact toll taken by the epidemics. According to these two partial estimates, then, at the very least, fifty-four people had died at these two posts, and in all probability there were many more. Estimates of the populations of Lac Seul and Osnaburgh House as of the 1830s were, respectively, 319 (in 1838) and 279 (in 1830). At a minimum, almost nine percent of the people had died in this one year alone.106 This was a tremendous loss. It is impossible to verify Charles McKenzie's suggestion that epidemic disease spread throughout the country east of Lake Winnipeg, particularly that part north and west of Lac Seul and Osnaburgh, and to the south of Trout Lake. It is not known, for instance, if either measles or dysentery diffused into the East Winnipeg Country, although it seems likely. Certainly, there was considerable opportunity for diffusion to the eastern side of Lake Winnipeg. At least one Berens River Ojibway man succumbed

THE EPIDEMICS OF 1846 229 while employed on the brigades, and boats from the Berens River outpost arrived at Norway House during the epidemic period on two occasions, June 13 and August 7. Moreover, free traders from the Red River Settlement traded among these people during the winter of 1845-46, a pattern probably repeated the following year. Likewise, Aboriginal people from both the Red Lake (Ontario) and Osnaburgh areas had been known to spend time on that river.107 Connections among the Aboriginal people living elsewhere in the interior of the Petit Nord also favoured the spread of epidemic disease. According to Charles McKenzie, at least seven of the people from Rat Portage on Lake of the Woods wintered with the Cat and Crow's Nest Lake bands north of Lac Seul. Farther north, the Aboriginal people did indeed contract a fatal disease. One group, the Cranes, experienced sickness and several deaths during the winter of 1846-47.The Cranes, who wintered to the north, at Round Lake, traded at Trout Lake in October and at Osnaburgh in January and June of 1847. Such movements exposed them to measles and dysentery, both from the north and the south.108 Whatever the fate of the people of the deepest interior of the Petit Nord, it is clear that neither disease was able to make much progress down the Albany River from Osnaburgh House. Here they remained free of all epidemic disease in 1846. In January of 1847, Thomas Corcoran, Chief Factor at Albany, received news of the devastation at Lac Seul and Osnaburgh, as well as of affairs at Martin's Falls, via the winter mail packet. In his journal entry for January 28, he wrote: At Lac Seul + Osnaburgh they have been severely scourged during the last summer + autumn with measles, dysentery + bilious fever, which proved fatal to many of the Indians of both places + to two of our most youthful + active servants—Robert Gill + Wm Sabiston at Lac Seul.The evils that proved so disastrous at the above two posts have not reached Martins Falls where everything goes on as favourably as could be expected.109

Even as late as this, there was not a hint of any of these diseases as far down the Albany as Martin's Falls, nor would they ever reach this post. In fact, the Martin's Falls journals for the period from 1846 to 1849 reflect what can only be described as a remarkably healthy period, and at Albany, Corcoran could only comment on the sickness from a distance. Even at Moose the people were free from any significant infectious disease at this time. Although the traders at Martin's Falls and Albany might sympathize

230 CHAPTER NINE with Charles Mackenzie and George McPherson, sickness and death on the scale occurring among the Lac Seul and Osnaburgh House people were almost certainly beyond their experience.110 To a certain extent, the same was true of the country north of Lake Superior. With the possible exception of influenza, none of the major epidemic diseases appeared in 1846.111 There was a good reason why the people of this area were spared these diseases. By the mid-1840s, the Aboriginal people of Lake Superior had, for the most part, settled into a pattern of movement that revolved around the shore of Lake Superior and journeys only a short distance into the interior.Trips to Manitoulin Island and Sault Ste. Marie combined with lake fishing, as well as visits to American settlements and HBC posts, all kept the people around the lake during the critical summer of 1846. That fall, they dispersed into smaller, more isolated, winter hunting parties with even less contact. The decline of fur-bearers and game animals in the Lake Superior region also tended to keep the Ojibway near the lake. Long before 1846, beaver and other big game had begun to disappear from the region to the north of Lake Superior. As a result, some of the people started to remain for extended periods of time along its shores, where fish could be readily found at certain seasons. Many now spent a longer part of the year along the shore, rather than trapping in the interior, where subsistence might be far more precarious. In 1846 this general pattern of movement was reinforced by the arrival of mining companies who were surveying promising locations along the north shore. During the early to mid-1840s, there had been a substantial rise in the number of non-Aboriginal people travelling to Lake Superior, fuelled first by commercial fishing and later eclipsed by the growing interest in its mineral wealth. After a treaty in 1842 opened up the south shore of the lake, hundreds of American miners entered the region. By 1846, twenty-four companies employed 500 men along the US shore, and the Americans had at least five schooners and a steamboat in operation on Lake Superior to transport men as far as the mines at La Pointe.That same year, miners began to appear on the Canadian side in substantial numbers. These mining companies employed many of the Ojibway of the area as guides and canoemen. Having little communication with the Aboriginal people to the west and northwest of Lake Superior, where the sicknesses reigned during the summer and winter, there was almost no chance of these Ojibway contracting these deadly diseases.112 Unlike those living along the lower reaches of the Albany River, however, the Lake Superior people were by no means free of epidemic disease in 1846. They were exposed to several other afflictions that were

THE EPIDEMICS OF 1846 231 comparatively localized and, with one exception, were of limited severity. As we have seen, mumps spread from Grand Portage to the Fort William area and on to Lake Nipigon, where it was joined by a severe but unidentified affliction characterized by delirium and vomiting of blood. Nevertheless, no deaths occurred at either post. Later, in the fall of 1846, a considerable number of the Lake Nipigon people became seriously ill while visiting the miners of the Montreal Mining Company at Point Gourgon on Lake Superior, and had to be attended by the company's representative. Again, there is no indication that anyone perished.113 Farther east, at Long Lake, there was a far more destructive sickness during the summer and ensuing autumn of 1846.John Swanston explained in February of 1847 that "sickness was very prevalent at Long Lake last Autumn amongst the Indians, and proved fatal to 17 individuals, man woman and children shortly after having received their supplies for the winter, and Mr Laronde was apprehensive that he would hear of some other deaths, as there were some others very low late in the autumn."114 Three more casualties were reported at the Pic post. At Michipicoten, Swanston and his men suffered from a very severe respiratory disease, accompanied by a cough, early in the summer of 1846, and during the fall they "suffered somewhat" with dysentery. The first disease was likely influenza,115 but it is not clear if it was connected to the epidemic that was then racing through the country north and west of Lake Winnipeg. Certainly, this was not the same devastating dysentery that had killed so many people beginning in June of 1846, as it lacked both the severity and explosive diffusion characteristic of shigellosis. Thus, in 1846, the people living along the northern coast of Lake Superior suffered from infectious disease, in some cases fatally, but they appear to have escaped the worst of what was extant at the time. Although the mining companies on Lake Superior played a role in preventing the spread of the diseases from the west in 1846, in the long run their presence threatened to make such diffusion possible. The miners represented a disruptive force to the fur trade, and a threat to the influence over the Aboriginal people that the company had cultivated since the merger of 1821. More specifically, they offered employment opportunities, which in turn encouraged the trappers to abandon the fur-trading lands in favour of Lake Superior. People from as far away as Lac Seul might be inclined to travel eastward to hire on with the miners during the summer, providing epidemic disease with a chance to spread in both directions.With little real coercive power, Governor Simpson recommended fighting back through the power of persuasion. He counselled Thomas Corcoran of Albany that:

232 CHAPTER NINE Should these reports have reached the Indians of the upper parts of the [Albany] River it would be proper to let them know that such demand for labor was merely temporary while the operations were going forward, but now that the shores of the lake are thoroughly examined in reference to mining purposes it is not possible that the Indians will be furthered employed in that way, and instead of benefiting by a visit to Lake Superior, they are more likely to injure themselves and their families by harsh treatment on the part of the miners who feel no interest in their welfare, while the whole race would in due time be destroyed by the diseases contracted in their intercourse with strangers.116

Given the HBC's role in spreading epidemic disease, in 1846 and in the past, this was ironic advice indeed!

The epidemics that spread through the Petit Nord with great frequency during this era likely affected the relationship between the Aboriginal people and the HBC. Certainly, they may have turned a few people away from the fur trade because of the traders' role in spreading disease. For others, however, the epidemics may have increased their dependency on the company. Those who had closer ties to the traders often had a better chance of survival than those who chose to follow a more independent lifestyle. Some of the factors that led to this differential in mortality were identified during this epidemic by Laurence Robertson, the manager at Oxford House, and are worth examining in some detail, for the light they shed on the impact of this new era of disease. On July 29 Robertson learned that a band of Cree people encamped at nearby Trout Fall were refusing his aid and advice, despite their great suffering. Over the course of the next month, he commented frequently in the journal regarding the fate of these people, particularly in contrast to the fate of those who camped near the fort, and who readily accepted both relief and advice. On August 25 he wrote: The sickness amaung the natives of this place has been and is very heavy, but those in the neighbourhood of the Fort, being well cloathed and having tents, they have recovered, very few Deaths occurring:—But those from the Out Post who camps at the Trout Falls, being almost destitute of cloathing + tents - and Sticks close by their own ways of "Conjuring" has and is suffering and many dying. Every possible help has been and is offerded them, but advice or medicine except their own they refuse. I

THE EPIDEMICS OF 1846 233 again visited them to day + find a great many very lo,- and 5 men 7 wives & 5 + children has Died.117

The trader identified two key factors that exacerbated the health problems of the people at Trout Fall. The first was the lack of clothing and shelter available to these people, and the shortfall of these necessaries would have complicated the course of their sickness by exposing the victims to the elements. In fact, given the increasing scarcity of animals that could supply fur and leather at this time throughout much of the Northwest, these effects were most likely widespread. Related to this was the need for traders to provide food to the ill, for, as Robertson later observed, the epidemics had had a deleterious effect on the Aboriginal people's quest for provisions, even after the sickness had passed, since it had disrupted their normal seasonal pattern of activity. Thus, he wrote, the people were "suffering for a want of food, being kept from their usual fishing + hunting lands owing to the lateness of their getting winter supplies, last autumn and the effects of the past Summer Sickness is greatly felt by the Indians all over."118 This was not merely unfounded speculation on Robertson's part.The failure to supply simple medical assistance, even as basic as providing the victim with warmth and water, has been identified by epidemiologists as a contributing factor in the excess mortality observed during measles epidemics among isolated societies.119 The second factor, and one that has long been implicated in the massive mortality of Aboriginal people during post-contact epidemics, was the use of certain traditional treatments. Long before the arrival of the Europeans, the people of the Americas had developed indigenous methods of medical treatment that, though varying by culture, environment, and the local health concerns, would have been admirably effective within the context of their pre-contact disease load. Indeed, their knowledge of medicinal plants and surgical practices would have compared favourably to that of the Europeans, who, from the beginning, sought out the medicines and advice of the Aboriginal healers.120 With the introduction of the novel diseases from the Old World, however, some of these cures proved ineffective and, no doubt, even contributed to the excessive death rates seen during epidemics.121 When Robertson suggested that the Trout Fall people were dying in part due to reliance on "their own ways of'Conjuring,'" he was observing the same deadly relationship that many others had witnessed before him. Two of the most widespread treatments among the Aboriginal people of the Americas were the sweat lodge and exposure to cold water, or some variation, and both could be fatal under these conditions.122 For those at Trout

234 CHAPTER NINE Fall in 1846, treatment revolved around attempts to relieve the terrible fever that is characteristic of measles and many of the other Old World diseases. On August 28, Robertson went down to the Trout Fall... on arriving there I find 3 men + several children dead.—and all the others very low.—about the time the Measles is broke out on any one they then resort to the horrid custom of Cooling the Boy [meaning body?] by covering their naked Body up in wet moss—or lay exposed to the rain or if able plaing [playing] in the water nothing can persuade them against such and this is what makes their Sufferings & Death.123

On the other hand, those who accepted the trader's simple medical advice, and eschewed some of the more harmful (in this context) traditional cures, were much more likely to survive.124 A related outcome was that those Aboriginal people who remained in the vicinity of the posts throughout the year also had a better chance of survival, as the traders could provide medical aid and subsistence when needed.125 The company sought to provide the sick with shelter, food, and clothing, and no doubt the HBC men helped to save many lives in this way. However, those who were out of reach had to make do on their own, and in times of severe and widespread epidemics, many died, and the differential could be significant. Speaking of an influenza epidemic near Fort Chipewyan in the winter of 1836-37, the fur trader and northern explorer Thomas Simpson noted that that disease carried off nearly two hundred of the distant Chipewyans. I say distant, because all who were within reach of the establishments were sent for and carried thither, where every care was taken of them; warm clothing and lodgings were provided, medicines administered; the Traders and servants fed them, parting with their own slender stocks of luxuries for their nourishment.126

In a period when severe epidemic disease had become an almost annual event, as it had in the 1840s, the trading posts increasingly came to be seen as refuges by some Aboriginal people. Robertson's observations suggest that many people had, temporarily at least, come to rely on the HBC post for clothing, medical assistance, food, and shelter during this epidemic, a frequent pattern of behaviour whenever epidemic disease struck the Aboriginal people of the Canadian Northwest during the fur-trade era. While this dependency on the traders was a short-term measure, it also may be that a more permanent reliance upon

THE EPIDEMICS OF 1846 235 the trading posts was developing among some Aboriginal people as a result of these epidemics. If the epidemics of 1846 favoured the survival of non-traditionalists, they also seem to have induced changes to certain long-standing customs among some groups. These would not have been the result of this single year, though. Rather, they must have stemmed from the deep despair and hopelessness felt by these people after years of relentless epidemics, characteristic of this new era of epidemic disease. Perhaps most surprising was the abandonment of a pair of traditional mourning practices that were common in the early eighteenth century among some of the people of Norway House and elsewhere. Throughout much, if not all, of the Northwest, custom dictated that in the event of the loss of a close relative, the survivors either had to discard all their furs, and in many cases all belongings beyond what they needed for survival, or to refrain from trapping furs for an extended period of time, or both.Well established by 1737, when LaVerendrye's son witnessed the Cree of the Saskatchewan River throwing away their furs and those of their deceased relatives "according to their custom,"127 these behaviours were well known among the fur traders, and epidemics in which widespread mortality occurred were a major cause for concern on the part of the company, for the loss of the trade of not only the dead, but also of the living. On September 19 Donald Ross at Norway House wrote to George Simpson of some surprising developments. In reminding the governor of these mourning customs, he noted that the numerous deaths among the hunters would of itself occasion a serious falling off and amongst Indians the event extends much farther as most of those who survive generally lose all heart and energy and for months on end do little more than moan and mourn helplessly for their lost friends and relatives their little property is either recklessly destroyed or given away thus rendering themselves a great measure unable to hunt even after their fit of despondency may have passed away. 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.128

In fact, traders at several of the other Northern Department posts witnessed the same surprising changes. In July of 1847 Simpson briefed London on the epidemic and its aftermath, describing the great mortality that took place last summer among the natives which we

236 CHAPTER NINE were apprehensive would have distracted the survivors (as is usual in cases of mourning) from giving attention to the chase. The discontinuation of this usage, however, reflects much credit on the management of the gentlemen in charge of districts and posts, to whose influence with the natives may, in a great degree, be ascribed the abandonment of many of their old and useless customs.129

As much as Simpson attributed the transformation to the traders' influence, which indeed had been ineffective for over a hundred years, for the Aboriginal people the decline of their lifestyle was, no doubt, a more telling factor. With mortal epidemics now striking some groups on a nearly annual basis, the frequent loss of a family's material goods, combined with the inability to replenish them through hunting, doomed some to perpetual poverty, even if fur-bearing animals were plentiful. In a similar vein, some of the Aboriginal people abandoned their dead and dying relations during the time of greatest sickness, something that would have been unconscionable in previous years. At Oxford House, for instance, Laurence Robertson "met 3 Indians coming for a supply of ammunition, stating that if they had such they were going off, so as to shun the light of their Friends Death—and that of their own. I gave none but encouraged those in health to try + bring their Friends in reach of the Fort." Similarly, at Lac Seul, Charles McKenzie noted that "the Indians are going off as many as can having many at the point of death—Sons leaving their Fathers and Mothers—brothers leaving brothers—careless whether they can ever see them again."130 If such abandonment was unusual in a traditional sense, it was symptomatic of this new era of epidemic disease, an era in which self-preservation demanded the loss of some traditional ways of behaviour. In turn, these departures from past behaviour hint at a more fundamental transformation to belief structures that included no less than one's relationship with the living and the dead. As much as the deaths that came each year, this was a legacy of the epidemic transition in the Petit Nord.

Conclusion

THE DEVASTATION WREAKED BY OLD WORLD DISEASES UPON THE Aboriginal people of the Americas following the fifteenth century is well known by now. As these "new" sicknesses appeared and spread throughout the hemisphere, they left millions of casualties in their wake. Nevertheless, the epidemic history of each group, and of each region, was by no means the same. There can be no doubt that the timing and penetration of initial infection, the frequency of epidemics, and even the severity of their impact varied greatly across the face of the New World. In the Petit Nord, the historical record suggests that there was a tremendous increase in epidemic activity from the late seventeenth to the nineteenth centuries. Clearly, conditions within the region had changed completely. The process by which the Petit Nord's disease load intensified and diversified over this period illustrates how a population or region can shift from epidemic isolation to progressively greater inclusion within the disease frontier of formerly distant pools. Between 1670 and 1846, diverse changes occurred both within and beyond the region's borders, most relating to evolving patterns of human settlement and movement, and innovations in transport technology, and these changes enhanced the spread of

238 CONCLUSION epidemic diseases to the region. Initially, the increase in the disease load was modest. With the arrival of more French and English fur traders following the establishment of the HBC, the Petit Nord found itself within the frontiers of the European disease pools. These afflictions came mainly by way of overland diffusion from the growing Euroamerican colonies of northeastern North America, which acted as continental entrance points for disease as well as temporary pools, but there was also a lesser amount of disease introduced directly via the ships from Europe.Thus, occasional epidemics of varying severity struck the people of the region prior to 1780, signifying growing connections with the external sources of disease.1 In the late eighteenth century, the changes became more profound, the connections closer still. After 1780, greater numbers of fur traders than ever before appeared in the Petit Nord, carrying epidemic disease to the very corners of the region. As well, the risk of disease from the south also increased greatly through the elaboration of the Plains Aboriginal horse culture and the growth of the commerce between the village tribes of the upper Missouri and the traders from St. Louis. Perhaps most importantly, this era also witnessed the emergence of an American disease pool among the cities of the east, and the beginning of wholesale White settlement in the interior of the continent after the Revolution. Here was a potent combination of circumstances that harkened back to the sudden and catastrophic appearance of Old World diseases along the Atlantic coast during the first half of the seventeenth century. Finally, the era following 1821 brought an explosion of epidemic disease to the Petit Nord, which, by this time, was well entrenched within the frontier of the newly emerging eastern pool. The reasons for this were many. Internally, further structural and personnel changes in the fur trade helped to spread the crowd diseases, while the establishment of the Red River Settlement placed a temporary pool and disease redistribution centre on its western flank. More significant were the changes occurring well beyond the region. Beginning in the 1820s and 1830s, the American settlement frontier began to approach, and in places almost encroach upon, the eastern and southern margins of the Petit Nord. The resultant influx of settlers brought crowd disorders with unprecedented frequency. Moreover, it was at this time that the nature of travel in the east was transformed, and this had much to do with this new era of sickness. By 1846, the development of an elaborate system of canals in the interior of North America, combined with the transport benefits afforded by the widespread use of steamboats, carried settlers from the east farther, and faster, than had ever before been possible, favouring the diffusion of the diseases of civilization.

CONCLUSION 239 Epidemics in the Petit Nord were "remarkable" in their infrequency no more. Despite the ongoing changes that greatly favoured the spread of acute infectious diseases into the interior of North America, the Petit Nord did not fully complete the transition from a peripheral to a near region. In the end, the true crowd diseases did not penetrate into the region with sufficient frequency to render them full-fledged diseases of childhood, as, for instance, smallpox did in the smaller towns of Britain during the eighteenth century, or as measles did in Iceland during the second half of the twentieth. Although they were far more frequent than they had been, the crowd diseases remained irregular visitors, and therefore often struck the people of this region with greater severity than if the transition had been completed. There are at least two reasons why this may have been so. For one, the low population densities throughout the Petit Nord limited the frequency of return of these sicknesses. Typical gatherings were small, with even the largest of temporary assemblages numbering no more than a few thousands. Most of the time they counted in the tens or hundreds. The groups in the Petit Nord throughout this period, then, fell into the very low end of Bartlett's type III communities, those with less than 10,000 total population. Once a crowd disease swept through these communities, it was some time before a sufficient supply of susceptibles was built up for the disease's return, no matter how constant the opportunity for infection from an outside source. Until the number of susceptibles was replenished, and this generally occurred by new births, a crowd disease could not penetrate into the region. Consequently, for lightly populated regions, as was the Petit Nord, after a certain point the inter-epidemic period for diseases like smallpox or measles could not be lessened significantly by more frequent appearances among nearby groups.There simply was not sufficient fuel to maintain the epidemic fire. Equally important, there were restrictions on the spread of crowd diseases into the Petit Nord because of the immune status of the gateway populations, those people through whom the diseases spread into the region. In other contexts, large numbers of susceptibles, particularly children, carried disease from the pools into peripheral regions and, in so doing, transformed them into near regions. However, there was no such flow through the lands to the north and west of Lake Superior, where settlement bypassed the region until late in the nineteenth century. Instead, the seeds of epidemic disease arrived either with the few adult non-Aboriginal people who journeyed into the region and along its margins, or with

240 CONCLUSION Aboriginal people who ventured beyond its limits. In either case, there was little possibility for frequent reintroduction of crowd diseases since, once exposed, the people would have acquired immunity that prevented their contracting the disease a second time. On the other hand, these limitations of population size and herd immunity were much less of a constraint on the appearance of other diseases, most notably influenza and the myriad of discrete, upper respiratory tract infections known collectively as colds and catarrhs. The flu and sundry colds reappeared frequently by the mid-nineteenth century, perhaps annually (or more) among some groups, and came to dominate the disease load of the region. These diseases were also among the first arrivals in the Petit Nord. This pattern was probably seen elsewhere where acute infectious diseases were introduced into regions with progressively closer connections with the larger urban disease pools.2 The timing of disease introduction into the Petit Nord was not entirely random, nor, indeed, was the sequence in which each different affliction appeared. Instead, the timing and sequence reflected specific attributes of each disease, as well as the changing circumstances surrounding the region's communication with the external disease pools. Certain diseases appeared early and often, and others rarely and not until towards the end of the period. This pattern both supports and contradicts Ramenofsky's classification scheme. As expected, smallpox first struck the region during the early part of the contact period (Table 5), appearing on several occasions prior to 1800. Later epidemics were prevented by vaccinations, but it is likely that smallpox would have been a periodic, if not regular, visitor to the Petit Nord during the nineteenth century, had it not been prevented by artificial means. Measles arrived later, first breaking out in 1751 and then again in 1819-20,1828, and finally in 1845-46. Chickenpox (1835), mumps (1841), and scarlet fever (1843) were among the last to arrive, reflecting their more limited diffusion potential.The latter diseases arrived only during the period when large numbers of settler families began to move into the areas immediately south and southeast of the Petit Nord. Running contrary to the predicted order of arrival were the acute respiratory diseases, influenza, andrwhooping cough. Although colds and influenza have comparatively brief infectious periods, placing them in the third class of diffusion potential, according to Ramenofsky, they arrived early in the Petit Nord. Scattered colds broke out at Albany as early as 1715-16, with a larger outbreak in 1719, well before the first epidemics of measles (second class) and whooping cough (first class). By the 1750s, outbreaks or epidemics of colds or "great colds," some of them undoubtedly influenza,

CONCLUSION 241

Table 5: Order of Disease Introduction (* From Ramenofsky, Vectors of Death, 167)

were increasingly common among both the European and Aboriginal people around the HBC's bayside posts. By the third decade of the nineteenth century, influenza had emerged as the most frequent epidemic disease in the Petit Nord (excluding the colds). Conversely, whooping cough appeared far later in the epidemic record than would be predicted, based on its infectious period. It first broke out in 1806, long after the first appearance of measles and the colds, but returned at least once a decade after the 1819-20 epidemic. Of all the true crowd diseases, then, whooping cough came closest to achieving status as a childhood disease in the Petit Nord during this era. The divergence between the expected and the observed order of introduction indicates that other disease-specific factors, in addition to the length of the infectious period, helped to determine the order and frequency of appearance of the diseases from external sources. Trimble identified pathogenicity/virulence, infectivity/transmission, invasiveness, and stability of the disease agent as core factors affecting the spread of a specific disease in a given population, and these probably played a role in determining the order of introduction in the Petit Nord.3 Diseases with high rates of infectivity prolong a chain of infection, but highly pathogenic afflictions may actually hinder diffusion by preventing movement. In the past, this was especially important when humans provided the power for travel, such as when walking or canoeing, but became far less so as mechanized forms of mass travel were introduced, such as the steamboat and the train. Moreover, afflictions with longer incubation periods will have greater opportunity to travel longer distances from the initial point of infection before the onset of the disease (relocation diffusion), and thus to find new susceptibles. Finally, the immunological nature of the disease was also important in determining the timing and frequency of its introduction to more isolated regions.4 The list of

242 CONCLUSION possible factors influencing a disease's diffusion potential, therefore, is far greater than just the infectious period, and their impact is highly dependent upon the local conditions. In addition to the changes that occurred in the nature of the epidemics that struck the Petit Nord over time, we must also reconstruct epidemic histories on a local scale in order to understand the varying effects of the introduction of exogenous diseases in virgin soil populations. Indeed, it is sometimes necessary to consider the impact of these diseases on a family or band level, rather than at a regional or tribal scale. In no case did an epidemic strike all the people of the region at a given time and with the same force; inevitably, some were hit harder than others, while still others escaped entirely. These disparities in their impact on different populations led to social disparities. For example, secondary consequences, such as shifting balances of power, increased dependency, altered marriage and medical practices, and even divergent spiritual beliefs, could all result from variations in epidemic effects, either in the short term or over a succession of epidemics. One important secondary consequence in the Petit Nord was the movement of individuals or groups after some major epidemics, a pattern of post-epidemic migration that has been well documented for populations elsewhere in the New World. Such movements occurred as differential mortality created population vacuums or power imbalances, making former boundaries more permeable, or as surviving groups sought to maintain minimum viable sizes.

The decades immediately following 1846 were similar to the previous era.5 Acute infectious diseases continued to plague the people of the Petit Nord on occasion, although how frequently is not known. For example, smallpox returned to the region in 1876 when it struck at Berens River, and in 1905, when it surfaced to the north of Lake Superior.6 Measles appeared on several occasions, including a devastating epidemic that spread throughout northwestern Ontario in 1871, another at Osnaburgh House in 1879, and again at Norway House in 1905, an outbreak at Lac Seul in 1910, and yet another in the York Factory area in the mid-1920s, possibly accompanied by scarlet fever.7 Whooping cough struck at Osnaburgh House in 1882. Influenza and other respiratory diseases remained troublesome as well, in some cases exhibiting the same long-standing seasonal patterns that they had since the eighteenth century. Percy Mathews, who served as doctor at York Factory from the 1860s to the 1880s, noted that "in the month

CONCLUSION 243 of April ... an epidemic of catarrh, influenza, bronchitis, or, certainly, some malarial cachexia will very shortly make itself evident, giving rise to dyspesia, diarrhoea or dysentery."8 Influenza attacked at Fort Hope in 1911 and was apparently common on the Albany River at that time. Indeed, few epidemics from this era took as terrible a toll as the Spanish Influenza, which raced across the world at the end of the First World War. This truly global pandemic devastated many of the people of the Petit Nord, including those north of Lake Winnipeg and along the Albany, although it seems to have been much more severe at Norway House and Cross Lake than at nearby Oxford House and Island Lake.9 Seemingly, then, little had changed in terms of the burden of acute infectious disease in the Petit Nord. Towards the close of the nineteenth century, though, another disease began to gain prominence, one characterized by chronic infection potentially lasting years. Tuberculosis (TB) soon rose to the top of the ranks of health problems among the Aboriginal people. For instance, even as Dr. Mathews described the problems of acute infections at York Factory, he also identified TB in its various forms as the second leading cause of death among the York Factory Cree, accounting for thirty percent of all fatalities between 1864 and 1884. Extremely high rates of infection were observed among the Aboriginal people of northwestern Ontario during the first decade of the twentieth century, including at Albany (twenty percent), Martin's Falls (forty-five percent), Osnaburgh House (thirty-five percent), and Fort Hope (thirty-five percent), located on the Albany River just to the north of Lake Nipigon.10 By this time TB had eclipsed the acute infectious diseases in its impact, a fact noted by the Chief Medical Officer of the Department of Indian Affairs, Dr. Peter Bryce, in his annual report for 1905: The Indian bands ... suffer practically from only one disease (TB) to an extent greater than do the neighbouring white population. The infection, introduced some way or other as truly as small-pox was, into some bands, nay more, some families of some bands, just as amongst families of white people, has produced its logical consequences, 30,40, 50,60, even 70 of a death-rate per l.OOO.11

The rise of this chronic infectious disease brought with it an ironic and disturbing change in attitude regarding public health. During the era of the crowd infections, many Aboriginal people had, and justifiably so, identified the settlers as a primary source of disease. Even in those areas in which the settlement frontier had yet to penetrate, the possibility of the arrival of large numbers of intruders from the east was a cause for much concern. This relationship was turned on its head during the twentieth century,

244 CONCLUSION however. With the ascendancy of tuberculosis in western Canada, the tide turned and the settlers began to blame the newly settled reserves, which they perceived as reservoirs of infection. In 1936 Dr. David Stewart summed up the fears of the non-Aboriginal people in Manitoba, although not without some sympathy: Not only do we owe the Indian this fair treatment because we took and occupied his country, but especially because we brought him the disease, tuberculosis, and so should help him to fight it. Furthermore, intercommunications of all kinds between Indians and white people, on account of new means of transportation and in the opening up of the North, are steadily increasing, and ought to be.These Indian reservations and settlements never were water-tight or disease-tight compartments, and in a new day of easier travel are becoming less and less so. And it is true that any disease in any remote corner of a province is disease of the province; that the province will not be clear of any disease nor safe from its menace until every group is clear and safe; and that in health matters no man liveth unto himself and no man dieth unto himself.12

Within a few decades the Aboriginal people of the Petit Nord had graduated from fearing the threat of encroachment by the outsiders, to becoming a threat to the health of those same people.13 Still, tuberculosis did not remain the sole or even the main threat. With the introduction of effective antibiotic drug therapies, beginning in the 1940s, the morbidity and mortality rates due to TB plummeted across Canada, including among the nation's Aboriginal people.14 This marked the end of the age of dominance of infectious disease in the Petit Nord. All was not positive, however. In contrast to this decline in TB, the post-war period also witnessed fundamental changes to the lifestyles of these people that carried their own increased risk of negative consequences.15 Treaties with the Canadian government and the subsequent shift to sedentary life on reserves, with attendant changes in diet and a decline in living conditions, brought new disorders and medical conditions among the people. As infectious diseases fell offin importance, at least in terms of mortality, chronic (though non-infectious) and degenerative afflictions associated with modernization and dietary inadequacy increased greatly, especially diabetes and, to a lesser extent, certain forms of cancer, coronary heart disease, gallbladder disease, and cerebrovascular disease. At the same time, the profound social and cultural disruption that accompanied the era of government control brought social pathologies, or health issues related to accidents, violence, and alcohol abuse.16 Here, then, was a whole new set of health concerns to be addressed.17

Endnotes

Preface 1. Henry F. Dobyns, Their Number Become Thinned: Native American Population Dynamics in Eastern North America (Knoxville: University ofTennessee Press, 1983).This book built on earlier work by Dobyns, including an earlier paper he had written in the 1960s, in which he had called for a drastic upward revision in the estimated population of the pre-Columbian Americas (Henry F. Dobyns, "Estimating Aboriginal American Population: An Appraisal of Techniques with a New Hemispheric Estimate," Current Anthropology 7, no. 4 [1966]). 2. A recent summary of the ongoing debate can be found in Charles Mann's highly readable article,"1491" (The Atlantic Monthly 289, no. 3 [March 2002]). 3. Arthur J. Ray, "Diffusion of Diseases in the Western Interior of Canada, 1830-1850," The Geographical Review 66, no. 2 (1976): 142, fn. 4. 4. There are several recent works of excellence on the Pacific Northwest that illustrate this point, notably Harris's paper, "Voices of Disaster," and Boyd's The Coming of the Spirit of Pestilence (R. Cole Harris, "Voices of Disaster: Smallpox Around the Straight of Georgia in 1782," Ethnohistory 41, no. 4 [1994]); Robert T. Boyd, The Coming of the Spirit of Pestilence: Introduced Infectious Diseases and Population Decline among Northwest Coast Indians, 1774-1874 [Vancouver and Toronto: University of British Columbia Press, 1999]).

246 NOTES PAGES iii TO 5 5. A related problem is the inability, or unwillingness, of the writers to identify or even describe the symptoms of the diseases they observed. The written records are replete with entries about undifFerentiated sickness, the cause of which is impossible to identify. As such, this book is often forced to fall back on intellectually unsatisfying descriptions such as "widespread sickness" for want of a more precise diagnosis, and to adopt a cautious approach to assigning them to the body of afflictions that forms the subject of this study. 6. Those who would dismiss outright the value of fur-trade records for epidemiological research might temper their criticism on two grounds. First, although most fur-trade employees lacked even the rudimentary professional medical knowledge of the day, many of the records of the Hudson's Bay Company were written by men who had entered the trade as surgeons and who had subsequently risen in rank to take command of one of the major posts, or who had their own medical men to advise them. Secondly, the lay person of the fur-trade era, who had limited access to professional medical help and who instead relied on traditional knowledge and treatments, would have had a more intimate relationship with the major epidemic diseases than does an equivalent person today. A prime example of this comes from the case of smallpox: the English physician, Edward Jenner, who is credited with the discovery of vaccination in the late eighteenth century, based his experiments upon common folk-knowledge concerning smallpox and milkmaids, and may have been verifying vaccination procedures that were well established among non-professionals.

Introduction 1. Charles McKenzie entered the fur trade in the employ of the North West Company as an apprentice clerk in 1802, being sent to the country about the Red and Assiniboine rivers the following year, and his career was dogged by epidemics almost from the start. After serving a few years in the trade on the upper Missouri and at Lake Nipigon, he was transferred to the Lac Seul region where he remained, with the exception of a brief hiatus in the 1820s, until his retirement in 1854. Unlike many of his associates in the North West Company, he never rose above the rank of clerk, even after the merger with the rival Hudson's Bay Company in 1821. His reputation suffered severely for a number of reasons, especially the personal dislike held for him by his superior, Governor George Simpson, but Simpson's refusal to allow for the impact of epidemic disease on McKenzie's slipping returns no doubt contributed significantly. 2. HBCA B.107/a/14: 7d; B.107/a/22:13. 3. On the early good health of the Aboriginal people of Hudson Bay and the central subarctic, seeT. Kue Young, Health Care and Cultural Change: The Indian Experience in the Central Subarctic, reprint edition (Toronto: University of Toronto Press, 1991). 4. On the pre-contact health of the Aboriginal people of Canada, see James B.Waldram, D.Ann Herring, andT. Kue Young, Aboriginal Health in Canada: Historical, Cultural, and Epidemiological Perspectives (Toronto, Buffalo, and London: University of Toronto Press, 1995).

NOTES PAGES 5 TO 8 247 5. Alfred W. Crosby, The Columbian Exchange: Biological and Cultural Consequences of 1492, Contributions in American Studies (Westport, Conn,: Greenwood Press, 1972).There is no unanimity among scholars about which diseases were introduced from the Old World, and some, notably syphilis, have been flashpoints for debate. For a recent list of diseases that were probably indigenous to the New World along with the Old World imports, see Boyd, Coming of the Spirit, 15. 6. When identifying particular diseases, this study will refer to its ICD (International Classification of Diseases) number, the tenth version of a system of unique classification of disease established by the World Health Organization. For example, measles is classified as ICD-10 BOS (Abraham S. Benenson, ed., Control of Communicable Diseases Manual, sixteenth edition [Washington, DC: American Public Health Association, 1995]). Although for the sake of brevity I often refer to them as the epidemic diseases, they are by no means the only epidemic diseases to strike the Petit Nord. "Epidemic" simply means "the occurrence in a community or region of cases of an illness (or an outbreak) with a frequency clearly in excess of normal expectancy" (Ibid., 535), and chronic afflictions such as syphilis and tuberculosis, and environmental disorders such as snow blindness and food poisoning, could also assume epidemic levels. 7. Kelvyn Jones and Graham Moon, Health, Disease and Society: An Introduction to Medical Geography (London: Routledge, 1992), 147-148. Many other diseases that affect humans are not infectious, but instead are triggered by other factors such as environmental hazards or old age, or are the result of genetically inherited conditions. 8. An exception to this among the diseases being studied here is influenza type A, for which avian and swine populations may act as a reservoir. However, the vast majority of transmissions of influenza A to humans are via person-to-person spread. 9. Peter Haggett,"Sauer's 'Origins and Dispersals': Its Implications for the Geography of Disease," Transactions of the British Institute of Geographers (New Series) 17 (1992): 394; Boyd, Coming of the Spirit; William H. McNeill, Plagues and Peoples (Garden City, New York: Anchor Press/Doubleday, 1976), 62, 55; William H. McNeill, "Migration Patterns and Infection in Traditional Societies," in Changing Disease Patterns and Human Behavior, edited by N.F. Stanley and R.A.Joske (London: Academic Press, 1980), 29. 10. McNeill, Plagues and Peoples; McNeill, "Migration Patterns";William H. McNeill, "Historical Patterns of Migration," Current Anthropology 20, no. 1 (March 1979). 11. M. S. Bartlett, "Measles Periodicity and Community Size" Journal of the Royal Statistical Society, Series A 120 (1957): 48-70; M. S. Bartlett, "The Critical Community Size for Measles in the United States," Journal of the Royal Statistical Society, Series A 123 (1960): 37-44; Francis L. Black,"Measles Endemicity in Insular Populations: Critical Community Size and Its Evolutionary Implication,"Journal ofTheoretical Biology 11 (1966): 207; Francis L. Black,"Modern Isolated Pre-Agricultural Populations as a Source of Information on Prehistoric Epidemic Patterns," in Changing Disease Patterns and Human Behaviour, edited by N.F. Stanley and R.A.Joske (London:Academic Press, 1980), 43; Andrew D. Cliff, Peter Haggett, and Mathew Smallman-Raynor, Island Epidemics (Oxford and New York: Oxford University Press, 2000), 108. An exception to the requirement of large populations may be chickenpox, for which it has been estimated that the critical community size is only 1000, due to the varicella virus's

248 NOTES PAGES 8 TO 12 ability to hide within the human body for decades following an episode of chickenpox, only to re-emerge as shingles (Black, "Measles Endemicity," 210). 12. Cliff et al., Island Epidemics, 107-109; Peter Haggett, "The Invasion of Human Epidemic Diseases into Australia, New Zealand, and the Southwest Pacific: The Geographical Context," New Zealand Geographer 49, no. 2 (1993): 46. In general, cities have acted as reservoirs for large numbers of infections, including those that are normally unapparent to the residents (M. Burnet and D.O. White, Natural History of Infectious Diseases, 4th edition [Cambridge: Cambridge University Press, 1972], 119). 13. For a detailed discussion of such factors see Cliff et al., Island Epidemics, 93-101, 113115. 14. Bartlett, "Measles Periodicity," 59. 15. Black, "Modern Isolated," 44. 16. Andrew D.P. Cliff and Peter Haggett, Atlas of Disease Distributions: Analytic Approaches to Epidemiological Data, reprint edition (Oxford: Blackwell Publishers, 1993), 245; McNeill "Migration Patterns," 30. For example, measles erupted in three-year cycles in England and Wales by the mid-nineteenth century (Cliff et al., Island Epidemics, 183). 17. McNeill,"Historical Patterns," 95. 18. S.R. Duncan, Susan Scott, and CJ. Duncan, "Smallpox Epidemics in Cities in Britain," Journal of Interdisciplinary History 25, no. 2 (Autumn 1994).The close epidemiological relationship between London and the smaller communities of Great Britain can be seen in the words of the nineteenth-century medical historian Charles Creighton, who observed that during the late seventeenth century and throughout the eighteenth, "a high mortality in London in a certain year meant an epidemic general in England in that or the following year..." (Charles Creighton, A History of Epidemics in Britain, reprint edition [London: Frank Cass & Co. Ltd., 1965], 2: 457). 19. McNeill, "Migration Patterns," 31. In one sense, isolation from disease pools provides protection from acute infectious disease for a peripheral group, since they are not generally exposed to the disease. However, each epidemic will likely take a greater toll than if the disease were endemic. 20. Andrew D. Cliff, Peter Haggett, J.K. Ord, and G.R.Versey, Spatial Diffusion:An Historical Geography of Epidemics in an Island Community (Cambridge: Cambridge University Press, 1981), 48. 21. Bartlett, "Measles Periodicity." 22. This is not to be confused with another type of transition, called the "mortality" or "epidemiologic" transition, which refers to the health changes that arise from economic and social development. Perhaps the best-documented manifestation of this transition is the shift from pre-industrial to modern industrial western societies, which saw the decline of death and birth rates, and the rise of chronic and degenerative diseases at the expense of infectious diseases, with an upwards rise in life expectancy. 23. Between 1500 and 1700, much of Europe underwent its own transition, as more intense communication and transportation enabled the crowd diseases to circulate freely over large areas. During this period, McNeill wrote, "Devastating epidemics of the sort that had raged so dramatically in Europe's cities between 1346 and the midseventeenth century tapered off towards the status of childhood diseases, or else, as in

NOTES PAGES 13 TO 15 249 the case of both plague and malaria, notably reduced the geographic range of their incidence" (McNeill, Plagues and Peoples, 223-224). 24. See, for example, Noble David Cook andW. George Lovell, "Unravelling the Web of Disease," in "Secret Judgements of God": Old World Disease in Colonial Spanish America, edited by Noble David Cook andW. George Lovell, The Civilization of the American Indian Series, 205 (Norman and London: University of Oklahoma Press, 1992), 236; Haggett, "Sauer's Origins," 395; Haggett,"Invasion," 46-47; Mary E.Wilson, "Travel and the Emergence of Infectious Diseases," Emerging Infectious Diseases 1, no. 2 (AprilJune 1995): 39-46; and Gerald F. Pyle,"The Diffusion of Cholera in the United States in the Nineteenth Century," Geographical Analysis 1 (1969): 59-79. In their wideranging study of epidemics and the world's islands, Cliff et al. (Island Epidemics, Chapter 5) provided an excellent discussion of the role of changing transportation technology and patterns of travel in introducing epidemic disease from abroad. 25. Cliff et al., Spatial Diffusion, 48, 64, 79,116. A similar example is the frequency of measles among the people of the Faeroe Islands, located between Iceland and Scotland, during the period from 1781 to 1905 (Cliff et al., Island Epidemics, 54-61). Subsequent to an epidemic in 1781, the disease did not reappear for another sixty-five years, when in 1846 it attacked more than three-quarters of the islands' inhabitants. The disease disappeared until 1875, a gap of twenty-nine years. Seven additional waves occurred between 1875 and 1905, and the average inter-epidemic gap had plummeted to less than four years due to increased connections with external sources of disease. Likewise, Haggett ("Invasion," 47) identified the decline in the isolation of Australia, New Zealand, and the South Pacific as a major factor in an increase in disease in those areas. Changes in transport technology made them less peripheral than they had once been. 26.A.F. Ramenofsky, Vectors of Death: The Archaeology of European Contact (Albuquerque: University of New Mexico Press, 1987), 167. 27. See Stephen}. Kunitz, Disease and Social Diversity:The European Impact on the Health of Non-Europeans (New York City: Oxford University Press, 1996). Such variability in the effects and diffusion of Old World diseases has often been observed in the recent literature. For instance, Newson concluded that the epidemics that struck early colonial Ecuador were unlikely to have spread over extensive areas or to have been uniform in their impact (Linda A. Newson, "Old World Epidemics in Early Colonial Ecuador," in "Secret Judgements of God": Old World Disease in Colonial Spanish America, edited by Noble David Cook andW. George Lovell, The Civilization of the American Indian Series [Norman and London: University of Oklahoma Press, 1992], 108-109.) Harris ("Voices of Disaster," 615) found no common epidemiological history among the Aboriginal people of coastal British Columbia until long after the first epidemics had struck them. Aufderheide warned of the danger of "extrapolating isolated observations of disease-related demographic changes to the population of an entire region or even a continent" (Arthur C. Aufderheide, "Summary on Disease Before and After Contact," in Disease and Demography in the Americas, edited by John W. Verano and Douglas H. Ubelaker [Washington and London: Smithsonian Institution Press, 1992], 166). By the same token, Milner cautioned that applying mortality figures taken from one epidemic situation to another is problematic, as varying conditions affected the frequency and severity of the disease experience in North America. Moreover, he also suggested that it is unlikely that epidemics reaching the interior of

250 NOTES PAGES 17 TO 22 North America would have had a uniform impact throughout. Instead, some groups would have been devastated while others escaped entirely (George R. Milner, "Disease and Sociopolitical Systems in Late Prehistoric Illinois," in Disease and Demography in the Americas, edited by John W.Verano and Douglas H. Ubelaker, [Washington and London: Smithsonian Institution Press, 1992], 110-111). 28. James S. Gardner, "General Environment," in Subarctic, edited by June Helm, vol. 6 of Handbook of North American Indians (Washington: Smithsonian Institution, 1981), 7; John A. Alwin, "Mode, Pattern, and Pulse: Hudson's Bay Company Transport, 16701821," PhD diss., University of Manitoba, 1978,24,27; Victor P. Lytwyn, Muskekowuck Athinuwick: Original People of the Great Swampy Land (Winnipeg: University of Manitoba Press, 2002), 4-5. 29. On the Shield, spruce, balsam,fir,jack pine, and birch are dominant, with some occurrence of willow, alder, and poplar. The extreme southwestern part of the Petit Nord, corresponding to the Boundary Waters region, is part of the Great Lakes-St. Lawrence forest, a region of mixed pine, hemlock, and birch that has long been exploited by the pulp and paper industry.

Chapter One 1. There is considerable debate as to when the first epidemic struck the Aboriginal people of the New World. See David Henige, Numbers from Nowhere: The American Indian Contact Population Debate (Norman: University of Oklahoma Press, 1998), 169,170. 2. Cook and Lovell, "Web of Disease," 219; Crosby, Columbian Exchange, 39. 3. Percy M. Ashburn, The Ranks of Death (New York: Coward-McCann, 1947), 29,32,39; Cook and Lovell, "Web of Disease," 218; D. W Meinig, Atlantic America, 1492-1800, vol. 1 of The Shaping of America: A Geographical Perspective on 500 Years of History (New Haven and London:Yale University Press, 1986), 14.The same situation prevailed in Portuguese territory to the south. Alden and Miller documented the relatively frequent introduction of smallpox to Brazil via the slave trade between 1560 and 1831, mainly from Africa (D. Alden and J. C. Miller, "Out of Africa: The Slave Trade and the Transmission of Smallpox to Brazil, 1560-1831," Journal of Interdisciplinary History 18, no. 2 [1987]: 195-224). 4.W. George Lovell,'"Heavy Shadows and Black Night': Disease and Depopulation in Colonial Spanish America," in The Americas Before and After 1492: Current Geographical Research, edited by Karl W. Butzer, Annals of the Association of American Geographers, Special Publication, vol. 82, no. 3,1992, pp.426-443; Linda A. Newson, "Old World Epidemics in Early Colonial Ecuador," in "Secret Judgements of God": Old World Disease in Colonial Spanish America, edited by Noble David Cook andW. George Lovell, The Civilization of the American Indian Series, (Norman and London: University of Oklahoma Press, 1992), 84-112; Suzanne Austin Alchon, "Disease, Population, and Public Health in Eighteenth Century Quito," in "Secret Judgements of God": Old World Disease in Colonial Spanish America, edited by Noble David Cook and W George Lovell, 159; Hanns J. Prem, "Disease Outbreaks in Central Mexico During the Sixteenth Century," in "Secret Judgements of God": Old World Disease in Colonial Spanish America, edited by Noble David Cook and W. George Lovell, 45-46.

NOTES PAGES 23 TO 25 251 5. Dobyns, Their Number, 13,15; Henry F. Dobyns,"More Methodological Perspectives on Historical Demography," Ethnohistory 36 (1989): 172; Henry F. Dobyns, "Native Historic Epidemiology in the Greater Southwest," American Anthropology 36 (1989): 294. 6. Dobyns, Their Number, 324. 7. Kunitz, Disease and Social Diversity, 178. Kunitz also ably summed up the effect of Dobyns s theories on the literature: "The lesson is that extrapolation from the known to the unknown can be useful for indicating directions in which to look for explanations of population change, but it can also result in the creation of a procrustean bed in which the unknown is forced to conform to what we think we know." 8. For example, Russell Thornton, Jonathan Warren, and Tim Miller, "Depopulation in the Southeast after 1492," in Disease and Demography in the Americas, edited by John W. Verano and Douglas H. Ubelaker (Washington and London: Smithsonian Institution Press, 1992); Henige, Numbers from Nowhere. 9. Dean R. Snow and Kim M. Lanphear, "European Contact and Indian Depopulation in the Northeast: The Timing of the First Epidemics," Ethnohistory 35, no. 1 (1988): 20, 21; Dobyns, Their Number, 318-319. 10. Dean R. Snow and William A. Starna, "Sixteenth-Century Depopulation: A View from the Mohawk Valley," American Anthropologist 91 (1989): 144,147; Bruce Trigger, "Ontario Native People and the Epidemics of 1634-40," in Indians, Animals and the FurTradeiA Critique of Keepers of the Game, edited by Shepard Krech, III (Athens, Georgia: University of Georgia Press, 1981), 22; Bruce G.Trigger, The Children of Aataentsic:A History of the Huron People to 1660 (Kingston and Montreal: McGillQueen's University Press, 1987), xxxi. 11. Dobyns, Their Number, 313-325. 12. H.P. Biggar, ed. and trans., The Works of Samuel De Champlain in Six Volumes, Publications of the Champlain Society (Toronto:The Champlain Society, 1925), 204. 13. Dobyns, Their Number, 314; David Henige, "Primary Source by Primary Source? On the Role of Epidemics in New World Depopulation," Ethnohistory 33, no. 3 (1986): 302; Snow and Lanphear, "European Contact," 18. Indeed, the two groups appear to have been suffering from different afflictions. Cartier's description of the symptoms makes it clear that the French were suffering from scurvy. The illness of the Iroquois was no doubt caused by something else, because they knew how to treat scurvy before it became life-threatening. Given what is now known about the Aboriginal disease load of the Iroquois, it could easily have been an indigenous disorder exacerbated by malnutrition, rather than an Old World complaint. Shelley Saunders, Peter G. Ramsden, and D.Ann Herring,"Transformation and Disease: Precontact Ontario Iroquoians," in Disease and Demography in the Americas, edited by John W. Verano and Douglas H. Ubelaker (Washington and London: Smithsonian Institution Press, 1992),117-125. 14. Dobyns, "Methodological Perspectives," 289. 15. Dean R. Snow and K. M. Lanphear,'"More Methodological Perspectives': A Rejoinder to Dobyns," Ethnohistory 36, no. 3 (1989): 302; David Henige, "On the Current Devaluation of the Notion of Evidence: A Rejoinder to Dobyns,"

252 NOTES PAGES 25 TO 27 Ethnohistory 36, no. 3 (1989): 304-307;Trigger, Children ofAataentsic, 194-195,214224. 16. Ramenofsky, Vectors ofDeath.The third group studied by Ramenofsky included the Aboriginal people of the lower Mississippi Valley. 17. Sarah K. Campbell, PostColumbian Culture History in the Northern Columbia Plateau:A. D. 1500-1900, facsimile reproduction of a PhD dissertation (University of Washington, 1989),The Evolution of North American Indians (New York & London: Garland Publishing, Inc., 1990), 186-187,190. 18. Henige, Numbers from Nowhere, 158-161. 19. A. P. Nasatir, ed., Before Lewis and Clark: Documents Illustrating the History of the Missouri 1785-1804, 2 vols. (St. Louis: St. Louis Historical Documents Foundation, 1952), 299; Michael K.Trimble,"Epidemiology on the Northern Plains: A Cultural Perspective," PhD diss., University of Missouri-Columbia, 1985,75; John E Taylor, "Sociocultural Effects of Epidemics on the Northern Plains: 1734-1850," The Western Canadian Journal of Anthropology VII, no. 4 (1977): 79. Both Dobyns (Their Number, 310) and Ramenofsky (Vectors of Death, 130) have referred to this statement in support of protohistoric epidemics, however. 20. Most of the few attempts at colonization in North America during the sixteenth century proved short-lived. A Portuguese colony on Cape Breton Island during the 1520s and one settled by the French near Quebec in 1541 each lasted only about two years or less (Samuel Eliot Morison, The European Discovery ofAmerica:The Northern Voyages A.D. 500-1600 [NewYork City: Oxford University Press, 1971], 228-229; Bruce G.Trigger, Natives and Newcomers: Canada's "HeroicAge"Reconsidered, reprint edition [Kingston and Montreal: McGill-Queen's University Press, 1989], 124-125, 134). The Spanish were more successful in Florida, including the establishment of St. Augustine in 1566. The English first attempted to colonize North America with Roanoke in the 1580s, but were thwarted within a few years. There were reports of sickness among some of the Aboriginal groups neighbouring Roanoke (Henige, Numbers from Nowhere, 150-151). The period of sustained colonization in the northern part of North America began in the early seventeenth century. Settlements at Jamestown,Virginia (1607), and Quebec (1608) were followed by the arrival of the pilgrims at Plymouth in 1620 and the Dutch at New Amsterdam (New York) in 1624. There appears to have been epidemic disease among the people ofVirginia from the start. Typhus, and possibly bubonic plague, may have been rampant on the ships sailing for Jamestown in 1609 (Creighton, Epidemics in Britain, 1: 610).Earle concluded that dysentery and possibly typhoid fever occurred almost annually in summertime epidemics among the Jamestown colonists between 1607 and 1624 (CarvilleV Earle, "Environment, Disease and Mortality in Early Virginia," Journal of Historical Geography 5, no. 4 [1979]: 365-390). Initially, Old World diseases were probably more often carried to Virginia than to New England (Creighton, Epidemics in Britain, 1: 612), but this situation was reversed after 1630. 21. For example, see Catherine C. Carlson, George J.Armelagos, and Ann L. Magennis, "Impact of Disease on the Precontact and Early Historic Populations of New England and the Maritimes," in Disease and Demography in the Americas, edited by John W Verano and Douglas H. Ubelaker (Washington and London: Smithsonian Institution Press, 1992), 145-147.

NOTES PAGES 27 TO 31 253 22. Snow and Lanphear, "European Contact," 25-26. 23. Indeed, Snow and Lanphear ('"More Methodological Perspectives,'" 302) acknowledged the probability that colds and influenza were transmitted to the Aboriginal people, but that such afflictions remained localized around the point of introduction rather than becoming pandemics. Unlike true crowd diseases such as measles and smallpox, the influenza virus periodically mutates, rendering previously acquired antibodies ineffective against the new strain. As such, it does not become a disease of childhood even in the largest of human populations. 24. Reuben Gold Thwaites, ed., The Jesuit Relations and Allied Documents: Travels and Explorations of the Jesuit Missionaries in New France 1610-1791, 73 vols., third reprint edition (NewYork City: Pageant Book Company, 1959), 105. 25. Dobyns,"Methodological Perspectives," 291-292. 26.Virginia P. Miller, "Aboriginal Micmac Population: A Review of the Evidence," Ethnohistory 23, no. 2 (1976): 117-127. 27. Snow and Lanphear,"European Contact," 25-26. 28. Meinig, Atlantic America, 90; Robert D. Mitchell, "The Colonial Origins of AngloAmerica," in North America: The Historical Geography of a Changing Continent, edited by Robert D. Mitchell and Paul A. Groves (Totowa, New Jersey: Rowman and Littlefield, 1987), 104. 29. Meinig, Atlantic America, 110. 30.This process began in earnest in the 1630s, but initially it may have been more common in New Netherland and the English colonies than in New France. In his Relation of 1647-48, the Jesuit missionary Jerome Lalement stated that "It seldom happens that sickness breaks out in the ships that come to the country..." (Thwaites, Jesuit Relations, 32: 133). French ships brought smallpox in 1639 and carried unnamed but deadly diseases in 1640 and 1648 (Joyce Marshall, ed. and trans., Word from New France:The Selected Letters of Marie De LTncarnation [Toronto: Oxford University Press, 1967], 18;Thwaites,Jesuit Relations, 8:309; 32:133; 33:19; 69: 47). 3 I.John Duffy, Epidemics in Colonial America (Baton Rouge: Louisiana State University Press, 1953), 43-44, 45, 69,104; Creighton, Epidemics in Britain, 1: 613; Earnest Caulfield, "Early Measles Epidemics in America," Yale Journal of Biology and Medicine 15, no. 4 (1943): 533. Duffy (Epidemics in Colonial America, 69) noted that the normal course of diffusion was northwest from New York into the Great Lakes region and the St. Lawrence Valley, but that epidemics also spread southward from Canada to the middle and southern English colonies. 32. Mitchell, "Colonial Origins," 104; R. Cole Harris, "France in North America," in North America: The Historical Geography of a Changing Continent, edited by Robert D. Mitchell and Paul A. Groves (Totowa, New Jersey: Rowman and Littlefield, 1987), 75, 80. 33. Duffy, Epidemics in Colonial America, 69,104,105. 34. Trigger, Children ofAataentsic, 501, 526, 528, 588. The primary records of the seventeenth and early eighteenth centuries contain many descriptions of epidemics spreading into the interior through Aboriginal movements.Trois Rivieres, a major French fur-trading centre along the St. Lawrence, was an especially important locus of diffusion (John J. Heagerty, Four Centuries of Medical History in Canada and a Sketch of

254 NOTES PAGES 32 TO 33 the Medical History of Newfoundland, 2 vols. [Toronto: The MacMillan Company, 1928], 1:32). 35.A.E. Spiess and B.D. Spiess,"New England Pandemic of 1616-1622: Cause and Archaeological Implication," Man in the Northeast 34 (1987): 71-82; Herbert U. Williams, "The Epidemic of the Indians of New England, 1616-1620, with Remarks on Native American Infections," Johns Hopkins Medical Bulletin 20 (1909): 340-349. 36. Biggar, Works of Champlain, 2:207;Trigger, Children ofAataentsic, 279,499. 37. Trigger, Natives and Newcomers, 230; Sherburne F. Cook, "The Significance of Disease in the Extinction of the New England Indians," Human Biology 45 (1973): 491; Dean R. Snow, "Disease and Population Decline in the Northeast," in Disease and Demography in the Americas, edited by John W.Verano and Douglas H. Ubelaker (Washington and London: Smithsonian Institution Press, 1992), 178. 38.Trigger, Children ofAataentsic, 527. 39. Trigger, Natives and Newcomers, 230, 231; Snow, "Disease and Population Decline," 179. 40. Marshall, Selected Letters, 18, 75; Snow, "Disease and Population Decline," 179;Trigger, Natives and Newcomers, 231;Trigger, Children ofAataentsic, 588; Duffy, Epidemics in Colonial America, 44. 41. Conrad E. Heidenreich, "The Great Lakes Indian Basin, 1600-1653," in Historical Atlas of Canada, Volume I: From the Beginning to 1800, edited by R. Cole Harris, plate 35 (Toronto: University ofToronto Press, 1987);Trigger, Children ofAataentsic, 355. Serious outbreaks of infectious disease ceased among the Huron for a decade after 1639-40, returning only in the winter of 1649-50 (Trigger, Natives and Newcomers, 271). Nevertheless, several epidemics erupted in the Atlantic colonies and among other eastern Aboriginal groups during this period, including the Iroquois (Trigger, Children ofAataentsic, 602; Heidenreich, "Great Lakes Indian Basin").There is no indication that these afflictions approached the Petit Nord, and their absence among the Huron and other groups located near the region suggests that they failed to reach it. 42. See, for instance, John Duffy, "Smallpox and the Indians in the American Colonies," Bulletin of the History of Medicine 25 (1951): 329; Duffy, Epidemics in Colonial America, 115,186; Duffy, "Disease and Population Decline," 179-180; Heagerty, Four Centuries, 1: 58; Creighton, Epidemics in Britain, 1: 613; and Marshall, Selected Letters, 239, 265 301, 311. Some appeared beyond Lake Huron between 1650 and 1670. In 1666 a severe, contagious disease prevailed among the Potawatomi, then living on Green Bay (Louise Phelps Kellogg, ed., Early Narratives of the Northwest, 1634-1699, Original Narratives of Early American History, reprint edition [New York City: Barnes & Noble Inc., 1959], 127; Helen Hornbeck Tanner, ed., Atlas of Great Lakes Indian History, The Civilization of the American Indian Series [Norman and London: University of Oklahoma Press, 1987], map 6). While he was there, Father Claude Allouez was able to baptise 340 people, about 300 of whom died shortly after converting (Marshall, Selected Letters, 331). This fits a general pattern of missionary success followed quickly by the death of the initiate, witnessed on other occasions during epidemics in northeastern North America. Father Allouez also indicated that at least one Ottawa village in the Lake Superior area was ravaged by disease while he was there during the 1660s (Richard White, The Middle Ground: Indians, Empires, and

NOTES PAGES 34 TO 38 255 Republics in the Great Lakes Region, 1650-i815, Cambridge Studies in North American Indian History, reprint edition [Cambridge: Cambridge University Press, 1995], 41 fn. 71;ThwaitesJesMtf Relations, 50: 287). 43. Lytwyn, Muskekowuck, 74-76. 44. Daniel Francis and Toby Morantz, Partners in Furs: A History of the Fur Trade in Eastern James Bay 1600-1870 (Kingston and Montreal: McGill-Queen's University Press, 1983), 18;Thwaites Jesuit Relations, 54: 241-243. 45.J. B.Tyrrell, ed., Documents Relating to the Early History of Hudson Bay, facsimile edition (New York City: Greenwood Press, 1968), 3-4,6. With the exception of the ill-fated Danish mission to the Churchill River, led by Munk, all originated in England. Nute concluded that "daring mariners from [New England] penetrated to the bay soon after English seamen gave up their interest in it," but there is no evidence to confirm this (Grace Lee Nute, Caesars of the Wilderness: Medard Chouart, Sieur Des Groseilliers and Pierre Esprit Radisson, 1618-1710 [NewYork City: D. Appleton-Century Company, 1943], 286). 46. Rosen identified "infectious fevers, avitaminoses, pulmonary and cardiac complaints, rheumatic affections, and ulcerative conditions of the extremities" (George Rosen, "Occupational Diseases of English Seamen During the Seventeenth and Eighteenth Centuries," Bulletin of the History of Medicine 7, no. 7 [1939]: 754).The term "fevers" would likely have included several infectious diseases. 47. While the Hudson, Button, Munk, and James expeditions all sent men ashore, there is evidence only that Hudson and his men interacted with Aboriginal people. Prior to the mutiny, Hudson traded with at least one Aboriginal person in the vicinity of the Rupert River (Toby Morantz, "Oral and Recorded History in James Bay," in Papers of the Fifteenth Algonquian Conference, edited by Willam Cowan [Ottawa: Carleton University Press, 1984], 176).There is other testimony that, after being forced off the Discovery, Hudson and the members of his banished party were murdered for attempting to steal corn and other items from the Aboriginal people (Trigger, Children ofAataentsic, 275, 283-285). According to Young, some have thought that a contagious disease was passed from one of Button's ships to the Inuit living north of Churchill, who were then decimated (DelbertYoung, "Was There an Unsuspected Killer Aboard 'The Unicorn'?" The Beaver Outfit 304, no. 3 [1973]: 13). In his view, this was very unlikely.

Chapter Two l.The failure of the HBC ships to transmit Old World diseases to the Petit Nord during this early period did not extend to chronic infectious diseases, however. These were not as constrained by the lengthy voyage as were the acute infections, and such longterm afflictions as tuberculosis and venereal diseases were quick to spread to Hudson Bay from Europe.Venereal diseases, now termed sexually transmitted diseases (STDs), were a significant problem among the HBC men almost from the start. As early as 1682, Governor John Nixon was complaining that the men were "seek of the ould disease of licentiousness" (Quoted in E.E. Rich, "The Fur Traders: Their Diet and Drugs," The Beaver Outfit 307, no. 1 [1976]: 47,49). From then on,"poxed" employees

256 NOTES PAGES 40 TO 42 appear intermittently in the HBC records. For instance, in 1727, a labourer named John Murrill, who had been infected in England, was sent home "for fear he should Touch with the Natives which may prove of 111 consequence to the Company" (K. G. Davies and A. M.Johnson, eds., Letters from Hudson Bay, 1703-40, Publications of the Hudson's Bay Record Society, vol. 25 [London:The Hudson's Bay Record Society, 1965], 124-125). Such actions proved ineffective, as by the midpoint of the eighteenth century, venereal disease was common among the Aboriginal people who traded at Hudson Bay, passed on to them by both the HBC and Canadian traders (Glyndwyr Williams, ed., Andrew Graham's Observations on Hudson's Bay, 1767-1791, Publications of the Hudson's Bay Record Society, vol. 27 [LondonrThe Hudson's Bay Record Society, 1969], 143-144). Similarly, pulmonary tuberculosis, called consumption, was also present among both Aboriginals and Europeans, and became common among the Aboriginals as time passed (Rich, "The Fur Traders," 50). 2. In 1670 Sydenham described measles as "a disease mainly of young children (infants)..." in London (Creighton, Epidemics in Britain, 635). See Creighton, Epidemics in Britain, 1:660; II: 436, 532. 3. Each generation is measured from the initial time of infection to the point when infectivity ceases. 4. Snow and Lanphear, "European Contact," 25; Haggett, "Invasion," esp. 46-47.The average duration was calculated from the descriptions of ships, movements found in HBCA C.4/1 (Book of Ships' Movements, Microfilm 2ml35), in which entries commence for 1719.The point of final departure from Europe, whether London or the Orkney Islands, was used as it would be the last day of contact between the crew and passengers on European soil. 5.These factors do not preclude the transmission of acute infectious diseases but make them less likely. Given a generational period of between twenty-six and thirty days for smallpox, for instance, at least three susceptible individuals would be required to support that affliction on the average voyage to Hudson Bay, assuming the widest spacing of cases while en route. For measles, more than three generations would be required, given a generational period of seventeen to twenty-one days. Other diseases with shorter periods would have required an even larger number of cases in succession. Nevertheless, while the theoretical number of cases required need not be great, it is important to note that most disease agents of this type could not remain viable in a single individual throughout the long trans-Atlantic voyage. Each additional generational link made the diffusion more complex and less likely, and with few susceptibles on board, if any, the possibility was even more remote. 6. Haggett, "Invasion," 43. 7. Arthur J. Ray, "At the Cutting Edge: Indians and the Expansion of the Land-Based Fur Trade in Northern North America, 1550-1750," in The Early-Modern World-System in Geographical Perspective, edited by Hans-Jurgen Nitz (Stuttgart, Germany: Franz Steiner Verlag, 1993), 319-320; Arthur S. Morton, A History of the Canadian West to 1870-71 Being a History of Rupert's Land (the Hudson's Bay Company) and of the North-West Territory (Including the Pacific Slope) (Toronto: University ofToronto Press, 1939), 53,72; Nute, Caesars of the Wilderness, 147. The progress of this movement into the Petit Nord is illustrated graphically in Heidenreich's series of plates for the Historical Atlas of Canada showing the expansion of the fur trade into the interior (plates 37-39). Innis (The Fur

NOTES PAGES 42 TO 45 257 Trade in Canada, 41-43) also identified a major shift in the French fur trade with the demise of the monopoly in 1663, which led to "a rapid expansion of trade" into the interior. 8. Thwaites, JeswY Relations, 56:157. 9. Ray, Cutting Edge, 319-320; Conrad E. Heidenreich, "Expansion of French Trade, 16671696," in Historical Atlas of Canada, Volume I: From the Beginning to 1800, edited by R. Cole Harris, plate 38 (Toronto: University of Toronto Press, 1987). On the immediate impact of English competition see Thwaites, Jesuit Relations, 57: 21. 10. Reuben Gold Thwaites, ed., New Voyages to North-America by the Baron De Lahontan: Reprinted from the English Edition of i 703, with Facsimiles of Original Title-Pages, Maps, and Illustrations, and the Addition of Introduction, Notes, and Index, 2 vols. (Chicago: A.C. McClurg & Co., 1905), 1:152-153. 11. Pierre Margry, ed., Decouvertes et Etablissementes Des Francais dans L'Quest et dans le Sud de L'Amerique Septentrionale, 1614-1154, 6 vols. (Paris: D.Jouaust, 1876-86), 6: 20-31; Morton, History of the Canadian West, 73,98;Thwaites, New Voyages, 1:316, fn. 1; Norman Anick, The Fur Trade in Eastern Canada Until 1870, National Parks Branch, Manuscript Series, vol. 207 (Ottawa: Parks Canada, Department of Indian and Northern Affairs, 1976), 1: 29,49; 2:255; Heidenreich, "Expansion of French Trade." See Tyrrell (Documents Relating, 386-387) for evidence of the effects of such direct competition on the HBC at Moose Fort. William Warren, who compiled a history of the Ojibway people based on oral tradition, summed up the gradual progress of furtrade expansion by the St. Lawrence traders and its effects on the spatial movements of the Ojibway: "In the early part of the seventeenth century the Ojibways had already commenced the custom of yearly visiting Quebec, and afterwards Montreal, taking with them packs of beaver skins, and returning with the fire-arms, blankets, trinkets, and firewater of the whites. This custom they kept up for many years, gradually curtailing the length of their journeys as the whites advanced toward them step by step" (William W. Warren, History of the Ojibways, Based on Traditions and Oral Statements, reprint edition [Minneapolis: Minnesota Historical Society Press, 1984], 126).When the traders finally established themselves in the Lake Superior district, "these periodical journeys came comparatively to an end." 12.Tyrrell, Documents Relating, xiii; Morton, History of the Canadian West, 116,125-126; HBC Post History "Albany." The first extant Albany journal dates from 1705-06 and the first available York journal dates from 1714-15. Oldmixon's History of Hudson's-Bay, written in 1708, contains details from Thomas Gorst's journal of the early 1670s (Tyrrell, Documents Relating, 371-410). Gorst's journal of 1671, which is in the Guildhall Library in London, was published by Grace Lee Nute (Caesars of the Wilderness,Appendix 2).There are also a few extant HBC letters to London and a few French memoirs written at York during the period of French control. 13. Although the English had already settled Charles Fort, the French had yet to respond by moving in force into the interior at this time. Thus, the conditions of diffusion reflected those of an earlier era, when groups of Aboriginal traders travelled to Canada to trade, rather than the period when the French began to move into the Petit Nord in larger numbers. 14. C. W. Dixon, Smallpox (London:], and A. Churchill Ltd., 1962), 7, 57; Benenson, Communicable Diseases, 350, 352.

258 NOTES PAGES 45 TO 49 15. Benenson, Communicable Diseases, 350-352; Dixon, Smallpox, 171,299-309. 16. Benenson, Communicable Diseases, 352; Ramenofsky, Vectors of Death, 167; Steadman Upham, "Smallpox and Climate in the American Southwest," American Anthropologist 88 (1986). 17. In the 1740s, the historian Charlevoix wrote that it was the French who passed the disease to the Aboriginal people (P. F. X. Charlevoix, History and General Description of New France, six vols., translated by John Gilmary Shea [New York City: John Gilmary Shea, 1866], 3:154). Among the ships arriving at Quebec during the summer and fall of 1669 were two carrying numerous passengers and capable of transporting the disease across the ocean (Marshall, Selected Letters, 353).The first, from La Rochelle, carried men, young women, and families. The second, a Norman ship, carried 150 young women. These ships arrived sometime between late June and October (see Ibid., 348, 353). Before the epidemic ended, the Montagnais and the Algonquin of the nearby Sillery settlement suffered heavy losses, such that the Abenaki replaced them, making Sillery an Abenaki settlement. However, for some unknown reason, the Huron, who lived just outside of Quebec, suffered only a few fatalities, despite a high morbidity rate.ThwaitesJeswzY Relations, 53:124-125; Charlevoix, History, 4:44, fn. 1, quoted in Cook, "Significance of Disease," 500;Thwaites, New Voyages, 1:48. 18.Thwaites,Je?M/( Relations, 53: 43; Duffy, "Smallpox and the Indians," 330. 19.Thwaites JesMrt Relations, 52: 223-224, 227; 53: 93. 20. Ibid., 53:61-69,71,77. 21. Ibid., 56: 155.The French termpeste used in this context may be translated as "pestilence" or "plague," rather than "pest," in order to better convey Father Albanel's intended meaning. 22. Ibid., 56:177. 23.Tanner, Atlas, map 32; Charlevoix, History, 3:153;Thwaites,JiesMi'f Relations, 53:95. 24.Thwaites,Je?M/( Relations, 55:117,119-121. Symptoms included fever, inflammation of the throat, vomited blood, pain in the loins, paralysis, bloody flux, or dysentery, and the loss of both hearing and speech in one case. Father Dablon claimed that "the most common malady was the bloody flux [dysentery], which spread through the whole village, so infecting the atmosphere that even all the dogs were going mad with it, and dying" (Ibid., 55:123).This disease was epidemic in New York in 1669 (Duffy, Epidemics in Colonial America, 215), and may have spread to Sault Ste. Marie. 25.Thwaites,Jesuit Relations, 55: 123. In the past, the name Kilistinon and several similar appellations have been treated as equivalent to the now common identifier Cree. Recent research has called such broad identification into question, and so here I will use the terms used by the Jesuits. 26.Thwaites,_/e5Mi'f Relations, 55: 97; see also Heidenreich, "Expansion of French Trade." 27. Emma H. Blair, ed. and trans., The Indian Tribes of the Upper Mississippi Valley and Region of the Great Lakes, as Described by Nicolas Perrot, Bacqueville de la Potherie, Morrel Marston, andThomas Forsyth, 2 vols. (Cleveland:Arthur H. Clark, 1911-12), 1: 210, 211 James H. Coyne, ed. and trans., Exploration of the Great Lakes 1669-1670 by Dollier De Casson and De Brehant De Galinee - Galinee's Narrative and Map with an English Version, Including All the Map-Legends, Ontario Historical Society Papers and Records, vol. 4 (Toronto:The Ontario Historical Society, 1903), 71.

NOTES PAGES 50 TO 54 259 28.Thwaites Jesuit Relations, 55:125,127,129-131; Charlevoix, History, 3:158. 29.Thwaites Jesuit Relations, 55: 99,125-127; F.J. Paul Hackett,"The Monsoni and the Smallpox of 1737-39," in Pushing the Margins: Native and Northern Studies, edited by Jill E. Oakes, et al. (Winnipeg: Departments of Native Studies and Zoology,The University of Manitoba, 2001). 30.W.Vernon Kinietz, Indians of the Western Great Lakes: 1615-1760 (Ann Arbor: The University of Michigan Press, 1965), 323;Thwaites Jesuit Relations, 54:133-135; Harold Hickerson, The Chippewa and Their Neighbours:A Study in Ethnohistory, revised and expanded edition, edited by Jennifer S.H. Brown and Laura L. Peers (Prospect Heights, Illinois: Waveland Press, 1988), 40-43, 45; Charles E. Cleland,"The Inland Shore Fishery of the Northern Great Lakes: Its Development and Importance in Prehistory," American Antiquity 47, no. 4 (1982): 763. 31. Kellogg, Early Narratives, 105. In the spring of 1660, Radisson and Groseilliers were met by a party of Cristinaux at La Pointe, on the south shore of Lake Superior. When the two men subsequently travelled to the north shore, they met a larger assembly (Nute, Caesars of the Wilderness, 64-65). 32. Nute, Caesars of the Wilderness, 290. 33. Charles A. Bishop, "The First Century: Adaptive Changes among the Western James Bay Cree Between the Early Seventeenth and Early Eighteenth Centuries," in The Subarctic Fur Trade: Native Social and Economic Adaptation, edited by Shepard Krech, III (Vancouver: University of British Columbia Press, 1984), 28; Tyrrell, Documents Relating, 391,392. 34. Lytwyn, Muskekowuck. In 1672, Father Charles Albanel praised Akimiski (Ouabaskou) Island as "abounding in all kinds of animals," based on information gathered from the Aboriginal people (Jesuit Relations, 203-205). 35. Far from being the backwater that it has sometimes been characterized as, the Hudson Bay lowlands in this vicinity was a key area for inter-tribal communications between people from the north and south. In the spring of 1659, a Nipissing named Awatanik journeyed from Lake Superior to James Bay as part of a lengthy trading expedition. Near Akimiski Island he found several, remarkably large, Kilistinon villages located along the coast, some said to be in excess of 1000 men (Thwaites,Je5Wif Relations, 45: 219-229, 231).These villages were doubtless temporary assemblies for the purposes of trade that took advantage of the seasonably plentiful food resources. If Governor Bayley witnessed a "great Mortality" at the Ekwan River in 1674, probably he was observing the effects of the disease among one of these temporary gatherings. 36. Davies and Johnson, Letters from Hudson Bay, 24. 37. HBCA B.3/a/4: 34d. 38. HBCA B.3/a/9; Duffy, Epidemics in Colonial America, 192. 39.HBCAB.3/a/16:18. 40.T. S. Drage, An Account of a Voyage for the Discovery of a North-West Passage by Hudson's Streights, to the Western and Southern Ocean of America, Performed in the Years 1746 and 1747, in the Ship California. Capt. Francis Smith Commander, 2 vols. (London: Jollife, Corbett and Clarke, 1748), 1: 43-44. See also Lytwyn, Muskekowuck, 63. In placing the blame for their sickness on the Inuit, the Cree were demonstrating a disease etiology traditional among many Aboriginal peoples in North America.

260 NOTES PAGES 54 TO 56 41.HBCAB.3/a/18:16,17. 42. In the early 1740s LaVerendrye identified a group of Ojibway-speaking people residing at the latter place as the gens de la Baye d'Esturgeon or Sturgeon Bay people (Adolph M. Greenberg and James Morrison, "Group Identities in the Boreal Forest: The Origins of the Northern Ojibwa," Ethnohistory 29, no. 2 [1982]). Joseph La France, who travelled through Lake of the Woods during 1741-42, also identified these people as the Sturgeon people (Arthur Dobbs, An Account of the Country Adjoining to Hudson's Bay, in the North-West Part of America [London: J. Robinson, 1744], 34). As late as 1814, the Sturgeon people still occupied a position very near Lake of the Woods (Victor P. Lytwyn, "The Hudson Bay Lowland Cree in the Fur Trade to 1821: A Study in Historical Geography," PhD diss., University of Manitoba, 1993,123-124). Unfortunately, French expansion into the Lake of the Woods region under LaVerendrye came after this sickness, and there is no additional evidence to further illuminate it. 43. HBCA B.3/a/21: 8; B.239/a/15: 30d. 44. Morton, History of the Canadian West, 178. 45. Davies and Johnson, Letters from Hudson Bay, 180-181; Harold A. Innis, The FurTrade in Canada:An Introduction to Canadian Economic History, revised edition (Toronto: University ofToronto Press, 1956), 102. 46. HBCA B.239/a/l: 46d, 50d; B.239/a/2:21d, 22,45d, 58; B.239/a/3: 7,19d, 25, 25d, 28d, 32, 33, 33d; William B. Ewart, "Causes of Mortality in a Subarctic Settlement (York Factory, Man.), 1714-1946," Canadian Medical Association Journal 129 (1983): 573. 47.HBCAB.239/a/6:15. 48. K.G. Davies, "Henry Kelsey," in Dictionary of Canadian Biography, Volume 2, 1700-1740 (Toronto: University ofToronto Press, 1969), 308,311,312,313; Henry Epp, ed., Three Hundred Prairie Years: Henry Kelsey's "Inland Country of Good Report" (University of Regina: Canadian Plains Research Center, 1993); Arthur G. Doughty and Chester Martin, eds., The Kelsey Papers (Ottawa: Archives of Canada and the Public Record Office of Northern Ireland, 1929); Richard I. Ruggles, A Country So Interesting: The Hudson's Bay Company and Two Centuries of Mapping, 1670-18 70, Rupert's Land Record Society Series (Montreal and Kingston: McGill Queen's University Press, 1991). 49. Creighton, Epidemics in Britain, 2: 449; HBCA C.4/1: 3d-4. 50. Unfortunately, the crucial Albany journal for 1720-21 is missing. However, Lytwyn ("The Hudson Bay Lowland Cree," 356) concluded that the disease did not reach the Albany River area. 51. HBCA B.239/a/8: 7d. Lytwyn ("The Hudson Bay Lowland Cree," 354-356) considered this an extension of the 1720 smallpox epidemic. 52. HBCA B.239/a/8: 36.The journal covering the summer of 1727 noted the suspicious death of fifty families of Uplanders (HBCA B.239/a/10: 22d), and it is possible that these were also related to epidemic disease.

NOTES PAGES 59 TO 62 261 Chapter Three 1. Unfortunately, LaVerendrye's detailed journal for 1737-38 is missing. In its place, Burpee published a translation of the summary journal, which covers the major events of the period, though not in as great detail. Lawrence J. Burpee, ed., Journals and Letters of Pierre Gaultier De Varennes De La Verendrye and His Sons, with Correspondence Between the Governors of Canada and the French Court, Touching the Search for the Western Sea, The Publications of the Champlain Society, vol. 16 (Toronto:The Champlain Society, 1927), 40. 2. Burpee,J0Mma/5 and Letters, 256-257. 3. Duffy, Epidemics in Colonial America, 53, 54,101;William Johnson, The Papers of Sir William Johnson, 14 vols. (Albany:The University of the State of New York, 19211953), 1:57. 4. Duffy, Epidemics in Colonial America, 78-80; Meinig, Atlantic America, 100-110. 5. By contrast, a century of epidemic disease, warfare, and forced relocation had removed most of the Aboriginal population from the emerging American core, and the few who remained were relegated to small, isolated communities or to areas adjacent to the non-Aboriginal towns (Meinig, Atlantic America, 205-212; James T. Lemon, "Colonial America in the Eighteenth Century," in North America: The Historical Geography of a Changing Continent, edited by Robert D. Mitchell and Paul A. Groves [Totowa, New Jersey: Rowman and Littlefield, 1987], 125). 6. On the role of the Aboriginal people as a conduit for the intercolonial spread of epidemic disease, see Duffy, Epidemics in Colonial America, 69, 75; Reuben Gold Thwaites, The French Regime in Wisconsin i634-1760, in Collections of the State Historical Society ofWisconsin, edited by Rueben Gold Thwaites (Madison: The State Historical Society ofWisconsin, 1902-1908), 17: 172,175; E.B. O'Callaghan, Documents Relative to the Colonial History of the State ofNewYork; Procured in Holland, England and France, 15 vols., edited by John Romeyn Brodhead (Albany, New York: Weed, Parsons and Company, 1853-61), 5: 963, 9:1029,1036; Elizabeth Tooker, "The League of the Iroquois: Its History, Politics and Ritual," in Northeast, edited by Bruce G.Trigger, vol. 15, Handbook of North American Indians (Washington: Smithsonian Institution, 1978), 432; Gordon M. Day, "Nipissing," in Northeast, edited by Bruce G.Trigger, Handbook of North American Indians, 790; and Jean Lunn, "The Illegal Fur Trade Out of New France, 1713-60," in Report of the Annual Meeting of the Canadian Historical Society, 6176 (Toronto: University of Toronto Press, 1939), 61. 7. William J. Eccles, France in America (Vancouver: Fitzhenry andWhiteside, 1972), 120; Heagerty, Four Centuries, 1: 72-73; Harris, "France in North America," 85. 8.The Wea and the Piankeshaw were found along the Wabash River, while the Miami lived at the head of the Maumee River (Tanner, A tlas, 44,172). 9.Thwaites, French Regime in Wisconsin, 17:173,175;White, Middle Ground, x, 217;Tanner, Atlas, 44,172; Emily J. Blasingham, "The Depopulation of the Illinois Indians," Ethnohistory 3 (1956): 384,393.The case of Pied Froid was not unique. In the 1950s, Sister Mary Hilger was told by some Ojibway informants "of men who had been rewarded with chieftainship by the tribe for unusual courage in time of widespread illness, such as smallpox epidemics" (Mary I. Hilger, Chippewa Child Life and Its

262 NOTES PAGES 64 TO 69 Cultural Background, reprint edition [St. Paul: Minnesota Historical Society Press, 1992], 151). 10. Prern, "Disease Outbreaks," 26. 11. Jonathan Carver, Travels Through the Interior Parts of North America, in theYears 1766, 1767, and 1768, reprint edition (Toronto: Coles Publishing Co., 1974); James H. Howard, "Yanktonai Ethnohistory and the John K. Bear Winter Count," Plains Anthropologist 21, Memoir 11, no. 73.2 [1976]: 5, 31;Taylor,"Sociocultural Effects"; William R. Swagerty, "Indian Trade in the Trans-Mississippi West to 1870," in History of Indian-White Relations, edited by Wilcomb E.Washburn, Handbook of North American Indians (Washington, D.C.: Smithsonian Institution, 1988), 353. 12. Donald J. Lehmer, "Epidemics Among the Indians of the Upper Missouri," in Selected Writings of Donald J. Lehmer, edited by W. Raymond Wood (Lincoln, Nebraska: J and L Reprints Co., 1977), 106. 13. W. Raymond Wood, "Plains Trade in Prehistoric and Protohistoric Intertribal Relations," in Anthropology on the Great Plains, edited by W Raymond Wood and Margot Liberty (Lincoln: University of Nebraska Press, 1980), 106. 14. Henry E Dobyns, "Native American Trade Centers as Contagious Disease Foci," in Disease and Demography in the Americas, edited by John W. Verano and Douglas H. Ubelaker (Washington and London: Smithsonian Institution Press, 1992), 215. 15. John M. Cooper, Ethnology of the Otchipwe of Lake of the Woods and Rainy Lake, Anthropological Series (Washington, DC.: The Catholic University of America, 1936), 2. 16. BurpeeJowma/5 and Letters, 96,211, 262-266, 238. 17. Morton, History of the Canadian West, 11; Gary B. Doige, "Warfare Patterns of the Assiniboine to 1809," Master's thesis, University of Manitoba, 1989, pp. 79-80. 18. Burpee,Journals and Letters, 238. 19. Harold Hickerson, The Southwestern Chippewa:An Ethnohistorical Study, American Anthropological Association Memoir 92,1962, 2-3. 20. John E Taylor, "Sociocultural Effects of Epidemics on the Northern Plains: 17351870," Master's thesis, University of Montana, 1982 p. 35. 21. Burpee Journals and Letters, 242,249-255. 22. Ibid., 256-257. 23. Louis-Joseph had been sent with these people in March to help choose a site for a future French post, a post that was later settled on the Saskatchewan River near Cedar Lake. Martin Kavanaugh, La Verendrye His Life and Times, with Many Illustrations and Maps, second edition (Brandon, Manitoba: self-published, 1968), 134. 24. Burpee J0wr«a/s and Letters, 258-259. 25. On this mourning custom see F.J. Paul Hackett, '"A Very Remarkable Sickness':The Diffusion of Directly Transmitted, Acute Infectious Diseases in the Petit Nord, 16701846," PhD dissertation, University of Manitoba, 1999. 26. Burpee,Journals and Letters, 282. 27. Ibid., 242. Another Ojibway group living near the Monsoni also may have been spared the initial round of the disease, only to be caught the following year. The

NOTES PAGES 69 TO 71 263 Sturgeon, who lived on the east side of Lake of the Woods, were afflicted with some sickness at about this time. On June 7,1741, nine canoes of Sturgeon people appeared at Albany Fort from up the Albany River. According to the journal (HBCA B.3/a/30: 48d), they "brought letele [little] goods there crye was that they had been all starvd + sick + some kil'd att ye ware with ye Poets Indns."With no references to the Sturgeon in the Albany journals between 1737 and this date, it is possible that they had been attacked by smallpox, had later gone to war, and had not returned to Albany Fort until three years after the epidemic. 28. Burpee,Journals and Letters; Greenberg and Morrison, "Group Identities," 93. La Verendrye has left a crucial, but undated, manuscript, which provided the name, number of warriors, and linguistic affiliation of Aboriginal groups living west of Lake Huron. This important document was subsequently translated and published by ethnohistorical researchers Adolph Greenberg and Jim Morrison, but has never been dated with any confidence, the authors suggesting a range of from 1730 to 1740. By referring to the posts identified in the document, specifically Fort Bourbon, which was constructed in 1742, and La Verendrye's rank of lieutenant (he was promoted to captain in 1745), I have been able to determine that it was written some time between 1742 and 1745, and therefore after the epidemic (Hackett, "Monsoni"). I am indebted to Patricia Kennedy and Gilles Durocher, of the National Archives in Ottawa, who provided the information relating to La Verendrye's rank. 29. Susan M.Johnston,"Epidemics:The Forgotten Factor in Seventeenth Century Native Warfare in the St. Lawrence Region," in Native People Native Lands: Canadian Indians, Inuit and Metis, edited by Bruce A. Cox, Carleton Library Series (Ottawa: Carleton University Press, 1987), 23,25,27. See also Trigger, Children ofAataentsic, 286-287; Trigger, Natives and Newcomers, 260; Burpee, Journals and Letters, 380-381. 30. Dobyns, Their Number, 311. 31. W. Raymond Wood and Thomas D.Thiessen, eds., Early Fur Trade on the Northern Plains: Canadian Traders Among the Mandan and Hidatsa Indians, 1738-1818,'The American Exploration and Travel Series (Norman: University of Oklahoma Press, 1985), 8,74; Donald J. Lehmer,"The Other Side of the Fur Trade," in Selected Writings of Donald J. Lehmer, edited by W. Raymond Wood (Lincoln, Nebraska: J and L Reprints Co., 1977), 101. 32. Greenberg and Morrison,"Group Identities," 93;Arthur E.Jones, ed., TheAulneau Collection, 1735-1745 (Montreal: Archives of St. Mary's College, 1893), 73. 33. Harold Hickerson, "Ethnohistory of Chippewa of Lake Superior," in Chippewa Indians III (New York: Garland Publishing Inc., 1974), 42-43; Joan A. Lovisek,"The Political Evolution of the Boundary Waters Ojibwa,"in Papers of the Twenty-Fourth Algonquian Conference, edited by William Cowan (Ottawa: Carleton University, 1993). In a similar vein, William Warren noted that following the almost complete decline of the Sandy Lake Ojibway of Minnesota, due to the smallpox epidemic of 1779 to 1783, their numbers were greatly augmented by additions from Lake Superior (Warren, History of the Ojibways, 344). 34. HBCA B.239/a/21: 23d. 35. Ibid., 36. 36.HBCAB.239/a/20;21.

264 NOTES PAGES 72 TO 79 37. Lytwyn, Muskekowuck, 49. 38.Dobyns, Their Number, 15.

Chapter Four 1. Henry Ellis, who travelled to York Factory in 1746-47, observed,"... it must be owned their [the Aboriginal people's] Diseases are but few, and those chiefly arising from Colds, taken after drinking Spiritous Liquors ..." (Henry Ellis, A Voyage to Hudson'sBay by the "Dobbs Galley" and "California" in theYears 1746 and 1747for Discovering a North West Passage, 2 vols. [London: Printed for H.Whitridge, 1748], 2: 186-187). Ellis also observed that "They are pretty much subject to some Disorders of the Breast, but to no contagious Diseases" (Ibid., 188). 2.HBCAA.11/114:124. 3. Howard, "Yanktonai Ethnohistory," 33. 4.These diseases did not, apparently, extend to the Inuit. According to Andrew Graham, who resided at Hudson Bay from 1749 to 1775, "The small pox, measles, and other epidemic disorders frequent in Europe, are unknown amongst these people [the Inuit]" (Williams, Graham's Observations, 230). 5. On September 21,1753, Joseph Isbister noted that "many of our Indians are laid up with a great Cold which has put them off from shooting and also creates a Slow fever. Several of our best Hunters not able to do us any service" (HBCA B.3/a/46: 6d).The Seahorse arrived at Albany on August 28 (HBCA B.3/a/45: 29).This timing suggests that the disease was imported from Europe by the ship. 6.Tanner, Atlas, plate 32. 7.Thwaites, French Regime in Wisconsin, 3: 85. 8. Henry R. Schoolcraft, Summary Narrative of an Exploratory Expedition to the Sources of the Mississippi River in 1820: Resumed and Completed, by the Discovery of Its Origin in Itasca Lake, in 1832, reprint edition (Millwood, New York: Kraus Reprints, 1973), 578. 9. Heagerty, Four Centuries, 1: 38, 74; 2:319;E.Wagner Stearn and Allen E. Stearn, The Effect of Smallpox on the Destiny of the Amerindian (Boston: Bruce Humphries, 1945), 42; Eccles, France in America, 180;Thwaites, French Regime in Wisconsin, 3:67-68; White, Middle Ground, 207.This epidemic foreshadowed the coming era later in the 1750s when, during the Seven Years War, smallpox epidemics spread among the Aboriginal people of the Upper Country due to their participation in the eastern battles during the war. In turn, these epidemics influenced the number of warriors that these tribes were willing to provide their allies, the French (D. Peter MacLeod, "Microbes and Muskets: Smallpox and the Participation of the Amerindian Allies of New France in the Seven Years'War," Ethnohistory 39, no. 1 [1992]: 42-64). Following epidemic years, the number of western warriors declined drastically. 10. HBCA B.239/a/34: 38d, 39,39d; B.239/a/35: 4; B.68/b/l: 9d, 10. ll.J.V Neel, Health and Disease in UnacculturatedAmerindian Populations, in Health and Disease in Tribal Societies, CIBA Foundation Symposium 49 (new series) (Amsterdam: Elsevier/Excerpta Medica/North-Holland, 1977), 171. For an example of excessive mortality during a virgin soil measles epidemic, see Panum's description of the 1846

NOTES PAGES 80 TO 88 265 epidemic on the Faeroe Islands. Peter L. Panum, Observations Made during the Epidemic of Measles on the Faroe Islands in the Year 1846 (New York City: American Public Health Association, 1940). 12. Arthur J. Ray, Indians in the Fur Trade: Their Roles as Trappers, Hunters, and Middlemen in the Lands Southwest of Hudson Bay 1660-1870, reprint edition (Toronto: University of Toronto Press, 1988), 57; Dale R. Russell, Eighteenth-Century Western Cree and Their Neighbours, Archaeological Survey of Canada, Mercury Series (Hull, Quebec: Canadian Museum of Civilization, 1991), 147-48; HBCA B.239/a/34: 36d, 37, 38d. 13. HBCA B.239/a/34: 40d. 14.Wood andThiesen, Early FurTrade, 6;Taylor,"Sociocultural Effects," 37; Caulfield, "Early Measles Epidemics," 539-540;Thwaites, French Regime in Wisconsin, 3: 87; Blasingham, "Depopulation," 379. 15. HBCA B.239/a/35: 38,39; B.239/a/36: 3,14,16d, 18d, 37; B.239/a/37:14d. 16. HBCA B.239/a/42: 24d; B.239/a/44: 41d-42. 17. HBCA B.239/a/42: 36,36d, 40d, 41; B.239/a/44: 2,21,31. 18. MacLeod, "Microbes and Muskets." 19. HBCA B.3/a/58: 36d; B.198/a/9: 26d. 20. HBCA B.3/a/57:18d, 42-42d; B.135/a/40: 2; C.4/1; B.3/a/58:3,3d, 4d; B.135/a/40: 2,3d-4; B.3/a/59: 8d, lOd, 17,19,17d, 2d, 36d; B.3/a/60:10,12d, 14d, 15,15d; Johnson, Papers of Sir William Johnson, 11: 835; Benjamin E Miller and Claire Brackman Keane, Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, third edition (Philadelphia: W.B. Saunders Company, 1983), 886; Duffy, Epidemics in Colonial America, 184. 21. Morton, History of the Canadian West, 270; HBCA B.3/a/62: 34d; B.198/a/15:34d; B.211/a/l:23d,25. 22.HBCAB.198/a/ll:30;B.239/a/70:38d,40;B.86/a/21:25d-26;B.86/a/30:4d, passim; B.3/a/71: 9,10, lOd, 11). 23. HBCA B.198/a/12:24; B.3/a/65: 45,46d, 47,47d, 48; B.59/a/44:29d; B.86/a/19: 31-31d; B.239/a/73: 23; B.239/a/74: 37, 38;Jody F. Decker,'"We Should Never Be again the Same People': The Diffusion and Cumulative Impact of Acute Infectious Diseases Affecting the Natives on the Northern Plains of the Western Interior of Canada 1774-1839,"PhD diss,York University, 1989,p. 156. 24. Benenson, Communicable Diseases, 396-397. 25. Duffy, Epidemics in Colonial America, Chapter VI. 26. Benenson, Communicable Diseases, 245-247; Alfred W. Crosby, "Influenza," in The Cambridge World History of Human Diseases, edited by Kenneth F. Kiple (Cambridge: Cambridge University Press, 1993), 807. 27. Type A influenza exists in animal reservoirs, although transmission of the virus occurs almost exclusively between humans. It is thought that periodic antigenic shifts that create new subtypes, to which all humans are susceptible, are caused by recombination of human and animal (usually swine and duck) antigens (Benenson, Communicable Diseases, 247).

266 NOTES PAGES 88 TO 95 28. Benenson, Communicable Diseases, 246; Crosby, "Influenza," 808; John S. Mackenzie, "Possible Future Changes in the Epidemiology and Pathogenesis of Human Influenza A Virus Infections," in Changing Disease Patterns and Human Behavior, edited by N.E Stanley and R.A.Joske (London: Academic Press, 1980), 144. 29. Burnet and White, Natural History, 125,209. 30. Crosby, "Influenza," 808, 809; William Currie, An Historical Account of the Climates and Diseases of the United States of America (Philadelphia :T. Dobson, 1792), 100-101; 103n. 31. In 1771, for instance, the Seahorse brought an ARD to York Factory, having taken fifty-nine days to sail from the Orkneys to Hudson Bay, and other crossings implicated in the trans-oceanic diffusion of disease were similarly lengthy. HBCA C.4/1. 32. HBCA B.3/a/63: 4d, 5d, 7, 9; B.239/a/62: 4d, 21. 33. HBCA B.239/a/65: 50; C.4/1:10d-ll; C. 1/104:24d;B.239/a/66:14d, 15d, 21,25d, 29, 30, 30d, 39, 45, 52; B.198/a/15:16d, 18, 21d, 40, 52; B.42/a/83: 26, 27d, 32, 32d, 33, 38. 34. HBCA B.3/a/75:1; C.4/1; B.86/a/32:16d, 21d; B.78/a/4; B.239/a/76: 9,10. 35. M.J. Holmes andT. R.Allen,"Viral Respiratory Diseases in Isolated Communities:A Review," Bulletin of the British Antarctic Survey 35 (1973); D.A.J. Tyrrell, "Aspects of Infection in Isolated Communities," in Health and Disease in Tribal Societies, Ciba Foundation Symposium 49, new series (Amsterdam: Elsevier/ Excerpta Medica/ North-Holland, 1977), 142; Creighton, Epidemics in Britain, 2: 431. For an examination of the phenomenon see Cliff et al., Island Epidemics, 387-390. 36. Burnet and White, Natural History, 132,133.

Chapter Five I.Michael K.Trimble, "Chronology of Epidemics Among Plains Village Horticulturalists: 1738-1838," Southwestern Lore 54 (1988): 7. 2.W. George Lovell, Conquest and Survival in Colonial Guatemala:A Historical Geography of the Cuchumatan Highlands, 1500-1821 (Montreal: McGill-Queen's University Press, 1985), 154;Juan A.Villamarin and Judith E.Villamarin, "Epidemic Disease in the Sabana de Bogota, 1536-1810," in "Secret Judgements of God": Old World Disease in Colonial Spanish America, edited by Noble David Cook andW. George Lovell, The Civilization of the American Indian Series (Norman and London: University of Oklahoma Press, 1992), 115,128-129. 3. Joseph Robson, An Account ofSixYears Residence in Hudson's-Bay, From 1733 to 1736, and 1744 to 1747 (London: Printed for J. Payne and J. Bouquet, 1752), 21. 4. Ross Cox, The Columbia River: Or Scenes and Adventures During a Residence ofSixYears on the Western Side of the Rocky Mountains Among the Various Tribes of Indians Hitherto Unknown; Together with "A Journey Across the American Continent," 2 vols., third edition (London: Henry Colburn and Richard Bentley, 1832), 284; quoted in Robert T. Boyd, "Smallpox in the Pacific Northwest:The First Epidemics," BC Studies 101 (1994): 24. 5. Donald B. Cooper, Epidemic Diseases in Mexico City, 1761-1813, Latin American Monographs, vol. 3 (Austin: Institute of Latin American Studies,The University of Texas, 1965), 99-102.

NOTES PAGES 95 TO 100 267 6. Sherburne E Cook, "The Smallpox Epidemic of 1797 in Mexico," Bulletin of the History of Medicine 7, no. 8 (1939): 940. 7. Cooper, Epidemic Diseases, ix, 56, 68-69, 86; Dobyns,"Estimating," 441; Ramenofsky, Vectors of Death, 130; Ann L.W. Stodder and Debra L. Martin, "Health and Disease in the Southwest before and after Spanish Contact," in Disease and Demography in the Americas, edited by John W.Verano and Douglas H. Ubelaker (Washington and London: Smithsonian Institution Press, 1992), 66; Marc Simmons, "New Mexico's Smallpox Epidemic of 1780-1781," New Mexico Historical Review 41 (1966): 321-323. 8. Ray, Indians in the Fur Trade, 87-89; Frank Raymond Secoy, Changing Military Patterns on the Great Plains (17th Century Through Early 19th Century), Monographs of the American Ethnological Society (Seattle and London: University ofWashington Press, 1966), 2,105; William R. Swagerty, "Indian Trade in the Trans-Mississippi West to 1870," in History of Indian-White Relations, edited by Wilcomb E.Washburn, Handbook of North American Indians (Washington, D.C.: Smithsonian Institution, 1988); John C. Ewers, The Horse in Blackfoot Indian Culture, Bureau of American Ethnology (Washington, D.C.: Smithsonian Institution Press, 1955). 9.Trimble, "Epidemiology on the Northern Plains," 79. 10. Ramenofsky, Vectors of Death, 167; Swagerty, "Indian Trade," 353; Ewers, Horse, 3,171172; Boyd, "Smallpox in the Pacific," 25; Wood, "Plains Trade," 106; Frank Gilbert Roe, The Indian and the Horse (Norman:The University of Oklahoma Press, 1968), 178,379; Diamond Jenness, The Indians of Canada, reprint edition (Toronto: University of Toronto Press, 1989), 129. During the eighteenth century, the trade in horses influenced the Cree and Assiniboine to join the Blackfoot in their warfare with the horse-rich Shoshone, Kutenai, and Flathead (Doige, "Warfare Patterns," 128,132, 151). In turn, the Blackfoot fought battles on many fronts and travelled great distances once they had acquired horses, in one instance raiding the Spanish in what is now the southern United States, but also crossing the Rockies and, later on, fighting the Cree and Assiniboine to the east (Ewers, Horse, 171-172). Conversely, Ewers noted that Blackfoot oral tradition claims the Shoshone as their only enemy during the prehorse period. Farther east, at least by the end of the eighteenth century, the desire for horses led the Cree to begin stealing from the Mandan and Hidatsa, from whom they had long obtained horses through trade (John S. Milloy, The Plains Cree: Trade, Diplomacy and War, 1790 to 1870, Manitoba Studies in Native History, vol. 4, reprint edition [Winnipeg: University of Manitoba Press, 1990], 58). 11. Edward Umfreville, The Present State of Hudson's Bay..., reprint edition, edited by W. Stewart Wallace (Toronto: Ryerson Press, 1954), 47-48. 12. J. B. Tyrrell, David Thompson's Narrative of His Explorations in Western America 17841812, Publications of the Champlain Society, vol. 12 (Toronto:The Champlain Society, 1916), 336-337. 13. HBCA B.239/a/80: 74. 14.Tyrrell, Thompson's Narrative, 321,322; E. E. Rich and A. M.Johnson, eds., Cumberland and Hudson House Journals 1775-82, Second Series, 1779-82, two vols., Publications of the Hudson's Bay Record Society, vols. 14-15 (London:The Hudson's Bay Record Society, 1952), 223-224, 262; Richard Glover, "Introduction," in E. E. Rich and Alice M.Johnson, eds., Cumberland and Hudson House, viii.

268 NOTES PAGES 100 TO 106 15. HBCA B.49/a/12:14d, 16,17,18,19,19d; B.239/a/80: 63-64, 68. 16. HBCA B.239/a/80: 79d, 90d, 91, 93-93d. 17.HBCAB.198/a/28:3. 18. Ibid. At Cumberland House William Tomison took the added precaution of disinfecting the goods from Hudson House with sulphur, along with isolating the victims (C. Stewart Houston and Stan Houston, "The First Smallpox Epidemic on the Canadian Plains: In the Fur-Traders'Words," Canadian Journal of Infectious Disease 11, no. 2 [March/April 2000]: 113-114). 19. HBCA B.239/a/83: 5,36d. 20. HBCA B.198/a/28:14d-15. 21. Ibid., 15. 22. R. Douglas, andJ. N.Wallace, eds. and trans., TwentyYears ofYork Factory 1694-1714: Jeremie's Account of Hudson Straight and Bay (Ottawa: Thorburn and Abbott, 1926), 35, fn. 55. 23.HBCAB.49/a/12:17. 24. HBCA B.239/a/80: 84, 87. 25.HBCAB.198/a/29:26. 26. Ibid., 44d. See also HBCA B.198/a/29: 36-36d. 27. For examples see HBCA B.198/a/29: 34d, 36-36d, 37, 38-38d, 45-46d. 28. Donald B. Gunn and Charles Tuttle, History of Manitoba from the Earliest Settlement to 1835 (Ottawa: Maclean, Rogers and Co., 1880), 87. 29. HBCA B.198/a/29: 44d; B.3/a/84: 32d, 52; E.E. Rich and A.M.Johnson, eds., Moose Fort Journals 1783-85, Publications of the Hudson's Bay Record Society, vol. 17 (London:The Hudson's Bay Record Society, 1954), 294. 30.Tyrrell, Thompson's Narrative, 322-323; Richard Glover, ed., David Thompson's Narrative 1784-1812, Publications ofThe Champlain Society, vol. 40 (Toronto:The Champlain Society, 1962), 236. 31.Tyrrell, Thompson's Narrative, 109,336-337. 32. Warren, History of the Ojibways, 17, 45-46,138,260; Henry R. Schoolcraft, Information Respecting the History, Conditions and Prospects of the Indian Tribes of the United States: Collected and Prepared Under the Direction of the Bureau of Indian Affairs, Department of the Interior, 6 vols., reprint edition (NewYork City: Paladin Press, 1969),V: 426,427; Lovisek, "Political Evolution," 293-294. For more on Flatmouth see Leo Waisberg, "An Ethnographic and Historical Outline of the Rainy River Ojibway," in An Historical Synthesis of the Manitou Mounds Site on the Rainy River, Ontario, edited by W. C. Noble (Manuscript in National Historic Sites Branch: Parks Canada, 1984), 202204. 33. Warren, History of the Ojibways, 179, 261. 34. Ibid., 179,261. 35. Ibid., 261. 36. Warren was not the only one to identify this path of diffusion. Alexander Mackenzie noted that "it was generally supposed to be from Missouri, by a war

NOTES PAGES 106 TO 109 269 party..." (W. Kaye Lamb, ed., The Journals and Letters of Sir Alexander Mackenzie [Toronto: Macmillan of Canada, 1970], 75). Similarly, Dr. Douglass Houghton wrote that this was the common belief of the Ojibway who had been afflicted by this disease. He observed that: "The most western bands of Chippewas relate a singular allegory of the introduction of the smallpox into their country by a war-party, returning from the plains of the Missouri, as nearly as information will enable me to judge, in the year 1784" (Schoolcraft, Summary Narrative, 579). Although Houghton had mistaken the date of infection, these accounts confirm Flatmouth's statements to Warren. 37. Warren, History of the Ojibways, 40,261. 38. Elliott Coues, ed., New Light on the Early History of the Greater Northwest, The Manuscript Journals of Alexander Henry and of David Thompson, 1799-1814,2 vols., reprint edition (Minneapolis: Ross and Haines, 1965), I: 46. 39. John C. Ewers, ed., Five Indian Tribes on the Upper Missouri: Sioux, Arickaras, Assiniboines, Crees, Crows (Norman: University of Oklahoma Press, 1961), 115. 40. Donald Gunn, "Indian Remains Near Red River Settlement," in Annual Report of the Smithsonian Institution (Washington: Smithsonian Institution, 1867), 399-400. 41. On the unburied remains, see, for example, Gunn andTuttle, History of Manitoba, 87; Lamb Journals and Letters, 122; HBCA E.3/3: 69; Umfreville, Present State, 8; and Taylor, "Sociocultural Effects," 39. 42. HBCA B.78/a/7: 24;Waisberg, "Ethnographic and Historical Outline," 126-130,243, 133; NAG MG 21 Add. Mss. 21758: 213;Warren, History of the Ojibways, 262. 43. Lamb,Journals and Letters, 103,107. 44. Ibid., 103,107, 111. 45. Although Douglass Houghton gave a date of 1770 for this outbreak, it was almost certainly part of the epidemic of 1779 to 1783 (Schoolcraft, Summary Narrative, 579). 46. Warren, History of the Ojibways, 262, 344; Reuben Gold Thwaites, ed.,"Cadotte's Letter to Gautier," in Letters from Southwestern Posts (Wisconsin Historical Collections, 9,1888), 170. Cadotte's letter states that:"7o«5 les sauvages dufond du Lac, lac de la Pluie, lac des Sables et autres endroits circonvoisine sont marts de la picotte" (NAC MG 21 Add. Mss. 21758: 213). 47. Warren, History of the Ojibways, 344. 48. Ibid., 262. 49. Louis-P. Cormier, ed.Jean-Baptiste Perrault Marchand Voyageur Parti de Montreal le 28e de Mai 1783 (Montreal: Boreal Express, 1978), 51. Perhaps not surprisingly, then, a Captain Robertson at Michilimackinac wrote to Lieutenant-Governor Haldimand in July of 1784, stating that he had not had a single Aboriginal visitor from the Mississippi although he had had several from Lake Superior and Lake Huron (NAC MG 21 Add. Mss. 21758: 268). 50. Warren, History of the Ojibways, 262. 51. Schoolcraft, Summary Narrative, 579. 52. R. Douglas, ed., Nipigon to Winnipeg:A Canoe Voyage Through Western Ontario by Edward Umfreville in 1784 (Ottawa: Commercial Printing, 1929), 41.

270 NOTES PAGES 109 TO 113 53. NAG MG 19, C4,Vol. 53: 3. 54.HBCAB.107/a/24:10. 55. HBCA B.78/a/7: 21-21d. 56. HBCA B.78/a/8: 24d. 57. HBCA B.78/a/4: 5d. 58. John Long, Voyages andTravels of an Indian Interpeter and Trader, reprint edition (Toronto: Coles Publishing Company, 1974), 45,97-98; James Mooney and Thomas Cyrus, Handbook of Indians of Canada, reprint edition (Toronto: Coles Publishing Co., 1971), 379;Victor P. Lytwyn, The FurTrade of the Little North: Indians, Pedlars, and Englishmen East of Lake Winnipeg, 1760-1821 (Winnipeg: Rupert's Land Research Centre, 1986), 20-21, fn. 15. Chauvignerie in 1736, LaVerendrye in ca. 1742, and unnamed Montreal fur traders in 1766-67 all located the Ouases at Kaministiquia (O'Callaghan, Documents Relative, 9:1054; Greenberg and Morrison, "Group Identities"; PAM MG 10 F4, Microfilm reel M131,"A list of Indians living in the inhabited part of the Province of Quebec, as well as those residing in the South and Northwestern part of Canada as they stood in the years 1766 and 1767"). 59. HBCA B.78/a/8: 24d; B.78/a/8: 25d; B.78/a/10: 5; B.78/a/9:13; Charles A. Bishop, The Northern Ojibwa and the Fur Trade: An Historical and Ecological Study, Culture and Communities: A Series of Monographs (Toronto: Holt Rinehart and Winston of Canada Limited, 1974), 268. 60. Overall, the impact of the epidemic on Sheawaquannep's people was probably less than on other nearby bands that were universally susceptible. In 1784, James Sutherland of the HBC made a journey to Pashkokogan Lake from Gloucester House and met the two main trading captains from that lake, Sheawaquannep and Connamatchie, and their adherents, which included fifteen men in addition to women and children (HBCA B.78/a/ll: 5d). Moreover, the Canadian returns at that lake in 1783-84 amounted to 1200 MB, not an inconsiderable amount (HBCA B.78/ a/11: 6), and Pashkokogan Lake was one of only three Canadian houses in the country about Gloucester House not abandoned in 1784 (HBCA B.78/a/10: 3d). Sheawaquannep's gang has been identified as being one of the largest trading at Gloucester House and later Osnaburgh House, consistently bringing twelve to fourteen canoes to trade prior to and long after the epidemic (Bishop, The Northern Ojibwa, 268). An excellent example of selective mortality due to prior exposure may be found among the Fall, or Atsina, people who, having been struck severely during the epidemic of 1779 to 1783, suffered substantial losses among their youngest people in 1801. Peter Fidler wrote, "The smallpox the same spring [1801] also came amongst them from the Southwards towards the Mississoury river + cut off 100 principally of Children" (HBCA E.3/2: 71). 61. HBCA B.78/a/9: 21d, 23. 62. HBCA B.3/a/73:40,15d, 29d, 39d. 63. HBCA B.78/a/12:19d; Lytwyn, FurTrade, 30; Laura L. Peers, The Ojibwa of Western Canada, Manitoba Studies in Native History (Winnipeg: The University of Manitoba Press, 1994), 30. 64. HBCA B.78/a/8: 25d. 65. HBCA B.78/a/10: 3; B.78/a/16:31d; Lytwyn, FurTrade, 48.

NOTES PAGES 66 TO 121 271 66.HBCAB.198/a/28:24. 67 HBCA B.78/a/9: 7,12d, 13d. 68. HBCA B.78/a/7: 25d-26. 69. HBCA B.78/a/8: 25d-26; B.78/a/10: 3d; B.78/a/l 1:13. 70. Lytwyn, Muskekowuck, 164-165. 71. HBCA B.135/B/12: 26d-27. 72. HBCA B.86/a/36: 52d; B.3/a/80: 20d; 21. 73.William B. Ewart,"Thomas Hutchins and the HBC:A Surgeon on the Bay," The Beaver (August/September 1995). 74. HBCA B.3/a/81:1-ld; B.3/a/81: 2d; B.3/a/82: 9d-10; B.3/a/82: 9d. 75. Crosby, "Influenza," 809; Burnet and White, Natural History, 203; Creighton, Epidemics in Britain, 2: 363, 364. 76. HBCA C.l/1047: 7, 33d; C.4/1. 77. HBCA B.3/a/82: 46. 78. Lytwyn, Muskekowuck, 10-11. 79.HBCAB.198/a/33:39. 80. Lytwyn, Muskekowuck, 165,171. 81. HBCA B.3/a/81: 29; B.198/a/33: 34, 34d. 82. HBCA B.3/a/83: 2. 83. Morton, History of the Canadian West, 424. 84. HBCA A.I 1/44:162d. 85. Shepard Krech, III, "Disease, Starvation, and Northern Athapaskan Social Organization,'Mmen'ow Ethnologist 5, no. 4 (1978): 712; Harris, "Voices of Disaster," 605,606, 615; Lovell, Conquest and Survival, 156-159;Taylor,"Sociocultural Effects," 38-39;Trimble, "Chronology," 8.

Chapter Six 1. Lytwyn, FurTrade, 84; cf. Arthur J. Ray, "Bayside Trade, 1720-1780," in Historical Atlas of Canada, Volume I: From the Beginning to 1800, edited by R. Cole Harris (Toronto: University of Toronto Press, 1987), Plate 60. 2. For a brief period, between 1799 and 1805, a second, major Canadian company, called the XY or New Northwest Company, traded in the Northwest from Montreal (Lytwyn, FurTrade, 82).This heightened the competition for furs, and contributed to the tremendous growth in the number of posts in both the Grand Nord and the Petit Nord at this time (D.Wayne Moodie, "The Trading Post Settlement of the Canadian Northwest, 1774-182 \" Journal of Historical Geography 13, no. 4 [1987]: 360-374). Following the merger of the two Canadian companies in 1805, the number of posts located in the Petit Nord declined significantly for several years, and then increased once again about a decade later (Moodie, "Trading Post Settlement," 366).

272 NOTES PAGES 121 TO 124 3. Lytwyn, FurTrade, 98,101-102,104; 114,115;Victor P. Lytwyn,"Transportation in the Petit Nord," in Historical Atlas of Canada, Volume I: From the Beginning to 1800, edited by R. Cole Harris (Toronto: University ofToronto Press, 1987), plate 63; Moodie, "Trading Post Settlement," 364, 368. 4. E.E. Rich, Hudson's Bay Company, 1670-1870, 3 vols. (Toronto: McClelland and Stewart, 1958-60), II: 291, 314, 315. 5.Trimble,"Chronology," 10;Trimble,"Epidemiology on the Northern Plains," 36-37, 39. 6. David J.Wishart, The FurTrade of the American West 1807-1840: A Geographical Synthesis (Lincoln: University of Nebraska Press, 1979), 41-42;A. P. Nasatir, "Anglo-Spanish Rivalry on the Upper Missouri (Part I)," Mississippi Valley Historical Review 16 (1929); Nasatir, Before Lewis and Clark; Harold A. Innis, The FurTrade in Canada, revised paperback edition (Toronto: University ofToronto Press, 1964), 190-192. For example, Donald McKay, a Canadian trader stationed on the Assiniboine River, traded in the Hidatsa villages in April of 1781, just prior to the smallpox epidemic (HBCA E.223/ 1:20-34). 7. Duffy, Epidemics in Colonial America, 178; Currie, Historical Account, 4-5, 94,96, 99. 8. However, Cliff et al. suggested that endemicity in the northeastern United States came much later, during the nineteenth century (Andrew D. Cliff, Peter Haggett, and Mathew Smallman-Raynor, Deciphering Global Epidemics: Analytical Approaches to the Disease Records of World Cities, Cambridge Studies in Historical Geography [Cambridge: Cambridge University Press, 1998], 44). 9. Lemon, "Colonial America," 122-123; Ralph H. Brown, Historical Geography of the United States (NewYork City: Harcourt, Brace and Co., 1948), 99-100,103; Meinig, Atlantic America, 348,363. 10.J.R. Borchert,"American Metropolitan Evolution," Geographical Review 57 (1967): 314,315. 11. Even as late as 1800, Philadelphia (69,403), New York (60,489), Baltimore (26,114), and Boston (24,937) all had insufficient populations to host the crowd diseases endemically (Meinig, Atlantic America, 364). 12. Currie, Historical Account, 65,99. 13. Caulfield, "Early Measles Epidemics," 548, 555. 14. For instance, see Map 3 for the pattern of measles and smallpox epidemics in Boston up to 1800. 15. As of the initial federal census of 1790, there were an estimated 100,000 settlers living beyond the Appalachian Mountains. By 1800 there were 325,000 Americans living in the interior states of Kentucky and Tennessee alone, and the lands along the Ohio and south of the lower Great Lakes were beginning to fill with non-Aboriginal people. Twenty years later there were some two million people living in the interior, almost one quarter of the nation's total population. Meinig, Atlantic America, 287,348, 364365; Samuel B. Hilliard,"A Robust New Nation, 1783-1820," in North America: The Historical Geography of a Changing Continent, edited by Robert D. Mitchell and Paul A. Groves (Totowa, New Jersey: Rowman and Littlefield, 1987), 149,165. 16. Crosby, "Influenza," 809.

NOTES PAGES 125 TO 129 273 17.This included "colds" in 1784,1785,1787, and 1792.There was also an outbreak of "sore throats" in 1787. Of the twelve years between 1784 and 1795, during at least six there was an acute infectious disease in the Albany area, for a total of seven separate sicknesses. 18.The sicknesses at York were bowel complaints among the HBC men in August of 1786, and an epidemic disorder among the Lowland Cree in the fall of 1793 (HBCA B.239/a/86: 52d, 53d; B.239/a/96: 25-25d). Neither of these appears to have been severe. The illnesses at Severn were also minor, and included a widespread ailment that struck the Homeguard Cree and the Winisk River people during the winter of 178990, some unidentified ailment forcing the Aboriginal people to remain on the Severn plantation in December of 1794, and a sickness among both the Aboriginal and HBC people at Severn in August of 1795 (HBCA B.198/a/40: 33d, 34d, 35; B.198/a/46: 18; B.198/a/47: 5). As at York Factory, these do not seem to have been mortal in any case. 19. These included a severe disorder among the York Homeguard Cree in the fall of 1793 (HBCA B.239/a/96: 25-25d), and an epidemic that broke out among the Albany people the following fall (HBCA B.3/a/96: 5, 6d, 26d, 27d). 20. HBCA B.78/a/12: 21d; B.78/a/16: 27d, 28, 29, 31d; B.155/a/l: 2. 21.White, Middle Ground, 418; Stearn and Steam, Effect of Smallpox, 49;Tanner, Atlas, 173, map 32. 22. HBCA B.145/a/2: 4d-5. 23. Ibid., 6. 24. Ibid., 6-6d. 25. Ibid., 15d,24d-25,26. 26. HBCA B.145/a/2: 24d-26. 27. Ibid., 29d; HBCA File "Suweawamenica Settlement." 28.HBCAB.155/a/4:26d. 29. HBCA B.78/a/18: passim, 18d, 19,20d; B.86/a/43:16,45,47d; B.86/a/45: 3, 8,9, 12d, 15d,32. 30. Crosby, "Influenza," 809; Currie, Historical Account, 2. 31.HBCAB.166/a/l:2d. 32. HBCA B.105/a/3: Id, 17d, 32. 33. HBCA B.3/a/96: 26d, 27,27d. 34.This included outbreaks of "colds" or "catarrh" in 1796,1804,1805,1806,1807, and 1809. Some sicknesses that broke out in the Petit Nord during this period do not clearly indicate a source by their timing. For example, there was an unknown disease circulating among the Aboriginal people to the north ofYork Factory in the spring of 1798, and epidemic colds among the Albany men and the Lowland Cree in February of 1800 (HBCAB.3/a/101:18d;B.3/a/103:13d, 21d). 35.These included a sickness among the HBC men in July of 1798, another among the crews from the inland posts in June-July of 1800, and colds and sore throats among the York men and some Aboriginal people in July 1802 (HBCA B.239/a/102: 50, 52; B.239/a/104: 45,45d, 46, passim; B.239/a/106: 37d, 38d, 39d).

274 NOTES PAGES 129 TO 133 36. HBCA B.3/a/108: 3d; B.3/a/109:17d, 18; C.4/1:16d-17; B.3/V97: 32, 33d, 34. 37. As well, in September-August of 1808, sickness broke out among many of the HBC men travelling from Osnaburgh House to Sandy Lake, and those at Albany, and subsequently among the Albany Cree (HBCA B.193/a/3: 2d, 3,3d;B.3/a/lll: 5,12, 18;B.123/a/13:2d). 38. HBCA B.3/a/104: 20,20d, 21,21d; B.3/a/106: 25d, 43d; B.123/a/8: 32. 39. HBCA B.135/a/83: 28, 28d. 40. HBCA B.198/a/49:44b; B.3/a/97: 32,33d, 34, 34d; B.135/a/84:44; B.3/a/98:11, 3d, 4d, 6,12d; B.123/a/3:14d; B.135/a/84: 47d. 41. HBCA B. 123/a/3:10; B.3/b/34: 5d-6, 8d; B.86/a/52: 4d. 42. HBCA B.64/a/2:14d; B.105/a/4: 20,20d. 43. HBCA B.64/a/3: 3, 7d, 8,16. 44. HBCA B.192/a/l: 4d, 5, 5d, 7, 7d, 8, 8d, 9. 45. HBCA B.3/a/104: 20, 20d, 21, 21d; B.135/a/88a: 78; B.23/a/8: 5d.The identity of this disease is not clear. Although referred to by John Hodgson and others as a bowel disease (and as the bloody flux), it seems to have been much more. At one point Hodgson suggested that the symptoms were similar to those of yellow fever (ICD-10 A95), an extremely severe, acute, infectious viral disease transmitted by mosquitoes, generally Aedes aegypti (Benenson, Communicable Diseases, 519). However, victims of yellow fever do not typically experience problems with excessive loose bowel movements, but instead suffer from a myriad of other symptoms, including fever and headache, both of which plagued the HBC trader (HBCA B.3/a/23, 24). 46. Tanner, Atlas, 173, map 32. The evidence for the presence of smallpox at Lake of the Woods was not cited, but there is certainly sufficient evidence of the disease among the Sioux at this time. Taylor ("Sociocultural Effects," 45-47) suggested that at least three major epidemics may have been circulating on the northern plains between 1800 and 1803, including undifferentiated respiratory infections, smallpox, and a possibly concurrent (with the smallpox) epidemic of measles. 47.HBCA B.3/a/106:25d, 43d; B.123/a/8:32,33; B.135/a/91:38d, 39;Tanner, Atlas, map 32. 48. Lytwyn, Fur Trade, 113; Metropolitan Toronto Reference Library, Baldwin Collection, George Nelson MS, Journal, 1805-06:16. 49. Coues, New Light, 1: 343. 50. Louis F. R. Masson, ed., Les Bourgeois de la Compagnie Du Nord-Ouest: Recits de Voyages, Lettres et Rapports Inedits RelatifAu Nord-Ouest Canadien, reprint edition, 2 vols. (New York: Antiquarian Press, 1960), 1: 371. 5I.Trimble,"Epidemiology on the Northern Plains," 52-53; Lucy Kramer Cohen,"Swift Bear's Winter Count," Indians at Work 9, no. 5 (1942): 19; NAG MG 19 A8,Vol. 8 (Part III)—David Thompson Papers: 278,279. Thompson wrote that the Kutenai were "3 days march hence + that many y them are very sick + several children dead, it seems by the Hooping Cough." 52. Benenson, Communicable Diseases, 347-348; Ramenofsky, Vectors of Death, 149-151; Miller and Keane, Encyclopedia, 1213-1214.

NOTES PAGES 134 TO 141 275 53.HBCAB.39/a/15:8. 54. Duffy, Epidemics in Colonial America, 179; Creighton, Epidemics in Britain, II: 670; Currie, Historical Account, 6, 99. 55. HBCA B.155/a/27: 6d, 8,10,13. 56. HBCA B.239/a/118: Id, 2, 3d, 5,19.

Chapter Seven 1. It may also have crossed the Rockies into the Pacific Northwest. See Robert T. Boyd, "The Pacific Northwest Measles Epidemic of 1847-48," Oregon Historical Quarterly 95, no. 1 (1994): 9. 2.Taylor,"Sociocultural Effects," 78; Ray, Indians in the FurTrade, 106-110; D. Morley, "Severe Measles," in Changing Disease Patterns and Human Behavior, edited by N.F. Stanley and R.A.Joske (London:Academic Press, 1980), 117; Panuni, Observations; Ramenofsky, Vectors of Death, 161; Francis L. Black, et al., "Epidemiology of Infectious Disease:The Example of Measles," in Health and Disease in Tribal Societies, CIBA Foundation Symposium 49 (new series) (Amsterdam: Elsevier/Excerpta Medica/ North-Holland, 1977): 120; F.J. Paul Hackett,"The 1819-20 Measles Epidemic: Its Origin, Diffusion and Mortality Effects Upon the Indians of the Petit Nord," Master's thesis, University of Manitoba, 1991, p. 132. 3. HBCA B.129/a/9: 6d, 7d, 8d, 9d. On this epidemic see Hackett," 1819-20 Measles Epidemic." 4.HBCAB.51/a/3:2. 5. HBCA A.10/2: 242; B.231/a/4: 27d. 6. Gordon Charles Davidson, The North West Company, University of California Publications in History (Berkeley: University of California Press, 1918), 204, 238;W. Stewart Wallace, ed., Documents Relating to the North West Company, Publications of the Champlain Society, vol. 22 (Toronto:The Champlain Society, 1934), 1. 7. Nicholas Garry, "Diary of Nicholas Garry...," Transactions of the Royal Society of Canada, Series 2, 6, section 2 (1900): 116. 8. HBCA B.105/a/27: 28; B.105/a/7: 29d; Edwin James, ed., A Narrative of the Captivity and Adventures of John Tanner During Thirty Years' Residence Among the Indians in the Interior of North America (London: Baldwin and Craddock, 1830), 255. 9.HBCAB.105/a/7:36d. lO.Waisberg,"Ethnographic and Historical Outline," 127;ThomasVennum Jr., Wild Rice and the Ojibwa People (St. Paul: Minnesota Historical Society, 1988), 143,163; HBCA B.105/a/7: 86d.The NWC men were consistent in blaming the HBC for the importation and diffusion of the sicknesses, as a means of antagonizing the Aboriginal people against their rivals. For instance, near Edmonton House, they "tried every means to [exasperate] the natives against us [the HBC], as well as against the Settlers at Red River, by impressing upon their mind that it was the Settlers who first brought those diseases to Red River, and that it was the English (as we are called) who brought them from there to this part of the country...." (HBCA B.60/e/3: 7. See also Masson, Bourgeois, 130.)

276 NOTES PAGES 141 TO 148 11. HBCA B.105/a/7: 38d, 43,49d, 50, 51d, 54d. 12.HBCAB.155/a/32:4d. 13. HBCA B.64/e/2: 2. 14.HBCAB.105/a/7:56d. 15. HBCA B.64/a/8: 4d; B.64/a/7: 20; B.64/a/8:20; B.64/e/2: 4d. 16. HBCA B.107/e/3: 2; B.107/a/25:12; B. 123/e/32d. In 1837-38 Charles McKenzie noted that the population of Lac Seul "is greatly on the increase since 1821... .At the above quoted date the population was small the Measles having carried off 7/10 of the natives a few years before which is the cause that there is not a very old man among them" (HBCA B.107/a/16: 28). 17. HBCA B.107/e/3: 2; B.107/a/6:26; B.3/e/15: 3; B.107/a/16: 28. 18. Bishop, Northern Ojibwa, 159-162. 19. Lytwyn, FurTrade, 159; HBCA B.107/e/2:2d; HBCA Post Histories "Escabitchewan," "Red Lake"; B.107/e/2: 3; B.107/a/2: 5; B.107/a/9: 24d; B.105/a/9: 68; B.107/a/12: 10d;B.107/a/13:4. 20. HBCA B.64/e/2: 3. 21. HBCA B.64/a/8: 3, 6d, 7, 7d; B.64/e/2: 4. 22. HBCA B.16/e/3: 2, lOd, 18; B.16/a/3:2; B.107/a/12: 3. 23.HBCAB.107/a/25:12. 24. HBCA B.16/a/3: lld;B.64/a/7: 7, 13;B.64/a/8:16.The impact of this epidemic on the Ojibway of the Berens River should not be underestimated. When surveyors laid out the reserve at the mouth of the river almost a century later, they identified on their maps the "old camping ground, graves of those who died from measles epidemic" (A. Irving Hallowell, The Ojibwa of Berens River, Manitoba: Ethnography Into History, edited by Jennifer S. H. Brown, Case Studies in Cultural Anthropology [Fort Worth: Harcourt, Brace and Company, 1992], 34). 25.HBCAD.l/2:lld. 26. This is probably in reference to Fort Lisa, at Council Bluffs on the Missouri, which was the supply depot of the Missouri Fur Company. According to a contemporary letter describing the trade of the upper Missouri in 1819, Lisa's Missouri Fur Company had several traders among the Sioux, and two others were trading with the Arikara. Although there were no permanent American traders at the Mandan villages at this time, it would have been a relatively short journey from the Arikara to their northern neighbours along the Missouri. In April of 1820, John Gale, at Council Bluffs, noted the downward progress of three boats from the Mandan trade laden with buffalo robes.Wishart, FurTrade, 41-42,46-47; Hiram Martin Chittenden, The American FurTrade of the Far West: A History of the Pioneering Trading Posts and Early Fur Companies of the Missouri Valley and the Rocky Mountains and of the Overland Commerce with Santa Fe, 2 vols., reprint edition (Stanford, California: Academic Reprints, 1954), 901-902; HBCA B.22/a/21:40; Roger L. Nichols, ed., The Missouri Expedition 18181820: The Journal of Surgeon John Gale with Related Documents (Norman: University of Oklahoma Press, 1969), 41, 84.

NOTES PAGES 148 TO 151 277 27. HBCA B.27/a/8: 31;B.51/a/2: 4,13. See also PAM MG 7 D13 Microfilm reel 1 Belleau Collection: Provencher to Amable Dionne, St. Boniface, 1 September, 1819. 28. Captain Grant, who was said to have emigrated from his home in the Severn region, lived with his people in Grant's Village, a small but thriving agricultural settlement located on the Assiniboine River halfway between Brandon House and Portage la Prairie. HBCA B.51/a/2: 6d; B.51/e/l: 18d; B.22/a/21: 34, 51; D.Wayne Moodie, and Barry Kaye," Indian Agriculture in the Fur Trade Northwest," Prairie Forum 11, no. 2 (Fall 1986): 175. 29.HBCAB.51/a/2:7. 30. Barry Kaye, "Birsay Village on the Assiniboine," The Beaver Outfit 212, no. 3 (Winter 1981): 21; HBCA B.51/a/2: 8. 31. PAM MG 7 D13 Microfilm reel 1 Belleau Collection: Provencher to Bishop Plessis, St. Boniface, 27 July, 1819. See also Microfilm reel 1 Belleau Collection: Provencher to Amable Dionne, St. Boniface, 1 September, 1819, and Provencher to Dionne PAM MG7D13. 32. C. Stewart Houston, ed., To the Arctic by Canoe 1819-1821 -.The Journals and Paintings of Robert Hood Midshipman with Franklin (Montreal and London: McGill-Queen's University Press, 1974), 36. 33. HBCA B.154/a/8: 6, 7, 8. 34. Robert S. Drews, "A History of the Care of the Sick Poor of the City of Detroit (1703-1855)," Bulletin of the History of MedidneVll, no. 7 (1939): 762. 35. Statements made by HBC employees implicate both the upper Missouri and Fort William as local sources for whooping cough. However, there is no supporting evidence for the disease in the eastern part of the Boundary Waters or among the brigades heading northward from Fort William (HBCA A.10/2: 242; D.l/2: lid). 36. HBCA B.51/a/2: 7; B.105/a/7: 29d, 71d; B.105/a/7: 18. 37.HBCAB.16/a/2:7,8. 38. HBCA B.93/a/2: passim, 3d. 39.HBCAB.93/e/l:2d-3. 40. HBCA B.239/a/126: 32, 33, 35. 41. Houston, To the Arctic, 33. Although Franklin was at York Factory in late August and wrote in his memoirs that the Lowland Cree about York Factory "were suffering under the combined affliction of hooping-cough and measles...," it is likely that only whooping cough struck the Cree of that area in 1819-20 (John Franklin, Narrative of a Journey to the Shores of the Polar Sea in the Years 1819-20-21-22 [London: John Murray, 1823], 25; see Hackett,"Remarkable Sickness," 298). 42. HBCA B.239/a/127: 23,24, 26; B.239/e/2: 2. 43. Houston, To the Arctic, 31; C. Stewart Houston, ed., Arctic Artist: The Journal and Paintings of George Back, Midshipman with Franklin, 1819-1822 (Montreal and Kingston: McGillQueen's University Press, 1994), 17.The timing of introduction is unknown due to a gap in the journal record between August 20,1819, and October 1,1820.There had been no indication of the sickness in the Oxford journal prior to that gap. Here again Sir John Franklin (Narrative of a Journey, 37) stated that the Cree were suffering from

278 NOTES PAGES 151 TO 156 both whooping cough and measles, while one of his men, George Back, recorded only whooping cough (Houston, Arctic Artist, 17). Since there is no evidence of measles in this part of the Canadian Northwest until the following November, when it spread to Norway House from the west, and because Back's journal appears to be the most reliable for this portion of the expedition, I have concluded that only whooping cough was present at this time. For more on this see Hackett, "Remarkable Sickness." 44. There are several extant records from Severn and its hinterland, and none mention any sickness that could be construed as either whooping cough or measles. In fact, neither the post journals (HBCA B.198/a/58a; B.198/a/59), nor the Severn district report for 1819-20, which includes data on the Trout Lake and Winisk River outposts (HBCA B.I 98/e/3), nor John Work's journal of an expedition up the Winisk River (HBCA B.198/a/58b), make mention of any disease among the Aboriginal people. 45. HBCA B.154/a/8: 6; B.105/a/7: 73; B.I 17/a/4: 5,6; B.117/a/5: 5,5d;B.129/a/10; B.3/a/124. 46. It is possible that these were reflective of pneumonia, although this is far from certain. 47.HBCA B.123/a/18;B.135/b/40: 55,18;B.155/a/32:11,14,14d, 18. 48.HBCAB.145/a/39:49. 49. Heagerty, Four Centuries, 212; HBCA B.145/a/41:14.

Chapter Eight l.HBCAB.129/a/18:7. 2.HBCAB.107/a/14:7d. 3. In his report for 1839-40, McKenzie noted, "The Indians were entirely free from any flying [acute epidemic] disease, to which they have been so much subject of late years..." (HBCA B.107/a/18:19d). 4. G. P. deT. Glazebrook, ed., The Hargrave Correspondence 1821-1843,The Publications of the Champlain Society, vol. 24 (Toronto:The Champlain Society, 1938), 461. 5. HBCA D.5/14: 242d. 6.HBCAA.12/3:137. 7. By the 1830s and 1840s it may be more appropriate to speak of American disease pools, for the Atlantic cities had grown tremendously. By 1830 New York City had a population of 200,000, while that of Philadelphia was 175,000 (Harry T.Williams, Richard N. Current, and Frank Freidel, A History of the United States [To 1877], second edition [New York City: Alfred A. Knopf, 1964], 343). A decade later, New York had about 360,000 citizens and Philadelphia over 220,000 (Paul A. Groves, "The Northeast and Regional Integration, 1800-1860," in North America: The Historical Geography of a Changing Continent, edited by Robert D. Mitchell and Paul A. Groves [Totowa, New Jersey: Rowman and Littlefield, 1987], 207). Given the additional population in surrounding towns and the annual input of emigrants from overseas, the crowd diseases were probably endemic within these major cities. 8. Glazebrook, The Hargrave Correspondence, 102. See also HBCA B.4/a/7:2d.

NOTES PAGES 157 TO 160 279 9. Epidemics threatened Detroit in 1813,1829,1831, and 1837 (Drews, "History of the Care," 762, 764,766,774). According to Harstad (PeterT. Harstad,"Disease and Sickness on the Wisconsin Frontier: Smallpox and Other Diseases," Wisconsin Magazine of History [Summer I960]: 54), "By the late 1830's the white population was so widespread in Wisconsin that the Indian continually came into contact with them; thus there were unlimited opportunities for exposure to smallpox." Moreover, "Throughout the 1840's and 1850's, [smallpox] was present somewhere in the [upper Mississippi] and few communities were spared an epidemic" (Peter T. Harstad, "Health in the Upper Mississippi River Valley, 1820 to 1861," PhD diss., University of Wisconsin, 1963, p. 218). The same was true of the adjacent country to the south of Lake Superior. For instance, this disease broke out in the area between Lake Superior and the upper Mississippi at least in 1842,1843,1846,1847,1849, and 1851 (HBCA D.5/7:229d; Harstad, "Health in the Upper Mississippi," 219,220; United States, Annual Report, Commissioner of Indian Affairs [Washington: US Government Printing Office, 1847], 91-92; United States, Annual Report, Commissioner of Indian Affairs [Washington: US Government Printing Office, 1848], 558; United States, Annual Report, Commissioner of Indian Affairs [Washington: US Government Printing Office, 1849], 111; United States, Annual Report, Commissioner of Indian Affairs [Washington: US Government Printing Office, 1851], 162,168). 10. PAM MG 2 Al Selkirk Papers, "Instructions to Miles Macdonell,"1811, p. 178; HBCA B.239/a/124: 73d. 11. HBCA B.51/a/2:13; HBCA A.10/2: 242; HBCA B.51/a/3: 5d. 12. HBCA D.5/5: 49-49d; see also A.6/2:158d. 13. HBCA B.3/a/145:1; B.123/e/14: 4; B.3/b/63: 27d; B.155/a/50: 20. 14.The factors that led to an increase in disease in the country to the north and west of Lake Superior did the same elsewhere across North America, including in the Pacific Northwest during the 1830s and 1840s. In his analysis of that region's epidemic history, Robert Boyd identified the rapid breakdown of isolation with the outside world as the precipitating factor in the onset of a new era of diseases during that decade. As large numbers of settlers flooded the region from the east, its disease load both increased and became far more varied.Thus, in a decade or less, the previously isolated Pacific Northwest was integrated into what Boyd called the larger Euroamerican disease pool (Boyd, Coming of the Spirit). A similar process has been identified for the plains during the first half of the nineteenth century (Taylor, "Sociocultural Effects," 56, 59-60), and there are certain similarities with the situation atTeslin Lake, in the Yukon. There, in 1942-43, the breakdown in isolation due to the arrival of construction crews working on the Alaska Highway meant a sudden influx of disease for the Aboriginal people of the area. See J.F. Marchand, "Tribal Epidemics in the Yukon," Journal of the American Medical Association 123, no. 16 (SeptemberDecember 1943).This continued during the following decades. 15. Henry Youle Hind, Narrative of the Canadian Red River Exploring Expedition of 1857 and of the Assiniboine and Saskatchewan Exploring Expedition of 1858, two vols. in one, reprint edition (Edmonton: M.G. Hurtig Ltd., 1971), 100. 16. George Catlin, Letters and Notes on the Manners, Customs, and Condition of the North American Indians, 2 vols., reprint edition (Minneapolis: Ross and Haines, 1965), 1:6061.

280 NOTES PAGES 160 TO 162 17. Harstad, "Health in the Upper Mississippi," 209; Harstad, "Disease and Sickness," 254. 18. See, for example, HBCA D.5/14:138, and Taylor, "Sociocultural Effects," 59. 19. Brown, Historical Geography, 195;Thomas F. Mcllwraith, "British North America, 1763-1867," in North America: The Historical Geography of a Changing Continent, edited by Robert D. Mitchell and Paul A. Groves (Totowa, New Jersey: Rowman and Littlefield, 1987), 238-239. 20. Ronald E. Shaw, Erie Water West: A History of the Erie Canal 1792-1854 (Lexington: University of Kentucky Press, 1966), 273-274. 21. Borchert,"American Metropolitan Evolution," 303.There were perhaps 200 steamboats on the western waters in 1830 and about 600 in 1850 (Williams et al., History of the United States, 343). 22. Louis C. Hunter and Beatrice Jones Hunter, Steamboats on the Western Rivers: An Economic and Technological History (Cambridge: Harvard University Press, 1949), 29. 23. Andrew F. Burghardt, "Emergence of a Transportation System, 1837-1852," in Historical Atlas of Canada, Volume ILThe Land Transformed, 1800-1891, edited by R. Louis Gentilcore, plate 25 (Toronto: University ofToronto Press, 1993).The population of Upper Canada rose rapidly between 1825 and 1846, from 177,174 in 1827, to 321,145 in 1834, and to 432,159 in 1840 (Peter G. Goheen, Victorian Toronto, 1850 to 1900: Pattern and Process of Growth. Research Paper No. 127 [Chicago: The University of Chicago, Department of Geography, 1973], 48, 50; G. P. deT. Glazebrook, A History ofTransportation in Canada: Volume 1 Continental Strategy to 1867, 2 vols.,The Carleton Library [Toronto: McClelland and Stewart Limited, 1964],11: 60). By 1857, southern Ontario's population stood at one million (R. Cole Harris and John Warkentin, Canada Before Confederation: A Study in Historical Geography [NewYork City: Oxford University Press, 1974], 118,151). 24. Michigan became a state in 1837 and Wisconsin only in 1848. There was considerable immigration into Wisconsin during the 1830s and 1840s, and its non-Aboriginal population grew from 3245 in 1830 to about 200,000 by 1847, or just prior to gaining statehood (James L. Barton, Commerce on the Lakes: A Brief Sketch of the Commerce of the Great Northern and Western Lakes for a Series ofYears [Buffalo: Jenett, Thomas and Co., 1847], 55;John Perry Pritchett, The Red RiverValley 1811-1849:A Regional Study, reprint edition [NewYork City: Russell and Russell, 1970], 249). 25. The year 1843 was likely typical of this era. The HBC's John Ballenden noted that "This has been rather a gay Summer at the Sault [Ste. Marie]—Steamboats every fortnight, and often weekly," one of which brought 200 passengers (HBCA D.5/8: 412d). James Hargrave, who had been stationed in the village by the NWC prior to the merger, returned in 1851 and found it "changed by the advance of settlers" (Glazebrook, The Hargrave Correspondence, xviii-xix). In 1854 HBC Governor George Simpson stated simply that "This [Sault Ste. Marie] district may now be considered as within the limits of the 'civilised world,' the shores & islands being studded with growing villages & settlements while it is traversed in all directions by steamers. (HBCA D.4/74: 449-450). See also Robert M. Ballantyne, Hudson Bay, or, Everyday Life in the Wilds of North America During Six Years' Residence in the Territories of the Hon. Hudson Bay Company, reprint edition (NewYork City: Kraus Reprint Co., 1971), 297.

NOTES PAGES 162 TO 167 281 26. Hunter and Hunter, Steamboats, 30; Richard C.Wade, The Urban Frontier:The Rise of Western Cities, 1790-1830, Harvard University Monographs (Cambridge: Harvard University Press, 1959), 70; Pyle, "Diffusion of Cholera," 62, 67; St. Louis City Plan Commision, History: Physical Growth of the City of Saint Louis (St. Louis: The Commision, 1969); Harris and Warkentin, Canada Before Confederation, 152. 27. Haggett, "Sauer's Origins," 395; Haggett,"Invasion," 46-47; Peter Haggett, "Geographical Aspects of the Emergence of Infectious Disease," GeografiskaAnnaler76 B, no. 2 (1994): 102-103; Snow and Lanphear,"European Contact," 25-26.This was also the case in Canada during the twentieth century. In the 1960s,J.S.Willis noted of the Canadian north that "The improvement in transarctic communications in the mid-1950s added to the north-south air routes that became so well established during and after World War II, helped to carry new strains of organisms great distances in a short time and mix the strains already in the north." The result was the rapid spread of epidemics during the period from 1954 to 1959, and an increase in the infant mortality rate (J.S.Willis, "Disease and Death in Canada's North," Medical Services Journal, Canada 19 [October 1963]: 752). 28. As well, in the spring of 1847, Frederick Graham voyaged from Boston to Mackinac in less than two weeks, travelling by train from Boston to Buffalo and from thence to Mackinac by steamboat (Grace Lee Nute, "Westward with Sir George," The Beaver [December 1950]: 40-41). 29. John Richardson, Arctic Searching Expedition, 2 vols, (London: Longman, Brown, Green and Longmans, 1851), 1:51; Hunter and Hunter, Steamboats, 430-435; C.O. Paullin and J. K.Wright, Atlas of the Historical Geography of the United States (Westport, Conn.: Greenwood Press, 1975), plate 138.The classic example was the second pandemic of cholera, which from 1826 to 1832 spread from India to Europe, before entering North America in 1832 through New York City and Montreal. From these ports the disease penetrated along the main water routes leading far into the continent, often aboard ships that were densely packed with immigrants bound for the frontier communities. 30.HBCAB.129/a/16:18d. 31. John Strachan, A Journal of Visitation to the Western Portion of His Diocese, by the Lord Bishop of Toronto, in the Autumn of 1842 (London: Printed for the Society for the Propagation of the Gospel, 1844), 10-11; Anna Brownell Jameson, Winter Studies and Summer Rambles in Canada by Mrs. Jameson, 3 vols. (London: Saunders and Otley, 1838), 2: 275. 32. Garry,"Diary of Nicholas Garry," 109.According to Dr. Thomas Stratton, the numbers gathered at Manitowaning were: 3304 in 1839; 5057 in 1840; 3874 in 1841; 5812 in 1842; 3771 in 1843; 1887 in 1844; and 1852 in 1845.Thomas Stratton, "Contribution to an Account of the Diseases of the North American Indian," Edinburgh Medical and Surgical Journal 71 (1849): 272. 33.HBCAB.129/a/13:ld. 34. Henry R. Schoolcraft, Personal Memoirs of a Residence of Thirty Years with the Indian Tribes, reprint edition (NewYork City: AMS Press, 1978), 295. 35.HBCAD.5/10:219.

282 NOTES PAGES 167 TO 172 36. HBCA D.5/14:138. These deadly journeys by the Aboriginal people of Lake Superior continued until the signing of the Robinson-Superior Treaty in 1850. Thereafter, annuities were distributed at Michipicoten and Fort William. By the 1840s, sickness was so common among the Aboriginal people at the time of giving presents that the doctors in attendance could not record the number of cases. For eyewitness accounts see Stratton, "Contribution," 1849, and W. Winder, "On Indian Diseases and Remedies; With a Return of Sick Treated at the Indian Establishment, Great Manitoulin Island, Lake Huron, in 1841-42," British American Journal 1 (184546). 37. By 1824 its population numbered about 2000. By 1840 it had more than doubled to nearly 5000 (Barry Kaye, "Some Aspects of the Historical Geography of the Red River Settlement from 1812 to 1870," Master's thesis, University of Manitoba, 1967), pp. 38, 42-43,119; Innis, FurTrade in Canada, 288). As of the 1830s, according to historian Gerhard Ens, Red River was "an amalgam of small, largely metis, peasant communities of varying ethnic and religious orientations," situated along the Red and the Assiniboine rivers. Gerhard J. Ens, "Kinship, Ethnicity, Class and the Red River Metis:The Parishes of St. Francois Xavier and St. Andrew's," PhD diss., The University of Alberta, 1989, p. 74. Without a central core, the communication of infectious disease between these communities was often slow, prolonging the presence of disease in the colony. 38. Peers (Ojibwa of Western Canada, 123-124) identified the Red River Settlement as a "centre for communication among Ojibwa in the entire Northwest and Boundary Waters region." 39.Wishart, FurTrade, 87. 40.Trimble, "Epidemiology on the Northern Plains," 187. 41. John E. Sunder, The FurTrade on the Upper Missouri, 1840-1865 (Norman: University of Oklahoma Press, 1965), 19. 42.The phrase is Wishart's (FurTrade, 86). In 1832, after the first successful steamboat voyage from St. Louis to Fort Union, AFC trader Ramsey Crooks told fellow trader Pierre Chouteau, "You have brought the Falls of the Missouri as near comparatively as the River Platte was in my younger days" (quoted inWishart, FurTrade, 86). 43. Mentor L.Williams, ed., Narrative Journal of Travels Through the Northwestern Regions of the United States Extending from Detroit Through the Great Chain of American Lakes to the Sources of the Mississippi River in the Year 1820 (East Lansing: The Michigan State College Press, 1953), 430,466; Brown, Historical Geography, 301. 44. Quoted in Moodie and Kaye, "Indian Agriculture," 180. 45. HBCA D.5/6: 2d. 46. HBCA B.49/a/49: 35d-36. See also HBCA D.4/103:11; Jennifer S.H. Brown and R. Brightman," The Orders of the Dreamed": George Nelson on Cree and Northern Ojibwa Religion and Myth, 1823 (Winnipeg: University of Manitoba Press, 1988), 49-50. 47. Ray, "Diffusion of Diseases," 141,143; Innis, FurTrade in Canada, 290, 291,310. During the 1820s and into the early 1830s, sicknesses broke out at Norway House andYork Factory at least during July of 1824,1827,1828,1830, and 1831, coinciding with the arrival of the brigades from the interior (HBCA B.239/a/132: 27d; B.154/a/ 16: 7; B.239/a/141: 72, 75, 81; B.154/a/19: 2d; B.154/a/20: 8d; B.154/a/22: 8d). By

NOTES PAGES 174 TO 178 283 1835 minor epidemics were a common occurrence at York Factory during the late spring or early summer, when the brigades made their appearance (HBCA D.4/103: 13d). Indeed, Robert Ballantyne (Hudson Bay, 168) noted in his memoirs that the health ofYork was particularly bad during the summer but much better during the winter, a seasonal pattern that, in keeping with prevailing beliefs about disease causation, he attributed to the influence of climate. Over the following decade, many of the diseases being spread by the brigades were much more virulent. 48. John Weiler, Michipicoten: Hudson's Bay Company Post 1821-1904, Historical Sites Branch Research Report, vol. 3 (Ontario Ministry of Natural Resources, 1973), 5,17, 18,20,23. 49.Writing during the next decade when epidemics had become more common, Charles McKenzie expressed surprise at the later increase in diseases in the Northwest, "although the communication with Canada is less than formerly" (HBCA B.107/a/ 14: 7d). No doubt, he was well aware of the role played by the Canadian brigades in introducing infectious diseases to the Northwest. 50. HBCA B.162/a/2: 4,4d; B.149/a/ll: 16,18, 32; B.129/a/13: Id, 23d, 21d. 51. HBCA B.107/a/7:15d, 16,16d. 52. HBCA B.107/a/8: 3, 4, 7d, 14d. 53. HBCA B.124/e/3: 2d; B.70/e/3: 2d; B.135/a/128:15; B.135/e/15:1; B.3/e/12:2,2d, 7d; B.3/a/130: 12; Benenson, Communicable Diseases, 347. 54. HBCA B.156/a/10: 9d, lOd; B.235/a/9:13,13d, 14; PAM CMS C.l/M.l: 323 Microfilm Reel A77, "Reverend D.T.Jones's Journal from October 15,1826 to Oct. 15 1828"; Decker, "We Should Never," 103. 55. We also begin to see a level of preoccupation among the Aboriginal people over the appearance of epidemic disease. For instance, some of the Ojibway from Fort William visited Henry Schoolcraft at Michilimackinac in February and conversed with him on the subject of a tremendous meteor shower visible throughout much of North America on November 12,1833. Schoolcraft wrote, "They spoke of the meteoric phenomenon of November. I asked the leader of the party what he thought of it. He replied that it betokened evil to the Indian race-—that sickness would visit them calamitously" (Schoolcraft, Personal Memoirs, 466). 56. There are hints of something darker during this period, a severe disease that involved the brain. There was an outbreak of what was called "water on the brain" among the children at York Factory during the spring of 1844 (HBCA B.239/a/148: 18bd).The following year there was sickness among several people at Fort Alexander, mainly children, due to inflammation of the brain, and several deaths occurred due to "suffusion of the brain" at about the same time in the Red River Settlement (HBCA B.105/e/10:1; Glazebrook, The Hargrave Correspondence, 207). 57. Indeed, it was not unknown for colds to break out in consecutive years at a post or even twice in the same year. For instance, colds appeared at Michipicoten three times over the span of two years, in 1832-33 (HBCA B.129/a/16:18d; B.129/a/17: 3d, 6d; B.129/a/17:15; B.129/V18: 5d, 6d, 7). Unfortunately, we cannot identify how often they were breaking out, due to some large gaps in the documentary record. Not surprisingly, it was at this time that George Keith identified colds as a frequent visitor to Michipicoten (HBCA B.129/a/18: 7).

284 NOTES PAGES 178 TO 179 58.HBCAB.107/a/ll:2,3. 59. The people of Lac Seul were also struck by epidemic disease at this time, but this does not necessarily indicate a connection to the epidemic of 1832. Although we might argue that they had been attacked by the concurrent influenza epidemic, and thus there is no evidence that they lacked immunity, we could also argue that the two whooping cough epidemics were antigenically distinct, one being pertussis, the other parapertussis. Such are the pitfalls of researching a period in which epidemic disease was the norm. 60. Reuben Gold Thwaites, ed., Maximilian, Prince ofWied's Travels in the Interior of North America, 1832-1834, Early Western Travels, 1748-1846, vols. 22-24 (Cleveland: Arthur H. Clark Co., 1906), 23:236-237; PAM MG 7 D13 Microfilm reel 1 Belleau Collection: Bishop J.-N. Provencher to J. Signay, St. Boniface, 4 September, 1834; Same to Same, St. Boniface, 17 + 18 December, 1834;Glazebrook, Thetiargrave Correspondence, 148, 160,164,166,179. 61. HBCA B.154/a/25:49; D.5/4:98; Glazebrook, The Hargrave Correspondence, 166; Decker, "We Should Never," 108. Although there appears to have been some epidemic sickness at York in October of 1834, it wasn't whooping cough (HBCA B.239/a/148: 18bd). At Severn, only an "inward complaint" afflicted the Cree during the ensuing winter (HBCA B.198/a/71: 24). 62. HBCA B.105/a/19: 8d; B.105/e/10:1; Decker ("We Should Never," 105). In December Donald Mclntosh noted in the Fort William journal that "The most of the people + children in the Fort have been affected with a violent disease [influenza].We suppose it was brought here by the men who took Mr William Swanson to Lac la Pluie." In most cases this "fluenzy" manifested itself as a violent and painful cough accompanied in some cases by pains in the head, side, and breast, the last two probably the result of complications such as pneumonia. By Christmas almost all the HBC men at Fort William were labouring under its effects, and one had died. At the same time, the disease had spread to the Ojibway, including one band led by the Spaniard, a prominent figure who hunted to the south of the border. All suffered severely. By the end of January, however, everyone had fully recovered (HBCA B.231/a/14:12,14d, 15d, 16,16d, 17,18d; B.231/a/15: 2ad). 63. HBCA B.155/a/47: 2; B.107/a/13:11,14d, 18d, 20; see also B.211/a/7: 5d, 6, 7. If it was whooping cough at Lac Seul, then Charles McKenzie's history with the disease is little short of incredible. While among the Mandan during the epidemic of 1806, he had worried about catching whooping cough (Trimble, "Epidemiology on the Northern Plains," 52), suggesting that he had had no prior exposure to the disease. In 1819-20, he had escaped as it failed to spread the short distance northward from the Boundary Waters to Lac Seul. He also avoided contracting the disease in 1832, despite the fact that it struck the Ojibway around the post. Perhaps in 1834 his luck had run out. 64. For example, there were outbreaks in the Albany-Martin's Falls area in 1833, to the north of Lake Superior in the winter of 1833-34, and at Fort William in the winter of 1834-35, September of 1835, and again in the summer of 1836. In 1835 a devastating influenza epidemic swept the Northwest, and was followed by another in 1837. In the summer of 1839, the disease again afflicted the HBC people at Albany, Martin's Falls, and beyond. Finally, there were outbreaks of colds and coughs, likely influenza, at York

NOTES PAGES 180 TO 183 285 Factory in August of 1840.This had come from the interior, and seems to have also been among the Aboriginal people to the west of Lac Seul in September. References for these and many other epidemics from the period can be found in Hackett, "Remarkable Sickness." 65. PAM CMS C.1/M.2:143 Microfilm reel A77,"Rev. D.T.Jones'Journal, May 20/35 to July 20/36." 66. PAM CMS C.1/M.2:113 Microfilm reel A77, "Rev. W. Cockran's Journal, Aug. 14/ 34 to Aug 2/35"; PAM MG2 A6:101; Glazebrook, The Hargmve Correspondence, 207. See also Sarah Tucker, The Rainbow in the North: A Short Account of the First Settlement of Christians in Rupert's Land by the Church Missionary Society, fourth edition (London: James Nisbet, 1858), 75.The universal susceptibility and its extremely severe course suggest that this was a strain of type A influenza, the result of an antigenic shift in the disease. In turn, these characteristics invite comparison to the most infamous of influenza pandemics, the Spanish Flu of 1918-19.The latter sickness is well known for having caused tremendous mortality in its worldwide diffusion, its victims numbering in the tens of millions, but its case-fatality rate was actually low compared to many other epidemics, perhaps less than two percent (John H.Walters,"Influenza 1918:The Contemporary Perspective," Bulletin of New York Academy of Medicine 54, no. 9 [October 1978]: 860).We cannot calculate similar rates for the 1835 epidemic in the Northwest, but it seems likely that it surpassed the 1918-19 epidemic in the rate, if not in total numbers, of fatalities. 67. Glazebrook, The Hargrave Correspondence, 192; PAM CMS C.1/M.2:144 Microfilm reel A77,"Rev. D.T.Jones'Journal, May 20/35 to July 20/36"; HBCA B.154/a/26: 3, 5,6, 8, 9,10, 28, 31; see also HBCA B.154/e/8: 2. Boats arrived at Norway House from the Red River Settlement on the 8th, 9th, 16th, 17th, and 20th of June (HBCA B.154/a/26: 3, 5, 6). Here again we might see similarities with the influenza of 191819. The latter was often preceded by a relatively mild wave of the disease. For instance, in England and Wales there was a bout of the disease with a high attack rate but low mortality in June-July of 1918.This was followed by a second and far more deadly wave in October and November. A third wave of intermediate severity followed in February of 1919 (A.H. Gale, Epidemic Diseases [Harmondsworth, Middlesex, UK: Penguin Books, 1959], 49). Similarly, there were reports of less severe sickness preceding the more devastating wave of influenza at both Norway House (influenza) and York Factory (bowel and lung complaints) in 1835. 68. HBCA B.239/a/48: 61d, 66; B.198/a/73: 9; Richard King, Narrative of a Journey to the Shores of the Arctic Ocean, in 1833, 1834, and 1835; Under the Command ofCapt. Back, R.N, 2 vols. (London: Richard Bentley, 1836), 2: 219-220. 69. HBCA B.239/a/148:40ad, 41d, 44d, 48, 58, 59d, 60d, 66,66d; B.154/e/9:1; Ray, "Diffusion of Diseases," 142-143; King, Narrative of a Journey, 2:219-220. 70. HBCA B.107/a/14: page before 1,1,2, 2d. 71.HBCAB.231/a/15:2ad,7d;B.149/a/18:5;B.117/a/10:7d. 72. PAM CMS C.1/M.2 Microfilm reel A85, "Journal of Rev. Mr Cockran Aug/36 to Aug/37." 73. Heagerty, Four Centuries, 1: 213; Boyd, Coming of the Spirit, 136.

74. HBCA B.154/a/29: ll;B.156/a/17: 7d, 8, 9, lid.

286 NOTES PAGES 183 TO 188 75. HBCA B.107/a/14: 6, 6d. 76. R.Edgar Hope Simpson, "Infectiousness of Communicable Diseases in the Household (Measles, Chickenpox, and Mumps)," The Lancet Series 2 (September 20, 1952): 553; Benenson, Communicable Diseases, 87-89. 77.Boyd, Coming of the Spirit, 142. 78.HBCAB.107/a/14:6. 79. HBCA B.231/a/17: Id, 3d; 4, 4d, 5, 6. 80. Benenson, Communicable Diseases, 405, 407; Cliff et al., Island Epidemics, 62. 81. Benenson, Communicable Diseases, 315-316; Hope Simpson, "Infectiousness of Communicable Diseases," 553. 82. HBCA B.239/a/154: 65d; B.239/a/155: 23; D.5/6: 329d. 83. HBCA D.5/14: 190d, 299; PAM CMS C.l/0 Microfilm reel A84,William Cockran to the Secretaries of the CMS, Grand Rapids, Red River, no date but marked received April 3,1844; Stratton," Contribution"; Ray, "Diffusion of Diseases," 156: fn. 56; John Palliser, The Solitary Hunter; or, Sporting Adventures in the Prairies (London: George Routledge & Co., 1856), 84. 84. HBCA D.5/8: 435. 85. Winder, "On Indian Diseases," 255-256. 86. HBCA D.5/8: 59; D.5/14:138; United States, Annual Report, Commissioner of Indian Affairs (Washington: US Government Printing Office, 1842), 403; Stratton, "Contribution." 87. HBCA D.5/14:138; D.5/7: 372; D.5/8: 59. 88. PAM CMS C.l/0 Microfilm reel A96, "No. 2 Copy of Journal from Feb 1st to August 1st, 1836,John Smithurst, Indian Settlement"; C.l/0 Microfilm reel A86, Donald Gunn to William Cockran, Grand Rapids, July 6,1843; PAM CMS C.l/0 Microfilm reel A84, William Cockran to the Secretaries of the CMS, Grand Rapids, Red River, no date but marked received April 3,1844. 89. HBCA D.5/12: 563d; B.154/b/l: 30,48d, 53; PAM CMS C.l/M Microfilm reel A78, "Revd J. Hunters Journal from June 1 1844 to May 11 1845," 612, 620. As well, many of the Aboriginal people around Severn House were sick late in October of 1844, of an unnamed illness, and there was an outbreak of unidentified disease among the HBC men at Trout Lake in November (HBCA B.198/a/86: lOd; B.220/a/6:24). There was no such sickness at Island Lake, although the post manager, James Harrold, fully expected the Aboriginal people to fall ill at some point, suggesting that epidemic disease was becoming common in that area (HBCA B.93/a/7: 7d, 13). 90. Miller and Keane, Encyclopedia, 1002-1003; Benenson, Communicable Diseases, 438-443. There are some eighty serologically distinct strains of S. Pyogenes, and so repeated infections with different strains is possible. Of these, three are responsible for scarlet fever. 91. HBCA B.3/a/65: 47, 47d, 48; B.3/a/66:2d; Benenson, Communicable Diseases, 439; Anne Hardy, "Scarlet Fever," in The Cambridge World History of Human Diseases, edited by Kenneth F. Kiple (Cambridge: Cambridge University Press, 1993), 991-992; Stratton, "Contribution," 275.

NOTES PAGES 188 TO 189 287 92. HBCA D.5/9: 323, 373; PAM MG 2 C19 Bunn Papers,Thomas Bunn to Mrs. Ann Bailey, Red River, August 7,1844; PAM MG 1 C9 #6 HBC Duncan Finlayson to HBC Governor, Chief Factors and Chief Traders, Red River Settlement, December 2, 1843; John H. Pitezel, Lights and Shades of Missionary Life: Incidents and Missionary Efforts During Nine Years Spent in the Region of Lake Superior (Cincinatti: R.P. Thompson Printer, 1860), 76; United States, Annual Report, Commissioner of Indian Affairs (Washington: US Government Printing Office, 1843), 429. 93. PAM CMS C.l/0 Microfilm reel A96,W. Robert Smith to Reverend William Cockran, Middle Church School and House, August 1,1844; Reverend John Smithurst to the Secretaries of the CMS, Indian Settlement, Red River, December 22, 1843; Ens, Homeland to Hinterland, 107; HBCA D.5/9:373. 94. Ray, "Diffusion of Diseases," 151; HBCA D.5/9:381; Glazebrook, The Hargrave Correspondence, 452,461. 95. HBCA D.5/11:212; D.5/9: 313; B.107/a/22: 5d; B.107/a/21:16d; B.155/a/55:13d, 17. Another severe disease subsequently appeared among the Lac Seul Ojibway during the winter of 1843-44, one that rendered many of all ages crippled and unable to walk (HBCA B.107/a/21:13). McKenzie commented on how they had declined in size and robustness compared to their ancestors, an observation he claimed was shared by the elders (HBCA B.107/a/22:13).This suggests that the general level of health in the Lac Seul area had declined significantly since McKenzie first went there. 96. Boyd, Coming of the Spirit, 142. Beginning in 1841, and continuing each year until 1866, American settlers from the eastern half of North America departed from the Missouri River along one of the long overland trails leading to California or Oregon. In 1843 there were 1000 travellers on the trails. By 1850, the year of peak migration, there may have been as many as 55,000 (Lillian Schlissel, Women's Diaries of the Westward Journey, Studies in the Life ofWomen [New York: Schocken Books, 1982], 24). From an epidemiological perspective, the settlers moving along the Oregon and California trails represented the moving edge of the American frontier, the outer limits of the influence of the urban east and growing midwest. Like the introduction of acute infectious diseases to the Northeast by colony ships during the seventeenth century, settler caravans brought with them diseases such as measles, scarlet fever, typhoid fever, mumps, dysentery, smallpox, and cholera from the east (Georgia Willis Reed, "Diseases, Drugs, and Doctors on the Oregon-California Trail in the GoldRush Years," Missouri Historical Review [1944]: 269; Schlissel, Women's Diaries, 10-11,13, 15, 47, 60). Edwin Denig, an AFC trader stationed on the upper Missouri from 1833 until the mid-1850s, provides a contemporary perspective on the negative effect of the Oregon Trail on the health of the Aboriginal people of the American plains. Denig noted especially that the Brule Sioux, one of theTeton bands, had suffered greatly due to the presence of the migrants: "Since the emigration to California and Oregon has passed through the Sioux Country, the Brulees have suffered more from diseases thus introduced than any other portion of these [Sioux] Indians, they being situated nearest to the trail. Smallpox, cholera, measles, etc., have year after year thinned their ranks so that but a remnant of this once numerous band remains" (Ewers, Five Indian Tribes, 19). Similarly, the Oglala, another Teton division, had also "been much reduced in numbers by diseases contracted along the Platte Trail from passing immigrants," and

288 NOTES PAGES 189 TO 197 theYankton and theYanktonai suffered greatly from diseases from the same source (Ewers, Five Indian Tribes, 19,22,36,38). See also Taylor, "Sociocultural Effects," 60. 97. Boyd, Coming of the Spirit. 98. The number of fatalities is unclear, and there were estimates of twenty-three, twentyfive, thirty-six, and forty-four deaths. United States, Indian Affairs Report 1843,377; HBCA D.5/8: 356, 412,435d, 459, 514, 546d; D.5/10: 85,197, 219; D.5/14:138. 99. Ray, "Diffusion of Diseases," 147-148; HBCA D.5/7: 564d; D.5/8:450; D.5/9: 312, 381,361d; D.5/10: 411; D.5/11: Id; B.239/a/157:43d, 44,44d, ff.;B.156/a/23: 8d, 9, 11,13d, 17, if. 100. HBCA B.156/a/23:11,13d, 25d, 33d, 34d; B.198/a/85: 20d, 21d, 24d. 101. PAM CMS C.l/0 Microfilm reel A84,WiUiam Cockran to the Secretaries of the CMS, Grand Rapids, Red River, no date but marked received April 3,1844; HBCA D.5/9: 313. 102. HBCA B.155/a/55:13d, 17; B.107/a/22:12d, 15d. 103. HBCA B.107/a/23:1. 104.HBCAB.107/a/23:3. 105. HBCA B.107/a/23:1, 3d, 7, 8, 8d, 9d, 10, lid, 13d, 14; D.5/13:117,117d. 106. An undated letter from Charles McKenzie to Thomas Corcoran speaks of great sickness among the Lac Seul people, but it is unclear if it applies to the winter of 1844-45 or 1845-46. It states: "There was a fatal disease raging among the Lac Seul Indians all winter nor are they free from it to this day—to which no less than 6 fell victims—all young or middle aged men—more or less in debt—as well as several women and children—there was scarcely a family free from Sickness of some kind or other during the winter" (HBCA B.3/C/1: lad). 107. HBCA B.107/a/23:14,17d; B.107/a/24:1, Id. 108. HBCA B.107/a/24:1, 2, 4d, 5, 6d, lOd, 20; NAG MG 19 A40 1A,Thomas Corcoran to William Lane, Albany, January 1846. 109. HBCA B.107/a/24:25. 110. HBCA B. 107/a/24: lOd. 111. HBCA B.I07/a/24: 3, 5, 6d, lOd; E.I8/3: 52;B.3/C/1: Letter 8, Charles McKenzie to Thomas Corcoran, Lac Seul, August 30,1845. 112. PAM CMS C.l/M Microfilm reel A78,"RevdJ. Smithurst's Journal April 1st to July 31st 1845," 587. 113. HBCA B.154/a/45:2d, 3d, 7d. 114. HBCA B.154/b/3:2d; see also D.5/14: 226d. 115. HBCA B.239/a/161:47. 116. Ray, "Diffusion of Diseases," 149; HBCA B.239/a/161:27d, 44d, 47,47d, 48, 48d; D.5/13: 376d; D.5/14: 253d; D.5/16: 317d; B.198/a/88: 5d; B.198/a/86:26. 117. HBCA D.5/18:105; B.107/a/24:1, Id, 6d; B.155/a/57: 4d, 5d, 12,13. 118. David Anderson, The Net in the Bay, reprint edition (New York City: Johnson Reprint Corp., 1967), 202; HBCA B.123/e/14: 3d, 4, 4d.

NOTES PAGES 199 TO 205 289

Chapter Nine l.HBCAA.12/3:275. 2. PAM CMS C.1/M.4: 96 Microfilm reel A78, "Reverend J. Smithurst's Journal from Aug 1st, 1845 to March 31st, 1846"; Alexander Ross, The Red River Settlement: Its Rise, Progress, and Present State, reprint edition (Minneapolis: Ross and Haines, 1957), 362. See also PAM MG 2 C38 Peter Garrioch Journal: 68. 3. PAM CMS C.1/M.4: 96 Microfilm reel A78, "Reverend J. Smithurst's Journal from Aug 1st, 1845 to March 31st, 1846"; PAM CMS C.1/M.4: 62 Microfilm reelA78, "Reverend William Cockran's Journal from August 1845 to June 1846"; Ross, Red River Settlement, 362. The source of this disease is not mentioned in any of the records and remains unknown. Perhaps it had come from Pembina where the American trader Norman Kittson had a post frequented by smugglers from Red River. Kittson obtained his supplies from St. Paul, Minnesota, and this would have provided an excellent route for the virus to pass to the Red River. 4. HBCA B.107/a/24:19, 25. 5.HBCAB.107/a/24:25d. 6.HBCAB.155/a/57:20. 7. Attendance at the Aboriginal school at Grand Traverse Bay, on the east shore of Lake Michigan, was down substantially due to measles (United States, Annual Report, Commissioner of Indian Affairs [Washington: US Government Printing Office, 1845], 576). A family that had "wintered up the lake" had introduced the disease during the spring and it had begun spreading through the village. 8. Ibid., 503; HBCA D.5/14: 138, 298d; Frederick Augustus O'Meara, Second Report of a Mission to the Ottahwahs and Ojibwas on Lake Huron, Missions to the Heathen, vol. 13 (London: Society for the Propagation of the Gospel, 1847), 35,37. 9. John W. Garvin, ed., Wanderings of an Artist Among the Indians of North America from Canada to Vancouver's Island and Oregon Through the Hudson's Bay Company's Territory (Toronto: Radisson Society, 1925), 10,18. 10. O'Meara, Second Report, 34. 11. HBCA D.5/14:138. 12. HBCA D.5/14: 299. 13. HBCA D.5/14: 299-299d; D.5/15: 658-658d. 14. HBCA D.5/14:190d. 15. HBCA D.5/15: 84, 612d. 16. United States, Indian Affairs Report 1845, 503; HBCA D.5/16:115,135. 17. HBCA D.5/17: 214a, 246. 18. Minnesota Historical Society [MHS], American Board of Commissioners for Foreign Missions Papers Correspondence [A.B.C.F.M.],May 1844 to May 1848,MSS:No.29, BA10.A5126, Box 6: 8-9, F. Ayer to D. Greene, Red Lake, March 10,1846; Palliser, The Solitary Hunter, 84.

290 NOTES PAGES 205 TO 207 19.HBCAD.5/15:612d. 20. MHS, ABCFM: MSS No.29, F. Ayer to D. Greene, Red Lake, March 10,1846;Warren, History of the Ojibways, 335. 21. Howard, "Yanktonai Ethnohistory," 51. In the Annual Report of the US Commissioner of Indian Affairs for 1845, an undated extract from the report for the mission school at Lac Qui Parle (on the Minnesota River near Lac Travers) noted: "The measles and dysentery caused a great mortality among the Dakota last fall and winter. Out of a population of 400 souls who reside here some part of the year more than 30 have died within a year" (United States, Indian Affairs Report 1845, 564-565). Measles was also said to be among some of the families travelling along the Platte River Trails, during the spring or summer of 1845 (Merrill J. Mattes, Platte River Road Narratives: A Descriptive Bibliography of Travel Over the Great Central Overland Route to Oregon, California, Utah, Colorado, Montana, and Other Western States and Territories, 1812-1866 [Urbana and Chicago: University of Illinois Press, 1988], 64;Andrew Jackson Chambers, Recollections [Fairfield,Washington:Ye Galleon Press, 1975], 11). 22. For example, see Lucy Kramer Cohen, "Swift Bears Winter Count," Indians at Work 9, no. 6 (1942): 29; and James H. Howard, Dakota Winter Counts as a Source of Plains History, Anthropological Papers No. 61, Bureau of American Ethnology Bulletin 173 (Washington: Smithsonian Institution, 1960), 377-378. 23. James H. Howard, "Butterfly's Mandan Winter Count: 1833-1876," Ethnohistory 7 (1960): 32; Martha Warren Beckwith, Mandan-Hidatsa Myths and Ceremonies (New York: Kraus Reprint Co., 1969), 32. 24. Sunder, Fur Trade, 86; "Report of Thomas P. Moore Indian Agent for the Upper Missouri Agency, Sept. 21,1846," United States, Annual Report, Commissioner of Indian Affairs (Washington: US Government Printing Office, 1846), 78.The Arikara nation numbered about 600 prior to the epidemic (Sunder, Fur Trade, 83, fn. 12). Interestingly, several of the Arikara attributed the disease to the Whites (United States, Indian Affairs Report 1846,78). 25. Ray, "Diffusion of Diseases," 152. 26. Robert T. Boyd, "Demographic History, 1774-1874," in Northwest Coast, edited by Wayne Suttles, vol. 7, Handbook of North American Indians (Washington: Smithsonian Institution, 1990); Boyd, "Pacific Northwest Measles Epidemic"; Robert M. Galois, "Measles, 1847-1850:The First Modern Epidemic in British Columbia," BC Studies 109 (Spring 1996); Schlissel, Women's Diaries, 75, fn. 31; George Wood Ebbert,"Joe Meek'sTrip to Washington," Quarterly of the Oregon Historical Society 19 (1918): 264; RichardW Stoffle, Kristine L.Jones, and Henry F. Dobyns, "Direct European Immigrant Transmission to Numic Indians During the Nineteenth Century," The American Indian Quarterly 19, no. 2 (Spring 1995): 183. 27. Ross, The Red River Settlement, 362; PAM CMS C.1/M.4:68, Microfilm reel A78, "Reverend William Cockran's Journal from August 1845 to June 1846," May 24, 1846; PAM MG 7 D13 Microfilm reel 1 Belleau Collection: Bishop J.-N. Provencher to J. Signay, St. Boniface, 16 June, 1846. 28. HBCA D.5/17: 287. 29. PAM MG 7 D13 Microfilm reel 1 Belleau Collection: Bishop J.-N. Provencher to Bishop Ignace Bourget, St. Boniface, 16 June, 1846. The text reads: "Sir George

NOTES PAGES 208 TO 211 291 [Simpson] n'avait pas encore vu M. Belcourt qui est retenue chez lui par la maladie des sauvages; la rougeole a jete tout la monde sur la grabat; il m'a dit qu'il desirait le voir." 30. PAM CMS C.1/M.4: 68,107,108,109 Microfilm reel A78, "Reverend William Cockran's Journal from August 1845 to June 1846." Cockran's statement regarding the lack of prior exposure to measles is erroneous since the disease had raged in the Red River Settlement in 1819-20. However, the composition of Red River had changed substantially since that time, and so there may not have been a high degree of herd immunity in 1846. Nevertheless, there is no evidence that measles was responsible for excessive mortalities. Rather, contemporary observers agreed that it was the dysentery that followed that was responsible for most of the deaths during the epidemics of 1846. 31. PAM CMS C.1/M.4: 107-109 Microfilm reel A78, "Reverend J. Smithurst's Journal from April 1st to July 1st 1846." 32.Tenesmus is "ineffectual and painful straining at stool or in urinating" (Miller and Keane, Encyclopedia, 347, 1095); Benenson, Communicable Diseases, 421, 422. 33. Duffy, Epidemics in Colonial America, 202-203; Earle, "Disease and Mortality in Early Virginia"; Boyd, Coming of the Spirit, 139-142; Cliff et al., Island Epidemics, 139. As we have noted, there was a report of a severe form of dysentery at Lac Qui Parle, immediately to the south of the Red River Settlement, during the winter of 1844-45 (United States, Indian Affairs Report 1845, 564-565). 34. Ross, The Red River Settlement, 363. On the 28th of July Governor Simpson estimated that there had been 300 deaths in the settlement out of a population of roughly 6000, during a one-month period (HBCA A.12/3: 242). This amounted to the loss of about five percent of the total population in a span of about four weeks, and so comparisons with cholera were perhaps not unreasonable. 35. HBCA A.12/3: 275d. In Britain an epidemic of cholera killed perhaps five to ten percent of the total population in those towns that were hit hardest in 1832 (Robert John Morris, Cholera 1832:The Social Response to an Epidemic [London: Groom Helm, 1976], 12). 36. There was, in fact, an element of hyperbole, in that the mortality figures cited by most observers in the Red River Settlement rarely exceeded ten percent, whereas several earlier epidemics in the Northwest had mortality rates far in excess of that figure. Those epidemics were largely confined to the Aboriginal people, however, suggesting that the key factor in alerting observers in 1846 was not the number of deaths but the number of deaths among non-Aboriginal people. In this respect, there had been nothing like it before at Red River. 37.The American fur trader, Edwin Denig, who was stationed on the upper Missouri, attributed the mortality to measles alone (Ewers, Five Indian Tribes, 115). He stated, "The halfbreed settlement on Red River suffered severely at the same time [as the Cree] from the same distemper [measles]," and identified the well-known sequel of measles, pneumonia, as a major cause of death for those who succumbed during this epidemic. 38. PAM CMS C.1/M.4:148-149 Microfilm reel A78, "Reverend A. Cowley's Journal from August 1st to July 28th, 1846." In June Cowley had been at the Red River

2 2 NOTES PAGES 212 TO 213 Settlement before departing on his return for Partridge Crop about the middle of the month. While on board the boat taking the flour to the mission, two of the men fell ill of the measles. The ship reached the mission on June 29 and by July 11 the disease was widespread throughout the region (Ibid., 146-150). 39. PAM CMS C.1/M.4: 205 Microfilm reel A78, "Reverend Abraham Cowley to the Secretaries of the CMS, Partridge Crop, December 17,1846." After the epidemic had largely run its course in the settlement, Reverend John Smithurst informed his CMS superiors that: "Notwithstanding the alarming extent to which the measles prevailed the fatal cases among the Indians have been comparatively few, and those few for the most part have been occasioned by mismanagement or by the interference of their own Medicine men" (PAM CMS C.1/M.4:101 Microfilm reel A78, "Reverend J. Smithurst's Report for the Year ending Aug 1st, 1846"). 40. Ross, The Red River Settlement, 363. 41. Father Belcourt, who was at nearby Baie St. Paul until June 22, identified dysentery as the sickness that was devastating the Metis, although it seems likely that both diseases were then present (G.A Belcourt,"Lettre de M. Belcourt a Mgr. L'Archeveque de Quebec, Dated St. Paul 6 Aout 1846," Rapport sur les Missions Du Diocese de Quebec et Autres Qui en Ont Ci-Devant Fait Partie 7 [July 1847]: 70-71). 42. PAM CMS C.1/M.4: 113 Microfilm reel A78 "Reverend J. Smithurst's Journal from April 1st to July 1st, 1846." 43.The noted painter Paul Kane accompanied the Red River people on their hunt in June of 1846 and made mention of the death of his guide due to measles (I.S. MacLaren,'"I Came to Write Thare Portraits': Paul Kane's Journal of His Western Travels, 1846-1848," The American Art Journal 21, no. 2 [1989]: 28; Garvin, Wanderings of an Artist, 62-66). 44. Originally, Father Belcourt had intended to travel to the mission at Wabassimong on the Winnipeg River, but he was prevented from proceeding by the outbreak of dysentery among his guides in early June. Instead, he obtained permission to accompany the hunters onto the plains (Belcourt, "Lettre de M. Belcourt," 70). 45. Belcourt,"Lettre de M. Belcourt," 70-71, 75; G.A. Belcourt,"Letter from Father G.A. Belcourt to Bishop Loras Dated Pembina, 5 January 1849," The United States Catholic Magazine 1 (6 January 1849): 314;Joseph-Norbert Provencher, "Lettres de Monseigneur Joseph-Norbert Provencher, Premier Eveque de Saint-Boniface," Bulletin de la Societe Historique de Saint-Boniface 3 (1913), 258; Sunder, FurTrade, 101. Bishop Provencher, the sole remaining Roman Catholic priest in Red River after the departures of Fathers Belcourt, Aubert,Tache, and Lafleche, later wrote that sickness was killing many in the three missions of Baie St. Paul, White Horse Plain, and St. Boniface, and that he had had to bury as many as nine in one day, mostly children (Provencher, "Lettres," 258-259). 46. HBCA D.5/18: 89;A.12/3: 322d. 47. PAM CMS C.1/M.4:101,104,194,197 Microfilm reel A78, "Reverend J. Smithurst's Report for the Year Ending Aug 1st, 1846"; Reverend John Smithurst to the Secretaries of the CMS, Red River Settlement, 18 November, 1846. 48. At St. Peter's the disease was relentless: "Since I last wrote to you on the 1st of August I have had to pass through one of the most trying and anxious seasons that has ever

NOTES PAGES 213 TO 215 293 yet fallen to my lot. You will recollect that I then mentioned the prevalence of a very fatal disease, which was making great ravages throughout the whole settlement. During the last 12 days of July there were eleven funerals at the Indian Church, and eighteen in the month of August, making a total of twenty nine in six weeks, out of a population of about 450" (PAM CMS C.1/M.4:196 Microfilm reel A78, Reverend]. Smithurst to the Secretaries of the CMS, Red River Settlement, 18, November, 1846). There were also four more funerals in September for a total of thirty-three during this epidemic (Ibid., 197). Smithurst lost twenty of his students at the Sunday school during the epidemic (PAM CMS C.1/M.4:264 Microfilm reel A79, "Rev J. Smithurst's Report for the Year ending Aug 1847"). 49. For instance, after describing the well-being of his own family, Reverend Abraham Cowley wrote: "When I think of my family circle unbroken while so many around us have been called upon to endure the most distressing bereavements, e.g. the father of a numerous family the only survivor of which I think there were several instances in the R.R. Settlement. I also know of a whole encampment of Indians cut down by it [the dysentery] I think myself highly favoured & praise God for his goodness. Health has long since been established but as every where we have sickness & death warning us of hereafter" (NAC MG 19 E9 F.W. Rice Fonds, Rev. Abraham Cowley to F.W. Rice, Partridge Crop, July 20,1847). 50. PAM CMS C.1/M.4: 115 Microfilm reel A78, "Reverend J. Smithurst s Journal from April 1st to July 1st 1846." 51.HBCAD.5/18:113d-114. 52. A similar opinion was expressed by Adam Beatty and, on August 8, by Alexander Christie (HBCA D.5/18: 95,119). On the 1st Christie had informed Simpson to the contrary, stating that: "I am concerned to say the prevailing malady continues, with much about the usual daily deaths, our shop man at the Upper fort is no better, and another two of the men are taken ill this morning, we are hopeful that as the season advances health will be returned" (Ibid., 93d). See also Simpson to Governor and Committee,York Factory, 23 August, 1846 (HBCAA.12/3: 322d).There was, however, one more sickness in store for Red River later in the year. On December 30, Dr. John Bunn informed Governor George Simpson that "the health of the settlement is still far from good a troublesome fever causes much distress and some casualties" (HBCA D.5/18: 539d). 53. HBCA D.5/17:287;W. E. Ingersoll, "Redcoats at Fort Garry," The Beaver (December 1945): 15. 54. In fact, these first boats belonged to two private traders from the Red River Settlement, Edward Mowat and Thomas Sinclair, who acted as contract freighters engaged by the HBC in the transport to York Factory. Later in the summer, Reverend Cowley learned from the Swan River brigade that "the Measles have been carried in every direction by theVoyageurs who have suffered severely from it and that many Indians and others have died from it" (PAM CMS C.1/M.4: 274 Microfilm reel A79, "Rev.A. Cowley's Journal from July 25th 1846 to July 21st 1847"). 55. Ray, "Diffusion of Diseases," 151; PAM CMS C.1/M.4:144 Microfilm reel A78,"Rev. A. Cowley s Journal from August 1st 1845 to July 28, 1846"; HBCA B.154/a/46: 33d.

294 NOTES PAGES 215 TO 220 56. HBCA B.154/a/46: 4d, 5; B.154/B/3:17-17d; HBCA D.5/17: 414. 57.HBCAD.5/18:30a. 58. For instance, the Lac la Pluie brigade reached Norway House on June 10. HBCA D.5/18: 66d; B.154/a/46: 4, 8, 8d; Ray, "Diffusion of Diseases," 153. 59. Peter Jacobs, Journal of the Reverend Peter Jacobs, from Rice Lake to the Hudson's Bay Territory (Toronto:Anson Green, 1853), 30; HBCA B.154/a/46: 9,11, lid, 13d; D.5/ 17: 277d; B.154/b/3: 27; A.12/3: 320. Rossville was also the home of many of those who worked on the freight brigades between Norway House and York Factory. 60.HBCAB.154/b/3:23. 61. HBCA D.5/18: 539d; B.154/a/46:16-26d. 62. HBCA D.5/18: 66,430; B.154/b/3:18d. 63. HBCA B.156/a/25: 5d-6, 7. 64. HBCA B.156/a/25: 7; B.154/a/46: lOd. 65. HBCA D.5/18:180, 428, 430. 66. HBCA B.220/a/10: 18d; B.198/a/90: 31. And so, Ross felt it necessary to inform Nelson River outpost manager John Isbister not to draw upon any of the Norway House Aboriginal people, telling him: "At all events you must have nothing to do with any of the voyaging Indians of this place, their number is already greatly reduced by deaths and Sickness, and none of the Beren's River Indians are coming here at all next Summer" (HBCA B.154/b/3: 27).This was a refrain heard elsewhere in this part of the Northwest (e.g. HBCA D.5/18:195). For instance, the following year, the surviving tripmen at both Severn and Trout Lake declined hiring on for the next years journey to York (HBCA D.5/19: 420d; B.198/a/90:31,31d; B.220/a/10:18d). In turn, the elevated death rate among the exclusively male boatmen created another problem for the HBC. In 1847, Ross observed that "the lamentable mortality among the Indians last summer has left a vast number of widows and orphans unprovided for" (HBCA B.154/b/3: 21). 67. HBCA B.156/a/25: 3,4, 5, 7. 68. HBCA B.156/a/25: 7,13d, 16d; PAM CMS C.1/M.4:202 Microfilm reel A78, Reverend R.James to the Reverend R.Venn, Red River, 11 January, 1847. 69. HBCA D.5/18: 36,180. 70. HBCA D.5/18: 38-38d, 107. 71. Lois Halliday McDonald, ed., Fur Trade Letters of Frances Ermatinger Written to His Brother Edward During His Service with the Hudson's Bay Company (Glendale, California: The Arthur H. Clark Co., 1980), 271. 72. At one point Hargrave's children suffered from measles although, unlike many of the Aboriginal people, they recovered. HBCA D.5/18:130d; Margaret Arnett Macleod, ed., The Letters ofLetitia Hargrave, Publications of the Champlain Society (Toronto:The Champlain Society, 1947), 221-222; PAM CMS C.1/M.4:185 Microfilm reel A78, Reverend R.James to Reverend H.Venn,York Factory, 27 August, 1846. 73. The population about York Factory had declined considerably some years before, as many Cree had abandoned the lowlands for interior fishing stations or the settlement of Rossville near Norway House (HBCA D.5/11: 4).Thus, even the thirty-one

NOTES PAGES 220 TO 224 295 people whom Hargrave's men buried were in all likelihood a significant portion of the local Aboriginal population. 74. Macleod, Letters ofLetitia Hargmve, 221-222. 75.This route was an ancient one, but had only just come into use by the Trout Lake men(HBCAD.5/ll:2d). 76. HBCA B.198/a/90: 4-4d, 5; D.5/18:131d, 428. 77. HBCA D.5/18: 428; B.198/a/90: 4d. 78. HBCA B.220/a/9: 5d. 79. HBCA B.198/a/90: 5-5d. 80. HBCA B.198/a/90: 6d, 7,7d, 9,10,11,18d, 19,25,27,28d. 81. HBCA B.220/a/8: 35; B.220/a/9: 5d, 14; B.220/a/10: 20; D.5/19: 420; B.156/a/25: 37. 82. HBCA B.220/a/9: 24. Here again is evidence of the limited penetration of the 181920 measles epidemic into the northern part of the Petit Nord. 83. It is impossible to state the exact timing of this diffusion as there is, unfortunately, very little that survives in the way of primary accounts for this period. It is not likely that either disease appeared in the Boundary Waters prior to early June, however. As they did every year, large numbers of people began to gather on the Winnipeg River about the beginning of June, to celebrate the rites of the Midewiwin. In 1846 Paul Kane was at Fort Alexander on June 11 and attended a medicine ceremony where he was met by "grate swarems of Indanes" (MacLaren, "Thare Portraits," 24). Although he spent some time observing these people, the artist wrote nothing of sickness among them. 84.HBCAB.107/a/25:l. 85. Indeed, Father Belcourt was prevented from accompanying Father Aubert on the journey to Wabassimong by the outbreak of dysentery among his guides (Belcourt, "Lettre de M. Belcourt," 70). 86. HBCA B.154/a/46: 3d, 8; D.5/17: 287; PAM MG 7 D2 L'Esperance 1: 135; PAM MG 7 D13 Microfilm reel 1 Belleau Collection, Bishop J.-N. Provencher to Bishop Turgeon, St. Boniface, 4 December, 1847. 87. HBCA D.5/18:105. 88. HBCA B.107/a/25: 2d; B.107/a/25: 4. 89. HBCA D.5/18:19-20. 90. Ibid., 232. 91. Certainly measles was present well before August 17, as on that date Lac Seul trader Charles McKenzie noted the presence of measles among the Eagle Lake people who had contracted it while summering at Lac la Pluie. HBCA B.107/a/25:2;Waisberg, "Ethnographic and Historical Outline," 127. 92. HBCA D.5/18: 232; D.5/19:129d; A.12/3: 447d. In an earlier letter, Finlayson told Simpson that the Aboriginal people were mourning many of their friends and relatives who had succumbed. The reference to following the chase is, obviously, an allusion to the hereafter.

296 NOTES PAGES 225 TO 229 93.These women had departed Lac Seul on May 19. McKenzie wrote: "No less than 3 of our Ladies went off for Red River to visit their friends in that quarter— + the two young lads who passed the winter here—two only of these are to be back this summer—the other being the widow of the late Samuel Rat, is to remain "with her relations" (HBCA B.107/a/24:23d). 94.HBCAB.107/a/25:l. 95. HBCA B.3/b/73:12d, McKenzie to Corcoran, Lac Seul, 20 December, 1846; B.107/ a/25: 3d. 96.HBCAB.107/a/25:5. 97. HBCA B.107/a/25: 29, 6, 6d; B.3/b/73:12-12d, McKenzie to Corcoran, Lac Seul, 20 December, 1846. 98. HBCA B.107/a/25: 2, 5, 6d. In turn, this may suggest that those few Aboriginal groups in the region who had adopted agriculture had a better chance of survival if an epidemic struck when crops were edible, than those who relied on the chase. 99. HBCA B.107/a/2:14; B.107/a/25: 9; B.107/a/25: 9. 100. There are many ricing lakes in the area, and it is not known which one McKenzie referred to as Rice Lake. One clue is that in an earlier journal he stated that Rice Lake was Gull Lake (HBCA B.107/a/9: 5d). Gull Rock Lake lies along the route to Red Lake, a short distance to the northwest of Lac Seul, and this may be McKenzie s Rice Lake. In 1836 a Lac Seul trading party had left for Rice Lake on the llth of September and returned only three days later (HBCA B.107/a/15: 3d). 101. Although the people of Sturgeon Lake may have escaped the measles in 1819-20, those who resided there did not in 1846.These were not the same people, however. As at Lac Seul, new people had settled around the lake, in this case the Nipigon band who were moving westward (HBCA B.107/a/5d). 102. HBCA B.3/a/73:12d; B.107/a/25: 2,2d, 3, 4, 5, 9; B.155/a/587d. 103. HBCA B.155/a/58:7d, 8,1 Id; D.5/19:128; B.107/a/25: 2, 3d, 9,12, 26, 31; B.3/b/ 73:12. 104. HBCA B.3/b/73:12d. 105. On January 23, 1847, he wrote,"Two Cranes arrived they paid their debts and trade a little they are to start tomorrow, they report that six of their wives + children have died of the Measels," and on the 28th, "Kanandouray + two of his brothers arrived they bring very little. They report that 12 of that family have died, viz.WhiskeyJacob, Snake, 2 women + 7 children all of the measles" (HBCA B.155/a/58:12d). 106. Bishop, Northern Ojibwa, 157,160,162; HBCA B.3/b/73:12d.The percentage was undoubtedly much higher. There had been frequent epidemics since the earlier estimates had been made and the trend appears to have been downwards. Thus, the numbers of people trading at Lac Seul and Osnaburgh House may have been significantly less by 1846. As well, there seem to have been many victims who were not included in the fifty-four. 107. HBCA B.156/a/25: 7; B.154/a/46:4; B.154/a/46:11; D.5/17: 277d; B.107/a/24: 23; B.3/c/l:lad. 108. HBCA B.3/b/73:1 lad, 29d; B.155/a/58:12d, 21; Edward S. Rogers and Mary Black-Rogers, "Who Were the Cranes? Groups and Group Identity in Northern

NOTES PAGES 229 TO 234 297 Ontario," in Approaches to Algonquian Archaeology, edited by M. Hanna and B. Kooyman (Calgary: University of Calgary, 1982). 109. HBCA B.3/V152: 20d. See also HBCA D.5/19:128; B.3/b/73:16. 110.HBCAB.123/a/50-52;B.3/a/152-153;B.135/a/151. 111. Measles did strike Fort William on its westward course, late in 1845, and an unknown number of Lake Superior people were infected while at Manitoulin Island or Sault Ste. Marie the same year. 112. Glazebrook, The Hargrave Correspondence, 312;Jacobs,Jo«rmz/, 10; United States, Indian Affairs Report 1845,498; W. E. Logan, Remarks on the Mining Region of Lake Superior; Addressed to the Committee of the Honorable the Executive Council, and Report on Mining Locations Claimed on the Canadian Shores of the Lake (Montreal: Lovell & Gibson, 1847), 10; PAM CMS C.l/0, Microfilm reel A84, Reverend William Cockran to the Reverend R. Davis,Toronto, 11 August, 1846; HBCA D.5/8: 347d, 435d;A.12/3: 135d, 368d, 369d. 113. HBCA D.5/19: 318. 114. HBCA D.5/19:161d. 115. John Swanston wrote to Governor Simpson from Michipicoten on July 9,1846:"! am sorry to acquaint you that nearly the whole of the inhabitants of this Establishment are suffering severely from Colds, the cough attending which is most distressing and found by all more severe than the Influenza we had in '43—I have become so weak from its effects, that for a few days could scarcely manage to go about and altho far from being well, am improving a little" (HBCA D.5/18: 28d). 116. HBCA B.3/b/73:17-17d. 117. HBCA B.156/a/25: 7d, lOd. 118. HBCA B.156/a/25: 27. Of course, the trader's motives in providing aid was not purely humanitarian, as, Robertson explained, "These are great drawbacks to the fur hunting." 119. Black et al., "Epidemiology of Infectious Disease," 120. 120.John W.Verano and Douglas H. Ubelaker, "Health and Disease in the PreColumbian World," in Seeds of Change, edited by Herman J.Viola and Carolyn Margolis (Washington and London: Smithsonian Institution Press, 1991), 215-216. 121. It should be noted, however, that some of these indigenous treatments could have provided a degree of symptomatic relief from these new diseases, if only to make the victim more comfortable. 122. In his study of this same measles epidemic in the Pacific Northwest, Robert Boyd identified these treatments as major reasons for extreme fatalities among traditional groups, compared to those who took the simple medical advice and assistance of the Whites (Boyd, "Pacific Northwest Measles Epidemic," 41). Likewise, many died near the juncture of the Powder and Snake rivers, in eastern Montana, during the measles epidemic, due to the use of the cold plunge for treatment (Ebbert,"Joe Meek'sTrip," 264). The people of Fiji attempted to cool their bodies using almost identical treatments during a measles epidemic in 1875, with similar results (Cliff et al., Island Epidemics, 159). 123.HBCAB.156/a/25:ll.

298 NOTES PAGES 235 TO 238 124. Perhaps the most telling example of the high price paid by traditional groups was with smallpox vaccination. In the Pacific Northwest and on the plains, for instance, traditionalists championed opposition to the procedure. During the subsequent smallpox epidemic of 1837-38, many died among those who refused vaccination, and in the Pacific Northwest, at least, it was claimed that this "had the effect of increasing the influence of the missionaries" (Hiram Martin Chittenden and Alfred Talbot Richardson, eds., Life, Letters and Travels of Father Pierre-Jean De Smet, SJ. 1801-1873, four vols. [NewYork: Francis P. Harper, 1905], 1235; Ewers, Five Indian Tribes, 115). 125. Indeed, according to Governor George Simpson in 1836, the HBC posts spent considerable effort "administering to the sick and infirm, every Trading Establishment being in fact an Indian Hospital, where those who are unable to follow the Chase during the Winter months, are fed, clothed, and maintained throughout that inclement season with the most tender solicitude..." (HBCA E.18/3:11).This was another facet of the company's traditional paternalistic role in times of want, a role it continued to play into the late nineteenth century. See Arthur J. Ray, "Periodic Shortages, Native Welfare, and the Hudson's Bay Company 1670-1930," in The Subarctic Fur Trade: Native Social and Economic Adaptations, edited by Shepard Krech, III (Vancouver: University of British Columbia Press, 1984). 126. Thomas Simpson, Narrative of the Discoveries on the North Coast of America; Effected by the Officers of the Hudson's Bay Company During theYears 1836-39 (London: Richard Bentley, 1843), 67-68. 127. Burpee Journals and Letters, 258-259. 128. HBCA D.5/18: 466-466d. 129. HBCA A. 12/3: 444d. 130. HBCA B.156/a/25: lOd; B.107/a/25: 6d.

Conclusion 1. In identifying these earlier epidemics, this study has challenged a common belief in the secondary literature that the smallpox epidemic of 1779 to 1783 was the first significant or at least the first recorded epidemic in western Canada. An extreme example of this belief was expressed by James G.E. Smith (James G.E. Smith, "Review of Keepers of the Game: Indian-Animal Relationships and the Fur Trade," American Ethnologist 7, no. 4 [November 1980]: 811), who stated that "the Hudson's Bay Company archives do not provide evidence of epidemic disease [among the Cree and Chipewyan west of Hudson Bay] until the winter of 1781-82." Instead, it is necessary to look much earlier than 1781 for an epidemic baseline for the Canadian Northwest, and especially in the Petit Nord. Moreover, given the frequency with which epidemics struck the people of the Petit Nord prior to the merger of the HBC and the NWC, Young's (Health Care, 97) characterization of the "Early contact" period (1670 to 1821) as one of excellent health among the people of the central subarctic needs to be reassessed.

NOTES PAGES 240 TO 242 299 2. For instance, influenza seems to have been introduced to the islands of the Pacific long before measles, whooping cough, smallpox, and mumps made their appearance (Cliff et al., Island Epidemics, 131-245). 3. Michael K.Trimble,"Infectious Disease and the Northern Plains Horticulturalists:A Human Behavioral Model," in Plains Indian Historical Demography and Health: Perspectives, Interpretations, and Critiques, edited by Gregory R. Campbell (Plains Anthropologist, memoir 23, Part 2,1989), 42-43.The singular ability of the smallpox virus to survive for prolonged periods on fomites also enhanced its diffusion potential. Other characteristic or possible forms of transmission also aid or detract from a disease's diffusion potential. For instance, dust infected with diphtheria can cause disease after several weeks, and some people may act as chronic asyptomatic carriers for a few diseases such as typhoid and paratyphoid (Cliff et al., Deciphering Global Epidemics, 92-93). Both would certainly favour the appearance, and reappearance, of the disease, even in a smaller population. 4. This appears to have been the case with the crowd diseases and the Petit Nord. If most of the contact between the isolated population and the disease pools is through the movement of adult individuals who were born and raised in the proximity of a large urban area, then there would be limited opportunities for crowd diseases to spread to the region. Conversely, diseases that do not provoke a lasting immunity, including the respiratory diseases that flooded the Petit Nord after the 1820s, would have a much greater opportunity to arrive through these connections, since most of these people would be susceptible. 5. An excellent overview and analysis of the state of health of the Aboriginal people of the central subarctic after 1846 can be found in Kue Young's Health Care and Cultural Change. Young (40) noted that all of the most common diseases to strike the people of this region during the first decade of the twentieth century were infectious, including several acute infectious afflictions. 6. Canada, "Report of the Deputy Superintendent General of Indian Affairs," in Annual Report of the Department of the Interior for theYear Ended 30th June, 1877 (Ottawa: Government of Canada, 1878), 12; Canada, "Report of the Deputy Superintendent General of Indian Affairs," in Annual Report of the Department of the Interior for theYear Ended 30th June, 1876 (Ottawa: Government of Canada, 1877), 38; Canada, "Annual Report of the Department of Indian Affairs," Sessional Papers XL (Ottawa: Government of Canada, 1906), xxi, 23,191. The diffusion of smallpox was limited during this era, no doubt in large part due to the use of vaccine by the Canadian government, which assumed responsibility for the health of the Aboriginal people following the sale of Rupert's Land by the HBC. One of the main duties of the doctors who travelled with the treaty parties or visited Aboriginal communities during the annual annuity payments was to vaccinate the people (Young, Health Care, 101). 7. Canada,"Indian Affairs Report," 1906,191; Elizabeth Arthur, ed., Thunder Bay District 1821-1892:A Collection of Documents,The Publications of the Champlain Society, Ontario Series, vol. 9 (Toronto:The Champlain Society, 1973), 175-176; Flora Beardy and Robert Coutts, eds. and comp., Voices from Hudson Bay: Cree Stories fromYork Factory, Rupert's Land Record Society Series (Montreal and Kingston: McGillQueen's University Press, 1996), 61. Measles had also been present at York Factory at

300 NOTES PAGES 243 TO 244 some point between 1864 and 1884, and an outbreak of scarlet fever at the post in 1862-63 had claimed thirty-five lives (Percy W. Mathews, "Notes on Diseases Among the Indians Frequenting York Factory, Hudson's Bay," Canadian Medical and Surgical Journal 13 [1884-1885]: 459).Alanson Skinner ("Notes on the Eastern Cree and Northern Saulteaux," Anthropological Papers of the American Museum of Natural History 9 Part 1 [1911]: 161) noted that the Northern Ojibway had been swept by measles in the early 1890s.The measles at Norway House in 1905 was accompanied by mumps, scarlet fever, and diphtheria, yet another compound epidemic. 8. Mathews, "Notes on Diseases," 450. 9.Young, Health Care, 38-40; Bishop, Northern Ojibwa, 89; Skinner, "Notes on the Eastern Cree," 161; D.Ann Herring,'"There Were Young People and Old People and Babies Dying Every Week': The 1918-19 Influenza Pandemic at Norway House," Ethnohistory 41, no. 1 (1993). During 1919 the death rate at Norway House was 1467 1000 and at Cross Lake was 137/1000 (E. L. Stone, "Tuberculosis Among the Indians of the Norway House Agency," The Public Health Journal 16, no. 2 [February 1925]: 79, 80). Excluding this anomalous year, the death rate of the people of the Norway House Agency was about 25.5/1000 during this period. 10. Mathews, "Notes on Diseases," 450;Young, Health Care, 39. As well,Alanson Skinner, an anthropologist who travelled along the Albany River in 1909, identified "consumption"' as one of the most common diseases among the Aboriginal people (Skinner,"Notes on the Eastern Cree," 161). Herring and Hoppa (D.Ann Herring and R.D. Hoppa, "Endemic Tuberculosis Among Nineteenth Century Cree in the Central Canadian Subarctic," Perspectives in Human Biology 4, no. 1 [1999]) found that TB was endemic among the Cree at Moose Factory by the second half of the nineteenth century. 11. Canada, "Indian Affairs Report," 1906, 277.The situation remained bleak over the following decades, even in the north where mortality rates appear not to have been as high. In 1925 Dr. E.L. Stone, the medical officer for the Norway House Agency, noted that the disease was widespread among the people of his agency, claiming the lives of thirteen of the 700 people during the previous year (Stone, "Tuberculosis," 77). It should not be thought that acute infectious diseases ceased to be a significant health threat, however. Indeed, certain disorders, such as the respiratory infections, continue to be much more severe among these people than among the general population (Young, Health Care, 51-53). 12. David A. Stewart, "The Red Man and the Plague," Canadian Medical Association Journal (December 1936): 674. 13. Although the fear of reserves declined as effective therapies forTB were developed, it may be beginning to re-emerge. In recent years multiple drug-resistant strains of TB have surfaced among Aboriginal people in western Canada. Unless researchers approach this subject with sensitivity to the past, they may inadvertently repoliticize the disease, ushering in a new era of resentment as the reserves are once again treated as a source of disease for the mainstream population. 14. Nevertheless, researchers have noted that despite the availability of these effective drug therapies, the decline in morbidity has been neither as steep nor as complete among Canada's Aboriginal people as it has been among the remainder of the population. For instance, as of 1994 the incidence ofTB among registered Aboriginals

NOTES PAGE 244 301 in Canada was 47 per 100,000, greater than six times that of the Canadian population as a whole (Kathryn Wilkins, "Tuberculosis, 1994," Health Reports 8, no. 1 [Summer 1996]). Moreover, researchers have also identified significant variations in the provincial rates of TB among registered people, with the lowest rates found in the eastern provinces (7/100,000), and higher rates in British Columbia (52/100,000), the prairie provinces (79/100,000), and the Territories (97/100,000) (Vernon H. Hoeppner and Darcy D. Marciniuk, "Tuberculosis in Aboriginal Canadians," Canadian Respiratory Journal 1, no. 2 [March/April 2000]). See alsoT. Kue Young and I. Casson, "The Decline and Persistence ofTuberculosis in a Canadian Indian Population: Implications for Control," Canadian Journal of Public Health 79 (1988). IS.Waldram, Aboriginal Healthffoung, Health Care; T. Kue Young, "Changing Patterns of Health and Sickness Among the Cree-Ojibwa of Northwestern Ontario," Medical Anthropology 3, no. 2 (1979);T. Kue Young, The Health of Native Americans: Towards a Biocultural Epidemiology (Oxford and New York: Oxford University Press, 1994). 16. Young, Health Care. The decline of infectious diseases was accompanied by a general decline in mortality rates among Canada's Aboriginal people as the twentieth century wore on, fuelled in part by major improvements in health care. 17. Essentially, the period following 1846 in the Petit Nord saw these people undergo a variation of Omran's epidemiologic transition (A.R. Omran,"The Epidemiological Transition—A Theory of the Epidemiology of Population Change," Milbank Memorial Fund Quarterly 49, no. 4 [October 1971]).This took them from the "Age of Pestilence," when rampant infectious diseases yielded poor life expectancy and high mortality rates, to the "Age of Degenerative and Man-Made Disease," when life expectancy had increased substantially and the major epidemic diseases had ceased to be a dominant health concern, only to be replaced by the diseases of modern life. However,Young (Health Care) has pointed out that the plight of the Aboriginal people of the subarctic does not conform precisely to any of Omran's three models (Classical, Accelerated, or Contemporary), particularly with respect to the continued (though lessened) importance of infectious diseases and the staggeringly high death rates from accidents and violence. It may be, then, that a new variation on Omran's transition is needed in order to explain the recent changes in the health status and population dynamics of Canada's Aboriginal people.

This page intentionally left blank

Bibliography

Full bibliographic data is provided in the Endnotes with the first reference to the source cited. A complete bibliography is posted on the Web Site of University of Manitoba Press, at www.umanitoba.ca/uofmpress.

Primary Documents Hudson's Bay Company Archives (HBCA) The voluminous records of the HBC are housed in the Provincial Archives of Manitoba, in Winnipeg. Individual records are found within several sections, with numerous subsections in each. Documents cited in this book are taken from the following sections. Further information and an on-line finding aid may be found on the website of the Provincial Archives of Manitoba. Section A:

London Office Records

Section B:

Post Records

Section C:

Ships' Records

Section D:

Governor's Papers and Commissioner's Office

Section E:

Private Records

Section Z:

Miscellaneous Records

Citations of "HBCA Files" refer to search files compiled on a variety of subjects by the HBCA archivists. These files include information collected on a specific subject and may be consulted at the HBCA. "Post Histories" have been created for many of

304 BIBLIOGRAPHY the company's posts and forts and these are an excellent source of basic information about the posts. Provincial Archives of Manitoba (PAM) PAM CMS

Papers of the Church Missionary Society

MG 1 C9

Hudson's Bay Company 1719-1913

MG 2 Al

Selkirk Papers

MG 2 A6

Red River Settlement Papers 1823-1826

MG 2 C19

Thomas Bunn Papers 1804-1857

MG 2 C38

Peter Garrioch Papers 1838-1847

MG7D2

Sisters of Charity (Grey Nuns)

MG 7 D13

Belleau Collection

MG 10 F4

Minnesota Historical Society

MG 12 Al

Adams George Archibald Papers [1870-72]

National Archives of Canada (NAC) MG 19 A4

Alexander Henry — "Copy of a Letter from Alexander Henry to Sir Joseph Banks"

MG19A8

David Thompson Papers

MG 19 A40

William Douglas Lane Papers

MG 19 C4

Masson Collection

MG 19 E9

F.W. Rice Papers

MG 21

Frederick Haldimand Papers

Minnesota Historical Society (MHS) American Board of Commissioners for Foreign Missions Papers Correspondence [A.B.C.F.M.]

Index

A

Abbitywabino (trading captain), 110 Abbitywabino's son, 110 Abenaki Nation, 46 Acute Respiratory Diseases (ARDs), 4,75, 76, 87-89,122,125 diffusion potential of, 14 episodes of: Albany Fort, 90,129-130; Albany Lowland Cree, 77; Antarctic research stations, 90; Churchill, 90; Escabitchewan, 131; Gloucester House, 90; Henley House, 90,127128; Lac la Pluie, 131; Martin's Falls, 132; Moose Factory, 130; New Brunswick House, 152; Petit Nord, 175,176-178; Severn, 90; Spitzbergen, 90; Tristan da Cunha, 90; York Factory, 80-81,86-87,89-90 adenovirus(es), 87 Adhemar, Patrick, 225 Akimiski Island, 50 Alaska, measles in, 206 Albanel, Father Charles, 42, 48 Albany Fort, 44 disease episodes at, 114-115,128-129; ARDs, 90,129,195-197; conjunctivitis, 85; influenza, 86; pneumonia, 86; smallpox, 115-116; throat infections at, 86,115; whooping cough, 175-176 disease history of, 54-55,84-85,85-86, 125,135 and inland contacts, 120-121, 124-129 Algonquin Nation, 32, 46 American Fur Company (AFC), 169,178 American Revolution, 101,123-124

The Americas and indigenous diseases, 5,32, 247n5 Anderson, James, 204,205 Antarctic research stations, ARDs at, 90 antigenetic shift, 88, 180, 265n27, 285n66 Antikiskickwescam (trading captain), 113 Archekishick (Lowland Cree leader), 116 ARDs. SEE Acute Respiratory Diseases (ARDs) Arikara Nation, 70,148 disease episodes among: measles, 80, 206; smallpox, 67 disease history of, 26 Assiniboine Nation disease episodes among: measles, 80,138, 148, 207; smallpox, 97,107 Upper Missouri connections of, 169 wars of: GrosVentres, 105; Shoshone, 1781,99 Assup (Lowland Cree trading captain) ,115— 116 Atkinson, George, 143 Atsina Nation disease episodes among: measles, 138; smallpox, 99 Attikameque Nation, 46, 49 Aubert, Father Pierre, 223 Aulneau, Father Jean-Pierre, 65-67 Aulneau Massacre, 1736,65-67 Australia, emergence of epidemics in, 40 Ayer, Frederick, 171 B Ballendenjohn, 186,203-204 Bartlett, Maurice, 11,239 Basswood Lake, smallpox at, 108

306 INDEX Bayley, Thomas, 50 Beale, Anthony, 52 Bearjohn K., 77 Beauharnois, Governor of New France, quarantines Quebec, 61—62 Belcourt, Father George-Antoine, 212 belief systems, Aboriginal disease in, 283n55 Berens River scarlet fever at, 145-146,188 Biard, Father Pierre, 27-28 Bishop, Charles, 144,228 bison hunt, dysentery in, 212—213 Black, Francis, 8-9 Blackfoot Nation disease episodes among: measles, 138; smallpox, 97,99 Blood Nation disease episodes among: smallpox, 99 war of against Shoshone, 1781,99 Bolland, William, 126-127 BorcherJ.R., 162 Boston smallpox epidemic, 60-61 Bourassa, Rene, 66 Boyd, Robert, 189,210,279nl4,297nl22 Brandon House disease episodes at: measles and whooping cough, 148,150 Brazil, 138, 250n2 Bruguiet, Monsieur (at Fort Berthold), 213 Brule Sioux, 287n96 Brunswick House, 112 bubonic plague, 6,32,36 Bungee (Ojibway), 72,98,101 SEE ALSO Ojibway burial mounds at The Forks, 106—107 Button, Thomas, 36 C CadotteJean-Baptiste, 107,108 Calder, Marcus, 146 Campbell, Sarah, 26 Carrier, Jacques, 25 Cat Lake, 145,179 Catlin, George, 160 Caucaukes (trading captain), 111 Caughnawaga, smallpox at, 61—62 Caupermertissnewinnekee (trading captain), 112 Charles Fort, 38, 51 Charlevoix, Father, 50 Charlotte (HBC ship), 90 Chequamegon, 65 Cheyenne Nation, 96-97

chickenpox, 4,183 CCSof,247nll episodes of: Lac Seul, 183; Northwest, 183-184; Petit Nord, 156 childhood disease(s), 8-9 chincough. SEE whooping cough Chipewyan of Athabaska, 134 cholera episodes of: Britain, 291n35; Montreal, 281n29; world pandemic of 1826-32, 156,281n29 Christie, Alexander, 207,215, 217 Churchill, 101 disease episodes at: ARDs, 90; pneumonia, 90 HBC quarantine against smallpox, 101 Claude, Father Allouez, 254n42 Cliff, Andrew D., 13-14 clothing and Aboriginal health, 233 Cock, Robert, 152 Cocking, Matthew, 99-102 Cockran, William, 182-183,200,206,208, 291n30 cold water cure dangers of in treating imported diseases, 233-234 colonies, European, 252n20 Columbia River, disease episodes at, 189 Columbian Exchange, 5 Comanche Nation, 96—97 compound epidemics, 192 conjunctivitis, 85 Cook Islands, 210 Cooper, John, 65 Corcoran, Thomas, 202,228-229,231-232 coronavirus(es), 87 Cowley, Abraham, 211-212,215 Cox, Ross, 94-95 Cranes (Ojibway), 229 Cree, Albany Homeguard, 114,128-129 disease episodes among: ARDs, 89; influenza, 130 Cree, Knee Lake, 219 Cree, Lowland disease episodes among, 51, 54-55, 114; ARDs, 77,80; dysentery, 220; fever, 55; measles, 220; pleuritic fever, 85; smallpox, 93,103 Cree, Northern, 68 Cree, Severn River, 116 Cree, Upland disease episodes among, 77, 80, 86; smallpox, 100 Cree, Western (Keskachewan), 80

INDEX 307 Cree,York Factory Homeguard disease episodes among: smallpox, 71, 100-102 Cree Nation disease episodes among: measles, 138; smallpox, 97,99 Upper Missouri connections of, 169 war(s) of: GrosVentres, 105; Shoshone, 99 Creighton, Charles, 248nl8 Cristinaux (Cree), 70 critical community size (CCS), 8—9,11, 247nll Cromartiejohn, 191,194,220-221 Crosby, Alfred, 5,124 Crow Nation, 96-97,117 crowds and disease diffusion, 65,239 culture change, post-epidemic, 117-118 Cumberland House disease episodes at: influenza, 181; smallpox, 100; whooping cough, 176 D Dakota Nation, 290n21 Dakota Rendezvous (pan-Siouan trade gathering), 65 De Brehant De Galinee (French explorer), 49 de Noyon, Jacques, 44 Decker, Jody, 86-87 D'EgliseJacques, 122 Denig, Edwin, 106-107 Denys, Louis, Sieur de la Ronde, 66 Detroit, 64 diarrhoeal disease diffusion of: HBC brigades, 131; PresentGiving Ceremony, 186 episodes of: Martin's Falls, 131 diffusion of disease(s), 32, 249n27 by Aboriginal people, 31, 52, 95-100, 105-108,197, 207, 227, 229,238, 253n34 on fomites, 56,101, 299n3 mechanisms for, 14-15,119-124,124, 153; crowds, 65,165-167,170,188, 203-204,239; fur traders, 62-64,124, 129-130,131,138-139; inland expansion of fur trade, 59,85; migration, 13,22,28,126,189; population size, 122—123; post-epidemic panic flight, 78; trading networks, 65,9597,102; transportation systems, 31, 43, 49, 78,119-124,143,169,171174,178-181,183,195,214; travel, 13, 31,119-124,169; urban disease

pool emergence, 122—124; war(s), 78, 82-85, 97-100,105-106,148; wild rice harvest gathering, 141,224,227— 228 order of introduction, 240—241 in Petit Nord, 42-43,165-167,165171,167-171,238 at Present-Giving Ceremony, 165— 167,170,186,203-204 Red River nexus of, 167-170,180, 238 SEE ALSO critical community size (CCS) diffusion potential, 14—15 disease in Aboriginal belief systems, 283n55 disease pool(s), 7 emergence of in U.S., 118,122,238, 278n7 expansion of to Petit Nord, 137 Fort Clark, 169 London, 40 Massachussetts Bay, 29 MesoAmerican, 21—26 urban, 7, 9, 91 dispersion of communities and decline of disease episodes, 230 Dobyns, Henry on: post-Columbian disease diffusion, xi— xii, 22-26, 28, 65,72-73; postepidemic behaviour, 70,72,109 domestication of animals and disease transmission, 6—7 Druillettes, Father Gabriel on disease at Sault Ste. Marie, 1670,49 Ducharme, Dominique reports on whooping cough at Portage de 1'Isle, 1806,132-133 Duluth, Sieur, 43 dysentery described, 209-210 diffusion of, 190,209-214,216,223-230 episodes of: Albany Fort, 1765,85; bison hunt, 212—213; Lac la Pluie, 152; Lake Superior District, 175; N. Atlantic coast communities, 29; Norway House, 152,216,219-222; Oxford House, 219; Pacific Northwest, 210; Petit Nord, 178, 190-195; Red River, 207; Sault Ste. Marie, 1670, 49;York Factor, 135 E Eagle Hills, smallpox at, 100 Eastern seaboard. SEE North Atlantic Coast Ecuador, 22,249n27

308 INDEX Eliud,Jim (Ojibway chief, Lake of the Woods), 65-66, 67 epidemic transition, 12-14, 248n23 epidemic (s) compound, 137; Petit Nord, 185-187, 242-243; Red River, 186 consequences of: population vacuums, 72; sociocultural change, 235-236 defined, 247n6 factors affecting mortality in, 232-233 SEE ALSO post-epidemic behaviour epidemiological transition, 248n23 Erie Canal, 160 Ermatinger, Edward, 220 Ermatinger, Francis, 220 erysipelas, 122,187-188 Escabitchewan, 145 disease episodes at, 128;ARDs, 131; influenza, 131; measles, 146 Esh-ke-bug-e-coshe. SEE Flatmouth (Leech Lake Ojibway leader) Etechemins (New Brunswick Malecite), and smallpox, 46 evidence for historical epidemiology archaeological, 23-27,67 HBC records, xii-xiii, 37, 94-95,246n6 mnemonic pictographs, 65 oral tradition, 67,116 written records, 37 Ewart, William, 55 F Faeroe Islands, 138,249n25 Falconer, William, 102-103 febrile disease episodes at Lac Seul, 131 at Sandy Lake, 131 Fidler, Peter, 140,148 Fiji, 163 disease episodes in: measles, 138; smallpox, 41 Finlayson, Duncan, 188 Finlayson, Nicol, 141,152,223,224 Flatmouth (Leech Lake Ojibway leader), 105, 107 Fond du Lac, 108 Fort Clark, 169,178 Fort Prince ofWales. SEE Churchill Fort William, 182 Foxe, Luke, 36 French and Indian Wars. SEE Seven Years' War, 1756-63 fur trade companies competition among, 119,121, 129

merger of, 167 records of, xii-xiii, 37,94-95,246n6 fur traders disease diffusion by, 43, 49,62-64,129130,131,138-139 inland expansion of, 59, 85 G Gabriel, Father Druillettes, 34 Garbut.John, 86 Garden Island, 141 Garry, Nicholas, 140-141 Gaspesiens and smallpox, 46 gathering, ceremonial, at Great Lakes. SEE Great Lakes Present-Giving Ceremonies Gill, Robert, 225,226 Gloucester House, 107,121 disease episodes at, 127-128; ARDs, 90; smallpox, 112,125 Gloucester House Uplanders, 110 Goodwin, Robert, 127 goose hunt, 116 Gorst, Thomas, 50 Graham, Andrew, 84,86 Graham, James, 152 Grant, Captain. SEE Ookemowescume "Great Death," 85,128 Great Lakes Present-Giving Ceremonies disease diffusion at, 165-167, 170, 203204; diarrhoeal disorder, 186 Greater New England urban system, 61 Greysolon de la Tourette, 43 GrosVentres disease episodes among: measles, 138; smallpox, 99,105-106 Guatemala, epidemics in, 22 gun trading system and disease diffusion, 96 Gunn, Donald, 103, 107 H Haggett, Peter, 41 Hannah (HBC ship), 56 Hargrave, James, 194,217-223,219-225, 280n25 Hargrave, Letitia, 220 Harris, R. Cole, 117 Harstad, Peter, 160 Hawaii, 206,210 Heidenreich, Conrad, 33 Henige, David, 26 Henley House, 112,113,121 disease episodes at, 127-128; ARDs, 90; throat infections, 86 disease history of, 85—86 Henry, Alexander, The Younger, 94,106,133

INDEX 309 hepatitis, 122 Hidatsa Nation, 148, 272n6 disease episodes among: measles, 80, 206; smallpox, 105-106 Hind, Henry Yule, 157-159 Hodgkin, Thomas, 171 Hodgsonjohn, 102,132 Hood, Robert, 149,151 horse trading system, 95-96, 238,267nlO Houghton, Douglass, 78,109 Hudson, Henry, 36 Hudson Bay disease history of to 1670,36 Hudson House, 100 Hudson's Bay Company, 38,101,119-121, 121 attempts to alleviate disease impact, 100— 101,146,189, 203-204, 226, 234235, 268n8, 298nl25; quarantines against: scarlet fever, 189; smallpox, 101 and disease diffusion, 171, 200-202, 214, 219-223 epidemiological impact of in Petit Nord, 38,41 records of, xii-xiii, 37,94-95,246n6 reorganization of, 1810,121,135 ships of: and disease diffusion, 77, 89— 91,115,125,129 Southern Department of created, 121 transportation system of, 38-41,178179; and disease diffusion, 131, 171174,180-181,183,192-195, 200202,217-219,220-222 vaccination program of, 157 Hunter, James, 187 Huron Nation, 33-34,62,69-70 disease episodes among, 32; smallpox, 46 disease history of, 24, 254n41 Hutchins, Thomas, 86,114 I Iceland, measles in, 9, 13-14 He a la Crosse disease episodes at: influenza and measles, 216; mumps, 185; whooping cough, 176 Illinois Nation, 62 infections, chronic, 6, 27,28, 52,244,248n22 diptheria carriers of, 299n3 dysentery, 210 syphilis, 247n6 tuberculosis, 243, 247n6

infections, crowd, 5-15,21,26-29,31, 38,40,239-241,243 diffusion of, 14 transformation of to childhood diseases, 7,12 transmission of: direct (human to human), 5—6; vectored (animal to human), 6—7 influenza, 4, 6, 8, \92-\95passim, 247n8 antigenetic shifts in, 180 described, 88-89 diffusion of, 14, 88,182,190-195,200202,216, 287n96 episodes of: Albany Fort, 85,86,130; among Huron, 32; Boundary Waters, 179-183; Cumberland House, 181; Europe, 88,127-128; Fort William, 182; Henley House, 86; He a la Crosse, 216;James Bay, 33; Lac Seul, 200202; Long Lake, 231; Martin's Falls, 131; Moose Factory, 130; N.Atlantic coast communities, 29; New York City, 128; Norway House, 186,216; Oxford House, 1837,183; Petit Nord, 137-138,152-153,156, 190,199202; Rat Portage, 200; Red River, 180,182-183,186;York Factory, 5556,181,183 pandemic of: 1781-82,115; 1918-19, 285n66 International Classification of Diseases (ICD), 247n6 Inuit, 90 Iroquois, 23-26,31, 42,61-62,69-70 disease history of: Laurentian, 25; New York, 25-26 Isbisterjohn, 294n66 Isham, James, 71,78-82 isolation and epidemic transition, 11-14, 90, 117, 237,249n25 as limiting factor in disease diffusion, 12— 14, 21, 64, 90,195-197, 249n25, 279nl4 J Jacobs, Peter, 193,224 James, Robert, 219 James,Thomas, 36 Jarvis, Edward, 113—116 Jenner, Edward, 157,246n6 Jeremie, Nicholas, 102 Johnston, Susan, 69—70 Jones, David, 180

310 INDEX K

Kakouchac. SEE Montagnais Kaministiquia, 43, 111, 270n58 Kane, Paul, 203,292n43,295n83 Keith, George, 155,165,167,175,283n57 Kelsey, Henry, 55-56 Kilistinon, 49-50, 258n25, 259n35 King, Richard, 181 Kingfishers (Ojibway). SEE Berens River Kipling, John, 107,110,113 Knight, James, 55 Krech, Shepard, 117 Kunitz, Stephen, 23 Kutenai, Fort, 133 Kutenai Nation, 133 La Colle (Monsoni chief), 70 La Jonquiere, Marquis de, 77—78 LaVerendrye, Jean Baptiste, 65—66 LaVerendrye, Louis-Joseph, 68 LaVerendrye, Pierre Gaultier deVarennes, 44,59-60, 67-68, 69 Lac la Pluie disease episodes atrARDs, 131; dysentery, 152;"great death," 128; measles, 141 LacSeul, 143-144,155 disease episodes at: chickenpox, 183; compound epidemics, 192-194; coughing sickness, 179; dysentery, 224-226; febrile disease, 131; influenza, 182, 200-202; measles, 143-144,175,224-226; scarlet fever, 189; whooping cough, 178 disease history of, 3—4 population at, 1826-37,144-146 Lafleche, Father, 212 Laidlaw, Mr, 148 Lake Minnitaki, 112-113 Lake Nipigon, 113-114 Lake of the Woods, 132 disease episodes at: smallpox, 108,132; whooping cough, 150 Lake Sturgeon, 110-111 Lanphear, Kim, 24,40 Laperouse, Comte de, 101 Laronde, Monsieur, 231 Laughlin, Peter, 131 Lehmer, Donald, 65 Lisa, Manuel, 122,148,276n26 Little Bloodvein River, 150 Little North. SEE Petit Nord London, 39, 56 Long,John, 111

Long Lake, 231 Louisville, Kentucky, 124 Lovell, George, 117 Lytwyn,Victor, 72,114,116 M Macatoppishnew (Sturgeon Lake trading captain), 110 Mackenzie, Alexander, 94,108 Mackenzie River valley, 117 malaria, 6 Mandan Nation, 70,148,169 disease episodes among: measles, 80,147, 206; whooping cough, 133,150,178 trading connections of, 96,122,148, 169,207,276n26; horse trade, 267nlO Marten, Humphrey, 85, 86,101-102 Martin's Falls, 121,152,174,191-192,195, 197,229, 243 disease episodes at, 152,284n64;ARDs, 129,132; diarrhoeal disorder, 131; influenza, 131 Massachusetts Bay Colony, 28-29 Matagami, 138-139 Maurepas, Council of, 1737,67-68,69 McDonell, Aeneas, 109-110 McKay, Donald, 131 McKay, John, 131 McKay, William, 152,220-222 passim McKenzie, Charles, 143-147,155,179,182183,223,225-230 biography of, 246nl on disease diffusion, 175 epidemics described by, 3-4,228; chickenpox, 183; dysentery, 226-228; influenza, 200; measles, 146—147, 223-228; scarlet fever, 189; smallpox, 110; whooping cough, 133,178 influenza in brigade of, 192-195,200202 McKenzie, Mrs. Charles, 225 McKenzie, Roderick, 141,150 McNeill, William, 7,9-12 McPherson, George, 195,202,227-228,230 McTavish,W.,217 measles, German (rubella), 8, 40,184 measles (rubeola), 4,6,8-9,11,79-80,122, 138,256n5 diffusion of, 138-147,147-152,202209, 214-230 episodes of, 137-138,151-152; Alaska, 206;Arikara, 80;Assiniboine, 80,138, 148;Atlantic seaboard, 80;Atsina, 138; Blackfoot, 138; Brandon House, 148,

INDEX 311 150; Brazil, 138; Britain, 248nl6; Cree, 138; Ecuador, 22,249n27; Escabitchewan, 1819,146; Faeroe Islands, 138, 249n25; Fiji, 41,138; Garden Island, 141; GrosVentres, 138; Hawaii, 206,210; HBC Brigade, 217, 293n54; Iceland, 9,13-14; lie a la Crosse, 216; Lac la Pluie, 141,152; Lac Seul, 143-144, 224-226; 182829,175; Lowland Cree, 220; Mandan, 80,147, 206; Matagami, 1818,138139; N.Atlantic coast communities, 29; northern great plains, 80; Norway House, 149,215,219-225; Ojibway, 143-144; Oxford House, 218; Pawnee, 80; Petit Nord, 76,202; Point Meuron, 140; Portage de 1'Isle, 141; Red River, 149, 206-207,214215; Rice Lake, 227-228; Sault Ste. Marie, 138; Sioux, 138,206; St. Peter's, 209,292n48; Sturgeon Lake, 141; Swan River, 149;Teton Nation, 206; Vermilion, 141;Wichita Nation, 80; York Factory, 1751,78-80 immunity to increasing, 1840s, 211 and whooping cough, 137-138, 140 medical treatment, Aboriginal, 233-235 failure of in treating imported diseases, 232-234, 297nl22 medical treatment, Euroamerican rejected by Aboriginal people, 211—212, 298nl24 Meetwass (Albany trading captain), 113—114 Meinig,D.W.,61 Memphis, Tennessee, 124 Mesoamerica disease history of, 21-26 SEE ALSO Mexico; New Spain Me,ta,wiss (Catfish Ojibway), 111 Metewisito (trading lieutenant), 110 Metis, 167-168 Mexico, 22,93,95 Miami Nation, 62, 126 Micabanish House. SEE New Brunswick House Michigan, immigration into, 280n24 Michilimackinac, 85 Michipicoten, 77-78,126-127 Micmac Nation, 27-28 migration and disease diffusion, 13,22,28, 189,237 Miller, Virginia, 28 mining and miners, 230—232,231 Missouri Fur Company, 276n26

Missouri River, population decline at, 25— 26 Mohawk Nation, 42 disease history of, 24-25 Mohawk of Sault St. Louis, 61-62 Monin (free trader), 139 Monontague of Lake Minnitaki, 112—113, 125 Monsoni Nation, 69-71,107 Montagnais, 46, 48, 258nl7 Montreal disease diffusion from, 62,78,126-127, 130,140,190-191 Ojibway trade with, 257nll smallpox at, 49,62 traders from, 42,84,271n2 transportation system from, 48,126,140, 163,175 Moodie, Wayne, xii Moore,Thomas P., 206 Moose, John, 227 Moose Factory, 48, 51,116-117,121 disease episodes at:ARDs, 130; whooping cough, 175—176 mourning customs, 235-236 Mowat, Edward, 215,293n54 Mumim (Michipicoten trading captain), 126 mumps, 122 described, 184-185 diffusion of, 1845-46,205 episodes of, 231; He a la Crosse, 185; Petit Nord, 156,184-185,205,220, 231; Red River, 186 Munkjens, 36 Munsee Nation, 126 Murphy, John, 152 Murrilljohn, 255nl N Narragansett Nation, 24 Neauahe (Ojibway trading lieutenant), 111 Neeljames, 79 Nelson, George, 132 New Brunswick House disease episodes at:ARDs, 152; smallpox, 126 New England bubonic plague in, 36 disease history of, 24,40 New France, 28-29,62 New Jersey, 61 New Netherlands, 28-29 New Northwest Company, 271n2 New Spain, 95 New York, 61

312 INDEX New Zealand, 40 Nigonice (Lac Seul Ojibway man), 226-227 Nimica (trading captain), 126 Nipigon, 43 Nipissing Nation, 32, 33-34, 46 Nodowasis (Sioux), 108 Nonsuch (HBC ship), 36 North Atlantic Coast disease history of, 27—35 NorthWest Company (NWC),94,119,135, 275nlO and disease diffusion, 130, 140-141, 141 Northern Columbia Plateau, 26 Norway House compound epidemics at, 185-186, 216, 299n7 disease episodes at, 216—217; dysentery, 152,219-222; influenza, 180-181; measles, 149,219-225; scarlet fever, 187; whooping cough, 149,176,178 O Oglala Nation, 287n96 Ohio River Valley, 126 Ojibway, 105,169,171 Catfish, 111 disease episodes among: measles, 143— 144; measles and whooping cough, 148; scarlet fever, 145-146,188; smallpox, 65,68-69,78,93,100,102106,108 expansion of, 55,72,118,127,145-146 resist White settlement, 159 Oman, Mitchell, 100 Omrans epidemiologic transition, 301nl7 One Arm (trading captain), 131 Onondaga Iroquois, 46 Ookemowescume (Ojibway, Captain Grant), 148, 277n28 oral history, xii oral testimony, 78 Ord, James, 188 Oregon Trail, 189 Osnaburgh House, 121,127 disease history of, 135 O'tash'a'way'kee'shick (trapper), 127 Ottawa Nation, 33,62,118 dispersion of, 33-34 smallpox among, 49 Ottawa River Valley, 32 Oxford House disease episodes at: influenza, 181,183; measles, 218; whooping cough, 151,176, 178

P Pacific Fur Company, 94 Pacific Northwest, 117 Pacquette, Antoine, 140 PaUiser, John, 205 parainfluenza virus, 87 parapertussis, 133,284n59 Pawnee Nation, 80 Pennsylvania, 61 periodicity of disease(s), 8—11 PerraultJ.B., 109 Perrot (French fur trader), 49 pertussis, 284n59 Petit Nord (Little North), xii, 15-20,37, 52 disease history of, 19 0,130,155-157, 237-244 indigenous trade contacts of, 32—33 Petun Nation, 33-34 Piankeshaw Nation, 62,64 pictographs as evidence of epidemics, 65 Piegan Nation, 69, 99 Pitezeljohn, 188 Pittsburgh, Pennsylvania, 124 pleuritic fever at Albany, 85 Plymouth Plantation, 28 pneumonia, 204 episodes of: at Albany Fort, 86; Churchill, 90; Petit Nord, 178;York Factory, 90 follows other diseases, 79,88,133,178, 284n62 Point Meuron, 140 Polynesia, 210 Pontiac's Rebellion, 84 population(s) American Aboriginal, xi-xii Atlantic seaboard, 29-30,122-123 Columbia Plateau, 26 decline of in Missouri River valley, 25-26 and disease, 7-8,11,239 French colonies, 29-30 Monsoni, 1734,69 Petit Nord, 19 U.S.,272nl5 Portage de 1'Isle, 128,133,141 post-epidemic behaviour, 69-70,72,78, 117-118,235-236 abandonment of territory, 127 avoidance, 127 migration, 242 panic flight, 78 potatoes, 226 Potawatomi Nation, 62 Prem, Hans, 64

INDEX 313 Prince Albert (HBC ship), 185 Prince of Wales (HBC ship), 129 Prince Rupert (HBC ship), 80-81,90,185 Provencher, Father J.-N., 149, 207, 212-213 Pusquothecot (Lowland Cree leader), 116

Q

quarantine scarlet fever, 189 smallpox, 22, 61-62,101 Quesip (trading lieutenant), 114 Questach (Lowland Cree leader), 116 R Rainy Lake, 107,132 Ramenofsky, Ann, 14-15,25-26,45 Rat Portage, 200 Ray, Arthur J., xii, 138,206 Red Lake, 145,171 Red River Exploring Expedition, 157—159 Red River Settlement compound epidemics at, 186 disease episodes at: dysentery, 210—214, 212; influenza, 180,182-183; measles, 149, 206-207; whooping cough, 186,189 • as nexus of disease diffusion, 167—170, 180,238 respiratory diseases. SEE acute respiratory diseases (ARDs) respiratory syncytial virus (RSV), 87 "Retrenching System" of HBC, 121-122, 135 rhinovirus(es), 6, 87 rice. SEE wild rice harvest gatherings Rice Lake, 227-228 Richards, Joseph, 115 Robertson, Laurence, 217, 218, 219, 232234,236 Robinson-Superior Treaty annuity gatherings, 282n36 Robson,Joseph, 94 Ross, Alexander, 210-211,213 Ross, Donald, 155-156,185,191, 194, 235 on diseases at Norway House, 180-181, 189,215 Rossville disease episodes at: dysentery, 216; scarlet fever, 187 rubella. SEE measles, German rubeola (red measles) description of, 79 SEE ALSO measles, German Rupert River trading post, 48

S

Sabiston, William, 225 Sackawabish (trading captain), 126 Saguenay River, 48 Sandy Lake, 108,131 Santa Fe, 95 Saquot (Lowland Cree leader), 116 Sarsi Nation, 99 Saukamappee (Cree elder), 99 Sault Ste. Marie disease episodes at: measles, 138; smallpox, 49 as nexus of disease diffusion, 45, 165— 167,171,190-191, 202-205, 230 trade routes through, 42, 45,62,161163,174 Saulteur (Southwestern Ojibway), 49,66— 67 scarlet fever, xiv, 8 described, 187-189 episodes of: on Columbia River, 189; at Lac Seul, 189; Norway House, 187; Petit Nord, 187-189; Red River, 186, 188; St Lawrence and Ottawa valleys, 32 scurvy, 50 Seahorse (HBC ship), 77, 89-90 Seahorse II (HBC ship), 115 Selkirk Colony, 135-136 Seneca Nation, 24—25 settlement frontier, 157-164,243 American, 162-170,174,238,287n96 westward expansion of, 160,162—163 Seven Years' War, 1756-63, 82-85, 84,264n9 Severn Fort disease episodes at: ARDs, 90; smallpox, 101,102 disease history of, 85-86,125 Severn River, 102 sexually transmitted diseases (STDs), 255nl Sheawappennesscome (Ojibway trading lieutenant), 111 Shewequenap (trading captain), 111 shigellosis. SEE dysentery Shoshone Nation, 99, 103 Simpson, George, 199, 213, 231 Simpson, Thomas, 234 Simpson, Wemyss, 215 Sinclair, Thomas, 293n54 Sioux, Lower Yanktonai, 77 Sioux, Teton, 64—65 Sioux,Yanktonai, 65,77,205-206,287n96 Sioux Nation, 138 Sioux of the Prairie, 70 Six Nations. SEE Iroquois

314 INDEX Sixth Royal Regiment of Foot, 214 Skrimshire, Samuel, 79 slave trade and disease diffusion, 22,28, 250n2 smallpox, xiii—xiv, 4,122 diffusion of, 45, 64, 95-96,99,107, 299n3 diffusion potential of, 14, 45-46 emergence of in: Ecuador, 22; James Bay, 33; Mesoamerica, 21-22; N.Atlantic coast communities, 29—31; southwest Pacific, 40; St Lawrence and Ottawa valleys, 32 epidemics: 1669-70, 45-52, 46-50; 1720s, 56; 1737-38, 59; 1751-52, 77; 1770s-80s, 91, 94-95; 1770s-1780s, 99;1779-83, 103-109, 106-107, 127 episodes of, 59-69,60; at Albany River, 114; among Blackfoot, 87, 99; among Blood, 99; among Miami, 62,126; among Munsee Nation, 126; among northern Cree, 68; among plains peoples, 26; among Potawatomi, 62; in Britain, 9; in Guatemala, 117; at Lac Seul, 109-110; at Lake Huron/ Lake Erie, 126; at Lake of theWoods, 108,132; in London, 40, 56; in Mackenzie River valley, 117; in Mexico, 22; at Michipicoten, 77-78, 126; at Minnitaki, 112-113; in Petit Nord, 59-69, 61-63,77,125; at Rainy Lake, 132; at Sault Ste Marie, 45 incubation period of, 256n5 origins of, 6, 59-60 in Seven Years'War, 82-85 vaccination against, 157,240,246n6, 298nl24 Smithurst, John, 200,209,212,213 Snake Nation, 99 Snodie.Adam, 151 Snow, Dean, 24,27, 40 Southwest Pacific, 41 Spanish Flu, 1918-19, 285n66 Spitzbergen, ARDs at, 90 St. Louis, Missouri, 122,147-148 St. Peter's, 209,292n48 St Lawrence River Valley, 32 Stadacona epidemic, 25 Starna, William, 24 starvation, 223-224,226 steamboats, 161-162,169 Stewart, Andrew, 139 streptococcal infections, 187—188 SEE ALSO throat infections Sturgeon Lake, 141,145

Sunder, John, 169-170 Susquehannock Nation, 32 Sutherland, Donald, 150 Sutherland, George, 85,112 Sutherland, James, 128 Swain, James, 150 Swan River, 149 Swanstonjohn, 204,231 sweat lodge, 233 syphilis, 6, 247n5

T Tache, Father, 212 Tadoussac, 48 Tait.Tom, 202 Tanner, Helen Hornbeck, 132 Taylorjohn, 67,138 Tekouerimat, Noel (Sillery chief), 46 territorial change, 117-118 Teton Nation, 206 Teton Sioux. SEE Sioux, Teton Their Number Became Thinned (H. Dobyns), xi, xii Thorn, Adam, 213-214 Thomas, John, 130 Thompson, David on smallpox, 1779-83,94,99,103,105 on whooping cough at Fort Kutenai, 1807,133 throat infections at Albany, 115 Tomison, William, 84 on smallpox, 100,102 trade routes, 34—35 diseases spread through, 33,95—97,102, 124 to Petit Nord, 42-43 trade with Montreal, 257nll trading posts, French, 43 transportation and travel in disease diffusion, 13, 28, 143, 151, 160-163,165, 169,171-174, 178181,183,195, 214, 223, 228-229, 237-238 Treaties, Indian disease changes resulting from, 244 Treaty of Paris, 1763, 84 Trigger, Bruce, 24,33 Trimble, Michael, 96,122,169 Tristan da Cunha ARDs at, 90 Trout Lake, 172,195,220-221,226,228229,286n89, 294n66 Truteau,Jean Baptiste, 26,122 Truthwaite, Jacob, 152-153

INDEX 315 tuberculosis, 6,178,243-244 Turner, Frederick Jackson, 160 Turner, Philip, 117 Type A influenza, 265n27, 285n66 typhoid, 29 typhus, 6, 29 U Umfreville, Edward, 99,109 Upper Canada, settlement of, 162 urban disease frontier, 9,11,13,43,46,57, 123,134 "near" populations, 9—11 "peripheral" populations, 10—11 urban disease pool(s). SEE disease pool(s), urban Utrecht, Treaty of, 44 V vaccination, 240,246n6,298nl24,299n6 HBCuseof, 157 varicella, 247nl 1 SEE ALSO chickenpox variola (smallpox), xiv, 56,111 SEE ALSO smallpox Vavasour, Lt. Mervyn, 156 vectored diseases, 6-7 Vermilion, 141 Virginia Colony, 29 W War of 1812,148,160 Warre,Lt. Henry, 156 Warren, William, 105-106,107,109 war(s) Aboriginal: and disease diffusion, 105— 106 and disease diffusion, 78, 97-100,105106,148 post-epidemic behaviour and, 69-70 SEE^LSO SevenYears'War, 1756-6 "water on the brain" outbreak,York Factory, 283n56 Wea Nation, 62,64 Welland Canal, 161 Wenro Nation, 32 Weskerini people, 32 White Horse Plain, 212 whooping cough, 4, 122 described, 133-134 diffusion of, 133,150-152,151,186-187 diffusion potential of, 14 episodes of: among Mandan, 133; Athabaska Chipewyan, 134; Boundary Waters, 179; Columbia River, 189; Fort Kutenai, 133; Lac

Seul, 178; Norway House, 178,186; Oxford House, 178; Petit Nord, 132, 156,175-176,178-179,186 and measles, 137-138,140 population required to sustain (CCS), 8 wild rice harvest gatherings as nexus for disease diffusion, 141, 224, 227-228 Willdridge, Peter, 101 Williams, Roger, 24 Williams, William, 147 Winder, W, 186 Winnebago Nation, 33 Winnipeg River, 223 Wisconsin, 280n24 Witchita Nation, 80 Wood, Raymond, 65 Wyandot Nation, 126 X XY Company, 271n2

Y Yanktonai Sioux. SEE Sioux.Yanktonai yellow fever, 6,274n45 York Factory, 101,121,129 disease episodes at, 55-56,80-82; ARDs, 86-87,90; compound epidemic, 219-220; influenza, 181,183; pneumonia, 90; smallpox, 56; whooping cough, 151 disease history of, 85-86,125,135 York Fort, 44 Z zoonoses, 6