02whole Dowling

"A Great Deal of Sickness"1
Introduced diseases among the Aboriginal People of

colonial Southeast Australia 1788-1900
Peter J. Dowling
January 1997
A thesis submitted for the degree of Doctor of Philosophy of the Australian National
University, Canberra
1
Buttfield 1874
Except where otherwise stated in the text, this thesis represents my own original work.
Peter J. Dowling
For Dianne
Saal na saol
Tús gá deiredh
Tá muid beo
Dá deo
Life of lives
Beginning without an end
We are alive
To the end of time
(Enya & Ryan 1987)

Abstract
Palaeopathological studies have sought to build up a picture of Australian Aboriginal health

before European settlement in 1788, and epidemiological studies of Aboriginal health in the
twentieth century are now legion. But, despite a growing body of literature on Aboriginal
history in the intervening colonial period, this remains an under-studied period from the
viewpoint specifically of Aboriginal health. This thesis is a contribution to filling that gap
through an examination of documentary and skeletal evidence on the changing bio-medical
situation experienced by Aboriginal populations of Southeast Australia from 1788 to 1900.
This thesis examines one of the major biological components of this change - the diseases that
were introduced into Australian Aboriginal populations during the process of colonisation. The
epidemiology, timing, diffusion of diseases are considered with specific attention given to
infectious and respiratory diseases that were responsible for causing major epidemics of
morbidity and mortality.
A medical model for the contact period in the late 18th and 19th centuries is proposed. This
model considers three major stages in the disease environment of Aboriginal populations in
Southeast Australia; a pre-contact stage with endemic pathogens causing chronic diseases and
limited epidemics, an early contact stage where introduced exotic human diseases cause severe
epidemics of infectious and respiratory diseases among Aboriginal populations, and a third
stage where remaining Aboriginal populations were institutionalised on government and
mission settlements and were subjected to a high level of mortality from the introduced
diseases.
The major epidemic diseases during the early contact stage were smallpox, syphilis,
tuberculosis, influenza, and measles. Each of these diseases were responsible for excessive
morbidity and mortality. During the period of institutionalisation infectious and respiratory
diseases were responsible for over 50% of recorded deaths on 8 separate Aboriginal settlements
in Southeast Australia. The major diseases recorded as causes of death were tuberculosis,
bronchitis, pneumonia, diarrhoea and dysentery.
Aboriginal and non-Aboriginal Australian infant mortality rates are calculated to provide an
indicator to compare the state of health of the two populations. Aboriginal rates were high
when compared to the non-Aboriginal populations of Victoria and South Australia. The rates
reveal a substantial health differential between Aboriginal and non-Aboriginal populations.
Aboriginal infant mortality has improved into the latter quarter of the twentieth century but the
corresponding improvement in non-Aboriginal infant mortality has been at a much higher rate.
The gap between the health status of each has widened rather than narrowed over the last one
hundred years.
Acknowledgments
When I first began this project I was warned by several colleagues that finding nineteenth
century information regarding the impact of introduced diseases on Aboriginal populations
would be difficult. The sources of information I would need, if they existed at all I was warned,
would most likely be scattered throughout archival texts in several capital cities and much of it
would not be readily obtainable through current archival referencing aids. They were correct.
Much of the material obtained came after seemingly endless days of searching through bundles
of files, often without any success, in the libraries and public records offices of five capital
cities. In order to find them, understand them, use them in the way I wished, cope with all the
inevitable setbacks, and finally put them all together in what I hope is a coherent story required
the help of many people.
At the top of the list is my wife Dianne. Once again she had to cope with this thing called a
thesis which invaded her life just as much as it did mine. Without her understanding, help in
the archives, and support throughout the good times and the bad times, this thesis would never
have been written.
My supervisory team require a large thank you for their guidance, criticism, and encouragement
throughout the processes of research, analysis, writing and rewriting. Dr Robert Attenborough
bore the biggest burden and his kind help, together with a role of devil's advocate and
administrator were greatly appreciated. Professor Isabel McBryde's depth of knowledge of
Australian Aboriginal history helped me understand the material all the better. I also thank her
for those 'spiky bits'. Dr Alan Thorne's advice, particularly in the initial stages, was
appreciated. On the medical side I thank Dr Bryan Furnass who had just retired from the
campus medical centre only to find a more demanding patient with a chronic disease we
eventually called thesisitis. His advice, interest and encouragement helped me over many
hurdles. Thanks also go to Professor Richard Wright who advised me on the use and
interpretation of multivariate statistics.
Big thanks go to those who volunteered to read and comment on various drafts of the thesis;
John Harrison, Dr Judith Littleton, Dr David Cameron and Dr Mary Jane Mountain. I was only
too glad to accept their help.
I would also like to thank Dr Barbara Tyler from the Wanniassa Medical Centre, who always
showed interest in the project during my medical checkups. I spent several extended
consultations with her discussing the symptoms and epidemiology of infectious and respiratory
diseases, none of which were the reason for my visits.
Another big thanks goes to Peter Figg with whom I met almost every Wednesday for lunch and
a precious pint of Guinness. I was often asked to explain my work in elementary terms thereby
making my own perceptions all the more clearer.
And then there was the extended family. My son Michael and daughter-in-law Deborah who
patiently listened to me as I begged for help after creating another glitch on my computer;
David, Angela, Ashley Jean and Marcus for regularly bringing me noisy, chaotic but totally
enjoyable diversions; the South Australians: Joan and Bill Johns, Beverley Dowling, Gilly and
Beth Dowling, Colin and Glad Dowling and all those of the following generation for the
interest they took and the support they gave; Geoff and Barb Banks for their long friendship
and concern; the Tasmanian in-laws Colin and Marj Walters who have come to appreciate the
Aboriginal past by farming the land surrounding the Little Swanport midden; Judy Belbin who
showed more concern for the writer than the thesis; Chris and Bob Robson who, although not
always here, were never really far away; and the Harrison clan with whom we spent many a
pleasant afternoon and evening.
I owe a special thanks to Dr Judith Littleton and Dr Jan Klaver who have been my helpers and
critics, but most of all my friends for over a decade.
I must also thank Dr Goran Şevo to whom I often turned for advice on diseases, their
symptoms, epidemiology, and diagnosis even though he may have been on the other side of the
world or just the other side of the room.
I also value the friendship of my other colleagues Dr Aubrey Parke, Dr Keiko Tamura, Dr Mark
Hudson, Dr Kate Stockhausen, Dr David Cameron, Tom Knight, Dr Ben Evans, and Dr Judith
Caton with whom I shared room LG23 at one time or another. I thank them for having the
grace, while in the midst of their own theses, for listening to me.
For those many days and evenings spent in archival rooms in five cities I must thank the
librarians, archivists and library staff, whose names I never knew, for guiding me through the
collections.
And finally Taia whom I think approved of this thesis only because it meant I was often at
home and the house was warm on those cold Canberra days.
Go raibh míle maith agat.

Table of Contents
List of Tables
List of Figures
List of Plates
Chapter 1: Introduction 1
1.1 Introduction 1
1.2 Research to date 2
1.3 Aims 7
1.4 Scope 8
1.5 Significance of thesis 10
1.6 Sources and methods 11
1.6.1 Historical sources 11
1.6.2 Skeletal evidence 14
1.7 Origin of diseases 17
1.8 Organisation 17
Chapter 2: Disease Environments and Epidemiological Considerations 18
2.1 Introduction 18
2.2 A medical model for contact in Southeast Australia 19
2.3 Epidemiological considerations 22
2.3.1 Pre-contact disease 23
2.3.2 Post-contact epidemics 31
2.4 European and Aboriginal concepts of disease and curing 39
Chapter 3: Smallpox 46
3.1 Introduction 46
3.2 Biology of smallpox 48
3.3 Smallpox among the European population of Southeast Australia 51
3.4 Small pox among the Aboriginal populations - Source material 52
3.4.1 The first epidemic û 1789 54
3.4.2 The second epidemic - 1828-32 66
3.4.3 The third epidemic - 1866-67 83
3.5 Discussion 88
3.6 Conclusion 96
Chapter 4: Sexually Transmitted Disease 98
4.1 Introduction 98
4.2 Biology of sexually transmitted diseases 101
4.2.1 Syphilis 101
4.2.2 Gonorrhoea 103
4.3 Syphilis and gonorrhoea among the European population of Southeast Australia 104
4.4 Syphilis and gonorrhoea among the Aboriginal populations - source material 106
4.4.1 At the frontiers 106
New South Wales 106
Victoria (Port Phillip) 109
South Australia 117
4.4.2 Beyond the frontiers 121
Historical Evidence 122
Osteological evidence 126
An early introduction into South Australia 138
4.5 Conclusion 139

Chapter 5: Tuberculosis 141
5.1 Introduction 141
5.2 Biology of tuberculosis 142
5.3 Tuberculosis among the European population of Southeast Australia 149
5.4 Tuberculosis among the Aboriginal populations - source material 152
5.4.1 Early contact and diffusion (Stage II) 152
5.4.2 Settlement and acculturation (Stage III) 158
5.4.3 Clinical features 162
5.4.4 Aboriginal treatment 165
5.5 Discussion 165
5.6 Conclusion 174
Chapter 6: Acute respiratory diseases 176
6.2 Biology of influenza & pneumonia 178
6.3 Influenza & pneumonia in the European population of Southeast Australia 179
6.4 Influenza among the Aboriginal populations - source material 183
6.4.1 Influenza and acute respiratory disease among Tasmanian

Aboriginal people, 1831-6 184
6.4.2 Influenza among the Aboriginal population of Port Phillip, 1839 199
6.4.3 Influenza and acute respiratory disease among Victorian Aboriginal

populations, 1845-90 203
6.4.4 Influenza and acute respiratory disease among South Australian

Aboriginal populations 207
6.5 Discussion 215
6.6 Conclusion 223

Chapter 7: Measles 225
7.2 Biology of measles 226
7.3 Measles among the European population of Southeast Australia 227
7.4 Measles among the Aboriginal population - source material 229
7.5 Discussion 242
7.6 Conclusion 249
Chapter 8: Diseases on Aboriginal Settlements 1876 to 1900 251
8.2 Source materials 256
8.2.1 Nature of the data 259
8.3 Methods of analysis 261
8.3.1 Proportional Mortality Ratios (PMR) 266
8.4 Results and discussion 267
8.4.1 Age range 0 to 4 years 272
8.4.1.2 Infectious diseases 273
Diarrhoea and dysentery 273
Other infectious diseases 279
8.4.1.3 Respiratory diseases 280
Bronchitis 280
Whooping cough (pertussis) 283
Other respiratory diseases 284
8.4.2 Age range 5 to 15 years 284
Tuberculosis 285
8.4.2.3 Digestive system diseases 287
8.4.3 Age range 15+ years 288
Tuberculosis 289
Hydatids 290
Enteric fever (typhoid) 293
Bronchitis 295
Pneumonia/inflammation of lungs 297
8.4.3.3 Digestive system diseases 298
8.4.4 Less frequent causes 299
8.5 Infant mortality 302
8.5.1 Method 303
8.5.2 Results and discussion 304
8.6 Conclusions 308
Chapter 9 Conclusions 312
An Afterword 315
References 317
Appendix A A1
Appendix B B1
Appendix C C1
List of Tables
2.1 Changes in health subsystems of Canadian Inuit during stages of culture contact. 20
2.2 Medical model for 18th & 19th century Aboriginal Australians. 21
2.3 Major characteristics of Aboriginal society and ecology (compared to Europeans)
exerting an influence on the pattern of disease. 25
2.4 Major characteristics of Aboriginal society and ecology (compared to Europeans)
exerting an influence on the pattern of disease. 27
2.5 Probable non-infectious disease profile of Australian Aborigines before contact
with Europeans. 29
2.6 Diseases suggested to have been introduced by European colonists into
Aboriginal populations of Southeast Australia (post 1788) and the Americas. 35
3.1 A classification of clinical types of variola virus infection. 49
3.2 Major smallpox outbreaks during nineteenth century in European population
of Australia. 52
4.1 Comments regarding syphilis among Aboriginal populations met by Chief
Protector Robinson during his journey through the eastern interior in 1844. 113
4.2 Treponemal infection in undated Australian Aboriginal crania. 129
4.3 Prevalence (%) of pathology in dated skeletal collections of Southeast Australia. 133
5.1 International Classification of Tuberculosis. 144
5.2 Factors relating to host/pathogen and the manifestation of tuberculosis symptoms. 144
5.3 Terms given by medical practitioners in the nineteenth century that may be
attributed to tuberculosis infection. 148
5.4 Extent of tuberculosis as the recorded cause of death on Aboriginal settlements
in the nineteenth century for which there are reliable data. 158
5.5 Summary of autopsy reports 1837-1838 from Wybalenna Aboriginal
settlement, Flinders Island, involving tuberculosis 163
6.1 Pandemics and periods of epidemic and unusually high morbidity from
influenza in Australia. 180
6.2 Mortality rates from 1890-91 influenza epidemic. 183
6.3 Total recorded deaths and cause from acute respiratory diseases at
Wybalenna Aboriginal settlement 1833 to 1847. 189
6.4 Periods of excessive morbidity from respiratory and possible respiratory
disease on Coranderrk Aboriginal Station between 1865 & 1875. 206
6.5 Evidence of influenza epidemics among Aboriginal populations in Southeast
Australia showing their relationship to Pandemics and localised epidemics. 217
7.1 Nineteenth century epidemic years of measles in the European population
of Southeast Australia by colonies. 227
7.2 Mortality from major epidemics of measles in European population of
Victoria and South Australia 1874-75 & 1893. 228
7.3 Official returns of estimated number of Aboriginal people in the settled
districts of New South Wales between 1835 and 1837 enumerated during
government blanket distributions. 230
7.4 Crude mortality rate from measles in European population of South Australia
for which there is information. 233
7.5 Number of Aboriginal deaths on Victorian Aboriginal settlements
attributable to the 1874-75 measles epidemic. 236
7.6 Estimated crude death rates (CDR) from 1874-75 measles epidemic
among Fijians and Aboriginal Australians. 246
8.1 Aboriginal settlements in Victoria and South Australia for which there is
reliable nineteenth century mortality data. 258
8.2 Number of deaths recorded on selected Aboriginal settlements in Southeast
Australia for period 1876-1900. 259
8.3 Breakdown of data set - extracted from records of Aboriginal deaths between
1876-1900 on selected settlements in Southeast Australia. 262
8.4 International Classification of Diseases categories and abbreviations
used (ICD.9.CM 1991). 263
8.5 Proportional mortality ratios (PMR) for disease categories on selected Aboriginal
settlements in Southeast Australia 1876-1900. 267
8.6 Frequency (%) of diseases in the infectious disease category (INF) recorded
as causes of death. 269
8.7 Frequency (%) of diseases in the respiratory disease category (RES)
recorded as causes of death. 269
8.8 Numbers of deaths and principal mortality ratios for age ranges 0 to 4,
5 to 14, and 15+ years for Aboriginal settlements in Southeast Australia
1876-1900 271
8.9 Reported occurrence of diarrhoea and dysentery as causes of death on Aboriginal
settlements in Southeast Australia 1876-1900 275
8.10 Infectious diseases less diarrhoea and dysentery reported as causes of death
in age range 0 to 4 years. 278
8.11 Respiratory diseases reported as causes of death in age range 0 to 4 years. 280
8.12 Causes of death from infectious diseases in age range 5 to 14 years. 285
8.13 Number of deaths from tuberculosis in age range 5 to 14 years. 285
8.14 Causes of death from respiratory diseases in age range 5 to 14 years. 287
8.15 Causes of death from infectious diseases in age range 15+ years. 289
8.16 Recorded cases of tuberculosis in age group 15+ years where both age
and sex were recorded. 290
8.17 Reported occurrence of hydatids as a cause of death on Aboriginal
settlements in Southeast Australia 1876-1900. 291
8.18 Causes of death in age range possibly attributed to typhoid. 294
8.19 Causes of death from respiratory diseases in age range 15+ years. 295
8.20 Breakdown by age of recorded deaths from bronchitis (male and female)
in age range 15+ years. 295
8.21 Causes of death from digestive system diseases in age range 15+ years. 298
8.22 Infant mortality rates of Aboriginal people living on settlements in
Victoria and South Australia 1876-1900 compared with selected pre-20th
and 20th century populations. 304
8.23 Infant mortality rates and differential rate ratios between nineteenth
and twentieth century non-Aboriginal and Aboriginal populations. 307
List of Figures
Linguistic groups of Southeast Australian Aborigines referred to throughout text.
1.1 Southeast Australia study area. Following Page 8

3.1 Reported sightings of smallpox and smallpox victims among
Aborigines of Southeast Australia Following Page 53
4.1 Approximate point of entry and spread of syphilis along Murray
River in pre-colonial South Australia Following Page 138
5.1 Mean annual death rate from respiratory tuberculosis per 100,000 in
England and Scotland Page 146
5.2 Tuberculosis as a percentage of the recorded causes of death on
Aboriginal settlements in Victoria and South Australia
1859 - 1900. Page 159
7.1 Reported presence and absence of measles among Aboriginal
communities during 1874-75 epidemic Following Page 233
8.1 Locations of Aboriginal settlements examined in this chapter Following Page 256
8.2 Relationship of ICD categories reported as causes of death
according to their occurrences on Aboriginal settlements
with respect to the first two component axes of
correspondence analysis Page 265
8.3 Proportional mortality ratios of ICD categories on Aboriginal
settlements in Victoria and South Australia 1876-1900 Page 268
8.4 Total recorded deaths (%) by age ranges for Aboriginal
settlements in Southeast Australia. Page 272
8.5 Age distribution of deaths from bronchitis among Aboriginal
populations living on settlements in Southeast Australia
1876-1900 compared to European population of Victoria
for the years 1876, 1880, 1890 & 1900. Page 281
List of Plates
4.1 Adult male cranium (A911 434) from Riverland region of South
Australia (Murray River) with frontonasal bone destruction
due to treponemal infection Following Page 126
Australia (Murray River), with destruction of nasal, frontal and
right parietal bones due to treponemal infection Following Page 126
Australia (Murray River) with areas of destruction on right
parietal and frontal bones due to treponemal infection Following Page 126
4.4 Adult male cranium (A531) from Lower Murray River region of
South Australia, with frontonasal bone destruction and focal
areas of destruction on right parietal bone duet to treponemal
infection Following Page 126
8.1 Lake Tyers Aboriginal settlement. A posed photograph of
Aboriginal residents outside their cottages
(La Trobe Picture Collection, State Library of Victoria) Following Page256
8.2 Residents of Coranderrk settlement. The picture depicts a mixture
of institutionalisation and tradition culture. European clothing
is worn by two and a government issued blanket is worn by
the elder of the two children. The woman carries a spear in
one hand and collected leaves in the other. The elder child
carries a steel axe (La Trobe Picture Collection,
State Library of Victoria). Following Page 259
CHAPTER ONE
Introduction
1.1 Introduction
This thesis begins an investigation and assessment of the disease environment
of the Aboriginal people of Southeast Australia during the colonial period 1788 to 1900.
Throughout, the discussion will centre around two propositions recurrent in biological
anthropology. The first is that hunter-gatherers who have had little or no contact with the
representatives of European industrial societies, their artefacts, ideas, and biology, tend to
have a society which is well adapted to their environments. They tend to have levels of
health that are able to sustain a state of population homeostasis with natality, mortality
and morbidity not threatening its internal state. The second is a condition of rapid
biological and social change. Almost immediately after such hunter-gatherer societies
begin extensive and continuous contact with European colonisation, and experience
sociocultural, medical and environmental changes, their relationships with their own
environment is disrupted and their health is jeopardised (Wirsing 1985: 303). The causes
of change are largely outside the control of the indigenous society, severe in their effects,
and there is often little time for social adaptation. The consequence is an imbalance to the
processes of natural and human control and the homeostatic state is lost.
The objective of this thesis is to examine one set of biological components of
this change - the diseases that were introduced into Australia during the process of
colonisation. The epidemiology, timing, and diffusion of diseases are considered with
specific attention given to infectious and respiratory diseases that caused major epidemics
of morbidity and mortality. This will be done mainly by examining historical documents
from the colonial period of Southeast Australia and to a lesser extent skeletal indications
of pathology.
Introduction
1.2 Research to date

While many researchers have recognized the value of investigating the history of
inter-racial contact in Australia, too few have sought to examine the nature of biological,
and in particular health, changes that occurred following contact between Aboriginal
societies and European colonists.
The first attempts were by Drs. J.B. Cleland (1928) and Herbert Basedow (1932).
Cleland was then professor of pathology at the University of Adelaide and Basedow was
Chief Medical Inspector, and for a short period Chief Protector of Aborigines, in Darwin.
Both had made periodic exploratory surveys into central and northern Australia as
naturalists and had medically examined Aboriginal people. Using historical sources,
contemporary medical literature, and their own observations both wrote extensive reviews
on diseases among Aboriginal communities. Both were concerned with the declining
population of Aborigines as was a common preoccupation at the time, and sought to gain
knowledge on the manifestation, symptoms and effects of introduced and endemic
diseases among Aboriginal people with no genetic admixture with Europeans. Their
coverage, while including many different diseases, was concentrated on populations in
central and northern Australia, and temporally focused in the early twentieth century on
Aboriginal communities who had had little contact with Europeans.
At the same time as Cleland and Basedow were writing on Aboriginal diseases,
J.H.L. Cumpston was writing on the health and diseases in Australia (Cumpston 1989).
His was a historically orientated, epidemiological review of diseases among the European
population of Australia. Cumpston's focus was not on Aboriginal people but in several
cases, for example when discussing smallpox, venereal diseases, and influenza, he briefly
2
Introduction
considered them in the context of the geographical dissemination of infectious disease
epidemics. His main work dealing with diseases among Aboriginal people was The
History of Smallpox in Australia, 1788-1908, (Cumpston 1914) which brought together
much of the historical literature dealing with three epidemics that affected the Aborigines
and the cases of smallpox among Europeans. Hackett (1936a, 1936b, 1936c) followed
with descriptions of treponemal infected bones, arguing that non-venereal syphilis and
yaws were long established endemic diseases throughout much of Australia.
In 1975 Reynolds began to examine the history of race relations in Australia, a
subject that had until then, been largely avoided by historians. His chapter 'Disease and
Deprivation' in Aborigines and Settlers, was concerned with the diseases of contact. He
acknowledged that exotic diseases caused severe mortality among Aboriginal populations
all over the continent (Reynolds 1975: 71) and briefly covered the topics of smallpox,
respiratory diseases, venereal diseases, malnutrition, mortality and morbidity, alcohol, and
fringe-dwellers. He presented, verbatim, a selection of previously published discussions
(often from secondary sources), and accounts by medical practitioners, missionaries,
Aboriginal protectors, and government inquiries in the nineteenth century and early
twentieth century. No analysis of the biomedical nature of these diseases was attempted.
Smallpox has continued to be the subject of most discussions and debates on the
early diseases of contact, and has remained a major emphasis of the study of introduced
diseases into Aboriginal Australia (Curson 1985: 41-53; Fenner 1984, 1985; Frost 1994;
Reynolds 1981, 1987; Watt 1989; Webb 1995: 284-7; Wilson 1985). In 1983 Butlin
published a controversial opinion on the origins and mortality of introduced diseases
among the Aboriginal populations of Australia. His book entitled Our Original
Aggression argued that the Aboriginal population, particularly that of Southeast Australia,
was severely and repeatedly reduced by diseases introduced by British colonists and that
3
Introduction
previous estimates of Aboriginal population in 1788 (then estimated to be approximately
300,000 for the entire continent) should be revised substantially upwards. He provided
demographic models based on life-table analysis to support his case. Butlin made three
assumptions to support his depopulation hypothesis: the first was that the 1789 smallpox
epidemic was the first to hit the Aboriginal population of Australia and that they had had
no previous exposure to the virus; the second was that the 1789 and the 1829-30 smallpox
epidemics affected almost all the Aboriginal people of Southeast Australia; the third was
that mortality in both epidemics followed the pattern of age-specific case fatality rates
seen in unvaccinated communities in India but at a much higher level. In a discussion on
the origins of the first recorded smallpox epidemic among Aboriginal populations in 1789
he suggested that it may have been started by deliberate release of the virus from the
government's store of variolous material.
These arguments elicited further discussion and protest on the origin and extent of
epidemic disease, particularly smallpox in early colonial Australia. Campbell (1983,
1985) argued that epidemics of smallpox originated on the north coast of Australia,
introduced by Macassan sailors on their annual visits to collect trepang, a hypothesis that
had previously been put forward by Cleland (1928, 1966). Curson (1985: 41-53) devoted
a chapter to the 1789 epidemic of smallpox observed in the vicinity of Sydney and
suggested that the disease may not have been smallpox but chickenpox and that the
mortality, duration, and geographical extent of the epidemic had been exaggerated by
previous authors. On the other hand, Frost (1994), also devoting a chapter to the 1789
epidemic, saw no reason to dispute the evidence that the disease was smallpox; an
opinion shared by most other authors (e.g. Butlin 1983, 1985; Campbell 1983; Fenner
1984, 1985).
4
Introduction
To the best of my knowledge there have been no attempts to document and discuss
in detail other serious diseases such as measles, acute respiratory diseases, or sexually
transmitted diseases, despite the effects they are perceived to have had on Aboriginal
communities. In the History of Tuberculosis in Australia, New Zealand and Papua New
Guinea (Proust 1991) the impact of tuberculosis among Aboriginal communities in
colonial Australia received only three and a half pages in a chapter entitled 'Tuberculosis
among Aborigines'. The majority of the chapter, however, dealt with tuberculosis in
twentieth century Aboriginal populations in central and northern Australia.
Two other recent books dealing solely with Aboriginal health have not attempted to
offer any substantial discussion on the colonial period. In one The Health of Aboriginal
Australia, ( ed. Reid & Trompf), Franklin and White (1991), in a chapter entitled 'The
history and politics of Aboriginal health', presented a brief review of earlier published
assessments on the demographic effects of introduced diseases before examining the
politics surrounding Aboriginal health and social status in the nineteenth and twentieth
centuries. Again, their emphasis was on smallpox. In the same publication Gray et al.
(1991) wrote on 'Early epidemics and introduced diseases'. Again the emphasis was on
smallpox and in particular Butlin's hypothesis on population decline. Brief mention was
accorded to other diseases. In the other recent book to examine the history of Aboriginal
health, Aboriginal Health & Society, Saggers and Gray (1991) tackled the topic of early
introduced diseases in a chapter entitled 'Colonisation and its consequences'. Their
concentration was on the changing social, economic and political impacts on Aboriginal
health in the last two centuries. A brief review of early published material on introduced
diseases was given as a backdrop to the main focus of the chapter.
Goldsmid (1984, 1988) provided an overview of the whole problem of the
international spread of disease, with special emphasis on Australia. He discussed
5
Introduction
diseases likely to have existed in precontact Australia and followed with a nine-page
discussion on the entry of pathogens into the Australian continent but has only a few
references to the effects of these disease on the Aboriginal people.
One writer to look further than the smallpox epidemics was Barwick (1971).
Barwick examined archival sources on introduced diseases but restricted her analysis to
Victoria and had population decline as her main issue. She argued that the spatial
dissemination and mortality from smallpox, particularly the 1829-30 epidemic, had been
exaggerated; and that other introduced diseases, particularly the chronic diseases such as
pulmonary tuberculosis, and other respiratory diseases were the major cause for the
decline in the population of Aborigines in Victoria (Barwick 1989).
Following on from Barwick, others have examined frontier contact in Victoria and
the causes of Aboriginal depopulation. Christie (1979) discussed the period of contact in
Victoria between 1835 and 1886 but only devoted a paragraph to diseases, preferring to
emphasise European violence as the major cause of Aboriginal deaths. Critchett (1990)
examined Aboriginal population decline in the western districts of Victoria between
1834-48. Her theme was directed towards the size of the Aboriginal populations just
prior to settlement; the strength of their opposition to European expansion; and the social
and demographic consequences of colonisation. Though she acknowledged that venereal
disease and influenza caused high mortality, Critchett was more concerned with arguing
for the presence of smallpox among Aboriginal groups of western Victoria than looking
at the effects of other introduced diseases. Cannon (1990) further contributed to the topic
of depopulation in Who Killed the Koories?, but made only brief references to diseases.
The theme of Cannon's book was an emotive one as the subtitle - The true and terrible
story of Australia's founding years - suggests.
6
Introduction
1.3 Aims
These studies just discussed have gone some way towards an understanding
of the changes in Aboriginal health during the nineteenth century. Smallpox has been the
most commonly studied disease, particularly the 1789 epidemic. But there are still large
gaps in our knowledge of the timing, dissemination, and effects of other introduced
diseases during the nineteenth century. For example, chronic diseases which, while not
killing swiftly in the way smallpox did, were nevertheless major causes of the ongoing
mortality and population decline among Aboriginal people last century.
The central aim of this thesis is to fill the gaps of our knowledge of these
diseases. A model (Table 2.2) of the changing medical circumstances in Aboriginal
populations that began with the colonisation of Australia in 1788 and continued
throughout the nineteenth century will be used as a structure in which to examine the
introduced diseases. While the emphasis will be on the major diseases - smallpox,
sexually transmitted disease (i.e. syphilis and gonorrhoea), tuberculosis, acute respiratory
diseases, and measles - other disease states will be considered.
Historical literature concerning these diseases, and to a lesser extent skeletal
evidence will be examined to:
 determine whether the epidemic events and annual outbreaks of introduced
diseases among the European population showed a similar pattern of events among the
Aborigines.
 establish in what regions and under what circumstances Aboriginal
populations were affected by introduced diseases and epidemic events.
 ascertain whether introduced diseases became endemic among the
sedentary groups on settlements between epidemic episodes
7
Introduction
 demonstrate and analyse the evidence for morbidity and mortality.
1.4 Scope
The spatial scope of this study is referred to as Southeast Australia (Fig 1.1)
covered today by the states of South Australia, Victoria, New South Wales, and
Tasmania. There were several reasons for choosing this area of Australia. The first is
that it covers the initial colonial settlement based at Sydney on the east coast and hence
the first contacts between Europeans and Aboriginal people. Apart from a penal
settlement on the Brisbane River (Queensland) established in 1825, the first thirty years
of colonial expansion were contained within this area. Expansion of the colonial frontiers
continued during the nineteenth and into the early twentieth centuries, with the north
western part of Southeast Australia being the last to be settled by Europeans (Williams
1969: 12-44). As a consequence, the Southeast of Australia contained the majority of
Australia's European population during the late eighteenth and nineteenth centuries, as it
does today.
The Southeast also contained the largest pre-contact Aboriginal population densities
of the continent (White & Mulvaney 1987:116-117) though they were concentrated in
differing ecological regions. The eastern and southern coast and hinterlands of the
mainland, the Murray Darling Basin, and the inland regions of the south, particularly
those in western Victoria, were the areas of high biomass able to sustain large Aboriginal
population densities (Butlin 1983; Lourandos 1983, 1987:293-307). In these areas
population densities in 1788 are estimated to have ranged between 1.5 to 3.9 persons per
square kilometre (Dowling 1990, Foster & Gara 1986, Lourandos 1987, Luebbers 1981,
Smith 1980). Archaeological and ethnographic evidence has indicated that in western
Victoria settlements consisting of stone hut clusters along water ways were occupied semi
permanently (Critchett 1990: 26-27; Lourandos 1976, 1977, 1980, 1983, 1987:293-307;
8
Introduction
White & Mulvaney 1987:116-117). In contrast with these high densities, the population
density of the desert areas of central and northern South Australia have been estimated to
be as low as 1 person per 50-60 square kilometres (Foster & Gara 1986).
The Southeast includes the whole or part of five of the eighteen proposed cultural
regions of the continent existing prior to European colonisation (Horton 1994: 935;
Peterson 1976: 50-72; McConvell 1990: 3-27). The population in the Southeast (the
states of New South Wales, Victoria, Tasmania, and South Australia) has been calculated
by Smith (1980: 69) at 82,500 or 26.2% of a total continental population of 310,000.
This figure, however, should be seen as a minimum estimate of population as White &
Mulvaney (1987:115-117), reviewing Butlin's (1983) calculations, have suggested a
continental population of c.750,000 with the Southeast having at least 250,000 or 33.3%.
A reasonable estimate of population in the Southeast would therefore lie between 85,500
and 250,000 or between 26 to 33% of the continental population.
Although I have included the present state of Tasmania as part of the Southeast,
much of the historical literature regarding introduced diseases from this area (main island
and Bass Strait islands) is restricted to those Aboriginal people confined on settlements
(e.g. Plomley 1966; 1987, Ryan 1996). Unlike the mainland, few documents about the
diffusion of introduced diseases among populations living beyond European frontiers
exist. Because a major part of this thesis is concerned with the period prior to Aboriginal
institutionalization on settlements, the available Tasmanian evidence on introduced
diseases is used mainly in a comparative sense against that existing for the mainland.
The period to be covered begins in 1788 with the establishment of the colony of
New South Wales and ends at 1900, the last year before Federation. The period of
sustained direct contact between Aborigines and Europeans in Southeast Australia is
9
Introduction
generally considered to have begun in 1788. Before the arrival of the First Fleet, sporadic
contact between Europeans had occurred on the east coast of mainland Australia and
Tasmania. Tasman sailed the southern coastline of Tasmania in 1642 and later
D'Entrecasteaux in 1792. There is, however, circumstantial evidence that Portuguese
mariners sailed down the east coast in the 1500s, but little is known of this venture (Frost
1987:369). British exploration began in 1770 when Captain James Cook in the
Endeavour sighted the eastern coast of Australia near the present border of Victoria and
New South Wales and then sailed north along the coast. In April of that year he sailed
into Botany Bay and stayed for eight days. He later had to spend seven weeks at the
mouth of the Endeavour River (the site of the present Cooktown), repairing Endeavour
before leaving Australia via the Torres Strait. His contact with Aboriginal people in these
places was limited and there is no record suggesting disease transferral.
The beginning of contact between Europeans and Aborigines differed in various
regions of Southeast Australia in accordance with the spread of colonial settlements.
After the establishment of New South Wales, Tasmania (Van Diemen's Land) was
colonised in 1804, followed by Victoria (Port Phillip) in 1835, and South Australia in
1837. Exploration and settlement of the inland regions continued throughout the first half
of the nineteenth century and the last Aboriginal groups to be contacted in were those of
the northern Spencer and southern Eyre regions during the last three decades.
1.5 Significance of thesis

The significance of this thesis is two-fold.
1. It begins an examination of the biological and medical impact on Australian
Aborigines in response to the changing social and cultural conditions that
resulted when Europeans colonised the continent.
10
Introduction
2. It adds to the growing body of literature regarding the biological consequences
indigenous populations were subjected to as a result of the expansion of
European powers into the Pacific and New World.
1.6 Sources and methods

The evidence used in this thesis comes primarily from European historical
and ethnohistorical documentary sources and to a lesser extent from skeletal collections.
For the most part quantitative evidence on morbidity and mortality could only be used
after 1876 when recording of the Aboriginal population's vital statistics became more
precise.
1.6.1 Historical sources

The major fund of information on the diseases and health of the Aborigines last
century comes from a range of written sources. They include official correspondence of
government bodies, parliamentary inquiries, reports tabled in colonial parliaments,
journals and diaries of explorers, pastoralists, and travellers, letters and reports of
missionaries and superintendents of Aboriginal settlements. Newspapers were a
particularly productive source. They contain many of the government reports on
Aboriginal matters reproduced verbatim in full or in part; letters to the editors from
writers whose impressions of Aborigines were based on anything from long-standing
personal contacts to a casual observation; and editorial opinions and judgements of
European attitudes towards the Aboriginal people and the responses by Aboriginal
people. These documents are housed in State Archives and State Libraries, in Sydney,
Melbourne, Adelaide and Hobart; the National Library of Australia in Canberra; and the
Institute of Aboriginal and Torres Strait Islander Studies in Canberra.
11
Introduction
A two stage method of selection of suitable material from such sources was utilised
in order to obtain the maximum information on the diseases from the most reliable
observers. The first stage used a 'shot-gun' approach, i.e. any reference to disease or state
of health of the Aborigines was noted regardless of its source or of its possible
inaccuracy. The second stage involved culling this material in an attempt to establish
some degree of accuracy and reliability in the reporting and the authority of those who
observed or commented on diseases. This was done by selecting material originated by

various sources:
 Reports by medical practitioners, particularly those who had cause to examine ill
Aborigines on more than one occasion. Many of these reports originated during routine
visits to Aboriginal missions and stations; others were on specially requested visits when
higher than normal morbidity began to cause concern. They provide first-hand accounts
of diseases and symptoms by contemporary qualified observers. In the majority of cases
these reports were considered the most reliable of sources dealing with diseases.
 Routine reports by Aboriginal protectors, sub-protectors and mission
superintendents appointed by the colonial governments. Reports were submitted to the
colonial heads of the colonies covering either a three-monthly, six-monthly or annual
period depending upon the official requirements of the time. Many of the references to
disease in this material were by the protector or sub-protector who in most cases had no
medical background. Often, however, they appear to have originated from either a verbal
or written observation by medical practitioners and were often included verbatim or as
statements within the body of the report.
12
Introduction
 Reports by Aboriginal settlement superintendents. The majority of the mission
settlements were under the administration of the various mission bodies who appointed
their own superintendents. Regular (quarterly, annually) reports were submitted to the
mission heads and to colonial officials responsible for the Aboriginal people. While the
majority of missionaries had little or no medical training one stands out in his
observations of diseases. George Taplin who founded the mission at Point McLeay on
the Lower Murray River in South Australia spent twenty years (1859 to 1879) among the
Narrindjeri until his death. Although he had no formal medical training his reports on the
diseases experienced by these people provide a valuable insight on their changing health
status and the timing and prevalence of the major introduced diseases in this region of the
colony.
 Explorers who initially contacted Aboriginal groups. In a few cases explorers
documenting the interior and coastlines of Australia paid particular attention to the
Aboriginal people whom they met and recorded their observations in diaries, journals and
letters. Although they often had no formal medical training themselves they were on
occasions the first Europeans to see the clinical symptoms of active epidemics (as in the
case of Charles Sturt who documented an epidemic of syphilis on the Murray River in
1829) or saw the sequelae of past epidemics (as in the case of Major Mitchell who
recorded facial scarring from smallpox on the Darling River in 1836).
 Where none of the above sources were available, comments by observers who
had no medical background or secondary advice; who had limited contact with Aboriginal
people, or whose personal knowledge of the Aborigines could not be ascertained, were
used. These came in the form of letters to the editors of newspapers, verbal statements to
government representatives, or personal letters and diaries. In such cases I have used
these sources only when they have been substantiated by other more reliable material.
13
Introduction
For example, during epidemic years of influenza and measles a reasonable reliance could
be ascribed to these sources when they refer to the same diseases which had been
observed in the near vicinity during the same period by a more reliable source.
There were several problems in using the historical data. One of the major hurdles
was that disease pathogenesis was poorly understood (and often misunderstood) by many
members of the medical profession last century. This has led to symptoms of one disease
often being diagnosed incorrectly as another entirely different disease. A case in point is
sexually transmitted diseases. Often, the early symptoms of gonorrhoea were thought to
be an aspect of the same disease entity as those of syphilis, mainly because of their
common venereal means of transmission and the organs involved in their primary
clinical symptoms. These two diseases, along with other sexually transmitted diseases,
were often referred to by the medical profession by using the term 'venereal disease' or
'the venereal' This problem is further exacerbated by the very few surviving detailed
clinical descriptions of these diseases.
Like all historical material written by Europeans that is used to reconstruct aspects
of Aboriginal history, they must be used in a cautious and critical manner. An awareness
of the ideological contexts in which they are written, and the character and background of
the author should always be taken into consideration when using a source for evidence.
When investigating the nature of diseases, which were poorly understood by the medical
writers themselves, one must be additionally cautious.
1.6.2 Skeletal evidence
While the use of human skeletal remains in pathological interpretations of
precontact and contact populations is well advanced, it is of limited value for this present
14
Introduction
topic for a number of reasons. The main shortcoming is simply that the diseases that are
of chief interest in this study either have no effect on the skeletal system, or infect the
skeleton in only a small percentage of individual cases. For example, two of the major
diseases causing high morbidity and mortality were smallpox and tuberculosis. In some
cases of smallpox infection osteomyelitis variolosa occurs mainly in the three long bones
(humerus, radius, and ulna) that meet at the elbow joint (Jackes 1983: 75, Zimmerman &
Kelley 1982:109) and small necrotic foci involving the spine, sternum, and bones of the
wrist and ankle. Zimmerman & Kelley (1982) found osteomyelitis variolosa occurring in
as little as 2 to 5% of cases and almost entirely restricted to children under the age of
fifteen. The severity of the disease also had no bearing on the extent of bone changes.
The main reason for smallpox's restricted skeletal involvement is that it was often rapidly
fatal, particularly in an immunologically vulnerable population, with death occurring
often within 1 to 10 days of infection (Benenson 1990:395) giving little time for
osteological infection and destruction.
Skeletal involvement in tuberculosis is usually a secondary development of
the disease emanating from a primary focus in the lungs or lymph nodes. Steinbock
(1976: 175) reviewed the incidence of bone lesions in tuberculosis patients and found it
occurred in approximately 5 to 7% of cases. The most common form of skeletal
involvement is Pott's disease of the lower thoracic and upper lumbar vertebrae, and
inflammation and destruction of the articular surfaces of the knees and hips.
Previous palaeopathological examinations of skeletal collections in Australia
(Dowling 1990; Webb 1984a, 1989, 1995) have failed to identify any smallpox or
tuberculous lesions in bone. One reason for this lack of evidence for smallpox is the low
frequency of osteomyelitis variolosa in smallpox cases and therefore the small likelihood
of it appearing in skeletal collections. The likelihood of tuberculosis lesions being
15
Introduction
represented in osteological collections is also low. Tuberculosis did not become a serious
cause of morbidity among the Aboriginal people until the second half of the nineteenth
century (see chapter five) when the greater part of the population was living permanently
or temporarily on mission and government settlements. The majority of Aborigines dying
from tuberculosis were buried within the grounds of these establishments and these
individuals are not represented in the osteological collections.
Another problem in using skeletal remains in Australia is that the majority of
the collections housed in museums were not excavated under strict archaeological control
and are therefore poorly provenanced and dated. In many collections it has been difficult
and often impossible to establish with clarity which individuals can be attributed to the
precontact period and which come from the post contact period. This can only be
resolved by individual dating of selected remains, a process that is destructive and largely
undesired by both museum curators and Aboriginal custodians.
Syphilis, on the other hand, presents a clearer picture in the Australian
skeletal collections (Dowling 1990; Webb 1984a; 1989, 1995). Untreated syphilis often
develops from a primary infection located at the point of entry of the treponeme into a
chronic systemic disease with severe lesions (gummatous osteoperiostitis) of the skeletal
system. The frequency of bone involvement is greater than smallpox and tuberculosis,
ranging from 10 to 20% of cases at the tertiary stage (Steinbock 1976: 109), probably
higher when first introduced into virgin-soil populations. The lesions caused by the
treponeme, particularly in the tertiary phase of the infection, can be readily identified in
dry bone (Hackett 1976). Venereal syphilis was almost certainly one of the first diseases
to have been introduced into Australia by European colonists and rapidly established
itself throughout the Aboriginal populations of Southeast Australia. I have therefore
limited the use of skeletal remains in this investigation to the discussion on venereal
16
Introduction
syphilis along the Murray River. The material used is housed in the South Australian
Museum and had been previously examined by me (Dowling 1990) and Webb (1984a,
1989, 1995).
1.7 Origin of diseases

This thesis is not about who was responsible for introducing new infections into the
Aboriginal populations. This topic has been the subject of some contention among
historians for some time (Butlin 1983; 1985; Campbell 1983, 1985) and continues to be
debated (Frost 1994). For example, the case of who was responsible for the first
introduction of smallpox in 1789, just one year after the British colonisation, has not been
resolved. There is, however, little doubt that most of the exotic diseases introduced into
Australia came with British colonisation and that these diseases were reintroduced several
times over until effective quarantine methods were enforced.
1.8 Organisation
Chapter Two introduces a three stage medical model for late 18th century and
19th century Aboriginal Australians which acts as a framework for the remaining
chapters. The first stage of the model deals with the pre-contact medical conditions
which is discussed in Chapter Two. Chapters Three, Four, Five, Six, and Seven cover
stage two of the model, the early contact period and diffusion of disease. Each of these
chapters is concerned with a particular disease or group of diseases which reached
epidemic proportions and caused wide-spread morbidity and mortality among the
Aboriginal people. These are smallpox, sexually transmitted diseases, acute respiratory
diseases, tuberculosis, and measles. Chapter eight is concerned with the third part of the
medical model and discusses the principal diseases responsible for mortality of
17
Introduction
Aboriginal people living on eight settlements in the colonies of Victoria and South
Australia. Conclusions are presented in Chapter Nine.
18
CHAPTER TWO
Disease Environments and Epidemiological Considerations
2.1 Introduction
There can be little doubt that the Aboriginal people of Southeast Australia
suffered severely from the stress brought about by European colonisation. They suffered
the destruction and depletion of traditional food resources; epidemics of exotic diseases
from which they had little or no immunological protection; wide-spread physical violence
and genocide; the forced dispossession of lands; and in the later stages of contact, the
confinement on settlements. Some groups could not recover from such a multi-pronged
attack and ceased as culturally distinct units. Many other groups survived. After first
suffering initial decline in population in the second and third stages of the contact period,
the population reached a nadir which was sufficient for eventual recovery. Populations
that recovered were nonetheless subject to considerable health problems and a severe
reduction in individual psychological well-being.
This chapter presents a medical model in an attempt to identify the processes
involved and the impact of new diseases that occurred among the Aboriginal populations
of Southeast Australia after their contact with European colonists. The model has three
stages relating to the colonisation of Southeast Australia. The first stage of the model
(pre-contact) is discussed in this chapter and the second (early contact and diffusion) and
third (settlement and acculturation) stages are the subjects of the remaining chapters.
2.2 A Medical Model for Contact in Southeast Australia
McElroy and Townsend (1989) developed a medical model based on changes
in Canadian Inuit health subsystems during the 19th and 20th century that were brought
about by European contact (Table 2.1). The table lists four stages of contact on one axis
and the epidemiological, demographic, nutritional, and health care subsystems on the
other axis. The circumstances presented by McElroy and Townsend in stage II and III are
in many ways typical of the development of changes brought about by colonial
occupation throughout the Americas (Verano & Ubelaker 1992) and the Pacific
(McArthur 1967) - epidemics of exotic diseases following closely on the heels of colonial
expansion, leading to extreme morbidity and mortality; population decline and in some
cases a collapse beyond the threshold of survival; a collapse of long-standing social
infrastructures; a decline in nutritional intake, leading to starvation in some cases;
institutionalisation often away from traditional homelands; and a loss of control of
individual and group lifestyles.
I have adapted the model to the Southeast Australian situation for the late
18th century and 19th century (Table 2.2). An extra subsystem representing changes to
socio-economic circumstances has been added. This subsystem outlines the severe and
often sudden changes to long-standing social and economic ways of life that occurred
with the arrival of European colonists. Omitted from the model is McElroy &
Townsend's Stage IV the equivalent of which began in Southeast Australia in the
twentieth century (and to a large degree can be seen to exist today) and so is outside the
scope of this discussion. The Aboriginal populations of Southeast Australia fit
sufficiently well into the model proposed by McElroy & Townsend of indigenous decline
and survival that followed colonisation.
19
Table 2.1 Changes in health subsystems of Canadian Inuit during stages of culture contact
(McElroy & Townsend 1989: 312).
Stage I Stage II Stage III Stage IV

Pre-Contact Early Contact Settlement Modernization
and Diffusion and and
Acculturation Assimilation
Epidemiologica Few pathogens Epidemics of Hyper- Endemic
l in ecosystem; infectious endemic infectious,
subsystem low immunities diseases infectious and nutritional, and
to infections nutritional stress-related
diseases diseases
Demographic Births  deaths, Births< deaths, Births > deaths Births ò deaths,
subsystem population population population slow population
stable decline growth growth
Nutritional High protein, Carbohydrate High High

subsystem low supplements; carbohydrate, carbohydrate,
carbohydrate; famine low protein; low protein
fluctuating interacting with food supply supply and
supply epidemics steady but quality varies by
nutritionally socioeconomic
poor status
Health Shamans and Shamans Government & Modern

resources midwives fulfil discredited in missions medicine
subsystem limited medical epidemics; provide continues; birth
& psycho- missions provide modern control
therapeutic relief medical care; increases; health
needs health needs care and ethnic
greatly politics
increased interconnected
20
Table 2.2 Medical model for 18th & 19th century Aboriginal Australians (after McElroy &
Townsend 1989).
Stage I Stage II Stage III

Pre-Contact Early Contact and Settlement and
Diffusion Acculturation
Epidemiology Pathogens in Epidemics of exotic Hyper-endemic

ecosystem, chronic infectious & infectious and
rather than epidemic; respiratory diseases respiratory
low immunities to diseases
exotic diseases
Demography Population Sharp population Lessening

homeostasis decline due to population decline
epidemics
Nutrition Adequate or more Traditional food High refined

than adequate sources disrupted; carbohydrate, low
nutritional lower protein & protein; food
requirements; often higher refined supply steady but
higher in carbohydrate intake nutritionally poor
carbohydrates than with introduction of
protein; fluctuating sugar & flour; famine
supply interacting with
epidemics
Socio-economic Hunter-gatherer Economic disruption; Reliance on

economy; society displacement from government &
based on kinship & land; social mission food
spiritual ties to land disintegration due to distributions
deaths from denial of land;
epidemics social breakdown
& destruction
Health care Traditional medical Traditional medical Health needs

practices fulfil practices unable to greatly increased;
psycho-therapeutic cope with epidemics governments &
needs & increased health missionaries
needs provide limited
but often
ineffective
medical care;
21
22
The pre-contact stage I is similar for each subsystem apart from the diet which
was higher in carbohydrates for the Australian Aborigines than the Inuit (McElroy &
Townsend 1989: 312). Stage II also shows a similar sequence in the subsystems but for
the epidemiological subsystem where infectious and respiratory diseases were the main
components for Southeast Australia. Stage III departs from McElroy and Townsend's
model in the demographic sub-system. Population decline continued after Aboriginal
people became institutionalised on mission and government controlled settlements. The
official reports from these settlements show a common and continuous trend of declining
population throughout the nineteenth century, with deaths continuing to outnumber births
(Barwick 1971; Butlin 1983; Dowling 1990; Smith 1975, 1980). The respective colonial
governments and missionary organisations in Southeast Australia were convinced of the
eventual extinction of Aboriginal people. Population decline continued into the first
decades of the twentieth century when the trend began to reverse (Smith 1975, 1980).
In accordance with the aims of this thesis which focus on introduced diseases
the following discussion will centre on the epidemiological subsystem of the model.
Discussions relevant to the other subsystems are incorporated within the following
chapters.
2.3 Epidemiological Considerations
An infection, defined simply, is the invasion and multiplication of a infectious
agent into body tissues (Benenson 1990: 501). If the invasion results in cellular injury
and the manifestation of symptoms in the host an infectious disease is the result. The
infectious agents (pathogens) capable of causing infectious disease range from minute and
structurally simple viruses to large, structurally complex helminthic parasites. It is
important to note, however, that infection by a specific pathogen does not necessarily
23
result in disease. The progression from initial infection by an agent capable of causing a
pathogenic response in the host to the clinical symptoms of the disease depends upon a
number of intervening variables. These include the pathogenicity of the agent, the route
of transmission of the agent to the host, and the ability of the host's immune system to
combat the infectious agent. All these factors, in turn, are affected by the natural and
social environments in which the agent and host are juxtaposed; in some cases, the
environments may promote the transmission of the agent to the host (e.g. crowded and
poor hygienic living conditions), while in other cases it may limit or even prevent such
transmission (e.g. small settlements and contact with fewer people). The transmission of
tuberculosis provides a good example of such conditions.
2.3.1 Pre-contact disease.
In order to comprehend the effects of these previously unknown infections
and how they influenced the colonial experience of Aboriginal people we must first
delineate the disease environment that existed before Europeans arrived.
Traditional models of pre and post-contact health and disease proposed by
anthropologists and historians have made two assumptions. The first is that indigenous
populations, particularly those of the New World and Pacific, lived in a mainly disease-
free environment prior to the arrival of Europeans with demographically and culturally
stable populations (e.g. Bushnell 1993: 19-20; Ubelaker & Verano 1992: 279). This
assumption has been based on an extensive body of recorded observations beginning at
the times of initial contact between Old World and New World populations (Lucas
Powell 1992: 41). In Australia the assumption was again made when early European
observers consistently compared the poor state of health of Aboriginal people who had
been in close contact with the colonists to the more healthier populations beyond the
settlement frontiers. The latter were often described as strong, well-shaped, clean-limbed,
24
powerful, noble, and generally healthy (Marshall 1993: 483; Moodie 1973: 1; Sturt 1833:
126). The second assumption is that contact with Europeans was destructive to the health
of indigenous people with epidemics sweeping through large regions and destabilising
them demographically. While I have no quarrel with the second assumption (it is the
subject of this dissertation) the first is deceptive.
The epidemiology of diseases in pre-agricultural hunter-gatherer populations
has been frequently studied (Black 1980; Buikstra 1992; Cockburn 1971; Cohen 1989;
Cohen & Armelagos 1984; Dobyns 1983, 1992: Fenner 1980; Lucas Powell 1992; Merbs
1992; McKeown 1991; McNeill 1976). Webb (1984a, 1984b, 1989, 1995) has discussed
in depth the paleopathology expressed in the skeletons of Aboriginal Australians prior to
European arrival. While these have largely put to rest the assumption of a 'disease-free
paradise' (Ubelaker & Verano 1992: 279) among New World populations the assumption,
however misleading, still lingers for Aboriginal Australia (Franklin & White 1991:3;
Marshall 1993: 483).
Here I wish only to outline briefly the epidemiological nature of the pre-
contact disease environment in Southeast Australia. In Stage I of the medical model
(Table 2.2) I have summarised the disease environment as having autochthonous
pathogens causing disease but rarely reaching an epidemic level. The epidemiology and
mortality of infectious diseases and their effects on the demography of hunter-gatherer
societies are inextricably linked to their social systems and the ecosystem in which they
exist (Polunin 1977). The major characteristics of Aboriginal society and ecology which
would have exerted an influence on the pattern of disease are summarised in Table 2.3.
25
Table 2.3 Major characteristics of Aboriginal society and

ecology (compared to Europeans) exerting an influence on the
pattern of disease (Polunin 1977:7).
Population Lower population density

distribution Smaller residential/foraging groups
Wider spatial distribution
Large group aggregation occurs infrequently
Greater residential mobility
Shorter range of individual movements
More contact with fewer people
Stability Greater resistance to changes

Greater vulnerability to external influences
Complexity Fewer formal roles and occupations

More rigidity in maintaining social and
subsistence roles
Simpler technology
Ecology Closer association with, and adaptations to

the ecosystem
Less close association with other animal
species
Less degradation of ecosystem
26
The main characteristic of Australian Aboriginal epidemiology before
European contact would have been the presence of human and zoonotic pathogenic agents
causing endemic diseases (Cockburn 1971; McNeill 1976; Black 1980; Fenner 1980;
Verano & Ubelaker 1992). Epidemics may have occurred but they would have been
limited temporally and spatially (Black 1975,1980).
The evolution of the relationship between humans and disease in Australia
spans the 50,000 years (Roberts et al. 1990) to 116,000 years (Fullagar et al. 1996) of
human occupation of Australia. The first human diseases to enter would have been those
already well established in the populations of Southeast Asia. Humans arriving on the
Australian continent would have brought with them many of the pathogens that were able
to be transmitted directly from one human host to another and able to be maintained
among the groups moving across the island chains to the Australian continent. They
would have left behind all the zoonoses and infections that required vectors, or obligatory
alternative hosts found only in Southeast Asia. When they arrived in Australia the first
people encountered the marsupials, a completely new type of fauna. The infectious
diseases carried by the marsupials would have differed considerably from those of the
Asian mammals and as a result the zoonotic diseases acquired would have been of a kind
not previously experienced (Cockburn 1971: 48). After many years of interaction
between the human hosts and the infectious agents a state of equilibrium would have then
resulted. Many of the diseases would have contributed, either on their own or
collectively, to mortality among Aboriginal people; usually at low levels of incidence and
mainly to the very young and the elderly. Only under exceptional circumstances would
diseases have reached epidemic proportions and caused excessive mortality among the
infected population. It was left to another group of humans arriving in Australia from
Europe to introduce new and lethal pathogens and thus upset the balance.
27
Table 2.4 Probable major infections of Aboriginal communities of

Southeast Australia prior to European contact (Benenson 1990;
Goldsmid 1984, 1988; Merbs 1992; Stevenson & Hughes 1980).
Disease Reservoir/Host
Worldwide
Herpes Human
Mononucleosis Human
Hepatitis B Human
Trachoma Human
Whipworm Human
Roundworm Human
Ringworm Human
Scabies Human
Pediculosis - lice infection Human
Streptococcal diseases Human
Staphylococcal diseases Human
Diarrhoea, acute bacterial Human
Salmonellosis Human/Animals
Tetanus Human/Animals/Soil
Autochthonous
Hydatids? Dingo/kangaroo
Botulism Spores in soil/fish
Australian encephalitis (MVE) ?Mosquito eggs
Ross River Fever (RRV) Macropods
Query Fever (Q fever) Bandicoots
Cryptococcosis Human
Scrub Typhus Mites
Queensland tick typhus Ticks
Leptospirosis Bandicoots, marsupials
28
Table 2.4 lists probable major infections of Australian Aborigines prior to
European contact. The list consists of worldwide diseases that are known, or have been
suspected of, having a long association with humans to the extent that humans are the
major reservoir for the pathogens, and pathogens that are known to infect humans and are
autochthonous or suspected to be autochthonous to Australia.
Many of these infections are capable of inflicting illness ranging from mild to
acute life-threatening symptoms in individuals. Chronic infection may have caused
anaemia in up to 45.6% of individuals as diagnosed by Webb (1995: 122) in one area of
the central Murray River prior to European arrival. In some cases localised epidemics
infecting a number of people simultaneously were likely to have occurred, particularly
among communities on the east coast and the Murray, Murrumbidgee, and Darling River
corridors where population densities were high and people were becoming more
sedentary (Luebbers 1978; Webb 1995: 274-291).
Absent from this list are the 'urban' or 'crowd' infectious diseases that were
endemic among the populations of Europe and Asia - smallpox, measles, influenza,
chickenpox, poliomyelitis, typhoid; and the chronic diseases syphilis and tuberculosis.
There is no evidence, circumstantial or otherwise, that these latter diseases existed among
the Aboriginal population of Southeast Australia before 1788 (see following chapters).
Table 2.5 lists non-infectious disease states that were likely to have affected
Aboriginal populations in Southeast Australia. Webb (1984a, 1984b, 1989, 1995) has
documented the wide-spread prevalence of nutritional and degenerative diseases, and
trauma in the form of cranial fractures, trephination and broken limbs and ribs in skeletal
collections Australia wide. Neoplastic disease in the form of multiple myeloma,
metastatic carcinoma, nasopharyngeal carcinoma, and osteomas (benign neoplasms) have
29
been identified in at least five Australian Aboriginal skeletons (Webb 1995: 217-234).
Evidence of neoplastic disruption of bone tissue in prehistoric skeletal samples is rare
(Ortner & Putschar 1981), mainly because the death of the individual usually occurs with
the destruction of vital soft tissue before the bone is affected. The prevalence of
neoplasms in precontact Australia can then be expected to be more than is represented in
the skeletal collections.
Table 2.5 Probable non-infectious disease profile of Australian Aborigines

before contact with Europeans (Thomson pers comm.).
Disease type Occurrence

Metabolic Some
Nutritional Some deficiencies, anaemia (famine, parasitic)
Traumatic Non-intentional - falls, bites, stings, burns
Intentional - human aggression
Degenerative Arthritis, dental attrition
Neoplasms Little - idiopathic, viral
Allergies Little
Toxic Some
Psychological Some
Psychiatric Some
The extent and prevalence of the other states are unknown, but on the basis
that they are known to be present in all historic and modern human populations there is
no reason to assume their absence in precontact Australia.
Saunders et al. (1992: 117-118) suggest that the acceptance of pre-contact
health has lead to the distorted use of the epidemiological concept 'virgin-soil epidemic'
(Crosby 1976) by many researchers. Virgin-soil populations have often been described as
having had no previous exposure to particular pathogens and thus lacking the necessary
immunological response when infected. Mauser and Bahn (1974: 27), however, define
30
virgin-soil populations as those 'in which an organism has not been present for many
years, if ever'.
When an infectious disease occurs in a population it will usually cause death
or leave the survivors immunologically protected. If the protection from the disease is
long-term and the disease does not reappear, future generations will have had no exposure
to the disease and will be unable to develop antibodies to the pathogen. This new or
younger virgin-soil population is then susceptible to the disease should it reappear, while
the older generations may still be able to produce antibodies to the pathogen and escape
serious clinical disease.
An example of a new virgin-soil sub population being created is cited by
Black (1990: 59) among the Amazonian Parakana after exposure to hepatitis A. The
Parakana were first exposed to hepatitis A in 1927 which was then present in a
neighbouring and rival tribe which they continually raided for a period of ten years before
breaking off contact and isolating themselves in the forest. In 1984, after they emerged
from the forest and re-established contact, Black and his team were able to test them
immunologically. The results showed an age specific pattern in positive reaction to
hepatitis A. They found that everybody over the age of fifty had antibody to hepatitis A
but nobody younger. The virus had not persisted in the Parakana after the raiding period
when they lived isolated in the forest and a new virgin-soil subgroup of the population
susceptible to hepatitis A had been created within the next generations.
We do not know whether the Aboriginal people of Southeast Australia had
any previous experience with an introduced disease before the arrival of Europeans in
1788. Diseases such as smallpox and tuberculosis may have been introduced to Australia
from Asia (Butlin 1983, 1985). If they had, the excessive morbidity and mortality that
31
later resulted from diseases such as these after European settlement, strongly suggests that
they had little or no immunological protection and that any experience with these diseases
would have been long in the past. The Aboriginal people of Southeast Australia had no
herd immunity to the introduced diseases and the region was virgin-soil for many
pathogens endemic among the Europeans.
The epidemiological concept of a virgin-soil population can therefore cover
situations where contact with a particular pathogen has caused an epidemic, but the
disease did not become endemic among the populations and eventually ceased to exist.
The herd immunity or immunological protection to the pathogen would have been
lessened and eventually lost with the succeeding generations having little or no exposure
to the pathogen (Saunders et al. 1992:117).
To conclude I can see no problem with the assumption that new pathogens
caused increased morbidity and mortality to Australian Aborigines. No-one can dispute
the fact that the diseases introduced into the New World populations were horrifically
destructive to the indigenous people because of their lack of immune experience with the
new pathogens.
2.3.2 Post-contact Epidemics
The process by which an epidemic of an infectious disease develops and the
period for which it can sustain a high level of incidence, are dependent on several factors
which are related to the success of the pathogen's ability to invade, establish itself in a
new host, multiply, and then spread into a new host.
32
 The presence of a source of the fully virulent microorganism. Introduction
and maintenance of the source of pathogens is often through actual cases, convalescent
cases, and apparently healthy carriers able to pass the pathogens on to further susceptible
individuals. Once introduced, the pathogen may be able to reside in animal hosts, re-
emerging when conditions are favourable, to infect human victims.
 The release from the source of infection of a large number of viable
pathogenic agents. The larger the number of agents able to be released from an infected
host, and the longer the period of time the host remains infectious, the greater the chances
are of the disease finding a new host and maintaining itself in a population.
 The survival ability of the pathogen outside the infected host. The
microorganism must retain its pathogenic ability between the time it leaves the host
source to the time it is able to enter and become established in the body of the new host.
 A high number of susceptible individuals must be present in the
population exposed to the pathogen; or put another way - the herd immunity to a
particular pathogen must be low enough to maintain it at an epidemic level. Many
diseases are density-dependent and need a high number of susceptible individuals in a
group or community to maintain their presence. Smallpox was an example of a density
dependent disease. If the disease is to maintain a high incidence within a population there
must be a large number of potential humans available who can host the pathogen. In turn,
their immune systems must allow the pathogen to multiply and to develop the ability to
exit one host and infect the next. If the herd immunity to a particular disease is high then
the chance of the disease becoming epidemic are low.
33
 The frequency of contact between infected hosts and susceptible
individuals must be suitable to the pathogen, enabling it to transfer from one to the other.
This may be achieved by direct means (e.g. person to person contact) or by indirect means
(e.g. an insect vector). The more personal contacts that are achieved, the greater the
period of time the contacts are maintained, and the more intimate the contacts, the greater
will be the spread of the pathogen from host to host and thus the better the ability to
maintain the development of the epidemic.
The effects of introduced infectious diseases upon an indigenous population
would vary according to several factors. Previous exposure to the pathogen, the point of
entry and route of transmission, the population density, and the health and nutritional
status of individuals would have strong bearings on the degree of morbidity and mortality
of a disease on the indigenous population. Cultural practices and intergroup social
relations also affect the dissemination of new pathogens.
Exotic diseases introduced into a population with no immunological
experience of them often display particularly high virulence of the pathogen and the
fulminate character of the symptoms (Crosby 1976; McNeill 1976). Black (1992: 1739-
40) has noted that an individual who catches measles from a family member or near
relative faces nearly twice the risk of death as an individual infected by someone
unrelated. His hypothesis for this is that the virus grown in one infected host is
preadapted to a genetically similar host and so increases its virulence. Histocompatibility
(MHC) antigens in a host infected by the virus present a restricted set of viral peptides to
the immune system which in turn selects against viruses with these peptide sequences.
Under natural selection the viruses that survive immune system attack are then preadapted
to a closely related host and are better able to survive the immune response and replicate
within the host. When the virus enters successive unrelated hosts it encounters a new
34
genetic background (new MHC genes) to which it is not efficiently adapted and while not
being as virulent within that host may nevertheless be able to survive and reinfect.
The cycle of adaptation and re-adaptation continues as a virus spreads
throughout the populations. Black (ibid) has estimated that among South Amerindians
there is a 32% chance that a virus will not encounter a new MHC type at either the A or B
locus when passing from one host to another. As new pathogens entered Southeast
Australia, the chances of finding successive closely related hosts with similar genomes
would also have been high. A gene pool more restricted among the Australian
Aborigines than among the Europeans together with many common lines of descent
within clans would have enabled many of the pathogens to retain a highly virulent state as
they passed through the populations.
In examining the biological consequences of New World colonisation Crosby
(1986), Dobyns (1983) and Ramenofsky (1987) identified eighteen viral, bacterial, and
protozoal diseases most likely to have been introduced for the first time to the indigenous
populations of the Americas. Table 2.6 lists these diseases and compares them with those
that were introduced into Southeast Australia during the nineteenth century.
With the exception of yellow fever which has not been recorded on shore in
Australia (Cumpston 1989: 221), malaria which when introduced was most probably
confined to Northern Australia (Black 1956: 136; Cumpston 1989: 221; Goldsmid 1984:
181), and bubonic plague which was first recorded in Australia in the initial months of
1900 (Cumpston 1989:192), all of the diseases introduced to the Americas were
subsequently introduced into Southeast Australia following the arrival of the First Fleet in
1788 (Black 1956: 136; Cumpston 1989: 221; Goldsmid 1984: 181).
35
Table 2.6 Diseases suggested to have been introduced by European colonists

into Aboriginal populations of Southeast Australia (post 1788) and the Americas .
Disease Post 1788 America America America

Southeast (Ramenofsky (Crosby (Dobyns
Australia 1987) 1986) 1983)
Chickenpox X X X
Dengue fever X X
Influenza X X X X
Measles X X X X
Mumps X X X
Rubella X X
Smallpox X X X X
Cholera X X X
Diphtheria X X X
Pneumonia X X
Pertussis X X X
Scarlet fever X X X X
Typhoid fever X X X
Anthrax X X
Plague X X
Malaria X X
Typhus X X X
Yellow fever X X X
Syphilis X
Gonorrhoea X
Tuberculosis X
36
There are, however, three notable diseases omitted from the Americas lists
which were introduced into Australia during the process of colonisation.
Treponematoses (venereal syphilis, non-venereal syphilis, yaws) has been the
subject of a long-standing debate concerning its endemicity in pre-Columbian America
(e.g. Cockburn 1961; Hudson 1963, 1965; Crosby 1969, 1972, 1986; Hackett 1963). The
debates have centred around the presence or absence of treponematoses in pre-Columbian
America, and their spread throughout Europe after the return of Columbous from the New
World. In her review on pre-Columbian disease environments Buikstra (1994) sees the
debate now swinging more convincingly to endemic forms of treponematoses in the
Americas having both a venereal and non-venereal mode of transmission. While the
debate is of interest to this project it is not a direct concern and I shall not contribute to it
here. I do, however, challenge the argument made by Webb (1984a, 1989, 1995) of an
endemic form of non-venereal syphilis in Southeast Australia prior to European arrival
(see Chapter Three).
Gonorrhoea is one of the oldest known and most common human diseases,
with a history dating back 5,500 years (Rothenberg 1993: 759). Its presence in pre-
contact Australia is unknown. An introduction cannot, however, be discounted in
Australia's north where contact between Macassan fisherman and Aboriginal groups
living on the coast was a frequent event, at least from the middle of the eighteenth century
and before European colonisation of the region (Macknight 1976; Mulvaney 1989: 22).
The third omission from the Americas lists is tuberculosis. This is a disease
transmitted mainly by airborne droplets carrying the bacilli and is often characterised by
acute and chronic symptoms. In the crowded and confined spaces of shipboard life
tuberculosis was an excellent traveller and was carried across the world time and time
37
again (Proust 1991a: 5-26). Erosive spinal, longbone and rib lesions in skeletal
populations dated to c.2,000 BP have now confirmed the presence of tuberculosis as an
endemic disease in pre-Columbian America (Buikstra 1981, 1994: 311; Lucas Powell
1992). There is no such evidence of the disease among pre-contact Australian
populations (Dowling 1990; Webb 1984a, 1989) and it was almost certainly absent in
Southeast Australia before 1788 (Thomson 1991:62). Again, it may have been introduced
into north Australia before 1788 through the long-standing annual contact between
Macassan fishermen and Aboriginal people but there is no positive evidence for this.
Most of the infectious diseases introduced into Australia would have
originated from Britain. The length of ocean voyages, the place of departure and
subsequent ports of call, however, are other major considerations of transcontinental
disease dissemination. The First Fleet left Portsmouth on 13 May 1787 and sailed into
Port Jackson on 27 January 1788, a voyage lasting thirty-six weeks; a period probably too
long for diseases with short periods of infectivity originating in Britain to retain their
communicability. On its passage the First Fleet called in at Rio de Janeiro in August
1787 and the last port of call was Capetown before a nine week crossing of the Indian
Ocean to the east coast of Australia. It is conceivable then that some short-term
infectious diseases may have originated from South Africa. Chronic infectious diseases,
such as tuberculosis and syphilis, could have survived the journey from Britain.
Once the colony had become established in the nineteenth century the
frequency of ship arrivals increased and improved sailing technology reduced the time of
passage between ports of origin and destination (Blainey 1982a: 173) allowing the short-
term infectious diseases a better chance of surviving the trip. This allowed a chain of
infection to become established, throughout the initial colony and into other new
38
settlements which, until effective quarantine practices were in place, would have been
difficult to break.
Throughout the nineteenth century the European population of Southeast
Australia increased and movements across that part of the continent became complex.
New settlements were established at Hobart in 1803; Melbourne in 1835, and Adelaide in
1836. The spread of pastoralism in the new colonies opened up the interior lands,
extended the European frontiers and increased contact with Aboriginal communities.
During the 1850s a population boom occurred following the discovery of gold. The
European population of Victoria increased three-fold during the decade and in New South
Wales it more than doubled between 1851 and 1861 (Blainey 1982c: 158-163). Also, in
1852 and 1853 a total of about 18,000 Chinese arrived in Victoria, and by the late 1850s
more than 40,000 lived on the diggings (Blainey 1982c: 164-165). The frequency of
disease entry into Australia would have increased with migrant arrivals and the new
diseases became established in the high population centres leading to endemicity of
introduced pathogens.
Historical documentation provides ample evidence of the impact of
Europeans on the Aboriginal people. Dispossession of their lands, addiction to tobacco
and alcohol, loss of access to traditional foods and incarceration in government and
mission institutions often in unhygienic conditions, predisposed them to severe mortality
and morbidity from the new diseases. Chronic malnutrition completed the well
established connection between social disruption and infectious diseases. The new
diseases flourished in the environment of unestablished immune responses and decreased
immuno-efficiency of individuals, often suffering from multiple chronic and acute
infections.
39
2.4 European and Aboriginal concepts of disease and curing
When the European colonisation of Australia began in 1788 both they and the
Aborigines had well established sets of beliefs in regard to sickness and curing. It is
therefore important to sketch the underlying concepts regarding disease and curing of
both western Europe and Aboriginal Australia because together they helped to determine
firstly, the Aboriginal response to the invasion of Old World pathogens and secondly, the
response by the European colonial system and its attitude towards the diseases among the
Aborigines.
Every human society is subject to illness in one form or another. Each in turn
has evolved concepts that define the various physical and psychological conditions that
effect personal well-being, explain the cause of illness, and proffer cures. While the
European and Aboriginal medical systems, as they were in the late 18th century, differed
in many respects, both were more socially than medically therapeutic. Neither could
adequately cope with the morbidity and mortality of infectious diseases and neither could
offer an effective cure to those infected.
At the time of colonisation, the arriving European medical community largely
subscribed to the long standing humeral theories of sickness and health. These had been
first advanced by Hippocrates in the fifth century BC, and later championed by Galen to
such an extent that they became a part of a quasi-religious dogma (Duin & Sutcliffe 1992:
22; McNeill 1976: 218-219). The idea that minute organisms might be the cause of
disease ('germ theory') had been postulated as early as the second century but it had little
impact on the medical establishment's conception of disease aetiology (Duin & Sutcliffe
1992:56). It was not until the nineteenth century breakthroughs of Pasteur and Koch that
the role of microbes in the causation of disease began to be accepted. These theories did
40
not go unchallenged in Europe and the medical profession was slow to come to terms
with the new ideas of illness and the new ways of treatment. The concepts were even
slower to become accepted in the distant Australian colonies (Cumpston 1978: 1-8). The
'tyranny of distance' (Blainey 1982a) which so often influenced the political, social and
commercial history of Australia in the nineteenth century also encumbered the
dissemination of medical knowledge. So, at the beginnings of the colonial period and
well into the nineteenth century, the understanding of disease aetiology and therapy was
still based on the long-held theories of humeral causes (Cumpston 1978: 1-8).
The traditional view held by Galen was that the four humours; blood, phlegm,
white bile and black bile, present in the body, coincided with the four elements that
comprised the world; air, water, fire, and earth. Each of the humours had qualities of
hot/cold and wet/dry. As the theory passed through the centuries it became subtly altered
and adorned with new connotations but the core concepts persisted. Illness in a
previously healthy person was perceived to be the result of an imbalance between the
bodily humours brought about by changing climatic or environmental factors (Howe
1972: 7; Duin & Sutcliffe 1992: 56). Most epidemic diseases were understood in much
the same way. But some, for example smallpox, were seen to be rather different and
appeared to result from a tangible contagion that was passed through the air from an
infected person to others. This was the presumption underlying the development of
variolation in the early eighteenth century and later Jenner's idea of inoculation. An
infective agent was also suspected by some to be the cause of tuberculosis (Ruddock
1873; Johnston 1993:1064).
The underlying principle behind treating the ill and affecting a cure was to
restore the balance of the humours. One of the most common practices up to the late 19th
century was to bleed the patient to expel the corruption within. This may actually have
41
been extremely deleterious to the health of the patient because it reduced the body's own
ability to fight the infection by the loss of the very medium, the blood supply, that carries
the antibodies to the infected area. Other methods used to restore the bodily balance were
medicinal. The drugs used for the treatment of diseases were, however, generally
ineffective in combating the infectious agents and in most cases had only limited effect on
the symptoms. For example, a range of drugs was prescribed for the treatment of
diarrhoea. Acute bacterial diarrhoea was a prevalent complaint of the times, mainly due
to the lack of knowledge regarding the cause of putrefaction and the poor hygienic
conditions that commonly prevailed. Conversely, drugs purported to relieve constipation
were used for almost all the non-specific illnesses e.g. debility, headache, anxiety,
rheumatism etc. Along with the practice of blood letting, purgation was considered to be
one of the best treatments to rid the infectious matter from the body and restore the
balance of the body humours (Duin & Sutcliffe 1992).
In many cases drugs were prescribed to relieve pain symptoms. Before
modern analgesics, the most effective were opium and its derivative morphine, often
causing problems of dependence and withdrawal symptoms when the drugs were no
longer available (Duin & Sutcliffe 1992). Others were given for the relief of respiratory
symptoms, e.g. coughs, colds, and the effects of bronchitis, influenza, and tuberculosis
(Potterton 1983). Perhaps the most dangerous of the forms of chemotherapy of the time
was the use of mercury, particularly in the treatment of syphilis symptoms. Until the
introduction of arsenic derivative treatments and the development of penicillin antibiotics
in the twentieth century, mercury chemotherapy had been the mainstay of treatment for
syphilis for four hundred years. Despite such a long faith by the medical profession in its
effectiveness, the drug had little effect on the symptoms of syphilis and was completely
ineffective against the causative agent of the disease. But if taken over a long period, as it
customarily was by the sufferers of chronic syphilis, it induced severe iatrogenic illnesses,
42
the cause of which frequently went unrecognised by doctors and often resulted in the
victims' demise.
Many of the drugs used in the nineteenth century were patent medicines of
little use in reducing the symptoms of infection. A highly popular concoction of the day
was 'Holloway's Pills' reputed to cure gout, rheumatism, inveterate ulcers, sore breasts,
sore heads, bad legs and so on. 'Doctor Morse's Indian Root Pills' were another invention
that claimed to purify the blood and to be a positive and permanent cure for 'biliousness,
constipation, indigestion, headaches, kidney troubles, piles, pimples, and female ailments
etc' (Cumpston 1978: 3). Even as late as the turn of the twentieth century little effective
treatment was available for most of the known infectious diseases and doctors treating the
ill were helpless because of their lack of knowledge of the true causes of the diseases
(Cumpston 1978: 3).
At the time of colonisation and for many years afterwards, Western
anthropologists had little or no knowledge of Aboriginal medical theories. Because of the
rapid destruction or transformation of many Aboriginal societies, many of the then
existing medical practices and beliefs have been lost for ever. But by drawing upon more
recent anthropological studies of contemporary Aboriginal medical beliefs and practices
we can gain some insight into how diseases and their cures may have been perceived.
Aboriginal approaches to health and illness were most probably holistic ones, recognising
spiritual, physical, and biological aetiologies and therapies (Reid 1982: 91). For the most
part, however, the theories of illness were based on magicoreligious beliefs (Taylor
1977:423; Saggers & Gray 1991:47). Blame for an illness was often attributed to the
machinations of rivals or to the will of angry supernatural beings intent on revenge for the
alleged misdeed of the patient. Divine anger was seen by some as the cause of the 1828-
30 smallpox epidemic which swept along the river systems of south eastern Australia
43
(Dawson 1881:60). Others placed the blame on the first European they had seen. The
explorer Charles Sturt was present in the land of the Wiradjuri just as smallpox began and
was seen as the cause of the epidemic (Mair 1831). The Ngarrindjeri and Meru along the
Murray River in South Australia blamed those further upstream for unleashing the
epidemic (Chapter Three). Determining the cause was an important part of coping with
illness (Saggers & Gray 1991: 41-52). It allowed the victims or their families to vent
their anger and frustration and so alleviate their feeling of helplessness which often arose
from being unable to control the disease. Finding a cause also transferred the
responsibility for the condition to someone or something else (Goodall 1994: 68-72;
Mobbs 1991:303-308).
The practice of healing the sick was often vested in special people. Doctor-
sorcerers were able to evoke and control alternative supernatural forces to combat those
already causing the illness. Not all of these practitioners, however, used their skills for
healing. They in turn could use their power and knowledge to cause illness and death
among others. The pointing of a bone by a sorcerer accompanied by a magic ritual, chant,
or song was widely used across the continent to invoke an illness, or to cause the death of
the unfortunate recipient (Berndt & Berndt 1988: 307-322). Frequently the process of
healing involved an act of purification or cleansing, such as sucking the skin to remove
the underlying pathogen, blood-letting, rubbing and massaging the skin to purge the
illness from the body. Heat was often applied to the body by burying the victim in warm
sand and ashes or suspension over a fire. This induced perspiration which was to sweat
the illness out. In other methods the illness could be ritually transferred to another object
and then cast out.
More profane (and potentially dangerous) methods of treatment were used by
the doctor-sorcerers. During the 1830 smallpox outbreak in the Lachlan and Wellington
44
Valley region of New South Wales a victim had his hair scorched from his head, probably
in an attempt to relieve a severe headache which was a common symptom of the disease.
The Kradjee (healer), who had previously observed other cases of smallpox where the
pustules had burst, then began to prick the pustules with a sharp-pointed fish bone and
squeezed out the fluid contained in them with the flat part of the instrument (Bennett
1834: 154-156). The outcome of this treatment on the patient and the doctor-sorcerer is
unknown, but considering the highly contagious nature of the disease, a favourable result
for both would not be expected.
Patient's participation in their own or their family's treatment was a socially
important aspect of the healing process. This allowed the sick to assert some measure of
control over the state of their body and their future well-being. With the breakdown of
the social fabric following the incursions of European colonisation, and the loss of faith in
the powers of the healing doctor-sorcerers to cure the new illnesses, this was often the
only way open to healing. An extreme method was used by one Aboriginal group in
South Australia in the late 19th Century who were probably suffering from the
maculopapular rash of venereal syphilis. They approached a group of Europeans who
were treating a flock of sheep with an arsenic based dip. One of the men was in a poor
state and in jest it was suggested by the Europeans that he should be dipped like the
sheep.
The scabby black was put in the vat, and after a short time he became so ill
that it was feared he would not recover, and lost his hair, toe nails and finger
nails; but in time an improvement was observable. His skin peeled off, and
he was described as a magpie when moulting. Eventually he quite recovered,
his hair grew again, and his skin became as smooth and as glossy as marble.
When this became known among the tribes others having the same complaint
presented themselves at Cannowie, and begged to be "jipped like it other
feller;" but the experiment was considered too hazardous, and no one cared to
risk a trial for murder or manslaughter, if, as was by no means unlikely, a
patient should die under the treatment (Adelaide Observer 1904).
45
While sorcery and supernatural agents probably formed the most important
component of medical concepts, a relationship of physical cause, medical consequence,
and biological treatment was widely acknowledged. Accidental and deliberate trauma,
diet and weather fluctuations were seen as direct causes for certain medical conditions
and specific methods were used to reduce their effects on well-being (Scarlett et al. 1984;
Saggers & Gray 1991). Together with this knowledge Aboriginal societies could draw
upon an extensive knowledge of medical resources and treatments. Scarlett et al. (1982)
have documented medical practices of the Yolngu from northern Australia and have
revealed an extensive pharmacopoeia based mainly on plant species but also using animal
and mineral preparations. Preparations were used for the treatment of coughs, colds,
disorders of the lungs, eyes, teeth, and healing agents for surface and penetrating wounds.
Most of the people were aware of these 'bush medicines', in particular the elderly women
who regularly collected the species and prepared the medicines. Many of the treatments
were used on specific ailments, others had multiple uses, while others were more
generalised treatments.
Australian Aboriginal pharmacopoeia was quite adequate for dealing with
wounds, burns, bites, gastro-intestinal ailments and body aches that were likely to occur
in the daily life of any group. But there were no traditional remedies for the Old World
pathogens such as tuberculosis, influenza, and smallpox that caused high morbidity and
mortality after 1788. This is not to say that European medicine could cope any better
with these diseases. In reality the European medical system could offer no cure and very
little relief from the major infectious diseases.
46
CHAPTER THREE
Smallpox
3.1 Introduction
Until it was officially eradicated in 1979 (Fenner et al. 1988: vii) smallpox
had been a highly infectious and serious systemic disease of humans, erupting in
populations throughout the world in particularly fatal epidemic episodes. The
causative agent of smallpox, variola virus, now no longer occurs in its natural
environment and exists in only two laboratories, one in the United States and the other
in Russia.
The origin of smallpox is not clear. It most probably developed as a zoonosis
during the Old World Neolithic period when agricultural societies grew sufficiently
large enough to provide a supporting human reservoir for the virus (Crosby 1993a:
1008). The disease, as it was known in modern times (a human disease with no animal
reservoir), required a large population reservoir to maintain itself and so almost
certainly did not exist among the hunting and gathering peoples of the Palaeolithic
(Crosby 1993a: 1008).
Descriptions of smallpox, or a disease of a similar nature, are known from
China during the 4th century AD and south-west Asia in the 7th century AD. One of
the earliest victims of the disease may have been Ramses V of Egypt who died in 1157
BC (Crosby 1993a: 1009; Fenner et al. 1988: 209-211). As large centres of population
developed in Europe, Asia, and Africa and movement of people increased, smallpox
developed from the occasional epidemic to become a well established endemic disease
- one of the most deadly known to humans of the Old World.

Smallpox
Its trans-oceanic spread began in the early 16th century when it was carried
across the Atlantic by Spanish expeditions to the New World populations of the West
Indies, Mexico, South and North America (Crosby 1986: 196). Mortality among these
populations was extreme (Dobyns 1983: 251-289; Stannard 1992: 77-136). Early
Spanish estimates suggest a 25% to 50% case-fatality rate among the Indians of
Central America (Crosby 1993a: 1010). Similar rates, or higher, were consistently
reported throughout the continent for the next three hundred years. Among the
Amerindian populations, smallpox was reported to have devastating effects in the
Andes beginning in the early 1540s (Cook, N.D. 1992: 208-213); in Massachusetts
during the seventeenth century (Crosby 1986:198; Cook, S.F. 1973: 491); among the
Mohawk, Iroquois, and Huron of the Northeast of North America from 1634 on
(Snow 1992: 183); in the Southeast during the early sixteenth century (Thornton et al.
1992: 191-193); in the Southwest during the fifteenth and sixteenth centuries (Stodder
& Martin 1992: 67); on the Northern Plains and Missouri River Valley during 1837-
1838 (Trimble 1992: 257-264); and among Californian mission populations during
1844 (Walker & Johnson 1992: 135).
Molnar (1983: 225) estimates that 1.5 million deaths occurred in the large
population centres of Mexico following the arrival of the Spanish. Other high
estimates include 60% mortality among the Northern Plains and Great Lakes
populations (Joralemon 1982); 74% among the Hopi Indians of Arizona (Dobyns
1983: 13;), 85-90% in Texas (Aten 1983); 98% among the Cree of Ontario (Young
1979) and 62% among the populations of the Northwest (Boyd 1990: 144). In
reviewing the evidence for mortality from smallpox both Dobyns (1983: 13-14) and
Cook (1973: 501) suggest an overall figure of 75% case-mortality among the virgin-
47
Smallpox
soil populations for the first smallpox epidemics throughout central and northern
America.
The first known introduction into the western Pacific was to the Palau Islands
in 1783. In 1853 smallpox killed up to 8% of the indigenous population of Hawaii; in
the Carolines it was responsible for the death of up 40%; and on Guam 33%. Other
introductions were to Easter Island in 1863-64 and New Guinea sometime before 1872
and later in 1893 and 1895. Quarantining of ships allowed Fiji to escape the
introduction of smallpox and the disease killed only six in New Zealand when two
ships carrying active cases arrived in 1872 (Fenner et al. 1988: 241-242).
Smallpox among the Aboriginal people of Australia was first recorded soon
after the arrival of British colonists. The aim of this chapter is to document its spread
among the Aboriginal populations of Southeast Australia, compare its dispersion to
that of the European colonists, and make some assessment of the demographic effect
on the Aboriginal populations.
3.2 Biology of smallpox
Smallpox was an acute disease specific to humans which often led to death
within the first two weeks from the appearance of clinical signs. Those victims who
survived, however, obtained a lifelong immunity to the disease and neither chronic nor
recurring infection followed. Immunity to the disease was not as well guaranteed by
vaccination, but in vaccinated individuals who developed the disease, it often
expressed a much milder symptomatology and had lower case-fatality rate in its
victims (Fenner et al. 1988: 272). The disease could only become endemic within a
population when there was a large reservoir of susceptible hosts. This was regularly
48
Smallpox
achieved by new births and immigration of susceptibles in the larger population
regions of the Old World.
Two main clinical-epidemiological varieties of smallpox have been
recognized - variola major, the classic type of smallpox, and variola minor (Table 3.1).
Table 3.1 A classification of clinical types of variola virus

infection (WHO 1977; Fenner et al. 1988).
WHO Clinical Manifestation

Classification
050.0 Variola major
Ordinary type
Modified type
Haemorrhagic (pustular) smallpox
Flat type
Variola sine eruptione
050.1 Variola minor

(alastrim)
The two strains of variola virus differed quite significantly in their virulence
to humans. Variola minor, as its name suggests, causes mild symptoms in its human
host and produces a case-fatality rate in unvaccinated individuals ranging from 0.1 to
2%. The more virulent variola major strain is a life-threatening disease. It often
manifests severe symptoms, and produces a case-fatality rate among unvaccinated
victims up to and in excess of 50%.
The virus is transmitted from person to person with no other vector involved.
In most cases the virus enters the body via the oropharynx or respiratory tract passed
on by respiratory discharges from infected individuals. Other means of transmission
49
Smallpox
are: direct inoculation, as in variolation; by the skin lesions of patients, by material
which has been contaminated by the virus, by placental transmission, and by airborne
spread (Benenson 1976:440, 1990:396; Fenner et al. 1988:186). The period of
communicability is greatest during the first week of initial infection and continues for
approximately 21 days. Susceptibility to the disease is universal but long-term
immunity usually follows recovery and second attacks are rare.
There are five main sub-types of variola major (Table 3.1) distinguished by
their clinical symptoms and prognoses. Ordinary type variola major is the most
common. In typical cases of this type of infection there is an incubation stage that
ranges from seven to seventeen days but usually between ten to twelve (Benenson
1990: 396). During this period of infection the virus replicates and spreads throughout
the body via the lymphoid organs (spleen, bone marrow and lymph nodes). The onset
of clinical symptoms is sudden. Fever, malaise, headache, severe backache,
prostration and in some instances abdominal pain are the first to appear. These
symptoms can easily be confused with influenza, meningitis and pneumonia
(Benenson 1976: 443). After two to four days the fever is reduced and the
characteristic stages of the smallpox rash begin. Starting as maculopapules first on the
face, hands or forearms and then by centrifugal distribution to the trunk and lower
limbs. The lesions are more abundant on the face and extremities than on the trunk.
The papules then become vesicular within a day or two and then form pustules within
48 hours. The fever often returns during this stage. The pustules dry and begin
forming scabs within eight to ten days of initial eruption. The matured lesions may be
confluent, semi confluent, or discrete. Finally the scabs fall off at the end of the third
to fourth week if the patient has survived. This type of variola major has been
documented as having case-fatality rates of up to 62% (Rao 1972 cited in Fenner et al.
1988).
50
Smallpox
The flat type of variola major, distinguished by the lesions which project
little, if at all, above the surrounding skin surface, is relatively rare but has a case-
fatality rate reaching 98% (Benenson 1976:444; Fenner et al. 1988: 5). Equally as
fatal is the haemorrhagic type which causes, either late or early in its development,
subconjunctival bleeding, bleeding from the mouth, gums, nose, and blood in the urine
(haematuria). In this type of variola major pregnant females are more susceptible than
males and non-pregnant females. The modified type and variola sine eruptione are
rare and occur principally in vaccinated individuals (Benenson 1976: 444; Fenner et al.
1988: 22-38)
The symptoms of variola minor were similar but much less severe than
variola major. The onset was, like variola major, sudden with a fever, headache,
backache, and sometimes vomiting. The sequence of development, and distribution of
the skin lesions were also similar but their evolution was much more rapid. The eruptions
became vesicular on the third day after the appearance of the papular stage and developed
into pustules within twenty four hours. The final crusting stage was established on the
sixth or seventh day of the rash. The facial lesions were often more sparse than in variola
major and rarely reached the confluent stage. Secondary fever was rare and the victims
usually remained ambulant and less affected during the course of the disease (Fenner et
al. 1988: 38-39).
3.3 Smallpox among the European population of Southeast Australia
In 1984 Fenner stated that Australia has not loomed large in the global history
of smallpox. A major reason for this may be seen in the slight effect the disease had on
the European population of Australia. Since the arrival of the First Fleet in 1788 there
51
Smallpox
have been seven outbreaks of smallpox among the European population that could be
considered serious (Table 3.2).
Table 3.2 Major smallpox outbreaks during nineteenth century

in European population of Australia (Cumpston 1914, 1989;
Curson 1985).
Year Region Cases Deaths Case

Fatality
1857 Melbourne 16 4 25
1868-69 Melbourne 43 10 23
1871 Sydney, Melbourne 7
1881-82 Sydney 154 40 25
1884-86 Sydney, Melbourne, 123 10 8
Adelaide
1887 Launceston 11
1893 Perth 52 9 17
All the outbreaks were due to importations by passengers arriving by ship.
The 1881-82 outbreak which spread throughout the port suburbs of Sydney had the
highest number of individual cases and a case-fatality rate of 25%. Most of the other
cases were confined among ship's passengers who were quarantined. The containment of
the outbreaks was largely due to the success of the various colonial government bodies
who emphasized a strategy of quarantine and vaccination of victims and contacts rather
than the routine vaccination of children (Hopkins 1983: 134). While this strategy was
suited to a colonial population who had recently arrived from an endemic to a non-
endemic country where the major threat was the periodic importation of the disease by
sea, it was not suited to the Aboriginal populations who had no previous experience with
smallpox and no means of prevention.
3.4 Smallpox among the Aboriginal populations - source material
52
Smallpox
In great contrast to its minor presence among the European population,
smallpox has had a lethal history in Aboriginal Australia. Three unconnected epidemics
attributable to smallpox were recorded among the Aboriginal populations of Southeast
Australia (Fig 3.1). The first began in March or April 1789. A severe epidemic disease
was seen by European colonists to be causing high mortality among the Aboriginal
population living around the new settlement of Sydney (e.g. Butlin 1983: 63-68; Frost
1994: 190-210; Curson 1985: 41-53). It appeared quickly and lasted in the Sydney region
for a few weeks. Later evidence suggests that it occurred along the coast line both north
and south of Sydney.
Apart from a handful of written accounts by members of the First Fleet (e.g.
Collins 1798; Hunter 1793; Phillip 1790b; Tench 1793) little is known about this
epidemic. A few contemporary accounts survive, written by those who saw the disease
active among the Eora around Sydney Harbour, and its effects in surrounding groups.
The First Fleeters attribute the disease they saw to smallpox, although this diagnosis has
not always been accepted by historians (Watt 1989: 145). Most writers (e.g. Butlin 1983;
Cumpston 1914, 1989; Day 1996; Fenner 1984, 1985; Fenner et al. 1988; Frost 1994),
however, have accepted that the disease was indeed smallpox, but debates mainly
concerned with the origin of the disease, have continued (Butlin 1985; Curson 1985).
Several possibilities have been put forward including; the accidental or deliberate release
of variolous matter brought with the colonists of the First Fleet in January 1788 (Butlin
1983: 19-24; Day 1996: 62-64); a visiting French squadron which arrived at Botany Bay;
seasonal fishermen reaching northern Australia from Makassar where the disease was
endemic; and a type of 'native pox' presumed to be an endemic disease of Australia
(Tench 1793; Cumpston 1914; Butlin 1983; Fenner 1985; Curson 1985). While each in
turn have made articulate use of historical records citing evidence for their particular case,
and in some cases speculating on evidence that does not exist, no one author or theory has
53
Smallpox
in the end prevailed over the others and the question of origin has remained unresolved.
The limiting factor has been the historical records themselves which show no conclusive
evidence either way. As far as this thesis is concerned the origin of the first smallpox
epidemic, and indeed the subsequent outbreaks among the Aboriginal populations is not a
central issue. It is far more relevant to examine the nature of the epidemics and to
establish their spatial and temporal extent, and the demographic and social effects they
had on the Aboriginal populations than to deliberate about their origin on evidence that
does not sustain such an approach.
The second epidemic occurred forty years later, between 1828 and 1832 and
was documented more extensively. It was first observed by European exploration parties
(Sturt 1833 vol I: 93) on the river systems west of the Great Dividing Range in New
South Wales, beyond the limits of the European settlements. Later, as the frontiers
extended, observations of Aboriginal people bearing smallpox scarring, and oral accounts
from those who survived, revealed that the epidemic had extended further inland along
major river corridors to South Australia, and to the eastern coastline of the continent (Fig
3.1).
A third outbreak of smallpox was observed to be spreading among the Nawu,
Wirangu, and Banggaria people along the western coast and inland regions of South
Australia in 1866-67 (Fenner 1984: 732; Gething 1867). This epidemic was most likely
the southern extent of an outbreak which was spreading among Aboriginal groups on the
north and west coast of Australia and through the centre between 1860 and 1869 (Fenner
1984, 1985; Fenner et al. 1988; Cumpston 1989: 180).
3.4.1 The first epidemic - 1789
54
Smallpox
One year after the first European colonists established their settlement at
Sydney Cove they noticed a severe mortality among the Eora seemingly caused by a
deadly disease. The few contemporary accounts referring to the incident describe it as an
epidemic of smallpox.
The 1789 outbreak of smallpox among the Aboriginal people was the first
epidemic in Australia to be recorded. It remains among the most poorly recorded.
Potentially, the most informative sources on the epidemic would have been the medical
journals of the First Fleet Surgeons which to a large extent have not survived. The
majority of written records that have survived are by contemporary observers who had no
medical education or background and which generally consist of accounts within official
reports, personal memoirs and letters. Nevertheless, these diarists wrote accounts of the
epidemic based on their visual observations and on information they received from those
who were medically trained. They should be accorded some credibility.
In April 1789 the Judge-Advocate and Secretary of the Colony, David Collins
(1798: 53) wrote:
Early in the month, and throughout its continuance, the people whose
business called them down the harbour daily reported, that they found, either
in excavations of the rock, or lying upon the beaches and points of the
different coves which they had been in, the bodies of many of the wretched
natives of this country.
Almost every boat that sailed on the harbour going about the daily business of
the colony saw bodies lying about as if they had been abandoned where they had died.
Returning from the Cape of Good Hope in the Sirius, Bradley (cited in Cobley 1963: 35)
sailed in from the sea entrance of Port Jackson to the settlement at Sydney Cove and saw
'a great number of dead Natives ... in every part of the Harbour'. According to Newton
55
Smallpox
Fowell, a naval officer on board Sirius, in some cases the bodies were found with the
remains of small fires on either side of them and containers of water left within reach
(Irvine 1988: 113). Bradley saw none of the Aboriginal fishing canoes that had
previously been a common sight on the harbour. In fact, the waters and shores of Port
Jackson appeared to the Europeans to be devoid of any living Aboriginal person.
Collins visited the harbour shores to investigate Bradley's observations and
reported:
At that time a native was living with us; and on taking him down to the
harbour to look for his former companions, those who witnessed his
expression and agony can never forget either. He looked anxiously around
him in the different coves we visited; not a vestige on the sand was to be
found of human foot; ... not a living person was anywhere to be met with. It
seemed as if, flying from the contagion, they had left the dead to bury the
dead. He lifted up his hands and eyes in silent agony for some time; at last he
exclaimed, `All dead! all dead!' and then hung his head in mournful silence
(Collins 1798: 496).
The only Aboriginal people that were seen by Collins that day were the 'putrid bodies of
those who had fallen victim to the disorder' (ibid: 496).
At first the cause of the mortality was unknown but the repeated accounts of
Eora bodies about the settlement environs aroused the interest of the staff of the colony's
hospital. A number of bodies were collected and brought into the settlement for the
purpose of post mortem examination (Tench 1793: 145). No description of these post
mortems survives.
Tench, a marine captain, who accompanied Collins around the shorelines
gives a brief description of the symptoms in his account of the settlement:
56
Smallpox
On inspection, it appeared that all the parties had died a natural death:
pustules, similar to those occasioned by the small pox, were thickly spread on
the bodies... (Tench 1793: 146).
In mid April a small group of Eora was found suffering from the disease in a
cove near to the settlement. The Governor of the colony, together with a surgeon and
Arabanoo (a captured Eora then living in the settlement), went immediately by boat to the
place. Tench again recorded in his account that:
Here they found an old man stretched before a few lighted sticks, and a boy of
nine or ten years old pouring water on his head, from a shell which he held in
his hand: near them lay a female child dead, and a little farther off, its
unfortunate mother... eruptions covered the poor boy from head to foot; and
the old man was so reduced, that he was with difficulty got into the boat
(Tench 1793: 146).
The old man and the boy were then brought back into the settlement and
placed under the care of the surgeons. The old man lived only a few hours after being
brought into the settlement:
By the encouragement of Arabanoo, who assured them of protection, and

soothing behaviour of our medical gentlemen, they became at once reconciled
to us and looked happy and grateful at the change of their situation. Sickness
and hunger had, however, so much exhausted the old man, that little hope was
entertained of his recovery. As he pointed frequently to his throat, at the
instance of Arabanoo, he tried to wash it with a gargle which was given him;
but the obstructed, tender state of the part rendered it impracticable (Tench
1793: 146)
Despite being 'covered from head to foot' with eruptions when he was brought
into the settlement the young male survived the disease. Collins (1798: 54) attributes his
survival to the care he received from Surgeon White during the course of his illness.
There is no surviving record by White of this incident.
Towards the end of April Governor Phillip (1790b) records that two more
Eora, an elderly man and a young female of ten or eleven years of age, were brought into
57
Smallpox
the settlement suffering from smallpox. Tench (1793: 148) recorded them as 'a young
man, and the other his sister, a girl of fourteen years old'. Other accounts differ as to how
many Aboriginal people were found suffering with the disease and were brought into the
settlement. Collins (1798: 496) reported that 'two elderly men, a boy, and a girl were
brought up, and placed in a separate hut at the hospital'; and Hunter (1793:134) recorded
that 'two children, a boy of six or seven years of age, and a girl about ten, were lately
picked up labouring under the same disease; two old men; whom we had reason to
believe were the fathers of the two children, were picked up at the same time, and much
care taken of them.' Whatever the number may have been, it is recorded by Tench (1793:
147), Collins (1798: 53), and Phillip (1790b) that, despite the care afforded them, the
adults died of smallpox. Two children, however, showed signs of improvement soon
after their arrival in the settlement and survived the disease.
Although there are no surviving descriptions of the symptoms of the disease
by the surgeons who attended the Eora brought into the settlement's hospital, it is possible
to reconstruct, with some detail, the course of the symptoms from the diarists. Among
the first group of Eora brought into the settlement in mid April was the young male with
eruptions covering most of his body (Tench 1793: 146). If this observation is accurate
then the boy was past the initial symptoms of fever, malaise, and prostration which would
have occurred in the first two to four days of symptomatic onset. Tench's account is not
clear as to which stage the 'eruptions' were at, but because he was able to sit up and offer
some assistance to the adult male, and because they covered most of his body we can
assume that he was in an advanced stage of clinical signs with the lesions reaching
maturity and was over the worse stages of the disease. No more is said of him in this
respect other than that he recovered and was adopted into the family of the Surgeon-
General of the colony. The accompanying adult male may have been in about the fourth
day of clinical signs as Tench describes him in a condition of immobility and exhaustion
58
Smallpox
when he was brought in. The next day his condition deteriorated with the onset of
secondary fever accompanied by periodic bouts of shivering. He remained prostrate and
was unable to eat but drank water when it was offered. He remained conscious until he
died. Of the second pair that was brought into hospital we know less. We can assume
that they were in an advanced stage of the disease as Tench (1793: 148) describes them
both as being in 'a most deplorable state of wretchedness from the small-pox'. After three
days the young male died and the female recovered to be adopted into the family of a
clergyman (Tench 1793: 148).
Arabanoo, who had closely attended the dying Aboriginal patients, also
succumbed to the disease. He began to show the symptoms on May 12 and died six days
later (Tench 1793: 149; Phillip 1790b). An incubation period of between 7-17 days, most
commonly 10-12 days, before the onset of symptoms would suggest that Arabanoo caught
the infection from the second couple to be brought in. According to Tench (ibid: 148)
Arabanoo had shown more sympathy and care for them than he had for the former group
brought in, and most likely had had more physical contact with them. A period of six or
eight days followed during which the symptoms 'burst forth with irresistible fury' (Collins
1798: 54; Tench 1793: 149) before he died:
During his sickness he reposed entire confidence in us. Although a stranger

to medicine, and nauseating the taste of it, he swallowed with patient
submission innumerable drugs, which the hope of relief induced us to
administer to him. The governor, who particularly regarded him, caused him
to be buried in his own garden, and attended the funeral in person (Tench
1793: 150).
The infection was limited almost entirely to the Aboriginal population. The
only non-Aboriginal person to be infected was, according to Collins (1798: 496), 'a
North-American Indian', a sailor belonging to the Supply, who manifested symptoms on
May 2 and died a few days later (Phillip 1790a: 145). The source of his infection is not
59
Smallpox
known. Nothing is recorded of this man's movements in the days preceding his infection,
or of his contact with the Aboriginal people within and without the settlement. Nor is
there record of the treatment he received during his illness or whether he was isolated
from the rest of the community. But, even though the disease is highly communicable
during the first week after the onset of symptoms, there is no record of the sailor
transmitting the infection on board the Supply nor within the settlement.
That the settlement escaped the epidemic was largely due to the low level of
personal contact the Europeans had recently had with the Eora. Governor Phillip (1790b:
159) was concerned with the lack of friendly contact and rapport that had so far been
established. One of his tasks on establishing the settlement was to initiate a friendly
relationship with the Aboriginal people, to conciliate their affections, and to learn as
much about them as he could for the benefit of the colony (George III: 1787). At first he
was able to meet them on amicable terms but the Eora remained generally aloof from the
Europeans and avoided the settlement. No mutual understanding of their respective
cultures developed and soon the goodwill, which had at best been tenuous, deteriorated
into a series of violent skirmishes around the settlement lasting several years (Clark 1981:
116; Day 1996:: 49-68; Reynolds 1987: 32-40). Because of this poor relationship Phillip
had decided to capture one of the Eora and bring him into the settlement in order to break
down the communication barrier that had resulted and try once again to establish close
association. Arabanoo, then, was the first of several Eora whom Phillip captured.
Nor did the ill Eora who were brought into the settlement hospital transmit
smallpox further. They were immediately isolated in an unoccupied building next to the
hospital. The colonists were well aware of the contagious nature of smallpox as Collins
comments:
60
Smallpox
It was not a desirable circumstance to introduce a disorder into the colony

which was raging with such fatal violence among the natives of the country
(1798: 53)
It is not known how many of the Europeans (about 1,000 in all) were immune
to smallpox, having either previously survived an infection or having been successfully
inoculated against it. There was, however, one potentially susceptible group in the
settlement - the children and infants who had either been born in the settlement or on the
voyage out. There is no record of any inoculation procedure performed on them. Collins
(ibid: 53) reveals that:
Notwithstanding the town of Sydney was at this time filled with children,
many of whom visited the natives that were ill of this disorder, not one of
them caught it...
While the arrival of Eora in the settlement would have been the cause of great curiosity
for adults and children alike it is unlikely that they would have risked, or been allowed,
close contact with them when they clearly showed signs of a disease that was feared and
known to be highly contagious.
The epidemic existed in the Sydney region during March and April 1789 and
appears to have subsided by early May. Its extent, however, appears to have been far
greater than the environs of Sydney. Cumpston (1914: 2) refers to evidence of its
existence far to the south-west in South Australia and Butlin (1983: 24) refers to evidence
of its presence to the north in the Hunter Valley region; but neither author indicates a
source for these assertions. The diarists of Sydney no longer report seeing active cases of
smallpox among the Aboriginal people after May 1789, but the characteristic traces of the
disease were often seen in survivors.
61
Smallpox
In June 1789 Governor Phillip led an exploration party to Broken Bay, a large
inlet, and mouth of the Hawkesbury River, twenty five kilometres north of the settlement.
They left their boat and crew at the northern end of Port Jackson and travelled first along
the beaches then overland using the well established Aboriginal trails to meet their boat at
Broken Bay. Collins (1798: 52) writes that the path they followed 'was in many places
covered with skeletons, and the same spectacles were met with in the hollows of the rocks
of that harbour.' Hunter, who also accompanied the party, recounts their meeting with a
group who had been fishing in the waters of the bay. On seeing the boat approaching:
...they all made their escape, except this miserable girl, who had just
recovered from the small-pox, and was very weak, and unable, from a
swelling in one of her knees, to get off to any distance ... she appeared to be
about 17 or 18 years of age, and had covered her debilitated and naked body
with the wet grass, having no other means of hiding herself (Hunter 1793:
138-139)
Governor Phillip (1790b) commented that they had seen the traces of
smallpox wherever they had been. Further to the north-west in the Wellington Valley
some 300 Km from Sydney and on the western side of the Great Dividing Range, Mair, a
military surgeon, reported seeing three old men with pock marks when he was
investigating the second epidemic in 1830 (Mair 1830, & see below). Each claimed to
have had the disease when they were young and each in turn was among the few who
were not infected by this outbreak.
Well south of the Sydney-Botany Bay region the situation was similar. In
1803 Lieutenant Grant, aboard the Lady Nelson, entered Jervis Bay, 160 kilometres south
of Port Jackson. He remarked that many of the Aboriginal men and women he saw were
marked with smallpox scars (Grant 1803). In February of the same year Flemming of the
Cumberland was on a voyage of exploration between Sydney and King Island in Bass
Strait. He landed at Port Phillip Bay on the south coast where he met a group of eleven
62
Smallpox
Aboriginal people, probably Woiworung. Two of them he states appeared to be marked
with smallpox sequelae (Flemming 1878: 16). Although Flemming does not say so, the
scarred individuals he saw were most likely adults and probably males as they were
carrying spears. If these reports are accurate, and there appears little reason for doubt,
then these Aboriginal people would have been children when the 1789 smallpox epidemic
reached the lower east and south coast of Australia. It is highly likely then that they were
the survivors of the 1789 epidemic.
If these observations at Broken Bay, Wellington Valley, Jervis Bay, and Port
Phillip are correct, then smallpox appears to have spread among the Aboriginal
populations, at least as far inland as the Wellington Valley in the north and Port Phillip on
the southern coast. Both points were well beyond the European frontier in 1789. Apart
from Cumpston's (1914:2) assertion of the 1789 smallpox epidemic reaching South
Australia there is no evidence to suggest that this epidemic broke out of the coast and
highlands belt and penetrated into the interior of the continent (Curson 1985: 51).
The epidemic was severe for the Eora living around the Sydney settlement.
The First Fleet records leave us with a stark picture of high morbidity and mortality from
the disease. Governor Phillip (1790b: 159) wrote:
It is not possible to determine the number of natives who were carried off by
this fatal disorder. It must be great; and judging from the information of the
native now living with us... one half of those who inhabit this part of the
country died...
While this was a crude estimate by Phillip, it may have not have been so
inaccurate. If this was the first episode of epidemic smallpox among this population then
they would not have been immunologically protected against it and high morbidity and
63
Smallpox
mortality would be expected. The effects of variola major among other unprotected and
virgin-soil populations elsewhere in the world has resulted in extraordinarily high
mortality (Black 1975: 517; Butlin 1983: 65; Dobyns 1983; Fenner 1984: 730-733;
Fenner et al. 1988: 1069-1102; Snow & Lanphear 1987; and above). In these
circumstances the disease affects both sexes and all age groups of the population and
case-fatality rates ranging from 25 to 90% can be expected (Koplan & Foster 1979: 440;
Fenner et al. 1988:5)
How severe then was the mortality among the Eora around the Sydney
settlement? If we accept Phillip's estimate of 50% mortality then how many deaths does
this represent? In May 1788, just weeks after the settlement was established, Governor
Phillip (1788a) estimated the number of Aboriginal people living in the vicinity of Botany
Bay, Port Jackson and Broken Bay, to be '... no less than one thousand five hundred'.
There is no way of knowing how accurate this was, but once again Phillip may have been
close in his estimate (White & Mulvaney 1987: 115). More recent estimates by Kohen
and Lampert (1987: 345) based on area/density calculations suggest a population of
between two and three thousand people belonging to three main linguistic groups
(Tharawal, Dharug, and Kuring-gai) living between Jervis Bay in the south to Broken Bay
in the north. Other estimates (see Turbet 1989: 26-28) have a population of between
2,600 and 5,200 for an area of 1,300 square kilometres of coastal strip around the
settlement. While there are certainly inaccuracies in these estimates they point to a
substantial number of people inhabiting the coastal plains and hinterland either side of the
Sydney settlement. With a postulated fatality rate of 50% (similar to the Americas) a
likely number of deaths from the smallpox epidemic would therefore lay somewhere
between 750 and 2,600.
64
Smallpox
The realisation that many had died in this epidemic remained with the
European colonists. In 1822 a Russian visiting the Sydney recorded:
Many of those who had settled in close proximity to the English colonists
became infected with smallpox and thousands died, several generations
perished (Hotimsky 1967: 93).
Whatever the real extent of mortality may have been it was certainly high.
Apart from seeing the many bodies around the shores of Port Jackson, the colonists had
the accounts of the friendly Eora to rely on for an estimation of the severity of mortality:
As a proof of the numbers of those miserable people who were carried off by
this disorder, Bennillong told us, that his friend Cole-be's tribe being reduced
by its effects to three persons... (Collins 1798: 497).
Again in April 1791, when the first exploration expeditions reached the
Nepean River region some fifty kilometres inland from the settlement, they were
informed by their two Aboriginal guides that:
this part of the country was inhabited by the Bidigals, but that most of the
tribe were dead of the smallpox (Hunter 1793: 340-341).
The other writers seemed equally shocked by the epidemic and report indications of high
mortalities (Irvine 1988: 113; Tench 1793: 146-149). The mortality in regions further
away from the settlement remains unrecorded and so unknown.
The response to the epidemic by those who did not die immediately was to
abandon the coastal regions near the settlement. Immediately after the epidemic was
noticed by the Europeans Port Jackson and the environs of the settlement appeared
deserted by the Aboriginal people. How far and to where they fled is unknown, but
whatever the case it was not for long. Small groups of Aboriginal people were soon
65
Smallpox
sporadically sighted around Sydney and Botany Bay by exploration groups travelling
outside the settlement (Hunter 1793: 165-167). Some four to six weeks after the
epidemic Aboriginal people began to be seen again on the waters of Port Jackson. On
2nd June Bradley wrote in his journal that:
Twenty canoes passed Sydney Cove going down the Harbour; this was the
first time any number of them had been seen together since the small Pox
having been among them (Cobley 1963: 43).
In November Hunter (1793: 167) recorded a group of twenty to thirty on the shores in a
hostile encounter. Later that month a group was met under more friendly terms and two
males, Benelong and Colbee, were enticed back into the settlement. One year after the
epidemic a group of three hundred Aboriginal people, including Benelong and Colbee,
who had escaped from the settlement, was seen at Manly Cove, Port Jackson, feasting on
a whale that had recently become stranded on the beach (Collins 1798: 109; Willey 1979:
111). However high the mortality had been, it would appear that large numbers of
Aboriginal people were again occupying the coastal regions of Port Jackson, as little as
twelve to eighteen months after the epidemic was first noticed.
3.4.2 The second epidemic - 1828-32

In early 1829 the explorer Charles Sturt returned from an expedition into the
north west of New South Wales and brought back with him what was probably the first
indication of a second epidemic of smallpox among the Aboriginal populations. He and
his party had traced the course of the Macquarie River into the interior and had reached
the Darling River near the present town of Bourke. On February 5th while he was
following the Darling southward he encountered a group of seventy Aboriginal huts
which appeared to Sturt to be permanent habitations. Further on he encountered a group
66
Smallpox
of Barundji which he believed to be the inhabitants of the village. Sturt and his party
were approached by an elderly male. Sturt recorded:
As his tribe gathered around him, the old chief threw a melancholy glance
upon them, and endeavoured, as much as he could, to explain the cause of
that affliction which, as I had rightly judged, weighed heavily upon him. It
appeared, then, that a violent cutaneous disease raged throughout the tribe,
that was sweeping them off in great numbers. He called several young men to
Mr. Hume and myself, who had been attacked by this singular malady (Sturt
1833 vol I: 93)
Four or five days later while resting in camp another group of about seventy
approached Sturt's party. The women and children of the group passed the camp by, but
Sturt noticed that several of the men who came nearer were afflicted with what he
believed to be the same 'violent cutaneous eruptions' he had just recently seen. Sturt
believed that this disease was smallpox (1838: 147). He was of the opinion that it was
causing a severe decline in the population as the numbers of Barundji he saw on the
Darling River bore no comparison to the size and numbers of the huts he had seen (ibid:
105).
Further indications that a second epidemic of smallpox was occurring among
the Aboriginal populations west of the Great Dividing Range were brought to the notice
of the Colonial Government in 1830 (Mair 1831). In August of that year five Wiradjuri
were observed by a local pastoralist, Andrew Brown, suffering from what was thought to
be smallpox. Two were described as being in the incipient stages of the disease and the
other three in the more advanced stages. One of these was later seen with smallpox
sequelae on his body, and when questioned he indicated that the others had died. Two
months later, in October, the same symptoms, together with a high mortality were again
reported among the Wiradjuri. The disease was active until at least December (Mair
1831). In August of 1831 the same symptoms were again witnessed by Brown in three
67
Smallpox
Wiradjuri who had been in contact with others recently arrived from the Lachlan River to
the south. The disease was reported to be causing high mortality among the Lachlan
River Wiradjuri, many of whom were fleeing the region.
A further indication that the disease was smallpox was recorded by Mair
(1831). A European family residing near Bathurst was struck with the infection (Mair
1831). Four of the family showed eruptive and febrile symptoms and one, a two year old
female, died. The first of the symptoms to appear was the rapid onset of fever to be
followed by the successive stages of the rash reaching the confluent stage after ten days.
The child's eyes were closed after the sixth day and the eruptions extended over most of
her torso, feet, face. The eruptions were particularly severe on the gums, lips and tongue.
The mother described the disease as being like a number of scalds running into each other
and a discharge emanating from them (Mair 1831). The disease had arisen after the
family had sheltered in their house a Wiradjuri child, whose parents had died from a
disease with similar symptoms, and who likewise later died of the same disease.
A concerned New South Wales administration sent Dr John Mair, a military
physician attached to the 39th Regiment, to investigate and report on the disease in
October 1831. Mair was too late to witness first-hand the disease among the Wiradjuri
but from accounts by eyewitnesses, whom he deemed to be credible observers, he pieced
together the symptoms of the disease (Mair 1831). While there appeared to be a variety
of forms of the disease in different individuals, the following description of the clinical
symptoms were common to all. The initial pre-eruptive stages were characterised by a
general malaise and fever lasting from 2 to 8 days accompanied by loss of appetite,
headaches, chest and abdominal pains. The eruptive stage followed, with focal lesions of
small 'red spots' (papules) resembling 'flea bites' commencing on the face and gradually
spreading over the head, breast and extremities. Enanthema occurred at this time with
68
Smallpox
lesions developing on the tongue and lips. The rash spread and in many instances the
soles of the feet were observed to be studded with lesions. After the eruption had
developed, usually observed to have occurred in twenty-four hours, the fever subsided.
At this time the patient experienced pain in the throat, most likely from enanthema on the
pharynx, making it difficult to swallow solid foods. After three to eight days the 'red
spots' developed into raised vesicles containing a milky fluid in some, and in others a
'yellowish' or 'straw coloured' fluid. At their height the lesions were the size of a 'small or
large pea'. At this stage it was recognized by observers, who were familiar with smallpox
in England, to be that disease. Scabs formed from the vesicles at different periods
according to the length of time it took to reach maturation. These were occasionally
confluent on the nose and cheeks and frequently left permanent scars or indurations on
the skin. Mair observed these on some of the subjects and stated they 'cannot be
distinguished from the pits of Small Pox'.
Mair's conclusions were, however, not unchallenged. Dr George Busby
(1831) was also requested by the Government to furnish particulars on the epidemic. In a
report to the Inspector of Colonial Hospitals, Sydney, he concluded that the disease was
varicella and not smallpox. Busby's observations, however, were not as extensive as
Mair's. He saw only two Wiradjuri from the Bathurst district showing clinical symptoms
but could not determine the nature of their affliction. He based his diagnosis solely on the
symptoms he monitored in a European male, Titman, who was confined in the Bathurst
Hospital on August 6 1831 under Busby's care. Titman was 40 years old and had been
living in the same house as an Aboriginal person who had caught the disease and later
died. He informed Busby that he had suffered from smallpox as a boy, being one of a
family of six, all of whom had the disease at the same time. Titman's symptoms were
generally milder than those described by Mair in the Wiradjuri. He complained of
headache, pains in the back and limbs, lassitude, loss of appetite, nausea, and fever.
69
Smallpox
Primary fever was, however, severe and lasted until the eruptive phase which was
followed by secondary fever. The vesicles appeared earlier, achieved maturity quickly,
covering most of the body, and were particularly numerous on the face, shoulders, back,
and lateral surfaces of the legs. The symptoms lasted for fourteen days terminating in full
recovery (Busby 1831).
Busby's diagnosis was that the disease he had observed was not small pox but
varicella. His view was based firstly on the modified nature of the symptoms and
secondly on Titman's previous infection with smallpox. In response to the prevailing
epidemic among the Aboriginal population he concluded:
I am, upon the whole, at present disposed to regard the eruptive disease lately
prevalent among the black natives in this district as varicella, but possessing
by no means a malignant character, nor likely, under ordinary circumstances
of comfort and attention attainable in civilized society, to prove fatal in more
than a few instances; the mortality it has occasioned among the blacks being
sufficiently accounted for by the unfavourable circumstances in which they
are placed (Busby 1831).
Mair (1831), on the other hand, saw it as a case of secondary modified
smallpox because it passed through the regular stages, albeit quickly, of ordinary
smallpox. He also examined the patient about six weeks after his discharge from
hospital. He described the skin on Titman's face having a `mottled appearance of red and
white, burning scales were separating from it, and numerous small pits or depressions
could be discerned' some of which were recent and others older which further
strengthened his diagnosis.
Busby's conclusion that the disease affecting the Wiradjuri was varicella was
supported by the Inspector of Colonial Hospitals, Dr. James Bowman. Bowman (1831)
disputed Mair's diagnosis of smallpox and cast doubts upon the reliability and integrity of
70
Smallpox
his witnesses. Writing to the Colonial Secretary he claimed that Mair and Imlay were
incorrect in their diagnosis and had formed their opinions that the disease was smallpox
from information they received from persons incapable of determining so important a
point, despite Mair's assertions to the contrary . Bowman also suggested the disease
among the Wiradjuri was not smallpox but varicella which, while common in the colony
at that time was of little threat. He called it 'native pock' (incorrectly believed by some to
be a local form of varicella).
He presented these arguments to the Governor and members of the Executive
Council of the colony in December 1831 (Thompson 1831). The Council readily agreed
with Bowman and passed over the whole matter of the epidemic apart from
recommending a Government notice should be published stating that suspicion had arisen
as to the current prevalence of smallpox. They recommended that voluntary vaccination
could be obtained from any of the Colonial Surgeons. They also agreed that measures
should be taken 'generally to induce the Aboriginal Natives also to submit to vaccination'
(Thompson 1831).
Mair (1831) reported varied clinical symptoms among the Aboriginal
populations. Among those in the Wellington Valley the vesicles began to coalesce on the
face during the eruptive stage to be followed in a day or two by excessive salivation. An
escaped convict who had lived among these people before, and during the epidemic,
described 'water pouring from the mouth as they lay on the ground' (Mair 1831). About
the tenth or twelfth day after the initial symptoms were noticed, many patients were seen
to experience convulsions and the fluid discharge from the mouth became more bloody
and viscid in appearance. The bloody discharge from the mouth and its late onset may be
indicative of bleeding from the oral mucous membranes, a symptom of the more fatal
71
Smallpox
haemorrhagic type of variola major (Benenson 1976: 444, 1990: 395; Fenner et al. 1988:
38, 138-9).
Among the Wiradjuri living on the Lachlan River and Wellington Valley
regions, death generally resulted after the third day of the eruptive stage. Mair (1831)
reported that secondary fever was seldom observed amongst these groups, and when it did
occur he suggested it was due to local low ambient temperatures. The rarity of secondary
fever, which usually begins on the seventh or eighth days in severe cases (Fenner et al.
1988: 22), can be explained by the early fatality of most of the victims. Many were
reported to have died at the very onset of the disease before the beginning of the eruptive
stage.
Most of the eye-witnesses consulted by Mair remarked that the disease proved
chiefly fatal to adults and elderly, and seldom to children even though their length of
exposure to infected individuals was the same. It was, however, reported to Mair by
several of the observers that many adults who bore pockmarks on their skin, evidence of a
previous exposure to smallpox, escaped the disease altogether.
The usual duration of the disease was stated to be between fourteen to twenty-
one days in cases where the patient survived and was restored to health. Many patients
who did survive were unable to walk for a considerable time due to the separation of the
epidermis from the sole of the feet. In other survivors more of the characteristic forms of
smallpox sequelae were present. Severe keratitis and/or corneal ulcerations were reported
in several victims who recovered from the infection. Brown stated:
... I found one middle aged woman who had lost her sight altogether by it, one
who had lost an eye, and two children male and female who had each been
deprived of an eye by it (Mair 1831).
72
Smallpox
In others secondary infections left the sufferer with ulcerations in different parts of the
body where the smallpox lesions had occurred.
It had been noted by most of the eye witnesses of the epidemic that fatality
occurred chiefly among adults and the aged, and seldom among children. In others who
escaped infection it was observed that some had been exposed to smallpox before.
Brown, who observed the disease first hand (Mair 1831), noted that it extended to most of
the Aboriginal people he saw. He did, however, see three old men with 'evident marks'
who informed him that they had been infected by the same disease when very young.
Others who escaped infection had been vaccinated (or variolated) by European settlers,
several years prior to the epidemic. During the epidemic Mair vaccinated many of the
Aboriginal people he encountered. He met with little opposition among them, most of
whom had come to realize the benefits that the simple procedure conferred in the face of
the serious morbidity and mortality caused by the epidemic. After his return to Sydney,
Mair sent supplies of recent and dried vaccine lymph to the Colonial Assistant Surgeon at
Bathurst for future use (Mair 1831).
The government surveyor and explorer, Thomas Mitchell, also observed
Aboriginal people suffering from the epidemic. On December 5, 1831 Mitchell and his
expedition crossed the Liverpool Range, north of Bathurst, which at that time divided the
settled from the unexplored districts of the colony. He recorded:
We reached at length, a water-course called "Currungai" and encamped upon

its bank, beside the natives from Dart Brook, who had crossed the range
before us, apparently to join some of their tribe, who lay at this place
extremely ill, being affected with a virulent kind of small-pox. We found the
helpless creatures, stretched on their backs, beside the water, under the shade
of the wattle or mimosa trees, to avoid the intense heat of the sun. We gave
them from our stock some medicine; and the wretched sufferers seemed to
place the utmost confidence in its efficacy (Mitchell 1838 vol I: 26).
73
Smallpox
According to Mitchell these people he saw were from another region as they had little
knowledge of the countryside they were now in. Mitchell continued his journey to the
north reaching the Gwyder River but made no further mention of smallpox among the
Aboriginal groups he encountered.
From these districts the epidemic spread along the river systems far in front of
the colonial frontiers. First hand observations of the epidemic by Europeans were now no
longer possible. From the upper Darling it spread downstream. In 1835 Mitchell was
again exploring beyond the frontier following the southerly course of the Darling River.
On May 28 while at his base camp at Bourke he was visited by a group of Aboriginal
people. They consisted of four adult males, seven females, and children. Mitchell
remarked that most of them had visible smallpox scarring 'but the marks were not larger
than pin heads' (Mitchell 1838 vol I: 218). From Bourke, Mitchell and his expedition
continued along the Darling River as far as Menindee, 190 Km above its junction with the
River Murray. He turned back on July 12 after an affray with the Barkindji. He had seen
smallpox scarring on many of the Aboriginal people during the journey. At Menindee he
recorded:
These natives, as well as most others seen by us on the river, bore strong
marks of the small-pox, or some such disease, which appeared to have been
very destructive among them. The marks appeared chiefly on the nose, and
did not exactly resemble those of the small-pox with us, inasmuch as the deep
scars and grooves left the original surface and skin in isolated specks on these
people, whereas the effects of small-pox with us appear in little isolated
hollows, no parts of the higher surface being detached like islands, as they
appeared on the noses of these natives (ibid: 261).
Mitchell may have observed the sequelae of confluent type smallpox. He was of the
opinion that the disease had been severe and had caused a great mortality among the
groups living along the Darling River.
74
Smallpox
The epidemic did not reach the Murray River populations until at least the
second half of 1830. In January of that year Charles Sturt (1833 vol II), on his second
expedition of exploration, began a journey down the Murrumbidgee and Murray rivers.
He arrived at the termination of the river systems, at Lake Alexandrina in what was to be
the colony of South Australia, on 9 February, passing the Darling River junction on his
way. Sturt was an astute observer and documenter, describing the landscape, geology, the
people and their state of health in some detail (Beale 1979). Along the Murray he noted
that 'the most violent cutaneous eruptions' were affecting many of the Aboriginal people
he encountered and remarked on their 'miserable state of disease and infirmity' (ibid:
148). Sturt was in two minds as to what the disease actually was, describing it in one
instance as leprosy (ibid: 96) and in another as syphilis (ibid: 125). He made no
suggestion, however, that it was due to smallpox, a disease he was surely familiar with
among Europeans in Britain and had seen just one year before among the Aboriginal
populations of the upper Darling. Nor did he mention seeing any Aboriginal people with
smallpox-like sequelae that would have indicated a previous epidemic. In a later
comment on smallpox (see below), however, Sturt makes a strong implication that the
disease was smallpox. Sturt returned the way he had come, along the Murray and
Murrumbidgee system and arrived back in Sydney in late May.
In 1830 the middle and lower Murray River corridor was well beyond the
European frontier and the spread of smallpox went unobserved, and hence unrecorded by
Europeans. There is, however, some indication that the epidemic had reached the
populations of the lower Murray well before the first European settlement was established
on the Adelaide plains in 1836. In February 1838 Joseph Hawdon (1838) overlanded the
first herd of cattle along the Murray to the newly established settlement of Adelaide. On
February 11 Hawdon set camp near the present town of Swan Hill on the Murray and met
up with a group of Wadi Wadi:
75
Smallpox
In the evening some of the Blacks came to Swan Hill, where we were
encamped. After holding a little conversation with us across the river, they
swam over to us. They were fine, well-made men about five feet eleven
inches in height. Their faces were nearly all marked with smallpox, but
otherwise their features were pleasing (ibid: 27)
The next day Hawdon saw 52 men, accompanied by their women and children
and described them as 'not a good-looking set of men' and many of them 'blind in one eye'
(ibid: 28). Hawdon makes no further mention of smallpox sequelae although he met
several more large groups along his way.
Alone, Hawdon's observations of smallpox sequelae could not be accepted as
being reliable. However, later the same year (1838) Charles Sturt followed Hawdon's
trail along the Murray corridor, also bringing cattle to the colonists at Adelaide (Sturt
1839; Kenyon 1925: 178). His observations of smallpox sequelae support Hawdon's.
Approximately 5 kilometres below the junction of the Murray and Murrumbidgee rivers
he came across a large group of Aboriginal people:
... in the course of the forenoon we were joined by various parties from
different quarters that when united formed a considerable body of athletic and
well proportioned men. They came with the most peaceable intentions and
several of them assisted us in our work. I observed many of them as if pitted
by the Small Pox, or that would appear as the disease which was having such
a fearful effect upon them when I was on the banks of the Darling in 1828 and
the Hume [the Murray above the junction of the Darling] in 1829... It must
have committed dreadful havoc amongst them, since on this journey I did not
see hundreds to the thousands I saw on my former expeditions (Sturt 1838:
147).
Smallpox was present on the eastern coast by late 1831 (Mair & Imlay 1831).
In October of that year two Aboriginal men brought an ill convict, Richard Scarme, to the
European settlement at Port Macquarie. Scarme had escaped from the penal settlement at
Moreton Bay some time before and had been living with a group of Dainggatti near the
mouth of the Macleay River at Trial Bay, sixty kilometres north of Port Macquarie. He
76
Smallpox
stated that he had seen more than fifty ill with smallpox, a disease he had seen in England
before he was transported. The military officer in command of Port Macquarie, Captain
Smyth, stated that Scarme was recovering from a disease that bore a 'striking resemblance
to the Small Pox' (Mair & Imlay 1831). Scarme was held in custody and later sent to
Sydney where he was seen by Mair and Imlay. They examined him and reported that his
skin bore unequivocal marks of the recent epidemic of smallpox. Scarme said he had not
previously suffered from smallpox or cowpox and he bore no vaccination scar.
Six weeks after they had brought Scarme into Port Macquarie, the same two
Aboriginal men returned to the settlement. Captain Smyth, described them as covered
from `head to foot' with the disease. By late December the Dainggatti living around the
Port Macquarie settlement were in turn infected. Many of the worst cases recovered but
five died, all of whom were young and had previously been in good health. The disease
did not affect the European population. Smyth isolated the Dainggatti by keeping them
on the opposite bank of the river which flowed through the settlement (Mair 1831).
As the European frontiers expanded in later years many of the settlers noted
smallpox scarring among Aboriginal people with whom they had frequent contact
(Brough Smyth 1876: 253-257; Cumpston 1914: 147-162). Peter Beveridge, a squatter
who held a property on the Murray River below Swan Hill for 23 years from 1845, and
who acquired an extensive knowledge of the Aboriginal people, commented on the
smallpox epidemic and its timing:
All the very old aboriginals in the Colony [Victoria] show very distinct traces
of small-pox, and in speaking of the scourge which has so indelibly left the
marks of its foul presence, they say that it came with the waters, that is it
followed down the rivers in the early flood season (about July or August),
laying its death-clutch on every tribe in its progress...(Beveridge 1877)
77
Smallpox
Further evidence of the epidemic spreading along the Murray comes from
accounts by Aboriginal survivors. In South Australia a survivor of the epidemic, a
Ngarrindjeri woman named Clulwuwyrie (Jenny Pougie) died in 1911. She remembered
the first visit by Sturt to the Murray in 1830 when she was a child and related that the
disease, which left her with pock marks and carried off many of her people, came soon
after (Adelaide Observer 1911). Another woman, Kontinyeri (Louisa Karpeny), possibly
the niece of Clulwuwyrie, could also recount her experience of the epidemic (Stirling
1911). She lived most of her life on the southern shore of Lake Alexandrina and as a
small child could remember her first sight of white Europeans, soldiers arriving at the
lake at the time the colony of South Australia was established in 1836. She described to
Stirling the coming of the sickness which was several years before the arrival of the
soldiers:
The old black spoke of the coming of a strong West wind which made the
reeds all tremble, and this, she said, was taken as a sure sign that the sickness
was coming... She described how the faces of those affected with the disease
came out all over spots, and how that many died of it, including many
children (Stirling 1911: 18-19).
Another survivor, an old male named Malo, who lived at Moorundie on the
lower Murray, related that when he was a small boy there was a sickness amongst his
people which killed many and left him with scarring on his face. Doctor De Lisle of the
96th Regiment examined the scarring on Malo many years later and concluded that he had
undoubtedly suffered from smallpox (Hawker 1901). Three old Aboriginal men from
nearby Swanport often spoke to Europeans about a great sickness which came along the
Murray causing a great number of deaths. Such was the scale of mortality that the living
could not cope with disposal of the dead. They describe that those who were inflicted by
the disease broke out in spots all over their bodies (Stirling 1911: 17). Another account
comes from a thirty-five year old male from Lake Alexandrina who bore smallpox
78
Smallpox
sequelae on his face. He related to Stirling that as a small boy a 'big one wind' came from
the east carrying the sickness and caused the marks on his face (Stirling 1911: 19).
George Augustus Robinson noted the presence of smallpox sequelae during
his journey through the southern highlands. In 1844 he spent three days among a group of
300 Aboriginal people near the present town of Yass. He noted, 'the virulent effects of
Variola or Small Pox was apparent' (Robinson 1844; Mackaness 1941:26). Near
Gundagai he reported that the Aboriginal populations in the Murrumbidgee valley and
surrounding highlands were 'strongly marked with smallpox' (Robinson 1844; Mackaness
1941:28). Robinson does not give the ages of the individuals he saw bearing smallpox
sequelae but as his sightings came a decade after the last epidemic as opposed to 55 years
since the first, the former occurrence of the disease would most likely have been the
cause.
As the European frontiers extended north into Queensland many of the
colonists saw the tell-tale sequelae on the faces of the survivors. During the 1850s and
1860s pockmarked Aboriginal people were regularly seen and reported along the coastal
regions as far as the Gulf of Carpentaria. Inland the extent of the pock marking was seen
north of the Darling, along its tributaries and near Cloncurry (Butlin 1983; Campbell
1983 & 1985).
There is little evidence of the severity and extent of the epidemic south of the
Murray River and its Victorian tributaries. There is no evidence at all that the 1830s
epidemic reached the Kurnai people living in the Gippsland ranges in eastern Victoria,
and indeed this region appears to have escaped altogether (Butlin 1983: 23; McBryde
1984: 277). Sharp social, political, linguistic, and economic boundaries between the
Kurnai groups of Gippsland and surrounding populations, resulting in mutual hostility
79
Smallpox
prior to European contact, have been demonstrated by several researchers (Howitt
1889,1904; McBryde 1978, 1984; Smyth 1878). This disjunction of the Gippsland
populations from their neighbours would most likely have acted as a deterrent to other
Aboriginal groups fleeing the epidemic to enter their territories and so acted as a barrier to
the transmission of smallpox.
The epidemic also seems to have missed the groups living in South Australia's
mallee districts south of the River Murray valley. Unlike inland New South Wales, no
active cases of smallpox were seen by the early settlers in Victoria. This is not surprising
as the European settlement was only permanently established in 1834 at Port Phillip Bay
(Melbourne) well after the epidemic was at its peak. A few of the settlers do, however,
report seeing Aboriginal people bearing the characteristic sequelae which would be
expected if there had been a previous severe epidemic of smallpox.
Before this settlement there had been a failed attempt to establish a southern
outpost of the colony of New South Wales in September 1803 at Port Phillip Bay.
William Buckley, a convict at this settlement, escaped in that same year and lived with
the Wathaurong near the present city of Geelong for 32 years. After his return to
European life he became known as the 'wild white man'. He recollected:
I never observed any European contagious disease prevalent in the least

degree; and this I thought strange. There was at one time however, I now
recollect, a complaint which spread through the country, occasioning the loss
of many lives, attacking generally the healthiest and strongest, whom it
appeared to fix upon in preference to the more weakly. It was a dreadful
swelling of the feet, so that they were unable to move about, being also
afflicted with ulcers of a very painful kind (Morgan 1852: 94-95)
Buckley's description of the disease is vague. Although there is no other
evidence for it he may be referring to an epidemic that had preceded his association with
80
Smallpox
the Wathaurong and one he had heard about through their recollections. Smallpox does
affect the soles of the feet (Benenson 1990:395; Fenner et al 1988: 38-39) and if
secondary bacterial infection occurs could cause the ulceration and swelling that Buckley
describes. Such a symptom, one among the many of smallpox, may be all that Buckley
was informed of, or all that he could recollect being told. There are other problems with
Buckley's account. The record of his life among the Wathaurong was written for him
after his return to the European colonists by Morgan, who had interviewed Buckley at
length and it is impossible to discern just how much Morgan's impressions and
conceptions misconstrue Buckley's reminiscences. Therefore, any diagnosis of smallpox
made upon this evidence can only be uncertain at best; yet it is still intriguing that
Buckley did not identify the disease as smallpox.
Several of the early colonists of Victoria do refer to smallpox south of the
river systems. Dawson (1881), in describing the Aboriginal populations of western
Victoria, briefly discussed smallpox and thought the epidemic had caused high
mortality on the south coast, particularly on the coastal dunes to the east of Port Fairy.
It was, however, a common misconception of the time that many of the extensive
Aboriginal burial areas in the coastal and riverine dune systems, often with exposed
skeletons on the surface, contained the victims of smallpox and were a direct
consequence of the high mortality wrought by the epidemic (Moulden 1877; Dawson
1881; Stirling 1911; Cleland 1914). Radiocarbon dates from several of these burial
sites have since shown an extended antiquity (Blackwood & Simpson 1973; Pretty
1976; Dowling 1990), in some cases dating back into the late Pleistocene (Pretty
1977), indicative of a long and consistent use for burial purposes (Pardoe 1988).
Edward Curr (1886), a Victorian pastoralist, compiled two volumes on the Australian
Aborigines. He discussed smallpox among the Aboriginal populations but cited no
81
Smallpox
strong evidence for the 1830s epidemic in Victoria and relied mainly on secondary
evidence from New South Wales and the Murray River corridor for his information.
As well as leaving marks on the faces of the survivors the epidemic left its
traces in the oral traditions of the Aboriginal people. Among the Aboriginal groups
affected by the epidemic, smallpox was given many names (e.g. Curr 1886; Cleland
1928: 67-70). In the river districts of central and western New South Wales, where the
epidemic was first recorded, it was called Booert, and on the Darling River where the
first active cases were seen by Sturt it was called Mungga. North of the Darling
among the Muruwari of the Narran River region it was called Dunnerh-Dunnerh
(Langloh Parker 1905: 39). The Wiradjuri from the Wellington Valley referred to the
disease as Danna-Danna and to the sequelae as Gulgog-Gulgog. In the western
districts of Victoria the epidemic was called Meen Warann (Dawson 1881:60), and
among the Dhiari of northern South Australia it was called Moora Moora. Years after
the event a song or chant, known as Mallae Mallae in Victoria and Nguyapalti in
South Australia, was performed by many groups in remembrance of the epidemic and
the many who died from it throughout south eastern Australia (Dawson 1881: 60;
Reynolds 1981:57).
The assignment of blame for the epidemic, by the Aboriginal people was
attributed in some instances to the Europeans, in others to the malevolent magic of
neighbouring tribes, and to mythical entities. Like the other major diseases of syphilis,
gonorrhoea, influenza, and tuberculosis, that had severe effects on the Aboriginal people,
they often associated the occurrence of smallpox as a direct result of the arrival of
Europeans among them. Sturt was blamed by the Wiradjuri of the Wellington Valley
(Mair 1831). He and his expedition passed through that region in 1828 just as the
smallpox epidemic was advancing along the river systems. Others in the same region
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Smallpox
placed the blame for the epidemic on Darrawirgal, a mythical entity who lived far to the
west of Wellington. They believed that Darrawirgal was angry for the want of a
tomahawk and so sent the disease among them. When the epidemic subsided they
assumed that he had finally obtained one and the disease would therefore not return
(Wilkes 1845: 197 loc. cit. Campbell 1985: 341). The malignant power of the Rainbow
Serpent Mindye, was believed to be the source of the disease in Victoria (Reynolds 1981:
57). Ahead of the colonial frontiers, where Aboriginal groups had yet to have direct
contact with Europeans, the blame was apportioned to neighbours. Among the Muruwari,
traditional enemies were claimed to have sent the disease on the winds which hung it on
trees over camps where it dropped on to its victims (Langloh Parker 1905: 39).
Clulwuwyrie, the last Ngarrindjeri survivor from the lower Murray, often spoke of a
peculiar wind-like noise immediately preceding the arrival of smallpox which came
among her people from the people to the east (Stirling1911).
3.4.3 The third epidemic - 1866-67

Smallpox made its appearance again in epidemic form in late 1866. It was
observed during a six month period among Aboriginal people living on the arid west
coast of South Australia on the periphery of European settlement and spread into the
inland regions (Figure 3.1).
The first reports of this third outbreak were made by police in the remote
regions of Streaky Bay and Venus in late October and early November of 1866. They
noted an epidemic disease among the Wirangu and Nawu which was causing damaging
skin eruptions on many who regularly visited the settlements (Gething 1867).
83
Smallpox
When informed, the initial reaction of the medical authorities in Adelaide was
that it was just another outbreak of the 'native pock' and therefore of little concern to the
colonists. (Native pock was a contemporary euphemism given to impetigo contagiosa, a
staphylococcal disease of the skin common amongst Aboriginal people, and while
sometimes confused with smallpox, has no relationship with the latter). The Vaccination
Board of South Australia was, however, more cautious. Its primary concern was to
protect the colony from any outbreak of smallpox that may occur by a program of
vaccination aimed at rendering the whole population immune. Any outbreak of smallpox
in the colony whether among the European or Aboriginal communities, was therefore to
be given immediate attention. The Board instructed a government medical officer, Dr.
Robert Gething, to leave at the earliest opportunity to investigate the outbreak and carry
out a vaccination program among the European and Aboriginal populations (Gething
1867).
Gething spent 21 days travelling the coastal regions between the two bays
meeting Aboriginal groups and vaccinating as many as he could. On January 12 1867,
approximately 30 miles (48km) from Streaky Bay, Gething met a group of Wirangu
suffering from the disease:
which had all the characteristics of having been pure variola; but which in
these cases seemed to have been singularly mild, as there could be only three
or four deaths distinctly traced to that cause
Although his report to the Vaccination Board did not describe clinical signs,
Gething was in no doubt that the disease he saw in these people was smallpox and not
'native pock'. His initial diagnosis of smallpox was soon strengthened:
The next day the natives I had seen the previous day came down to me at the
Bay, bringing with them others who had had the disease somewhat more
recently, thereby enabling me to see it in another phase. This strengthened
84
Smallpox
my opinion as to the nature of the disease, which was confirmed on a after

occasion [sic] (Gething 1867).
Gething vaccinated as many Wirangu as he could and then proceeded south to
Venus Bay. There he met a group of Nawu suffering from the disease, one of whom was
a young female in the stages of secondary fever 'suffering unmistakably from pure
variola'. This particular case was probably exhibiting the earliest stages of smallpox signs
that Gething had so far encountered.
The extent of the smallpox epidemic may have extended further than the bay
regions visited by Gething. To the west of Streaky Bay, and at the limit of European
occupation, a hut-keeper at Fowlers Bay, wrote to the South Australian Register
informing them that the Wirangu there were 'very much diseased' and that many of them
had died (South Australian Register 1867). He queried why Gething, who had attended at
Streaky Bay, had not made his way further west.
More observations of the extent of the epidemic came from the Sub-Protector
of Aborigines responsible for a large portion of central and northern South Australia.
Sub-Protector Buttfield, a former Methodist minister, had only recently taken up his
position and had travelled extensively, meeting many of the Aboriginal groups living in
regions remote from European settlements. On the south east coast of Eyre Peninsula he
reported that during the first six months of 1867 the Nawu in the region of Port Lincoln
had been suffering from the same disease as that previously notified by Gething near
Streaky Bay (Buttfield 1867a). In the Mount Remarkable region, near the present town of
Port Augusta, Buttfield (1867a) reported to the Acting Protector that Aboriginal people
(Nukunu) were suffering from an eruptive skin disease 'resembling in some of its
characteristics, smallpox' (ibid). Buttfield reported no deaths from this disease and those
infected were convalescent. Buttfield was not a medical practitioner and was not entirely
85
Smallpox
sure that the disease was indeed smallpox; he thought it may have been a skin disease
caught from dogs 'covered with loathsome sores and vermin'. The timing and locality of
Buttfield's observation, while not strongly supporting a presence of smallpox, do give
some indication to the probable extent of the epidemic.
This epidemic was almost certainly associated with simultaneous outbreaks of
smallpox among Aboriginal populations in the north and west of Australia (Fenner 1984:
733). Well established trading and ceremonial lines existed among the Aboriginal
populations of central Australia prior to European contact linking the far north of the
continent to the southern coast and extending into the west (McBryde 1987: 253-273).
The movement of Aboriginal people along these routes may have facilitated the slow
spread of smallpox (Fenner 1984: 733). Throughout central Australia and on the north
coast periodic outbreaks of smallpox infected Aboriginal populations between 1860 and
1869 (Cleland 1914: 170). In 1984, Goodall (1994: 75, note 13), an anthropologist
working among the Pitjantjatjara and Yanykunytjatjara in the central desert regions, noted
that a number of people could recall their parents or grandparents talking about an illness
of plague-like proportions which may have been smallpox. Goodall states, however, that
it was extremely difficult to follow up these indirect statements.
The origin of these outbreaks have been loosely attributed to visiting
Macassan fishing fleets that frequented the northern coastline during the monsoonal wet
season, collecting trepang (sea-cucumber) (Fenner 1984:732; Cumpston 1914; Lewis
1989). Other sightings of active smallpox and facial scarring have been reported on the
central west coast and in the central arid regions north and south of the present town of
Alice Springs between 1865 and 1870 (Fenner 1984:732). During the same period
Aboriginal people on the west coast of Australia between Geraldton and the Gascoyne
86
Smallpox
River were severely affected by smallpox along with several European settlers (Cumpston
1914; Lewis 1989).
The degree of morbidity and mortality from the epidemic is impossible to
estimate. Gething's report suggests, however, that morbidity was high among the Nawu
and Wirangu along the south west coast of South Australia. After the disease first came
to the attention of the police at Streaky Bay in October and November 1867 it was
estimated that at least 30 to 40 Aboriginal people could be seen at any one time showing
active smallpox. By January of the next year, when Gething was investigating the
disease, between 200 and 300 had been infected at Streaky Bay and between 60 and 70 at
Venus Bay - a range of between 260 and 370 (Gething 1867). The number of Nawu and
Wirangu living in the area at this time cannot be enumerated with any accuracy and so no
estimates of relative population loss from the epidemic can be made. Given the previous
history of smallpox epidemics and the resultant mortality, however, it would be
reasonable to assume that the case-fatality was high.
A young male and female living on a property between the two bays were the
only Europeans recorded with smallpox during this epidemic. The effect of the disease
was mild and both survived, having been previously vaccinated. In each case the disease
left only a few scars upon the neck and face of each (Gething 1867).
The mortality among the populations along the coast and those inland beyond
the frontier of European occupation remains largely obscure. Gething had little idea of
the mortality caused by the disease and could account for only six to eight deaths. For an
epidemic of smallpox among a population who had not been vaccinated regularly, if at
all, such a figure would appear to be a gross underestimation. In all likelihood it was.
Gething had spent only twenty one days on the west coast and most of that in a restricted
87
Smallpox
region between Streaky Bay and Venus Bay. He had not gone beyond the borders of
European occupation. Unless he had travelled further he would have had no knowledge
of the extent and severity of the disease in the interior, nor would any of the European
settlers he used as informants. Further, he had observed the epidemic only in its earliest
stages, during January. According to Sub-Protector Buttfield the epidemic lasted for a
further five months among the Nawu in the Port Lincoln region alone; and it was his
opinion that the disease had 'threatened destruction to the native population' in that region
(Scott 1867: 665). The mortality would almost certainly have been more than that
reported by Gething.
3.5 Discussion
Despite the varied nature of the surviving historical documents there is strong
evidence that the three epidemics were indeed smallpox. This conclusion has been
challenged by both contemporary and modern writers particularly for the 1789 epidemic.
The little evidence we have pertaining to the 1789 epidemic in the Sydney region has left
some historians and medical writers (Crosby 1986; Cumpston 1914; Curson 1985;
Hingston 1985: 278) with doubts as to whether it was smallpox. Chicken pox (varicella)
has been proposed as the main alternative to smallpox (Hingston 1985:278), with others
suggesting that it was cowpox, a form of 'native pox', or some other fatal disease, not
specified.
All these alternatives can be eliminated from serious contention on several
lines of evidence which lead to smallpox. Firstly the First Fleet recorders of 1789 who
reported on the disease are unanimous in their opinions that it was smallpox. Some saw it
first-hand, others did not. Those who did not were in all probability basing their
comments on the general opinion of the settlement that smallpox was the disease
88
Smallpox
infecting the Aboriginal people. Most, if not all, the recorders would have had
experiences with the disease, known of its effects and would have been familiar with its
signs, as it was the most widespread and fatal disease throughout the British Isles in the
eighteenth century (Howe 1972: 143).
Secondly, although none of the journals or diaries from the First Fleet
surgeons survived (Gandevia & Cobley 1974: 111), we can surmise with confidence that
they were involved with the epidemic and their opinions were known (Frost 1994: 191).
This is indicated by accounts that describe Eora people being brought in to the settlement
and being treated for the disease in the hospital by the medical staff. Indeed, one of the
child survivors was later accepted into the household of Chief Surgeon White. There
appears to be little doubt that the medical staff had other experiences with those suffering
from the epidemic. When it was first brought to the attention of Governor Phillip in April
1789 that Aboriginal people were dying among the coves of Port Jackson he immediately
left the settlement with a small party including a surgeon to investigate (Tench 1793:
146). They saw first-hand the effects of the disease in the living and the dead. We can
then be equally confident, that when Phillip (1790a, 1790b) reported back to London that
the disease affecting the Aboriginal people was smallpox, he had been advised so by his
medical staff.
A further line of evidence that strongly links the epidemic to smallpox are the
sightings of Aboriginal people bearing visible smallpox-like sequelae, both facial scarring
and blindness, after the epidemic had passed. The epidermal damage done by smallpox
infection can be severe and residual scarring is common; up to 85% in unvaccinated
variola major cases (Fenner 1985: 278; Jezek et al. 1981: 801). In chickenpox the
epidermal damage is more superficial and in most cases quickly repaired after infection
and facial scarring is rare. In a study of 250 Somalia subjects who had recovered from
89
Smallpox
chickenpox Jezek et al. (1981) found 2.4% of cases who had five or more facial scars
indistinguishable from those seen among variola victims. This figure, however, may be
an overestimation as the recorders tended to include subjects with a severe varicella rash
rather than those with a mild rash (ibid: 802).
The reporting of residual scarring attributed to smallpox among Aboriginal
people was widespread after each the three epidemics. After the 1789 epidemic, sightings
were seen to the north and inland of the Sydney settlement, and in the coastal regions to
the south at Jervis Bay and Port Phillip Bay. The recorded sightings after the second
epidemic are more profuse. Explorers travelling beyond the frontiers of European
settlement and colonists establishing new grazing lands commented on seeing Aboriginal
people bearing facial scarring which they attributed to a previous epidemic of smallpox.
The sightings were spread over a large area of southeast Australia following the major
river systems and their tributaries. With a low rate of residual scarring chickenpox would
be an unlikely candidate for the epidemics. The observations by Mair (1831), a qualified
medical practitioner (attached to the 39th Regiment), are more reliable. Mair was in no
doubt that the scarring he saw on Aboriginal people 'of very advanced age' corresponded
'with the pits left by the Small Pox' and that it was a result of the 1789 epidemic.
The evidence for smallpox is more cogent for the second and third epidemics.
Both outbreaks were investigated by qualified medical practitioners who would have been
familiar with the disease if not from practical experience then most likely from their
medical training. From the clinical descriptions and the behaviour of the 1830s disease
provided by Mair (1831) there can be little doubt that it was an epidemic of smallpox and
not varicella (despite the opposition of the Inspector of Colonial Hospitals, Dr. James
Bowman), or another disease displaying similar symptoms. After his investigation Mair
concluded that the 'eruptive febrile disease' that had so affected the Aboriginal people
90
Smallpox
'approached more nearly in its symptoms to the character of Small Pox, than any other
disease'. The descriptions of the symptoms by those who observed the active disease, and
later compiled by Mair, closely match the progress and clinical features of ordinary type
confluent and semi confluent, variola major as outlined by Fenner et al. (1988: 4-22) and
Benenson (1976: 443-446). The symptoms suffered by the European male, Titman, on
the other hand are more indicative of a secondary infection of variola major in a person
who had been either previously vaccinated or who had been infected with the variola
minor. It would appear by his own account of a previous childhood infection and Mair's
observation of old and recent sequelae resembling pockmarks, that the latter was the case.
Gething (1867), who saw active smallpox among South Australian Aboriginal
people in 1866-67 leaves us with no clinical description of the disease. Nevertheless, he
was in no doubt himself that what he observed was an outbreak of smallpox, and not
chickenpox or some another non-specified exanthematous disease. According to his
report he saw on three separate occasions Aboriginal people suffering with what he
described as the unmistakable symptoms of the disease in its various clinical stages. The
residual sequelae from this outbreak were still noticeable on surviving Aboriginal people
some 15 years later. The Royal Society of South Australia was informed at its meeting in
June 1882 that the outbreak had passed through the Wirangu living near Streaky Bay and
Fowlers Bay leaving 'a great number of them dying', and that a few of the survivors were
'very much pitted, more especially an old lubra who was blind (Adelaide Observer 1882)'.
Sightings of Aboriginal people pockmarked by this epidemic were common throughout
the centre of the continent when the overland telegraph line was being constructed and
further north on the coast during the settlement of Port Essington and Darwin (Fenner
1984: 732).
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Smallpox
The three epidemics, although differing in their geographic and temporal
aspects, had common characteristics each compatible with the epidemic behaviour of
smallpox in a virgin-soil population (Benenson 1976: 435-440; Fenner 1984:729-733):
1. They were highly transmissible. Accounts of all three epidemics report
that the disease was spreading rapidly from person to person. This was later confirmed
when observers noted that exposure to a sufferer could result in infection (e.g. Arabanoo
caught the same disease as those whom he attended and a European family suffered the
same symptoms as an Aboriginal child after they cared for her within their home).
2. They were almost entirely confined to the Aboriginal communities. In all
three epidemics the disease was first noted to be spreading among the Aboriginal
communities either on the periphery of the European settlements or ahead of the frontier.
Despite the spread of European settlements and their ever increasing population,
particularly after the first epidemic, very few Europeans (or non-Aborigines) were
infected during the epidemics. The reason can be seen in the separation of the two
groups. From the beginning of the first settlement in 1788 the social and cultural
restraints particular to the two groups largely ensured that European and Aboriginal
people lived in separate domiciles with physical proximity restricted to a few individuals.
Infection by smallpox is usually a result of close contact such as would be expected of
individuals living in the same household who had regular contact with each other. The
disease is rarely spread by fomites such as contaminated clothing or bedding; or by
limited exposure to airborne agents (Fenner 1984: 729). Only in exceptional cases then
did the epidemiological conditions enabling the spread of smallpox to move freely
between the two societies exist. In most of the recorded cases of non-Aboriginal people
acquiring the disease there had been close and sustained contact with infected Aboriginal
people.
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Smallpox
3. The extent of each of the epidemics followed a course through regions
where Aboriginal population density was high and European settlement low or where
there were well established exchange and ceremonial networks (Figure 3.1). The
evidence surviving for the first epidemic indicates that it was largely confined to the
coastal and hinterland regions on the eastern side of the continent and did not extend far
inland. The second epidemic followed the courses of the inland river systems forming the
vast catchment area (1,036,000 Km2) of eastern Australia that terminates at the mouth of
the Murray River on the southern coast of South Australia. It appears to have bypassed
the region of Victoria below the Murray and most of the coastal populations. The regions
affected by the epidemics were resource rich coastal and riverine environments and had
carried high population densities ranging from 2.5 to 4.6 persons per km2 (Kirk 1983: 40;
Webb 1984a). The geographical extent of the third epidemic has been documented over a
large extent of Australia from the northern and western coasts through the arid centre to
the southern coast (Fenner 1984: 731). In Southeast Australia, however, it was confined
to the coastal and central inland regions where, during the 1860s, the major remnant
populations of Aboriginal people lived. In an 1861 census in South Australia, the
Western, Northern, and North Eastern Pastoral Districts accounted for 2,761 Aboriginal
people or 58.9% of the total population enumerated for the state. It was these groups who
bore the major impact of the epidemic and the smaller population groups living on the
fringes of the European settlements and along the River Murray who escaped.
4. The three epidemics caused severe mortality. A recurring observation by
all recorders is the stark reference to high mortalities among the Aboriginal populations
inflicted with smallpox. Just how high then was the mortality? The immediate answer,
using the historical descriptions of each of the epidemics, is that the mortality was severe
- but just how severe?
93
Smallpox
In his model of Aboriginal population decline, Butlin (1983: 65) suggested an
overall death rate due to smallpox from 25% to considerably in excess of 50% of the total
populations affected by the epidemics. Butlin based his estimates on the American Indian
populations on the west coast of the United States during the 1837-39 epidemic (Stearn &
Stearn 1945). Conservative estimates of 30% mortality or more in initial smallpox
outbreaks have also been suggested for the Americas (Boyd 1990: 137; Crosby 1972: 44;
Dixon 1962: 325). This estimate has often lead to the generalised acceptance of a
minimal figure of one-third of the population dying from initial exposure to smallpox
(Boyd 1990: 325). Can such rates be inferred for the three epidemics in Australia? The
answer is yes, but with some caution.
Throughout its historic association with humans smallpox has had a high
case-fatality, particularly among those who had not been protected from the disease either
by previous infection or by inoculation. Case-fatality rates from smallpox among
unprotected populations vary according to the clinical type, but in most cases are severe:
ordinary-discrete type, <10%; ordinary semi confluent, 25-50%; ordinary-confluent, 50-
75%; flat, >90%; and haemorrhagic type, almost 100% (Fenner et al. 1988: 5; Koplan &
Foster 1979: 440). The young, the elderly, and pregnant women are the most likely to die
from smallpox. The lethality of smallpox became graphically apparent when the disease
was introduced from Europe into the New World at the end of 1518 or early 1519
(Crosby 1986: 196). The effect of variola major among the unprotected and virgin-soil
populations in the Americas resulted in extraordinarily high mortality with estimates
ranging from 25% through to 90% or more (Black 1975: 517; Boyd 1990: 144; Dobyns
1983; Fenner 1984: 730-733; Fenner et al. 1988: 1069-1102; Ramenofsky 1987; Snow &
Lanphear 1988). By the end of the seventeenth century, nearly two hundred years after its
introduction, smallpox was largely responsible for reducing the population of Central
Mexico to an estimated 3% of its 1520 level (Snow & Lanphear 1988: 16). In just two
94
Smallpox
decades after the introduction of smallpox in the north east of United States the
indigenous populations had been severely reduced by a factor estimated to be between 67
and 95%.
The clinical descriptions we have for the first and third smallpox epidemics
do not allow us to discriminate precisely which types of variola major were present,
although the discrete type would be favoured because of the high mortalities indicated by
the reporters and diarists. Phillip estimated that the 1789 smallpox epidemic killed 50%
of the Aboriginal people living around the Sydney settlement. The descriptions of
smallpox by Mair (1831) during the second epidemic, and later by Mitchell describing the
smallpox sequelae of the Barkindji on the Darling River, however, indicate symptoms
which accord with confluent and semi-confluent clinical types. Mortality was estimated
by Mair to vary from one in three (33%), to one in five or six (17-20%) of infected cases.
He thought, however, that it could have been less if the victims had been able to have
access to medical care and shelter. A case fatality-rate of 25% (the lower limit proposed
by Butlin (1983: 65) is then plausible.
Although the general tone of the majority of reporting on the epidemics
strongly implies high mortality, caution is required in accepting any mortality estimate
categorically for all populations in the path of an epidemic. In the cases of all three
smallpox epidemics there are several unknown factors relating to the prevalence of the
disease and the mortality. In all three epidemics we would expect regional variation in
the number of people infected by the disease. Some groups would have had a high
proportion of their numbers infected and a resulting high mortality while other nearby
groups managed to avoid contact with carriers and so escaped the epidemic. Within the
infected groups there would have been a degree of differential resistance to infection. A
number of individuals would have had an active immunity to the disease in which the
95
Smallpox
body reacts specifically to the pathogen and is able to survive the course of the symptoms.
This would depend chiefly on the amount of exposure to the virus, the current health of
the individual and the ability of the immune system to combat the spread of the virus.
Also a genetically inherited nonspecific resistance to the virus by some groups cannot be
discounted (Cockburn 1971: 51-52).
Finally, and as a word of caution, there is no way of determining the number
of individuals who were infected by smallpox and the number who managed to escape
infection. It is one thing to consider the various case-fatality rates of smallpox and
another to equate those rates with mortality in one entire community or region. In all
epidemics there are a number of individuals, families, groups, who manage to escape
infection entirely. This can happen due to fortuitous circumstances such as living away
from other groups who become infected during the epidemic, or active avoidance of the
disease by gaining prior knowledge of its presence and fleeing its path. We simply do not
know what this number may have been for any of the epidemics, nor in any of the regions
they occurred. When using case-fatality rates to estimate population loss we must first
know, or have a reasonable estimate of the number of cases of smallpox infection. For
the three epidemics in Southeast Australia I can see no way of estimating a reasonably
accurate number of infected cases. Therefore any estimation of Aboriginal population
loss incurred by the three smallpox epidemics of Southeast Australia based on case-
fatality must be treated with caution.
3.6 Conclusion
Three major epidemics of smallpox affected the Aboriginal population of
Southeast Australia during the colonial period. Evidence for the first in 1789 suggests
that it was confined mainly to the coastal regions of New South Wales and Victoria. The
second epidemic occurred between 1828 and 1832 and was observed along the major
96
Smallpox
river systems. The third epidemic which was observed in the western coastal regions of
South Australia was most likely a southern extension of a more extensive series of
outbreaks that occurred in the north, west, and centre of the continent.
While smallpox had only a minor effect on the European population of
Australia, the same cannot be said for the Aboriginal people The effects of the three
epidemics in Southeast Australia caused excessive mortality and morbidity. The three
epidemics hit hard at Aboriginal communities who were immunologically unprepared for
the virus. By contrast, they had little effect on the European population. While no
tangible estimate of population loss can be derived from the historical literature it is
reasonable to expect that 30% or more population loss occurred in areas reached by each
of the three epidemics.
97
CHAPTER FOUR
Sexually Transmitted Disease
4.1 Introduction
This chapter discusses the dissemination of syphilis, and to a lesser extent
gonorrhoea, through the Aboriginal populations of Southeast Australia after colonial
settlement. I will examine historical documents covering the region as well as skeletal
evidence from the Murray River and will argue that these two diseases were repeatedly
introduced into Aboriginal populations at the interface of contact with European
colonists. I will show evidence for the introduction of syphilis initially from the founding
settlements of each of the colonies of New South Wales, Victoria, and South Australia,
then subsequent introductions following the course of colonial expansion. Finally I will
discuss the evidence for syphilis along the Murray River in South Australia before the
establishment of the colony.
In the historical accounts of treponematosis among Aboriginal populations in
colonial Australia the problem arises as to which of the diseases in this group is being
documented. Was it an endemic disease that existed before European contact which the
colonist are confusing with the more familiar venereal form of syphilis, or were the
colonists indeed describing just the introduced venereal form of the disease?
Previous authors have argued that two forms of treponemal disease existed in
Australia prior to European colonisation; an endemic form of non-sexually transmitted
syphilis (treponarid) and yaws. Hackett (1936a, 1936b, 1978) and Webb (1984a, 1984b,
1989, 1995) have reviewed oral, historical, and ethnohistorical evidence together with
skeletal samples displaying typical treponemal lesions and claim that both forms existed
Sexually Trasmitted Disease
among Aboriginal populations of northern Australia and in some areas of the arid centre.
The yaws spirochaete (Treponema pertenue) was endemic to the nearby tropical regions
of New Guinea, and Oceania before European contact (Cahil 1975: 160; Cilento 1942;
Kranendonk 1958). Its presence in nearby regions of Australia with similar climatic
conditions is then no surprise (Garner et al. 1972).
In contrast, the evidence for any of the forms of treponematosis in pre-contact
Southeast Australia is by no means certain (Dowling 1990; and see discussion below).
The area is far removed from the equatorial and sub-equatorial regions of northern
Australia that are suitable for the survival and non-venereal transmission of the
spirochaete (Benenson 1990: 484). If there was indeed an endemic form of the disease in
Southeast Australia it was most likely to have been of low prevalence and of little
concern to the Aboriginal populations. The problem then of which form of syphilis,
endemic or introduced, is being seen and documented by the early colonists is therefore
much reduced.
A further problem arises in the historical literature regarding this disease
through its confusion with other sexually transmitted diseases, particularly gonorrhoea
(Spink 1978: 309). Historically, the spread of syphilis and gonorrhoea has been strongly
linked with the increasing transcontinental travel and migration of human groups over the
last five millennia (McNeill 1976: 202). Because of their similar modes of transmission
these diseases have often accompanied each other during mass population movements,
each in turn spreading in epidemic patterns among indigenous populations. In such cases
the incidence of gonorrhoea has been up to ten times more than syphilis (Spink 1978:
312-315).
99
Although sexually transmitted diseases today are regarded as a diverse group
of human infections with different aetiological and epidemiological features, this has not
always been the medical understanding. Much confusion and controversy have
surrounded the understanding of sexually transmitted diseases for several centuries, with
medical scholarship being split regarding their aetiology; particularly gonorrhoea and
syphilis. The influential British physicians Thomas Sydenham and John Hunter believed
that gonorrhoea and syphilis were the same disease (Duin & Sutcliffe 1992). Hunter
(cited by Duin & Sutcliffe 1992:100) argued that the difference between the two disease
syndromes depended on the nature of the surface which was infected; it caused the
characteristic ulceration or chancre on the cutaneous surfaces but only a purulent
discharge when mucous membranes were infected. Hunter's influence on British medical
scholarship was such that many of those trained in Britain held to his view of a single
disease entity well into the nineteenth century. The frequent association of gonorrhoea
with syphilis also added to the confusion between the two diseases and led many of the
writers to regard the symptoms of gonorrhoea, the 'clap', as an early stage, and the
symptoms of syphilis the more advanced stages, of a single disease. The controversy over
the two diseases began to be cleared during the 1830s when the French venereologist
Ricord distinguished the developmental stages of the diseases (Arrizabalaga 1993:1031-

1032). During the second half of the nineteenth century Ricord's concepts were gradually
being accepted by the medical scholarship of Europe, but it was not until 1879 when the
gonococcus was isolated and identified as the pathogenic agent causing gonorrhoea, that
the symptoms were seen as separate diseases. The identification of the treponeme
causing syphilis then followed in 1905 (Arrizabalaga 1993:1031).
Although the two diseases were separately classified in the Victorian
Nosological Index of 1863 (Morgan 1987), confusion surrounding the aetiology of
syphilis and gonorrhoea persisted among Australian physicians well into the nineteenth
100
century (Farr 1854: 139). This was possibly because they were situated far from the
mainstream of the development of medical knowledge in Europe. Further, those
physicians dealing with Aboriginal people and reporting on their health were usually
practising in rural regions further isolated from the medical centres of the cities. While
the terms 'syphilis' and 'gonorrhoea' were used by some physicians and non-medical
observers throughout much of the nineteenth century when referring to the symptoms they
saw, others used the more general term of 'the venereal' revealing a persisting confusion
between the diseases.
The result of this confusion is that it can be difficult (and sometimes
impossible) when examining medical accounts from the eighteenth and nineteenth
centuries to differentiate between the two diseases. In the source material used below I
have used accounts where there appears little doubt that the observers are referring to a
sexually transmitted disease, and in most cases it can be accepted as syphilis because of
the more destructive and well recognized symptoms of this disease. But at the same time,
the presence of gonorrhoea cannot be dismissed even though it is rarely referred to.
4.2 Biology of sexually transmitted diseases
4.2.1 Syphilis
Syphilis is a complex disease caused by the spirochaete Treponema pallidum.
Other closely related spirochaetes which infect humans but through non-venereal means
are T. pertenue, the causative agent of yaws, and T. carateum which causes pinta.
Antigenic cross-reactivity between T. pertenue and T. pallidum is now well documented
and the subtle molecular differences between these organisms are known (Baker-Zander
& Lukehart 1981; Thornburg & Baseman 1983).
101
The development of syphilis has three stages. The primary stage presents as a
characteristic lesion (chancre) at the site of entry of the treponeme. After four to six
weeks even without effective treatment the chancre may spontaneously heal. A secondary
disseminated macular-papular rash involving the skin particularly the palms and soles and
mucous membranes follows two weeks to six months after the disappearance of the
primary chancre. Lymph nodes, stomach, and liver may be affected. A latent period
follows the secondary stage and can be succeeded by a more debilitating third and final
stage (tertiary syphilis) in untreated victims (Benenson 1990: 420-421; Connor & Gibson
1988: 353-356).
The sequelae of syphilis if left untreated are multiple and unpredictable.
Primary infections often heal spontaneously but can progress steadily to cause serious and
debilitating symptoms which may lead to death. Syphilis can cause blindness, aortic
impairment (cardiovascular syphilis), visceral disorders, loss of neuro-muscular control,
and serious destruction of bone, skin and mucosal surfaces (Benenson 1990: 420-421;
Connor & Gibson 1988: 353-356; Hart 1984:6; King & Nicol 1975: 13-127). A major
debilitating effect of untreated syphilis is its involvement with the central nervous system.
Neurosyphilis may occur during any stage of the disease and presents as acute syphilitic
meningitis during the secondary or early latent phase, meningovasular syphilis later, and
finally, fifteen to twenty years after initial infection, progressive degeneration of the
dorsal roots and ganglia of the spinal cord (tabes dorsalis) characterised by impaired sense
of joint position, ataxia, episodes of intense pain (tabetic crisis), impotence hyperflexia,
secondary degenerative arthritis, and dementia (Benenson 1990: 421; Brown et al. 1970:
17; Connor & Gibson 1988: 353-356; King & Nicol 1975: 77-98). In addition chronic
102
untreated syphilis is often a predisposing factor in the appearance of other infections and
illnesses.
Syphilis can be acquired in utero. Foetal infection occurs at a high frequency
in pregnant women with untreated syphilis. It frequently results in abortion or stillbirth of
the foetus and can be a factor in infant deaths due to premature delivery, low birth-weight,
and generalized systemic infection and destruction of tissue and bones. Surviving infants
may carry associated stigmata such as Hutchinson's teeth, sabre shins (boomerang shins)
saddle nose, keratitis and deafness (Benenson 1990: 421; Connor & Gibson 1988: 356;
King & Nicol 1975: 99-127).
4.2.2 Gonorrhoea
Gonorrhoea is caused by the gonococcal bacterium Neisseria gonorrhoeae.
Infection is usually limited to the epithelial tissues of the urogenital tract, most commonly
the urethra in males and the endocervix of females. In males symptoms present two to
seven days after infection and are characterised by dysuria and a purulent discharge from
the anterior urethra. The infection may be self-limiting or in some cases develop into a
chronic carrier state. In such cases acute prostatitis, epididymitis, urethral stricture and
sometimes male sterility can result (Benenson 1990: 185; Brown et al. 1970: 90; Connor
& Gibson 1988: 391; Hart 1984: 3-4; King & Nicol 1975: 188-207). In females most
infections are asymptomatic or mild enough to pass almost unnoticed. In cases of
untreated gonorrhoea, pelvic inflammatory disease and chronic acute salpingitis may
occur when the infection spreads from the cervical glands to the fallopian tubes (Cates et
al. 1990). In such cases infertility occurs when inflammatory adhesions close the
fallopian tubes blocking the descent of the ova and the ascent of the sperm.
103
While in most cases gonorrhoea is not life-threatening for either males or
females, repeated infection and the lack of effective treatment may result in extra-
urogenital involvement secondary infections, most commonly gonococcal septicaemia,
arthritis, meningitis, and endocarditis. Neonatal infection can arise from infected
amniotic fluid or an infected birth canal. Symptoms usually arise a few days after birth.
The major form of neonatal infection is gonococcal conjunctivitis which may lead to
permanent blindness. Other sites of gonococcal infection in neonates are the pharynx,
respiratory tract, vagina, anus, joints, and bloodstream (Connor & Gibson 1988: 391;
Brown et al. 1970: 90-91).
4.3 Syphilis and gonorrhoea among the European population of Southeast

Australia.
Sexually transmitted diseases were common among the crews of ships
exploring the Pacific in the eighteenth century. For example, Captain James Cook's crew
together with other European voyagers left a trail of sexually transmitted diseases,
particularly syphilis and gonorrhoea throughout the islands of the Pacific (Watt 1979:
148-151). Syphilis and/or gonorrhoea came with the First Fleet to Australia in 1788.
Before sailing from Britain, Phillip had been concerned about the medical fitness of the
future colony, realising that its success would largely depend on the health of all who
sailed. He made a special request to the Home Office that convicts selected for
transportation should be in a good state of health and free from sexually transmitted
diseases (Watt 1989: 139). His request was not given due consideration. With the ever
increasing number of convicts in the already overcrowded prisons the Home Office was
under pressure to increase the numbers of convicts to be transported and their health was
given little attention in the selective processes (Watt 1989: 139).
104
Sexually transmitted disease became an unwelcome passenger to Australia,
not only among the convicts but among the military contingent as well. By the time the
fleet had reached the Canary Islands, their first port of call after just three weeks at sea,
ten cases of 'venereal' had been reported by the surgeons; eight of them were convicts, the
other two were marines. Further cases were reported among both groups before the final
destination of Botany Bay was reached (White 1787: 16).
Attempts to keep the sexes apart while at sea met with some success, but
when landed their separation became impossible to ensure. Heterosexual liaisons began
soon after the arrival in Port Jackson, particularly among the convicts (Tench 1793: 39).
Within three months of the settlement's establishment the presence of sexually
transmitted disease among the convicts began to concern Phillip and his medical staff.
Not only was it becoming more prevalent but it was common for the sufferers to conceal
their condition. In a vain effort to flush out those with the disease and prevent it
spreading through the colony, Phillip ordered that any man or woman, found to be
concealing the disease should receive corporal punishment and be put on a reduced
allowance of provisions for six months (Collins 1798: 20). Marriage was also
encouraged by both the medical and religious authorities as a further attempt at inhibiting
the spread of the diseases (Wrogan 1978: 25). Neither method was successful in stopping
the spread of sexually transmitted disease throughout the colony. In a five year period
between November 1791 to September 1796 'Lues venerea' (another name for syphilis,
see e.g. Arrizabalaga 1993: 1028; Farr 1854:165; Morgan 1987: 28) accounted for 5 of
the recorded 137 deaths (3.6%) among the civilian, military, and convict contingents
(Collins 1798: 426).
It continued to be a major cause of morbidity among the colonial population
throughout the nineteenth century. Annual reports from the Sydney Dispensary and
105
Infirmary record that syphilis was the sixth most common disease in 1838-39, accounting
for 4.8% of all diseases treated. By 1859 it was the third most common disease occurring
at 7.0%, and by 1874 it had reached second at 6.5% behind the leading cause of
morbidity, accidents and violence (Curson 1985: 19).
4.4 Syphilis and gonorrhoea among the Aboriginal populations - source material
The source material used below is examined in two contexts. Discussed first
is the evidence of syphilis and gonorrhoea among Aboriginal people living in the vicinity
of European settlements. Secondly I will examine historical and osteological evidence as
to the spread of syphilis and gonorrhoea spread ahead of European frontiers.
4.4.1 At the frontiers
New South Wales
It remains unknown when sexually transmitted disease began to infect the
Aboriginal people in the Sydney region after the arrival of the First Fleet in January 1788.
Collins was the first to comment on its presence:
The venereal disease also had got among them; but I fear our people have to
answer for that; for though I believe none of our women had connection with
them, yet there is no doubt but that several of the black women had not
scrupled to connect themselves with white men (Collins 1798: 495-496).
Which disease Collins is referring to, and at what time after the arrival of the
First Fleet he saw it, remains unclear. Collins served in New South Wales from January
1788 until August 1796 and published his account of the colony in 1798, so he is
referring to the presence of one or more of the sexually transmitted diseases among
Aboriginal people during that eight year period. He then goes on to say:
106
It was by no means ascertained whether the lues venerea had been among
them before they knew us, or whether our people had to answer for having
introduced that devouring plague. Thus far is certain, however, that they gave
it a name, Goo-bah-rong; a circumstance that seems rather to imply a pre-
knowledge of its dreadful effects (ibid: 496).
By the term 'lues venerea' Collins, in this instance, most likely means venereal syphilis
rather than gonorrhoea (Arrizabalaga 1993:1028; Farr 1854:165; Morgan 1987: 28).
How quickly the diseases spread throughout the Aboriginal population is
unclear. It may not, however, have become a serious health problem among them until
after at least the first six months of settlement at Port Jackson because of the infrequent
contact between the two groups (Phillip 1788b). Governor Phillip's objectives towards
the Aboriginal people were twofold (Blainey 1982c:25; Clark 1981: 116). On the one
hand the function of the Port Jackson community was to establish a penal settlement in
New South Wales. It was therefore necessary to control the movements of the convicts,
who made up the bulk of the settlement's population, and to keep them from freely
fraternizing with the Eora. Phillip had also been instructed to foster a friendly
relationship with the Aboriginal people, to establish a system of trade with them, and to
teach them the benefits of his own civilization. In order to do this he had to meet with
them. The first contacts between the Eora and the colonists were, however, sporadic.
When they did occur misunderstanding and mistrust between the two often resulted in the
angry use of weapons. The Aboriginal response was to avoid the settlement and its
occupants (Blainey 1982c: 25; Clark 1981: 116; Day 1996: 60-61; Phillip 1788b).
Keeping the convicts from meeting with Aboriginal people outside the
confines of the settlement was however, a problem for the colonial authorities. Collins
(1798: 29) records:
107
In one of the adjoining coves resided a family of them, who were visited by
large parties of the convicts of both sexes on those days in which they were
not wanted for labour, where they danced and sung with apparent good
humour, and received such presents as they could afford to make them; but
none of them would venture back with the visitors
By the 1820s sexually transmitted disease was perceived by Europeans as a
serious problem among the Aboriginal people in the Sydney region. Cunningham, a
naval surgeon, who made five trips to New South Wales aboard convict transport ships
between 1819 and 1828 commented on disease among the Aboriginal people. He made a
distinction between gonorrhoea and syphilis although attributing one disease to females
and the other to males:
From their natural filthiness, the women soon become diseased with
gonorrhoea, and propagate this infectious malady among the convict-servants
who cohabit with them. I have often observed the men too, labouring under
eruptions of the skin resembling syphilis, and open tumours [sic] also in their
groins apparently of the same nature; but time with them cures all disorders
(Cunningham 1827).
In all likelihood gonorrhoea and syphilis were affecting both sexes.
Cunningham's view that time cures all disorders, while reflecting the state of
medical knowledge of the time, was correct in one point but incorrect in another. We
have already seen that gonorrhoea in males can be self limiting, and if no further infection
is acquired the individual may be entirely cured. On the other hand mild clinical
symptoms may appear in females for a short period but lead to the more serious pelvic
inflammatory disease. Cunningham also appears to be referring to the primary chancres
of syphilis which can spontaneously heal within four to six weeks of infection even
without effective treatment. The second and third stages of development of this disease
often lead to more serious life-threatening complications if effective treatment is not

provided.
108
Victoria (Port Phillip)
Sexually transmitted diseases among Aboriginal people soon began to be
noticed by colonists after the settlement of Melbourne was established on the southern
coast of Southeast Australia in 1835.
Within four years of the establishment of this settlement, syphilis was
recorded by several observers to be widespread among Aboriginal people. During the late
spring and winter months of 1839 an increasing group had been living on the banks of the
Yarra River, on the fringe of the new European settlement. Many of these people were in
a poor state of health and were suffering from a variety of symptoms including dysentery
and fevers (Cussen 1839a). After six had died Dr. Cussen was instructed by Chief
Protector of Aborigines, G.A. Robinson, to visit the group and offer what assistance he
could. He reported back to the Chief Protector that most of those who were ill were
suffering from syphilis (Cussen 1839b).
Syphilis had been present among the Aboriginal people of the colony
(principally the Woiworung, Boonwurrung, Wathaurong, and Kurnai) before this
incident according to Cussen - probably as early as 1837, two years after the settlement.
In the same report he noted:
From an experience of more than a year and a half of the tribes which
frequent this neighbourhood, I can assert that syphilis is (generally speaking)
committing the most extensive ravages amongst them, and shall most shortly,
if unchecked, render them extinct in a very few years. I have had several of
them from time to time under my care and they appear to receive with avidity
and gratitude any measures that are adopted for their advantage (ibid 1839a)
109
In May 1839 Assistant Protector Sievewright wrote to the Chief Protector
reporting that 'nine-tenths' of the Wathaurong under his administration around the present
city of Geelong on the western side of Port Phillip Bay were victims of syphilis. The
symptoms, he claimed, appeared in a more 'violent' form than even the most
'extraordinary' European cases (Sievewright 1839). Sievewright went on to report that
neither sex was exempt from the disease and those infected ranged from infants to the
aged.
His observations were later supported by Fyans who had moved to the region
as the police magistrate in 1837. He stated that 'large families of natives - husband, wife,
boys, and girls - were eaten up with venereal disease' and estimated that 'two thirds of the
natives' of the colony had died from this infection (Fyans (c1853) in Bride 1898: 181).
The disease in this district could have two sources. It may have been carried
along from the Melbourne settlement 60 km east with the movement of colonists and
Aboriginal people between the two settlements. Another potential source may have been
from the sealing and whaling ships that had been frequenting the southern waters of
Southeast Australia since the early 1800s (Critchett 1990: 133). If the latter, then syphilis
and possibly gonorrhoea may have been present among the Aboriginal groups in this area
for thirty years before the settlement of Victoria.
In 1840 syphilis was reported by Assistant Protector Parker among the Wadi
Wadi, Wemba Wemba, and Wergaia in the northern district of the Port Phillip colony.
From early December of that year an increasing group of up to 170 had been gathering at
the Loddon River Aboriginal Station. Parker (1840a) reported that he had found '...five
cases of syphilis of a very severe character.' The rest of the people appeared to be free
from syphilis. Parker was concerned about the frequent sexual fraternization between
110
Aboriginal women and European men. He saw the Aboriginal people '...sinking to a
lower degree of moral degradation by the pernicious intercourse which they have with the
vitiated portion of the lower classes in the colony' (Parker 1840b). He was concerned
enough to write to Chief Protector Robinson and request that it would be 'highly
desirable' for a medical officer to visit the station as soon as possible to instruct him and
his overseer on ways to administer to the disease. Medical help was not immediately
forthcoming and his predictions about the increasing problem of syphilis were realised ten
months later. In an urgent disposition he wrote again to Robinson:
The call for medical assistance is however rendered especially urgent at the
present time by the rapid and extensive spread of syphilitic affections among
the aborigines... At the present time I fear more than half the women are
infected, and the disease is rapidly spreading (Parker 1841).
Similar reports were made by a third Assistant Protector of Aborigines, James
Dredge, on the Goulburn River among the Taungurong. Dredge reported to the Chief
Protector:
...it is extremely difficult to convey a correct report of the awful amount of

disease amongst both sexes of every age, resulting from illicit and promiscuous
intercourse with the Whites, and with each other. This disease amongst the
natives originating, in every instance - as my observation goes - in their
intercourse with white men. For the cure of this loathsome and deadly
disorder, no medicines adapted for their use have been placed at my disposal
(Dredge 1840).
While neither the Assistant Protectors nor the Police Magistrate were
medically qualified, their reports of what would appear to have been an epidemic of
syphilis can be taken with some confidence. All three Assistant Protectors had close
contact with the Aboriginal people in their regions and were required to investigate and
111
report any disease among them. Moreover, there is a strong similarity between all their
reports and with the observations of Dr. Cussen who was convinced of a highly virulent
epidemic of syphilis present among the Aboriginal people of the colony.
The reports of Dr. Cussen and the three Assistant Protectors reveal several
features of the disease they observed:
 The disease was almost certainly syphilis. All but Dredge reported that
the symptoms they saw were due to syphilis and referred to it by that
name. Dredge, while not specifically naming the disease as syphilis,
states that he is certain that it was spread by sexual intercourse,
particularly when Aboriginal females and European males were
involved.
 By 1840 it was widespread throughout the colony. Cussen reports it
among Aboriginal people at the main settlement of Melbourne, many
of whom had come from areas further inland to camp on the fringe.
The Assistant Protectors observed the symptoms in the vicinity of the

European pastoral settlements in the southeast and the north of the
colony.
 All report that there was a rapid dissemination of the disease among the
Aboriginal groups.
 Morbidity and mortality were excessive. Both sexes and a wide spread
of age groups were observed to be affected. While the claims of ninety
percent morbidity and two-thirds of the Aboriginal population dying
112
from the epidemic may be exaggerations on the part of Sievewright and
Fyans, they lend support to Cussen's observations that syphilis was at a
high level among the Aboriginal people of the colony at the time.
What the actual mortality from the epidemic was is of course unknown,
but the general tone of the reports demonstrates that it was severe.
Further evidence of the extent, persistence, and severity of the epidemic is
available from the papers of Chief Protector Robinson. Between April and October 1844
Robinson travelled throughout the eastern interior of the colony. His purpose was to
examine at first hand the state and welfare of the Aboriginal people living near European
settlements and those in the regions not settled by Europeans. Table 4.1 lists Robinson's
journal comments on syphilis among the Aboriginal populations he encountered.
Table 4.1 Comments regarding the observation of syphilis among Aboriginal populations
made by Chief Protector Robinson during his journey through the eastern interior in 1844
(Robinson 1844; Mackaness 1941).
Area Comment
Lake Omeo A loathsome disease (Syphilis) among the Natives imparted by
Europeans is making ravages.
Southern Syphilitic and other European Disease among the Natives is
Monaro/Upper prevalent, and their numbers are rapidly decreasing.
Snowy River
Twofold Bay Two men died from syphilis
Gundagai ...numbers are suffering from syphilis among whom are several
bad cases.
Albury A large number of Natives had congregated at the Hume [Murray
River] ... they were greatly suffering from Syphilitic disease.
On his return Robinson reported that syphilis was 'almost general throughout
the land' and had 'extended [its] baneful influences to the remotest parts of the interior'
(Robinson 1844).
113
In the same year concerned settlers on the Murray River in the northern region
of the colony wrote to Robinson calling his attention to the state of the Aboriginal people
in their region:
At the present moment there are few stations in the District at which there are
not from one to three Aborigines suffering under the various stages of
Venereal; and besides the mortality it causes amongst the natives themselves
it is also the means of propagating the disease among the labouring men of
the District to a very great extent. There is, and we fear will be, until religion
gradually works a change, a great deal of promiscuous intercourse between
the Europeans and the Aboriginal native, the consequence of which is the
rapid increase of the disease in the District (Huon et al. 1844).
In 1848 while Robinson was visiting the Aboriginal Protectorate settlements
of the colony he reported that along the main road between Sydney and Melbourne there
were 'as usual a great number suffering from Syphilis' (Robinson 1848).
By 1860 reports on the health of Aboriginal people living in the Murray River
corridor began to indicate that the cases of sexually transmitted disease had lessened. In
the first report the Central Board for the Protection of the Aborigines, Thomas Goodwin
reported from the Yelta settlement near the junction of the Murray and Darling Rivers in
the north west of the colony that:
Venereal is not so frequent amongst the men as is generally supposed, I have

seen very few cases, but I believe many of the young women, and even girls
are afflicted with it (Goodwin 1861-62).
In 1864 and again in 1866 the reports of the Board indicate an improvement
in the general health of the Aboriginal people along the Murray and a decrease in the
numbers of sexually transmitted disease being observed (B.P.A.1864-65, 1869). Dr

Campbell (1867) who had been employed as a medical practitioner among the Aboriginal
114
groups on the Lodden River reported in 1867 that he had not seen sexually transmitted
disease among those residing or visiting the station during the past four years.
Nineteenth century medical descriptions of sexually transmitted disease
among Aboriginal people are not well represented in the historical records. Probably the
earliest surviving description of a sexually transmitted disease comes from Dr. W.B.
Wilmot, medical officer and coroner, at Port Phillip. He attended the sick at Nerra Nerra
Warren Aboriginal Station, forty kilometres south east of Melbourne. His diagnosis of a
'syphilitic disease', which he saw among Aboriginal people was based on his own
observations of the clinical signs of the disease in what he took to be its various stages of
development, from a few weeks through to six months after the suspected time of initial
infection:
It generally originates with a small cluster of irritable papulae on the inside of

the thigh or scrotum and perineum, which rapidly coalesce, and degenerate
into foul ulcers, terminating ultimately in a warty excrescence; in a few weeks
it spreads very widely, and the skin becomes at length affected with a scaly
eruption of a circular form, with a well-defined margin, giving it much the
same appearance as lepra vulgare.
The action of the virus [sic] is singularly modified by the habits and
constitution of the native as it does not appear to pass through the ordinary
channel of the lymphatic system into the constitution, but directly through the
general circulation or capillary vessels as only in one instance and of a
dubious kind did I meet with any appearance of specific glandular affection.
In no case did I find any other than the inguinal glands affected; in no case
was there any ulceration of the fauces [mouth and throat], nor did I meet with
a single instance of a venereal node (Wilmot 1842: 257).
The signs Wilmot describes are not compatible with the clinical signs of
syphilis or gonorrhoea. Primary syphilis typically presents as a single painless ulcer or
chancre at the site of inoculation usually on the shaft of the penis, vulva, labia or cervix.
The secondary stage of syphilis is characterised by a spreading maculopapular rash in a
variety of organs, most commonly the skin of the palms and soles, mucosa, lymph nodes,
115
stomach and liver. The rash is apparent in the moist genital surfaces as well as the mouth,
although in Wilmot's description the latter was not the case. Other secondary symptoms
include the broad flat plaques of condylomata lata located in warm moist areas, and
lesions around hair follicules, neither of which can be reconciled to Wilmot's description.
Gonorrhoea infections are commonly localised to the urogenital tract in both sexes with
males displaying the characteristic purulent discharge from the anterior urethra. No
cutaneous lesions are associated with the infection (Beneson 1990: 421; Connor &
Gibson 1988: 354-355).
The small clustering of 'irritable papulae on the inside of the thigh' is more
suggestive of genital herpes. Herpes simplex virus type 2 produces a spectrum of
vesicular and necrotizing lesions localised to the genitalia and immediate surrounding
regions. The principal sites of primary infection are the glans penis, cervix, and vulva
with recurrent disease involving the perineal skin, legs and buttocks. The degeneration of
the primary rash into 'foul ulcers' described by Wilmot may represent localised secondary
bacterial infection particularly if the Aboriginal people were living under unhygienic
conditions as was possibly the case. The 'warty excrescence' may represent genital warts
(Condylomata acuminatum). They commence as small swellings in the peri-genital and

peri-anal regions and rapidly grow into grouped pedunculated lesions. A number of
lesions may fuse into a cauliflower-like mass (King & Nicol 1975).
A final possibility is that the pustular lesions may be due to chancroid
infection caused by Haemophilus ducreyi. This bacillus is highly infectious and invades
on contact through the skin or mucosa of the genitalia. A papule develops up to fourteen
days after inoculation, becomes pustular and ulcerates. The ulcers are usually small but
large mutilating ulcers can occur. Multiple ulcers are common. The lesions may spread
locally to the perineum, anus, scrotum, thighs or lower abdomen (Benenson 1990: 81-82).
116
From examining Wilmot's description it is not possible to come to any firm
conclusion in identifying the disease, or indeed diseases, which he saw. I think, however,
that two of the most common sexually transmitted diseases of that time, syphilis and
gonorrhoea can be ruled out as contenders in this case due to the incompatibility of the
symptoms. This then leaves the other possibilities, herpes simplex, genital warts, or
chancroid. The latter is unlikely because the disease is mostly confined to the tropical
and subtropical regions of the world (Benenson 1990:81); although introduction by
infected sailors recently arrived via a tropical port is a possibility. An outbreak of herpes
simplex possibly accompanied by cases of genital warts seems the most likely .
South Australia
The initial introduction and dissemination of sexually transmitted disease
among the Aboriginal groups of South Australia differs from the two other colonies
discussed above. As I will discuss below a disease resembling syphilis was present
among the Meru and Ngaridjeri living along the Murray River and southern coast before
the arrival of permanent European settlers and the establishment of Adelaide in 1836.
Before doing so I will continue with the discussion of sexually transmitted disease
spreading into the Aboriginal populations at the edges of the European settlements.
There is little surviving evidence of syphilis among the Kaurna living around
Adelaide and the surrounding coastal plains during the early years of the settlement. Dr
Wyatt was the first Aboriginal Protector appointed in South Australia and held the post
for two years from 1836. In an inquiry into the state of the Aboriginal people of the
colony Wyatt remarked that he first became aware of sexually transmitted disease,
although 'manifested as very considerable difference in appearance and symptoms' after
117
his first year as Protector (SAPP 1860). It is not clear, however, whether Wyatt was
referring to syphilis, gonorrhoea or some other disease. Nor is it clear that he was
referring specifically to the Kaurna or to the Ngarrindjeri and Meru with whom he also
had contact. Protector, Dr. M. Moorhouse, appointed in June 1839, in a brief report on
the health of the Aboriginal people, indicated that syphilis was present among Aboriginal
people in Adelaide (Moorhouse 1844). Again there is some doubt as to whether he was
referring to the Kaurna or a visiting group. In 1843 Moorhouse estimated that there were
300 Aboriginal people in the Adelaide district in regular contact with the settlers but
many of these were Meru and Ngarindjeri who regularly visited the region following
European settlement (Moorhouse 1843a).
The diffusion of sexually transmitted disease into the Kaurna and its
subsequent morbidity and mortality among them may have been less than it had been
among the other Aboriginal groups living near the settlements of Sydney and Melbourne.
Summers (1986: 288) has argued that the more liberal, humanitarian background of the
first settlers to South Australia, and the more orderly nature of colonization had the effect
of creating amicable relations with the Kaurna. Also, the absence of convicts in the
colony may have had some effect in reducing sexual relations between the two groups and
consequently the prevalence of sexually transmitted disease. On the other hand, it would
seem highly unlikely that sexual relations between free European males and Aboriginal
women did not regularly occur. It was a common practice for Aboriginal women to be
prostituted in exchange for tobacco, alcohol, and food from the early days of the
settlement (Summers 1986: 299). The timing of sexually transmitted disease into the
Kaurna population of the Adelaide Plains is unknown.
Its timing and distribution north and west of Adelaide is more readily
substantiated. During the 1850s and 1860s European pastoral leases and settlements
118
became established on Eyre Peninsula and in the recently surveyed regions north of
Spencer Gulf (Williams 1969: 16-20). As early as 1852 sexually transmitted disease was
being reported as a serious health problem among the Banggarla and Nawu who had
contact with the pastoralists. Moorhouse reported to the South Australian Government
that there had been a 'considerable mortality' among the adults. Thirteen men and one
woman had died chiefly of 'secondary symptoms of venereal' (Moorhouse 1852b).
Moorhouse wrote that he could do little about the problem other than send twenty
blankets to be given to those suffering.
The process of settlement and Aboriginal dispossession north and west of
Adelaide continued into the final decades of the nineteenth century with recurrent releases
of pastoral land tracts at the head of Spencers Gulf and into the Flinders Ranges (Brock
1995: 220). Sexually transmitted disease among the Nukunu and Ngadjuri spread at a
comparable pace. In 1867 the newly appointed Sub-protector Scott travelled 2,000 miles
(3,200 Km) along the spine of the Flinders Ranges and between Lakes Frome and
Torrens. He met with the Banggarla, Adnyamathanha, and Kuyani and reported to
Protector Buttfield, with some ambiguity, that their general health was good but there had
been a great amount of 'sickness' among them (Buttfield 1867). Subsequent reports by
Protector Buttfield to the Commissioner for Crown Lands (now the responsible body for
Aboriginal affairs in South Australia) allude to a satisfactory state of health and make no
reference to any sexually transmitted disease present among them (Buttfield 1871a,b,
1872).
By the mid 1870s further pastoral development and an increase of the
European population altered the Aboriginal health situation. Buttfield (1874) now
reported that there was 'a great deal of sickness' and syphilis was one of the principal
diseases. Once established, syphilis was maintained among the Aboriginal people who
119
had frequent contact with Europeans. In his annual report on the state of Aboriginal
people in the northern district of the colony for 1887 Sub-protector Beasley recounted
that:
...there are a great many suffering badly from venereal disease, caused
principally by contact with Shearers and those from Town, this is a sad thing
for these unfortunate creatures, but what can we do. The evil cannot be
stopped, nor the disease cured in most cases, as they cannot be induced to use
or submit to the necessary Medicinal remedies... Consequently this terrible
disease is spreading (Beasley 1888).
By 1879 the pastoral frontier had moved north of the Flinders Ranges and was
now into the arid regions beyond Lake Eyre. Syphilis had spread with the northern
movement and was infecting the Dieri whose lands centred around Cooper Creek on the
edge of the Strezlecki Desert. The missionary, C.A. Meyer, at Kopperamana Mission
reported to the Sub-protector that:
The general health of the Aborigines has not been very good during the past
year as they all - with only a few exceptions - suffer from Syphilis [emphasis
in the original] it would therefore be very advisable to have medicines for
them (Meyer, C.A. 1880).
Syphilis developed into a major health problem among the Dieri with little or nor
treatment or help available to them. In some circumstances help for the inflicted was
actively denied. It was the policy of the Lutheran missionaries at the Killapaninna
Mission settlement to expel those suffering the disease because of their perceived
'immoral behaviour' (Stevens 1994:191).
The effects of chronic sexually transmitted disease on the fertility of the
Aboriginal groups cannot be assessed with any degree of precision from the historical
records since there is not enough quantitative demographic data. It is reasonable to
120
assume, however, that where there is a high prevalence of sexually transmitted disease,
particularly where it is likely to go untreated and the chances of reinfection are high, there
is a strong likelihood of associated infertility (Cates et al. 1990: 214). A hint of such a
situation is given by Meyer in 1885 among Aboriginal people at Kopperamana mission
settlement. Although Meyer kept no written record of births and deaths he observed that
there had been no increase among the sixty-five living on the mission settlement nor
among the forty or fifty living nearby (Meyer 1885). Whether this was an effect of a
reduction in the birth rate, mortality, or migration was not specified by Meyer. If it was
due to reduced births then gonorrhoea may have been involved. Tubal destruction from
pelvic inflammatory disease in females and epdidymo-orchitis in males are complications
of untreated gonococcal infection leading to sterility.
Several years earlier Taplin, in a report on the Ngarrindjeri living on the Point
McLeay settlement, stated that:
I am well aware that the temptations held out by white men to the native girls
are constant and attractive, especially to those who can earn so little money...
I notice that decent, chaste women among the natives almost invariably have
large families. I know of three who have had three children in five years
(Taplin 1868).
Taplin is referring mainly to those who were living on the Point McLeay
settlement and its outstation. Like most missionaries Taplin strongly opposed pre-marital
sexual relationships and encouraged monogamous marriages. Such a practice, if
maintained, would reduce the incidence of sexually transmitted infection. The
implication of 'decent and chaste' women having large families may then be an indicator
of the reduction of sexually transmitted disease, particularly gonorrhoea, and a reduction
of associated tubal infertility.
121
4.4.2 Beyond the frontiers
So far discussion has focussed on the introduction and spread of sexually
transmitted disease as a consequence of European frontier movements. Below I wish to
examine the evidence for the spread of what was most likely venereal syphilis ahead of
the European frontiers and before the settlement of South Australia. I will again use
historical literature as the main form of evidence but support it with the use of
osteological evidence from the Murray River diagnosed with treponemal lesions.
Historical evidence
During his exploratory expedition along the inland river systems in 1830
Charles Sturt (1833) reported the presence of a disease severely affecting many of the
Aboriginal people he encountered. Sturt began his exploration at the limits of European
settlement; first by tracing the Murrumbidgee River from its upper reaches westwards
into the interior, then entering the Murray River and following it to its termination at Lake
Alexandrina on the south coast of South Australia. The day following his entry to the
Murray, Sturt and his party were met by a group of eighty-three men, women and children
(either Latje Latje or Kureinji) whose appearance he described as being 'extremely

picturesque and singular' (ibid: 91). Two days later, after setting camp, Sturt was
approached by a group of thirty-five:
The most loathsome diseases prevailed among them. Several were disabled
by leprosy, or some similar disorder and two or three had entirely lost their
sight (ibid: 96).
Further downstream Sturt was again struck by the appearance of a disease,
this time among the Barkindji. He saw many more affected by it:
122
The most loathsome diseases prevailed throughout the tribes, nor were the
youngest infants exempt from them. Indeed, so young were some, whose
condition was truly disgusting, that I cannot but suppose they must have been
born in a state of disease; but I am uncertain whether it is fatal or not in its
result, though, most probably it hurries many to a premature grave. How
these diseases originated it is impossible to say. Certainly not from the
colony, since the midland tribes alone were infected. Syphilis raged amongst
them with fearful violence; many had lost their noses, and all glandular parts
were considerably affected. I distributed some Turner's cerate to the women,
but left Fraser to superintend its application. It could do no good, of course,
but it convinced the natives we intended well towards them, and, on that
account, it was politic to give it, setting aside any humane feeling (ibid: 125).
Crossing what is now the border of South Australia and into the territory of
the Meru, Sturt and his party were in daily contact with larger groups, now numbering up
to 200 or more:
Their sameness of appearance, the disgusting diseases that raged among them,
their abominable filth... combined to estrange us from these people, and to
make their presence disagreeable (ibid: 131)
Sturt and his party continued to observe the presence of this same state of
disease among Aboriginal people during their progress downstream towards Lake
Alexandrina. Finally he comments on the Ngarrindjeri he met on the lower Murray:
It would disgust my readers were I to describe the miserable state of disease

and infirmity to which these tribes were reduced. Leprosy of the most
loathsome description, the most violent cutaneous eruptions, and glandular
affections, absolutely raged through the whole of them (ibid: 148).
From Sturt's comments there can be little doubt that the Aboriginal people he
met were indeed suffering from some form of debilitating disease; but what disease (or
diseases) was it? Sturt alternately called the symptoms he saw leprosy and syphilis. His
confusion is understandable when the regions of the body displaying leprosy lesions are
compared to those affected by syphilis. Leprosy affects the cooler parts of the body.
Infection involving the nasal mucosa, upper respiratory tract, and anterior segments of the
eyes leave the victim with nodular-like distortions of the face which can be confused with
123
syphilitic destruction in the same areas (Benenson 1990: 243-244; Connor & Gibson
1988:397-400: von Lichtenberg 1989: 380-382). The testes can also be affected giving
the misleading presentation of a sexually transmitted disease to the inexperienced
observer. Because of their similar clinical features leprosy and syphilis have often been
confused by early writers.
I think that we can rule leprosy out. While this disease was a problem among
Aboriginal people in the northern Australia where it became endemic, no clinical or
palaeopathological evidence for this disease has come from Aboriginal people in the
southern half of Australia (Basedow 1932: 13; Cleland 1928: 57; Cumpston 1989: 208;
Elphinstone 1971: 300; Webb 1989: 90). The disease described by Sturt appears to be of
very high prevalence, affecting all ages. Leprosy, however, has a low attack rate and a
long incubation period ranging on the average from three to six years making its
communicability low with clinical consequences presenting in just a few individuals
(Arnold 1966; Steinbock 1976) Leprosy then, does not fit the description put by Sturt.
What then of syphilis? Sturt was an astute and methodical observer and
recorder during his expeditions but his descriptions of the disease he saw are those of a
lay person. Sturt's education was not in medicine but in classics, mathematics and the
natural sciences, from which he developed a 'superior dilettante acquaintance with botany,
ornithology, zoology and geology' (Beale 1979:11). We have little way of knowing how
experienced he was in identifying the clinical signs of diseases, although like others of his
time he would have had at least a passing knowledge of syphilis and its symptoms having
lived in England where it was a common disease of adults (Arrizabalaga 1993: 1029;
McNeill 1976: 203).
124
Nevertheless, Sturt's use of the term 'syphilis' cannot be seen as a firm
indicator that the disease existed among the people he saw along the Murray River. But if
we look more closely at his comments in an aetiological and epidemiological context,
several points emerge which indicate an epidemic disease, most likely syphilis, was
spreading along the Murray River populations at the time Sturt and his party were
exploring the river:
 The infected Aboriginal people Sturt saw were living in a region far
removed from any colonial settlements in a land that was largely
unexplored by the Europeans.
 The disease he saw was active between a point upstream of the Murray-
Darling junction (between the present towns of Robinvale and Mildura)
and the mouth of the Murray River at Lake Alexandrina.
 By Sturt's implication the prevalence of the infection was high among
the groups he saw.
 Both sexes and all age groups (infants, adolescents, adults, and elderly)
were infected.
 Infection was severe among all ages.

 Infection may have been congenital in some cases.
 Areas of the body involved were: integument tissue over much of the
body, soft tissue and bone of the nasal region.
 Blindness resulted in some cases.
The diseased state described by Sturt of the Aboriginal groups along the
middle and lower Murray River is indicative of an active epidemic of treponematosis with
a high prevalence among the populations. Destruction of the peri-nasal soft tissue and
bone would indicate that the disease is in its tertiary stage in some of the individuals. The
125
blindness seen by Sturt may be the result of tertiary syphilis of the central nervous system
(neurosyphilis) or interstitial keratitis, a condition of late congenital treponeme infection
affecting mainly the 4 to 30 years age group (King & Nicol 1975: 85, 133). The primary
and secondary stages, particularly the dissemination of skin lesions were most likely to be
the main representation of the disease, but this is not clear from Sturt's descriptions.
Foetal involvement also seems to be represented with infants displaying lesions to the
surface of the body similar to adults.
Osteological evidence
Further evidence linking the clinical signs seen by Sturt to an epidemic of
treponemal infection comes from examinations of Aboriginal crania from the Murray
River in South Australia. From a total of 94 (6.8% of sample) Murray River crania
diagnosed with treponemal lesions (see Webb 1984a, 1989, 1995 & below) two
specimens bearing severe osteological lesions of tertiary syphilis are described below.
The first is from the eastern limits of the Meru and was found in sand deposits bordering
the Murray River in the Riverland region. The second was found near the town of
Manum in similar deposits. Its location is at the southern limits of the Meru bordering
the Ngarrindjeri. In terms of river distance they are separated by 340 kilometres
(Engineering and Water Supply Department 1975). The extracts from Sturt's narrative
presented above indicated that he was constantly seeing active lesions among the Meru
during his transit of this section of the Murray River. The two specimens showed clear
evidence of gummatous osteoperiostitis and were diagnosed as treponemal according to
Hackett's (1976) diagnostic criteria for syphilis, yaws and treponarid in dry bone. It is
worthwhile presenting and describing these two crania with a view of showing the
pathogenic pattern and extent of destruction; tying it in with Sturt's descriptions, and to
eliminate other forms of treponemia. Neither cranium has been dated. It should be noted
126
however, that these two specimens represent probably the severest form of treponemal
disease and are not indicative all the crania diagnosed with the disease.
Skull A911 434, (South Australian Museum) an adult male showed a severe
pattern of lesions. Infection involved nasal, frontal and right parietal bones (Plates 4.1,
4.2, 4.3). The nasal bone has been completely destroyed and erosion has proceeded
below the anterior nasal spine to the superior edge of the maxilla. Located above the
lateral margin of the right orbits is an irregular centre of serpiginous cavitation (caries
sicca sequence 6, Hackett 1976: 42) involving the rim of the orbit and extending
obliquely towards the mid-line for a distance of four centimetres. The lower margin of
the cavity has a sharp edge and the upper margins are slightly raised and rounded. The
walls of the cavity are concave and the diploe and inner table of the skull have been
perforated. No bone remodelling indicative of healing was observed. Further up the
frontal two additional centres of cavitation (caries sicca sequence 6) have united to form a
crescent shaped region approximately four centimetres long and one centimetre wide
extending from the mid-line down towards the anterior zygomatic arch. The crescent
lesion has concave walls ending in sharp edges at the rim. Three shallow circular
depressions (caries sicca sequence 4 to 5) form a line parallel to the coronal suture. The
central one of the three has a sharp, ridged margin and is deeper with radial scarring
beginning. The other two depressions have less defined, flattened margins. No
thickening of the inner surface of the frontal is obvious below the depression nor were
there any other changes observed on this surface. The right parietal is more heavily
involved. Two shallow depressions, similar to those on the frontal, and at the same stage
of development (caries sicca sequence 4 to 5), are located on the superior-anterior aspect
of the parietal between bregma and vertex forming a line at right angles to the sagittal
suture. The more medial depression borders, but does not cross, the suture line. Both
depressions have flattened rims. No radial scarring or inner table involvement was
127
observed. On the posterior half of the same parietal a confluence of clustered pits leading
into serpiginous lesions has resulted in bone destruction and perforation of the diploe and
inner cranial surface in four distinct regions (caries sicca sequence 6). The cavitations
roughly follow the temporal lines. The ectocranial edges of the cavities are sharp with
sloping sides leading down to the perforations of the endocranial surface, the edges of
which are also sharp. Another similar sequence of five lesions has penetrated the dorsal
half of the parietal resulting in considerable bone destruction. Clustered pits (caries sicca
sequence 1) surround the areas of penetration. The nature and distribution of these
lesions is indicative of gummatous destruction beginning on the external surface of the
calvarium caused by and infection extending from the soft tissues of the pericranium.
Skull A351 (South Australian Museum), an adult male, shows a similar
pattern of bone destruction (Plate 4.4). Nasal destruction in this individual has occurred
and the frontal bone displays several regions of radial scarring (caries sicca sequence 5)
with bone healing evident on the floor of the lesions and flattening rim margins. One of
these lesions is visible on the right mid region of the frontal bone. The posterior region of
the right parietal was the most effected at time of death. Active bone destruction is
evident in two areas. A series of four foci of destruction forms a row along the inferior
temporal line ending at the lamboidal suture. The lesions have not progressed to the
occipital bone. A second area of two destructive foci is located inferior and follows the
temporal line at the junction of the lamboidal and squamous sutures. The occipital and
temporal bones are not involved. All six cavitations are irregularly rounded with sharp
edges on the ectocranial surface and sloping walls penetrating to the cancellous tissue of
the diploe. The most inferior of the lesions is circumscribed by newly regenerative tissue.
The destruction of bone tissue in this individual is progressing from right lateral inferior
region of the parietal progressing along the temporal lines.
128
The cause of the lesions in both individuals is from gummatous infection
eroding the ectocranial bone followed by a regenerative process laying down new bone
tissue. Gummatous osteoperiostitis, as displayed in these two skulls is a characteristic
lesion of tertiary syphilis (Hackett 1976; Ortner & Putschar 1981; Steinbock 1976).
Gumma forms as a combined result of the restriction of blood supply to the bone by
thrombosed vessels entering the cranium from the pericranial tissue, and the toxic product
of the treponeme (Steinbock 1976: 123). A diagnosis of chronic tertiary syphilis can be
supported.
Several important questions now arise. What type of treponemal infection
was affecting these skulls? Was it venereal syphilis, or a form of non-venereal syphilis,
or yaws? Was it introduced, or was it occurring naturally among Aboriginal populations?
How long had it been present and how long did it last among the Murray people? Why
was the disease restricted to the middle and lower Murray populations and absent from
those further east as Sturt stated?
Webb (1984a, 1989, 1995) carried out a comprehensive investigation of bone
pathology using several Aboriginal skeletal collections from most of Australia's

geographic and climatic regions. A substantial part of the investigation involved
collections from the upper, middle, and lower Murray River. Webb found that these
populations had the highest prevalence of treponemal bone lesions for the whole
continent (Table 4.2).
129
Table 4.2 Treponemal infection in undated

Australian Aboriginal crania (after Webb 1984a)
Area n Treponema Percent

River Murray 1374 94 6.8
South Coast 261 7 2.7
Desert 183 9 4.9
Tropical 154 6 3.9
Coast 219 4 1.8
He concluded that the disease Sturt observed was indeed a form of
treponemal disease but could not determine whether it was introduced venereal syphilis or
an endemic form of the disease transmitted by non-venereal means. His inability to
resolve the nature of the disease stemmed from two main considerations. Firstly, while
the diagnostic criteria for treponemal lesions in bone have been determined (Hackett
1976) the discrimination between venereal syphilis, non venereal or endemic syphilis, and
yaws has not. The second problem is related to the skeletal samples themselves. Most of
the skeletal collections are poorly dated. Webb had little or no temporal control on the
collections of individuals he diagnosed with treponemal disease, and in many cases had
difficulty in determining whether they were pre-European contact or post-European
contact. This is particularly the case with much of the Murray River collections which
were collected without detailed recording of their spatial or temporal integrity. He

concluded that the 'extent and prevalence of treponemal disease in pre-contact Australia
cannot be determined from skeletal material held in collections around Australia until
some of it is dated' (Webb 1989: 98).
In order to establish which form of treponemal disease was affecting the
Murray River groups we must now consider yaws, non-venereal syphilis (endemic
syphilis), and venereal syphilis. All can display clinical symptoms similar to those seen
by Sturt.
130
Yaws certainly appears to have been common until recent times in some
Aboriginal populations but its distribution is restricted to the tropical regions of central
and northern Australia (Elphinstone 1971: 297). Long standing endemicity of the disease
was noted by Cleland (1928: 144) in tropical northern Australia; by Hackett (1936)
among the Aranda of northern and central Australia; and by Basedow (1932) in the
Kimberley region of Western Australia, but no trace of active yaws has ever been found
among the Aboriginal groups of southern Australia (Cleland 1928: 141).
The temperate climate along the Murray River corridor does not favour yaws.
The yaws spirochaete is a fragile organism outside its host, highly intolerant of seasonal
changes, particularly seasonal cold and low humidity such as are characteristic of the
Murray River and southern inland regions of Australia. The optimum environment for
the organism and for the disease to become endemic in human populations is the humid
equatorial, lowland rainforests where all months have a mean temperature exceeding
180C and a rainfall exceeding 65 mm per month (Pirie 1972: 189). The contemporary
world-wide distribution of yaws in tropical and sub-tropical regions reflects this optimum
environment. On the basis of this geographical restriction it is unlikely that yaws was the
disease that Sturt saw or that is represented by the cranial pathology.
Yaws can then be excluded on a further number of points. It is primarily a
disease of children and adolescents (Cleland 1928: 144; Benenson 1990: 484) with males
being more frequently affected than females. It is usually contracted in infancy or early
childhood through surface contact with infected children or adults. The condition may
last for several years into adulthood, often in latent form (Steinbock 1976: 142). The
initial lesion commences as a large, rounded papule (mother yaw) at the point of
inoculation usually on the leg. It may also occur on the mouth of a suckling infant or on
131
the breasts of a nursing mother (King & Nicol 1975: 302). Within three to six weeks
after initial infection secondary eruptions occur and can extend over much of the body's
surface. In many cases the disease is self-limiting and does not progress into the tertiary
stage to involve skeletal and soft tissue organs, or the central nervous system. In later life
all that may remain of an infection is scarcely perceptible scarring in the areas affected.
Bone lesions in yaws occur in about 1% of cases (Ortner & Putschar 1981:
180) and are commonly confined to the limbs. The most frequent bone is the tibia,
followed by the fibula, and the distal third of the femur. Cranial involvement in yaws is
even less common and much less destructive than from syphilis (Ortner & Putschar 1981:
180). Steinbock (1976: 145) reports that of 119 cases of osseous yaws, the cranial vault
was affected twenty times (16.8%), and of these, only one approached the severity of
bone destruction that is found in syphilis. The main involvement in yaws was destruction
around the nasal region. The frontal bone may be involved, but only in rare cases of
tertiary yaws. When affected, the frontal bone usually displays shallow pitted depressions
which do not perforate the ectocranial surface and are not characteristic of the carries
sicca common in tertiary syphilis (Ortner & Putschar 1981: 180; Steinbock 1976: 145).
With yaws then seeming unlikely, the two remaining forms of treponema -
endemic non-venereal syphilis and venereal syphilis - remain. Could the disease Sturt
saw be an endemic form of syphilis that had flared up into an epidemic just as he was
proceeding down the Murray River? This is possible but again unlikely. Endemic
syphilis, like yaws, is a disease of childhood, usually contracted before the age of fifteen
years (Garner et al. 1972: 287; Steinbock 1976: 138) with self-limiting symptoms and a
low case-fatality rate (Benenson 1990: 425-6).
132
There is no definitive evidence of treponemia in Murray River skeletal
material dated before European contact. Table 4.3 displays the collections from
Southeast Australia that have been dated. All are from the Murray River apart from
Broadbeach which is an east coast sample.
Table 4.3 Prevalence (%) of pathology in dated skeletal collections of Southeast Australia
(Blackwood & Simpson 1973; Haglund 1976; Pretty 1977; Pretty and Kircun 1989; Prokopec
1979; Sandison 1973: 173; Thorne 1971, 1975).
Sample Cranial Post- Porotic Trauma

Treponema cranial Hyperostosis
infection
Roonka (n=144) 1 5 1 14
7000-50 BP
Broadbeach (n=139) 0 3 23 15
1390-50 BP
Chowilla (n=72) 0 0 0 2
6000-170 BP
Murray River Pleistocene 0 _ 17 14
(n=44)
>9500 BP
The first of these collections to be excavated under controlled conditions was

the Chowilla collection. It came from a series of burial places located in the Murray
Valley between the present towns of Mildura and Renmark and Lake Victoria
(Blackwood & Simpson 1973). Radiocarbon dates of organic content from bone of one
burial and on charcoal intimately associated with another at Chowilla Station (near the
border of South Australia and Victoria) put the antiquity of the burials between 4,000 and
6,000 BP. Pathological examination of this material showed no changes attributable to
treponemal disease (Sandison 1973: 173). The skeletal collections excavated from
Broadbeach (Haglund 1976) and the Murray River Pleistocene collection (Thorne 1971,
1975) have also shown no evidence of treponemal infection (Webb 1989).
133
A large burial site at Roonka Flat on the lower Murray was excavated by
Pretty (1977). Radiocarbon analysis of sample from its stratigraphic horizons established
a range of dates from 18,000 BP with skeletal material coming from horizons dated 7,000
-50 BP (Pretty 1977; Brown 1996). Prokopec (1979) carried out a biological analysis of
this collection examining 132 full and partial skeletons from excavated graves and
surface exposures. Although there were four cases of bone changes suspected to be from
treponemal infection he could not confirm the presence of the disease.
In a more recent re-examination of skeletons (n = 144) from Roonka,
including those examined by Prokopec, Pretty and Kircun (1989) observed periostitis,
osteitis, osteoperiostitis and chronic osteomyelitis in six post-cranial bones and cranial
lesions in one individual from the Roonka III horizon radiocarbon dated between 4, 000
and 220 BP (Table 4.3). They ascribed the lesions to either yaws or endemic non-
venereal syphilis. All the postcranial osseous changes however, can be grouped together
as nonspecific infections caused by various kinds of pathogens (e.g. Staphylococcus sp.)
reacting with the bone (Steinbock 1976: 60) and are not peculiarities attributed only to
treponemal infection. The main bones infected were the longbones of the arms and legs
all of which are susceptible to nonspecific osteomyelitis caused by primary and/or
secondary infection. While treponema is possible as one cause of the postcranial osseous
lesions seen in the Roonka individuals it is by no means the only possible cause (Dowling
1990: 59). The single case of cranial lesions attributed to yaws is in an adult male
cranium coming from Tomb No. 18. It has not been described by the authors nor has this
individual been firmly dated. A photograph of the cranium appears in Prokopec (1979)
and Pretty & Kircun (1989) papers but again is not accompanied with any written
description. In the latter paper the lytic lesions visible on the frontal bone are diagnosed
with some reservation as being due to 'treponarid infection yaws?'. The skull is intact
134
with very little sign of post-depositional deterioration and may well be of post-contact
origin coming from the later range of radiocarbon dating of the site. If so, then the
suspected treponemal infection may well be venereal syphilis acquired from Europeans.
It is realised that lack of evidence for pre-contact treponemia on the Murray
River does not prove that it had never existed there. This can only be resolved by a series
of reliable radiocarbon age determinations for existing skeletal material held by museums
displaying unequivocal diagnosed treponemia sequelae or by newly excavated samples
from stratigraphically sequenced deposits with reliable radiocarbon dates. There is at
present little prospect of the former as this is seen by Aboriginal groups and museum
keepers as culturally sensitive and inappropriate. They are therefore reluctant to sanction
such tests. Time may tell for the latter.
There are still problems with accepting endemic non-venereal syphilis as the
disease Sturt observed. Was it just by chance that it was, for some reason, in a severe
form of an epidemic phase, when Sturt passed through the region? How often an
endemic disease flares up into a severe epidemic is dependent on the number of
susceptible individuals in the community. In most cases of infectious endemic disease,

endemic syphilis and yaws included, those susceptible are the young who have not been
exposed to the pathogen and who have not developed immunity to the disease. Such a
scenario does not sound plausible for the Murray River populations. The disease Sturt
saw was affecting all the ages, both young and old and the symptoms were severe. This is
consistent with the two crania described above, both were adult and the treponemal
symptoms had reached a severe tertiary stage characterised by bone destruction.
A further problem in accepting the existence of endemic syphilis along the
Murray is that a considerable degree of cross-immunity to venereal syphilis is acquired by
135
infection from non-venereal syphilis. Schell et al. (1982) have shown that hamsters
infected with endemic syphilis (T. pallidum Bosnia A) were resistant to challenge from
other virulent treponemes causing yaws and venereal syphilis symptoms. A similar
indication of treponeme cross-immunity in humans has been observed in regions where
other forms of treponemia are endemic (Garruto 1981: 561). An example of this comes
from the Pacific Islands. Until yaws was largely eradicated in many Pacific Island
populations as a result of concentrated medical campaigns, venereal syphilis was virtually
unknown even after close contact between the indigenous populations and European
colonists had been well established (Pirie 1972: 192). If endemic treponemal infection
had been present along the Murray before the European contact we would expect to see a
low prevalence and attenuated clinical symptoms of venereal syphilis when it was
introduced. History shows us that this is not the case.
Venereal syphilis was just as common and severe among the Ngarrindjeri and
Meru as it was elsewhere in the colony. George Taplin, who spent from 1859 to 1879
among the Narrindjeri of the lower Murray and coastal regions as founder and
superintendent of the Point McLeay mission settlement, writes:
I have seen cases, even bad cases of syphilis amongst the natives. I am sure
the disease was imported among them; they knew nothing of it before the
advent of whites - this is the testimony of the natives. I have known fatal
cases, also cases where the tibia was affected, and bony excrescences on the
skin, with atrocious neuralgic pain (Taplin 1879: 46)
During his residency at Moorundie Aboriginal station from 1841 to 1843 as
Protector, Eyre observed many Meru and Ngarrindjeri inflicted with venereal syphilis.
His account (originally written in Latin) reveals more about the disease:
136
Of the diseases from which they suffer since the arrival of the Europeans by
far the most frequent and the most deadly is the venereal stain... Among the
natives this disease manifests itself in the same way as in many Europeans,
yet for various causes it is even more hateful, especially because round
pustules, commonly the size of an ounce weight, rise at the same time from
the skin. The centre of these is gradually filled with flowing pus, then as they
grow larger and larger and disperse, the surface of the whole body is affected
with wasting and scab which cause horror and disgust to those near them.
These ulcers sometimes may persist for six or eight months; but generally
when irritants or caustics are applied locally they are cured within three
weeks... After the first or second year the disease disappears, but sometimes
causes death (Eyre 1845: 379, translation in Cleland 1928: 142)
Eyre appears to be in no doubt that the disease was venereal syphilis and that
it followed a similar symptomatic course among the European population as it did among
the Aboriginal population. His description of 'round pustules' rising from the skin and
dispersing over the body corresponds to the secondary stage maculopapular rash which
disseminates in a variety of organs, most strikingly the skin over much of the body
surface. Secondary symptoms of syphilis often spontaneously disappear within weeks
and up to twelve months after formation so it is doubtful whether Eyre's 'irritants or
caustics' were effective. The disappearance of the disease symptoms after the first or
second year as noted by Eyre would equate to the latent period between the secondary and
tertiary stages of the disease. This observation is interesting because it suggests that Eyre
was seeing only the primary and secondary stages of the disease and not the third and
final stage. Symptoms of tertiary syphilis would indicate that the disease had been
present among them for some time and many would have been initially infected much
earlier than when Eyre was seeing the disease.
The most parsimonious explanation for the disease Sturt observed is in terms
of an epidemic of introduced venereal syphilis spreading along the Murray corridor. This
is supported by osteological evidence of treponemia and by further historical
137
documentation of venereal syphilis in the Murray population, elsewhere in South
Australia , and in the other eastern colonies.
An early introduction into South Australia
A final set of questions must now be addressed. If venereal syphilis was the
disease seen by Sturt it was present before the establishment of the colony of South
Australia. When was it introduced, by whom, and where? While these questions cannot
be answered unequivocally, a strong contender for the introduction of venereal disease is
the sealing and whaling industry that began around the islands in Bass Strait and off the
South Australian coast in 1803 (Fig 4.1). Settlements were established on Kangaroo
Island around this time (Moore 1923) by the sealers, and ships often visited the mainland
coast to kidnap Ngarrindjeri women for wives and slaves (Summers 1986: 285). In 1819
Captain Sutherland of the brig Governor Macquarie recorded in his diary while at
Kangaroo Island:
They have carried their daring acts to extremes, venturing on the mainland in
their boats, and seizing on the natives, particularly the women, and keeping
them in a state of slavery, cruelly beating them on every trifling occasion, and
when at last some of the marauders were taken off the island by an expedition
from New South Wales, these women were landed on the main with their
children and dogs, to procure a subsistence, not knowing how their own
people would treat them after a long absence (Moore 1923: 121).
There is no direct evidence for the entry of sexually transmitted disease at this
time, but a final point coming from Sturt's observations supports a southern coastal entry
(Cleland 1928:141). Sturt first recorded the symptoms of syphilis at a point upstream of
138
the Darling River junction, then continued to make similar observations among the
Aboriginal people he met along the remainder of the river to its mouth. He makes no
mention of the disease among the Aboriginal communities before this point. An origin
from the east then seems unlikely. Discussing the origin of syphilis along the Murray
Cleland (1928:141) concluded that 'It is possible that from such a source syphilis may
have been introduced first amongst the Encounter Bay natives [the Ngarrindjeri] and then
have spread to those of the lakes [L. Alexandrina and L. Edward] and up the Murray'.
Sturt had observed the disease in 1830, twenty-seven years after the first European
contact with the Ngarrindjeri. This is an acceptable time frame, I would think, for
venereal syphilis to spread from the coast to the point from where Sturt began to observe
it.
4.5 Conclusions
The observations by the colonial writers document the spread of sexually
transmitted disease, particularly venereal syphilis, among the Aboriginal populations
throughout the European settled regions of Southeast Australia and beyond their frontiers.
Considered together they reveal several epidemiological factors.
Sexually transmitted disease, particularly syphilis, spread among the
Aboriginal populations in epidemic waves; in one instance together with the expansion of
European settlements, and in the other ahead of the frontier. The major foci of
introduction and spread of syphilis were from the settlements of Sydney (1788),
Melbourne (1835), and Adelaide (1836). Once these centres were established the colonial
settlement pushed inland and along the coast with a concurrent introduction and
dissemination of syphilis among the Aboriginal populations. A possible secondary point
of introduction was from the coast of South Australia in the vicinity of the Murray River
mouth and Lakes Alexandrina and Edward sometime after 1803 and prior to the
139
establishment of the colony. The most likely cause of this introduction was the
establishment of the sealing and whaling industry. By 1830 the disease had spread from
the coastal Aboriginal communities into the communities along the Murray River corridor
to a point just below the junction of the Darling river.
Both sexes were infected by sexually transmitted disease. While the most
common introduction of syphilis into the Aboriginal communities would have been
through sexual contact between European males and Aboriginal females it readily spread
within the Aboriginal communities by further sexual relationships. A high rate of early
and late congenital syphilis symptoms among pre-pubescents would be expected to have
occurred.
The fulminating signs that syphilis exhibited among the Aboriginal people of
Southeast Australia are similar to those recorded when introduced into other
immunologically unprotected communities in the past. Initially the disease appears to
have been highly infective with severe and life-threatening symptoms. An unusual degree
of severity of clinical symptoms was commonly noted among the Aboriginal groups
compared with its pathogenesis among the Europeans. This suggests that it was a new
disease in a population whose individuals had little effective immunological resistance to
its effects. A similar pattern of infectivity and severity of symptoms was documented in
the early 16th century when syphilis reached epidemic proportions in Europe (McNeill
1976: 63); in the post-contact period in America (Crosby 1972, 1986), and the Pacific
Islands (Marshall 1993: 490).
Although not always detectable from the historical literature, gonorrhoea most
likely accompanied the transmission of syphilis and quite likely was of higher morbidity.
Its effects on the fertility of males and females can be assumed to have been serious.
140
The arrival of syphilis to Australia with the First Fleet in 1788 and its spread
into the indigenous population of Australia represents the final continental introduction
and establishment of this disease.
141
CHAPTER FIVE
Tuberculosis
5.1 Introduction
Tuberculosis and humans have had an association stretching back at least
8,000 years (Merbs 1992: 17). It is not known, however, just how much longer this
association has been. One school of thought presents the view that tuberculosis and the
genus Homo have evolved together - the chronic nature of the disease enabling it to be
supported and transmitted within small populations. A second view is that the disease
evolved from a bovid zoonosis to a human disease during the early agricultural periods in
Europe and Asia when people began to domesticate and live closely with cattle (Dubos &
Dubos 1953; Johnston 1993: 1062; McKeown 1991: 38, 49). Whatever its origin,
tuberculosis was present among most people worldwide by the end of the prehistoric
period. Notable exceptions to this were the Maori of New Zealand (Bryder 1991: 80;
Johnston 1993: 1062; Wells 1991: 97) and the Aboriginal populations of Australia
(Basedow 1932: 16; Thomson 1991: 62; Webb 1984a, 1989, 1995; and below).
Using eighteenth and nineteenth century literature pertaining to tuberculosis,
this chapter will examine the effect this disease had on Aboriginal communities. The
examination will consider both stage II (early contact and diffusion) and stage III
(settlement and acculturation) of the medical model (Table 2.2). A further examination of
tuberculosis and its epidemiological nature is presented in Chapter Eight which deals
exclusively with stage III of the model. In this chapter the timing and dissemination of
tuberculosis throughout the Aboriginal communities and its morbidity and mortality
among them will be discussed.

Tuberculosis
5.2 Biology of tuberculosis
Tuberculosis is a chronic communicable disease caused by infection from
various species of Mycobacterium. The disease usually infects the lungs causing chronic
pulmonary tuberculosis in approximately 75% of cases (Bannister 1983: 166) but may
cause lesions in any other organ or tissue of the human body (Table 5.1) notably in
cervical and axillary lymph nodes; liver, spleen, and intestines; in the skeleton and in the
genitourinary system.
Table 5.1 International Classification of Tuberculosis

(ICD.9.CM 1991).
Classification Clinical Manifestation

Code
010 Primary tuberculosis infection
011 Pulmonary tuberculosis
012 Other respiratory tuberculosis
013 Tuberculosis of meninges and central nervous
system
014 Tuberculosis of intestines, peritoneum &
mesenteric glands
015 Tuberculosis of bones and joints
016 Tuberculosis of genitourinary system
017 Tuberculosis of other organs
018 Miliary tuberculosis
771.2 Congenital tuberculosis
Disseminated or miliary tuberculosis, where the disease is spread throughout
the body by the lymphatic system and the bloodstream, and tuberculous meningitis, where
the meninges surrounding the brain and the spinal cord are infected, are the two most
rapidly lethal forms (Sutherland 1977:175).
In humans the main species causing tuberculosis is M. tuberculosis but the
disease can be caused by infection from other species particularly M. bovis. The main
142
Tuberculosis
route of infection is from person to person by aerobic droplets transmitted in the air by
sneezing and coughing. In this case the portal of entry of the bacillus into the body is
usually the respiratory tract and initial infection begins in the lungs. Infection can also
take place through the digestive tract and the skin. The digestive tract is the main route
for M. bovis which can be ingested by humans through the milk of infected cows.
Ingestion by humans of infected milk may result in extensive tuberculous disease
(Youmans 1980: 371). Infection by the bovine tubercle in humans has now been virtually
eliminated in Western countries by the pasteurization of milk. Infection through the skin
occurs rarely under natural conditions and is usually a result of handling infectious
material (Youmans 1980: 371)
Two main types of tuberculous infection are recognized, primary and
reinfection or reactivated tuberculosis. Primary tuberculosis is the result of infection by
the organism in a person who has had no previous contact with M. tuberculosis and has
no developed cellular immune response to tubercular protein. The disease is
characterised by rapid multiplication of the tubercle bacilli followed by a wide
dissemination of the organism by the lymphatics or the bloodstream with no extensive
necrosis. Reinfection tuberculosis, on the other hand, is the disease occurring in a person
who has previously developed an immune reaction to tubercular protein because of a
previous exposure to M. tuberculosis. In this case the disease usually remains localised in
the lungs causing early and extensive necrosis. Dissemination to other parts of the body
is usually absent unless a bronchus or blood vessel is broken, in which case the bacilli can
be transported to other parts of the body (Bannister 1983; Cotran et al. 1989: 374-380;
Youmans 1980: 374-375).
Mycobacteria are among the oldest taxonomic groups on earth. M.
tuberculosis has become well adapted to living in humans who are its major reservoir
143
Tuberculosis
(Proust 1991a: 1; Youmans 1980: 371). Most people who are infected by M. tuberculosis
remain asymptomatic and show few or no clinical signs of the disease throughout their
life. In such cases the most common result is a minor pulmonary lesion which heals
spontaneously, leaving no serious sequelae but giving an increased resistance to further
infection. Only a fraction (around 5%) of people infected develop the clinical symptoms
of the disease (Cotran et al. 1989: 374). All infected asymptomatic persons, however,
remain indefinitely at risk of developing the disease throughout their life.
Progression of the disease into serious and life-threatening lesions depends on
several factors relating to the general health, socioeconomic status, nutrition, age of the
host and the amount and time of exposure, and the virulence of the bacillus (Table 5.2).
Table 5.2 Factors relating to host/pathogen and the

manifestation of tuberculosis symptoms.
Factors favouring disease Factors favouring host

Large dose of pathogen Low dose of pathogen
High virulence of pathogen Low virulence of pathogen
Poor nutritional state Good nutritional state
Poor health Good health
Low socio-economic status High socio-economic status
Inefficient immune system Efficient immune system
Young and old age groups Mid-age groups
The importance of social changes cannot be underestimated in the
epidemiology of tuberculosis. During periods of acute socioeconomic decline, as in
widespread warfare and colonization, outbreaks of tuberculosis commonly occur in those
communities most disadvantaged. For example, in Europe during the two World Wars,
epidemics of tuberculosis became rampant among refugee groups and prisoners of war
(Dubos & Dubos 1953; McElroy & Townsend 1989:243) even though the disease had
144
Tuberculosis
probably been endemic for thousands of years. A similar picture can be seen on the
American continent. Although it is now widely accepted that tuberculosis was present
throughout most of the Americas prior to 1492 (e.g. Allison et al. 1973; Armelagos 1990:
132; Arriaza et al. 1995; Buikstra 1981; Lucas Powell 1992: 41-53; Merbs 1992:17;
Stodder & Martin 1992: 63) skeletal collections and historical documents have shown a
high susceptibility of Amerindians to tuberculosis following contact with Europeans
during the processes of colonization and forced resettlement (Arriaza et al. 1995; Carlson
et al. 1992:143; McElroy & Townsend 1989: 308; Walker & Johnson 1992: 132). Clark
et al. (1987: 45) have argued that the high susceptibility of Amerindians to tuberculosis
following colonization was largely due to the socioeconomic changes enforced upon them
rather than an innate genetic susceptibility to M. tuberculosis (Cotran et al.1989: 374).
Tuberculosis infection has fluctuated during the last three hundred years. In
Europe, tuberculosis was the paramount cause of morbidity and mortality in the
seventeenth and eighteenth centuries (McElroy & Townsend 1989: 150) and was
probably responsible for 20% of all deaths (Smith, F.B. 1988:4). In an extensive review
of the disease in 1815 Thomas Young (cited in Dubos & Dubos 1953: 9) stated:
Of all hectic affections, by far the most important is pulmonary consumption,

a disease so frequent as to carry off prematurely about one-fourth part of the
inhabitants of Europe, and so fatal as often to deter the practitioner even from
attempting a cure.
In London alone during the middle and late seventeenth century the death rate
from all forms of tuberculosis was estimated at 1,300 per 100,000 (Smith 1988:4). By
1850 the mortality rate of respiratory tuberculosis had reached a peak in England and
Scotland and began to decline, but still remained one of the primary causes of death
throughout the rest of the century (Figure 5.1).
145
Tuberculosis
The fall in the mortality rate in Europe is not fully understood, but the gradual
improvement of working conditions, the development of social measures aimed towards
the relief of poverty and distress, the generalised betterment of living conditions (Long,
E.R. 1940; McKeown 1991), and the decline in family size (Smith 1988:8) are considered
to have had an effect.
Figure 5.1 Mean annual death rate from respiratory tuberculosis

per 100,000 in England and Scotland (after Smith 1988:7).
300
250
200
England
150 Scotland
Ireland
100
50
0
1851 1861 1871 1881 1891 1901 1911 1921
The last decade of this century has seen an increase in mortality from
tuberculosis surpassing any other period in history (WHO 1996). On a global scale
deaths have risen from 2.5 million in 1990, to an estimate of 2.9 million for 1995, and the
146
Tuberculosis
trend is expected to last to the end of the century when 3.5 million deaths annually are
predicted (WHO 1994a, 1996). The major cause for the increase is the association of
tuberculosis with HIV infection. The World Health Organization has estimated that a
person with TB/HIV infection is nearly thirty times more likely, in any given year, to
become sick from tuberculosis than a person who is only infected with the tuberculosis
bacillus (WHO 1994a). In Asia, where nearly half of the people are infected with the
mycobacterium, the deaths from co-infection of TB/HIV are doubling every three years.
A second cause for the increase of tuberculosis globally is the impact of recent political,
social and economic changes in Eastern Europe (WHO 1994b). After a steady decline of
the disease for the last forty years tuberculosis has began to increase in Eastern European
and former Soviet Union countries. Large cities are the most affected. Annual mortality
in Moscow has increased from 27 cases to 50 cases per 100,000 population in two years.
In the Siberian city of Tomsk the rate is 200 cases per 100,000 population, a level of
incidence usually only found in the most severely affected populations in the world
(WHO 1994b).
In Australia tuberculosis in all its forms is a minor cause of mortality. For the
years 1979 and 1990 the mortality from tuberculosis was 0.5 and 0.4 per 100,000 of
population respectively (Bennett et al. 1992).
Because of its long association with humans and its ability to attack a variety
of organs and tissues, tuberculosis infection has been known by several names in the
English speaking world (Dubos & Dubos 1953: 3-10; Farr 1854: 141; Morgan 1987).
147
Tuberculosis
Table 5.3 Terms given by medical

practitioners in the nineteenth century that may
be attributed to tuberculosis infection (Murray
1830; Registrar General 1863; Ruddock 1873;
Smith 1988:3-5; ).
Abscess in the pelvis or abscessus

Cachexia
Consumption
Consumption of the bowels
Decay
Decline
Dropsy of the brain
Enlargement of the glands (abdomen or throat)
Enlargement of the ometum
Gathering (abscess)
Haemoptysis
Abscess in pelvis or abscessus
Hives of the bowels
Hydrocephalus or water in the brain
Inflammation of the glands
King's evil
Phthisis
Pneumo-thorax
Psoas abscess
Scrofula
Scrofulosa
Struma
Swelling of the glands
Tabes
Tabes mesenterica
Tubercular disease
Tubercular peritonitis
Table 5.3 shows a variety of terms given by medical practitioners in the
nineteenth century that can be attributed to tuberculosis.
'Consumption' was the most common term used in the nineteenth century
referring to the most common form of the disease, pulmonary tuberculosis. Other
common terms were 'Phthisis' referring to the slow wasting away of the body; 'scrofula'
(tuberculous cervical lymphadenitis) referring to the direct extension of tuberculosis into
the skin from underlying lymph nodes (scrofuladerma). Tuberculosis has also been
148
Tuberculosis
known under other names, such as 'tabes' or 'tabes mesenterica' (tuberculosis in the
mesenteric glands of children resulting in progressive atrophy of the body or a part of it)
and 'lupus' (scrofuladerma) (Registrar General 1863:8; Waksman 1965: 7). Many of
these terms have largely been abandoned by Western medicine today. The actual name
'tuberculosis' was introduced during the first half of the nineteenth century to designate a
group of symptoms characterised by the presence of tubercles in different body organs.
More recently, it has come to mean any infection caused by tubercle bacilli, whether or
not tubercles could be found in the infected organs (Waksman 1965: 7).
5.3 Tuberculosis among the European population of Southeast Australia
The first recorded case of tuberculosis infection in Australia was before
European settlement. Forby Sutherland, a crew member of Captain James Cook's
Endeavour, was severely ill of pulmonary tuberculosis ('consumption') when the ship
entered Botany Bay on 29 April 1770. He died of the disease and was buried ashore the
next day (Cumpston 1989: 276; Proust 1991b: 5; Watt 1979: 138). Cook records in his
private log:
Last night departed this life Forby Sutherland, seaman, who died of a
consumption and in the a.m. his body was entard [sic] at the watering place.
The circumstance occasioned my calling the south point of this bay
Sutherland's Point (cited in Cleland 1938:257; Cumpston 1989: 276)
Sutherland was almost certainly not the only crew member to be suffering from the
disease when the Endeavour reached Australia (Watt 1979: 138).
When the First Fleet left its home port of Portsmouth for Australia in 1787,
tuberculosis was near its peak in the industrial cities of Britain. It is quite likely that it
149
Tuberculosis
was present among members of the First Fleet, and survived the long trip to Australia
particularly when considering the crowded and squalid living conditions of the convicts
(Bateson 1959: 60; Watt 1989: 138).
Although there are no surviving official medical statistics on tuberculosis, the
first reports of death among European settlers that could be attributed to tuberculosis
come several months after the arrival. John Easty, a marine private of the First Fleet,
recorded several deaths in his personal diary among which are cases that he considered to
be tuberculosis. He records for October 10th, 1788:
This Day John Jones A marine Departed this Life of a concumtion [sic] and
fever (Waksman 1965:106)
and for February 2nd, 1789:
This Night att [sic] 10 oclock Captn John Shea of Marines Departed this Life
after a Long illness of a Concumtion [sic] and was Buried the next Day in
Miliantary [sic] form very Neat and handsome (Waksman 1965: 108)
Easty also records four other deaths from long illness and fevers between June
1788 and June 1791 that may have been from tuberculosis. Little is known of Easty,
apart from his service in the marines, and he almost certainly had no medical education,
so his descriptions must be taken as a lay opinion only. Nevertheless, he was probably
recording the general opinions of the medical officers' diagnoses.
A sounder confirmation of tuberculosis in the new settlement comes from
records of the newly established Sydney General Hospital which listed in their 1803
returns of death, two males and two females dying of consumption during that year
(Jamison 1803). Tuberculosis, however, was responsible for just 4.2% of deaths recorded
150
Tuberculosis
in the hospital's register. The major cause of mortality in the settlement at this time was
due to dysentery which accounted for 52.1% of deaths recorded at the hospital.
The first recorded non-European death from tuberculosis was a Tahitian who
was visiting the new colony. 'Mowie', who had returned from a visit to England on HMS
Glatton, arrived in Port Jackson on the 11th of March, 1803, and died on the 6th August
before there was a ship available for his return home. The cause of death given was
'inveterate Scrophuli and decay' (King 1803: 370).
From the beginnings of European settlement in Australia tuberculosis was
constantly present among the first colonists. Governor Phillip considered that, up to
February 1790, about one-third of deceased convicts under his command 'died from
disorders of long standing, and which it is more than probable would have carried them
off much sooner in England'. Gandevia and Cobley (1974: 123) consider this comment
by Phillip to be based upon the observations of his medical officers and most likely to be
made in regard to pulmonary tuberculosis.
The disease was maintained in the population of the colony, being supported
by the new arrivals in the Second Fleet in June 1790 and in subsequent fleet arrivals
(Cumpston 1989:276; Proust 1991b: 5). Of the Second Fleet complement of 1026, 267
died enroute and 488 arrived at Port Jackson ill many requiring medical treatment (Clarke
1981: 123) McLeod (cited in Cumpston 1989: 276), writing in the fourth decade of
settlement says:
Consumption of the lungs (phthisis pulmonalis) is much more frequent than

from the mildness of the climate might be expected, and more in advanced
life suffer from this disease than in England. It is remarked that in people
who arrive in this Colony labouring under this complaint, it runs a much more
rapid course than it is observed to do in colder climates.
151
Tuberculosis
In 1860, when regular statistics began to be collected on the disease,
tuberculosis accounted for 146.6 deaths per 100,000 population in Victoria and ranked as
the third most common cause of death among the non-Aboriginal population. For the rest
of the century the disease maintained a high level of between 145.8 and 116.2 deaths per
100,000 of population (Government Statist 1904)
5.4 Tuberculosis among the Aboriginal populations - source material
5.4.1 Early contact and diffusion (Stage II)
Despite a long period of human occupation there is yet no evidence for
tuberculosis in Australia before European settlement (Basedow 1932:16; Cumpston 1989:
276; Thomson 1991: 62). Webb (1984a, 1989, 1995) conducted an extensive
palaeopathological study of Aboriginal skeletal collections covering most of Australia
and found no evidence of the disease. Other palaeopathological studies done on more
localised samples along the Murray River corridor in South Australia (Dowling 1990;
Pretty & Kricun 1989; Prokopec 1979; Sandison 1973) have had the same result.
This should not be seen as conclusive evidence for the absence of the disease
in Australia before 1788. Skeletal involvement in tuberculosis infection is uncommon.
With rare exceptions, skeletal tuberculosis results from secondary infection by the bacilli
spreading from either the lungs or the lymph nodes and just 5 to 7% of cases will show
discernible bone lesions (Steinbock 1976: 175). This substantially reduces the probability
of identifying tuberculosis infected individuals in skeletal collections. The probability is
further reduced when one considers the sites of skeletal involvement and the preservation
of the collections examined. The most frequent sites of infection are the lower vertebral
152
Tuberculosis
column, ribs and sternum, the proximal and distal articulations of the femur and the
proximal articulations of the tibia (Lucas Powell 1992: 42; Steinbock 1976: 178). Other
less involved sites of infection are the articulate regions of the shoulders, elbows, hands,
ankles, and feet (Steinbock 1976: 178). The skull is rarely involved. Many of the skeletal
remains examined in Australia for pathology consist of only the skull and/or incomplete
post-cranial bones and many are fragmentary and poorly preserved (Webb 1989: 10-14;
Dowling 1990: 12). It is not therefore surprising that palaeopathological examinations
have revealed no evidence of tuberculosis in Aboriginal Australia before European
colonization even if it had been present.
The first reference to tuberculosis among the Aboriginal people comes from a
visiting French expedition. R.P. Lesson, the second surgeon on La Cocquille which
visited the Sydney settlement from January 17th until March 20th 1824, noted that:
These natives are susceptible to a large number of illnesses, which their

miserable state makes them bear more readily than would the more robust
European. Most have chronic catarrh; some women are consumptive... (cited
in Royle 1973:950).
Although we cannot accept this observation at face value it is possible that
some of the Aboriginal people (both male and female) seen by Lesson were suffering
from tuberculosis. As discussed above the disease appears to have accompanied the First
Fleet colonists in 1788 and became established in the colony at that time, or soon
thereafter. The observation by Lesson was then some 36 years later, which is ample time
for the disease to have spread from the Europeans into the Aboriginal populations.
The first record of tuberculosis becoming a major health problem among
Aborigines is among those interned at Wybalenna settlement on Flinders Island in Bass
153
Tuberculosis
Strait (Plomley 1987: 917-947). In November 1831 the Tasmanian (Van Diemen's Land)
government moved one hundred and fifty Tasmanians from the main island to temporary
settlements on Flinders Island and later in 1833 the settlement of Wybalenna was
established. The mortality of the Aboriginal people was high and by 1847 when the
establishment was closed and the inmates were moved back to the main island, just forty-
seven had survived (Plomley 1987: 172; Ryan 1996: 203).
Before 1835 the causes of deaths on the main settlement and in the transit
camps went largely unrecorded. From October 1835 to February 1839, however, when
G.A. Robinson was in charge of Wybalenna, causes of death were recorded and thirty-two
autopsies were undertaken. After February 1839 the reporting of mortality again lapsed.
During 1837 and 1838 the autopsy reports show at least thirteen, or 35% of all autopsy
cases, involved extensive tuberculosis infection (Austin 1837; Walsh 1838; Plomley
1987: appendix II).
The number of deaths from tuberculosis in the settlement may have been
higher. Surgeon Allen stated he had been informed that most of the old and infirm
Aborigines had died of consumption and scrofula before he took up his position as
medical officer of the station (Allen 1837). The records do not give the cause of these
deaths, but in 1838 alone, the autopsy reports show that 9 (64.3%) deaths of the 14
recorded can be diagnosed as tuberculosis. After 1838 tuberculosis seemingly loses its
prominence in the records and influenza, pneumonia, catarrh, and 'pleuritis' were recorded
as the most common causes of death on the station (Plomley 1987: appendix II). This
does not, however, indicate that tuberculosis was becoming less of a problem. Mistaken
diagnosis of the cause of death and the underlying immuno-suppressant nature of chronic
tuberculosis could well have predisposed many of the Aboriginal people to life
154
Tuberculosis
threatening infections of influenza and pneumonia that were then recorded as causes of
death.
On the Australian mainland, for the first sixty years of European colonization,
tuberculosis appears to have had little impact on the Aboriginal population as there are
few references to it. Where it did occur, the morbidity was minor. With the instigation of
Aboriginal Protectorates in Port Phillip in 1835 and South Australia in 1836, reports on
the health status of Aborigines were sent by the Assistant Protectors from their various
stations in country and urban regions. In many cases the these reports allude in general
terms to severe and chronic diseases among the Aborigines. Few, however, make
reference to consumption, phthisis, tabes, or scrofula, the usual terms for tubercular
infection.
The disease is not mentioned as a major health problem among the large
groups that regularly left their homelands and congregated on the fringes of the major
settlements of Sydney, Melbourne, and Adelaide. One large group which collected
during April 1839 on the banks of the Yarra River flowing through the settlement of
Melbourne was described as being in a state of 'wretchedness and disease' by the
Assistant Protector of Aborigines for that area (Sievewright 1839). Doctor P. E. Cussen
was instructed by the Chief Protector of Aborigines to examine them and administer
treatment. He reported that they were suffering from dysentery, typhus, syphilis,
rheumatism, catarrh, and starvation (Cussen 1839a). He made no mention of any
tuberculosis infections
The disease also appears to have been uncommon among the Aborigines
living among the pastoral settlements of Victoria. In 1840, Watton, the medical officer of
the Mount Rouse Aboriginal Station, listed one case out of 142 presenting to him for
155
Tuberculosis
treatment that could be ascribed to tubercular infection. This was 'a very old woman' who
died while suffering from 'tabes' (Watton 1840). Of a further eighty-seven Aboriginal
people treated by Watton at Mount Rouse during the last four months of 1842, just two
(2.3%) were diagnosed as suffering from tuberculosis. One young female, aged eight
years was diagnosed with 'tabes mesenterica' and another female six years of age was
diagnosed with 'tabes' (Watton 1843). Doctors William Baylie and Neil Campbell
regularly examined Aboriginal people in the north east and north west districts of Victoria
between 1841 and 1845 while acting as medical officers for the Aboriginal Protectorate.
Neither diagnosed any as suffering from consumption or phthisis (Baylie 1841, 1841-42;
Campbell 1841, 1843, 1845) but Baylie (1841-42) described one case, a nine year old
male, suffering from 'inflammation of the mesenteric glands' which could possibly be
miliary infection
E.M. Curr, who compiled one of the most extensive accounts on Aborigines
last century, recorded the absence of tuberculosis among the tribes of the Murray River in
northern Victoria during the early period of European settlement:
During the first eight years of my residence amongst several large tribes near
Echuca, in 1841, I can recollect no instance of consumption; nor, though I
have made inquires on the subject of a few old residents who were good
observers, have I heard of more than one death of that disease at that period
(Curr 1886: 227)
In South Australia the situation was similar. Edward Eyre spent a decade in
close contact with Aboriginal people, during his residence in Australia, initially as a
traveller and explorer, but in particular during three years from 1841 to 1844 he spent as
Resident Magistrate and Protector of Aborigines at Moorundie, a police post and
Aboriginal depot on the Murray River . During this time Eyre made regular journeys
156
Tuberculosis
along the Murray as far as the Darling River and had frequent contact with many large
groups living along the river corridor. In regard to tuberculosis he records:
Phthisis occasionally occurs ... Scrofula has been met with, but rarely (Eyre
1845: 379).
Tuberculosis reporting among Aboriginal populations began to increase in the
second half of the nineteenth century when it became the major cause of death. William
Thomas (1861-62), a Victorian medical practitioner, reported that 'eight-tenths' of the
mortality he had observed among the Aboriginal people of the colony arose through
pulmonary disorders, mainly pleurisy, pneumonia and consumption. Thomas, like most
medical practitioners of that time, kept few or no health statistics on Aboriginal people he
examined so his statement must be seen as an impression based on his experiences.
Nevertheless, it suggests that tuberculosis was becoming a major cause of morbidity and
mortality among the Aboriginal people. He related these deaths to the Aboriginal
people's addiction to alcohol which, when coupled with infection, led, he believed, to
their deaths within days of showing the first symptoms (Thomas 1861-62).
The Ngarrindjeri who had their homelands extending along the lower reaches
of the Murray River and Coorong district of South Australia also became victims of
tuberculosis. This group had been in contact with Europeans since 1803 when sealing
enterprises began to be established on Kangaroo Island and the southern mainland coast
of South Australia (Moore 1923; Summers 1986: 285). They were soon infected with
syphilis and gonorrhoea spread by the sealers (Dowling 1990: 87-103; and Chapter 4) but
their early experience with tuberculosis is unknown. After eighteen years of close
association with the Ngarrindjeri, as well as other groups from further upstream on the
157
Tuberculosis
Murray, however, George Taplin (1876a) noted the importance of the disease amongst
them:
My observations have led me to the following view of the principal disease

from which the natives suffer with is evidently tuberculosis in its different
forms. I think that a large number of deaths arise from this cause. Of 50
deaths of Adults which occurred here [Point McLeay Settlement] between
1859 and 1869 twenty five were caused by tubercular consumption.
5.4.2 Settlement and acculturation (Stage III)
The extent of tuberculosis among the Aboriginal people in the latter half of
the nineteenth century is best seen in the records from the Aboriginal settlements (Table
5.4 and Figure 5.2). It should be noted, however, that tuberculosis was not confined to
Aboriginal people living on established settlements but affected those who were able to
live away from European settlements. In many instances migration of Aboriginal people
to and from the settlements would have facilitated the spread of the disease to those who
lived most of their life on their traditional homeland.
Table 5.4 Extent of tuberculosis as the recorded cause of death on Aboriginal

settlements in the nineteenth century for which there are reliable data..
Cause of death
Station Period TB Other Unknown Total % TB
Framlingham 1876-1883 4 14 18 22.2
Lake Condah 1876-1900 30 66 1 97 30.9
Lake Wellington 1876-1900 20 68 1 89 22.5
Lake Tyers 1876-1900 8 85 93 8.6
Coranderrk 1878-1900 22 49 71 31.0
Lake Hindmarsh 1876-1900 18 64 82 22.0
Point McLeay 1859-1900 60 226 94 380 15.8
Point Pearce 1880-1900 12 25 5 42 28.6
Total 1859-1900 174 872 19.9
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Tuberculosis
Data have been taken from the registers of births, deaths and marriages
compiled by each of the settlements during the latter half of the nineteenth century.
Those causes of death recorded in the registers as 'consumption', 'phthisis', 'phthisis
pulmonatis', 'tabes mesenterica', 'tubercular peritonitis', and 'tuberculosis', have been
extracted. Table 5.4 lists recorded deaths from tuberculosis on eight Aboriginal
settlements for varying periods and is compared with deaths from all other recorded
causes.
Fig 5.2 combines the data from the settlement records and expresses the
importance of tuberculosis as a cause of death among Aboriginal people living in
institutions throughout Victoria and South Australia between 1859 and 1900.
Figure 5.2 Tuberculosis as a percentage of the recorded

causes of death on Aboriginal settlements in Victoria and
South Australia 1859 - 1900.
159
Tuberculosis
68.5
Known other causes
Unknown
Tuberculosis
11.6
19.9
It can be seen from Table 5.4 and Figure 5.2 that tuberculosis was a major
cause of mortality among Aboriginal people living on the settlements accounting for
19.9% of all the recorded deaths. The records from Point McLeay, however, contain a
substantial number of deaths, (94 out of 380, or 24.7%) for which no cause was given.
This may have occurred because the cause was not known by the recorder or that it was
simply a failure to record the cause at the time of death. This has most probably distorted
the data for both tuberculosis as well as all other causes of death on this settlement and
for the combined total. In this case the extent of tuberculosis as a cause of death at 19.9%
of all deaths should be seen as an approximate figure only. I feel it may be an
underestimation because of the chronic nature of the disease making the sufferer more
susceptible to secondary infections, particularly respiratory, whose symptoms would be

more readily recognized by the recorders at time of death. In such cases tuberculosis
would most likely have been the underlying cause of death. An indication that this figure
may indeed be an underestimation comes from George Taplin (1876b), the superintendent
160
Tuberculosis
of Point McLeay settlement, who estimated that 50% of the deaths he observed among the
Ngarrindjeri of the lower Murray River between 1859 and 1869 were of those suffering
from tuberculosis. While this estimate should, of course, be taken with caution Taplin's
observations do intimate that tuberculosis was inflicting an excessive level of mortality
and by implication a high morbidity.
The prevalence of tuberculosis on Aboriginal settlements in South Australia
and Victoria had regularly been a point of concern for those in charge (e.g. Taplin 1876b;
Curr & LeSouef 1879). In 1878-79, however, it was causing high mortality among the
Aborigines on the Victorian missions. In 1878 Reverend Hagenauer of Lake Wellington
mission reported to the Board that the state of health of the residents had been poorer than
usual and the doctor who attended them had given up on several who had been suffering
from consumption (Hagenauer 1878). For the same period the superintendent of Lake
Tyers Aboriginal station reported that the past season had been a very trying one and there
had been more sickness during the year than at any other time (Bulmer 1879). The
superintendent at the Government's own settlement, Coranderrk, referred to the
morbidity and mortality caused by tuberculosis. There were approximately 80 Aboriginal
people living on the station and twelve deaths were recorded in the two year period. Of
these six were attributed to consumption, another one was attributed to 'softening of the
brain' and an infant died from 'low fever'. In July he reported to the Board that:
The health of the Aborigines is, I fear, much affected by the cold and damp
climate; scarcely any of them are sound, as they are the subjects of phthisis,
which is much promoted by their innate indifference to exposure to all kinds
of weather (Strickland 1879)
The Aborigines Protection Board responded by sending two members to visit
the stations at Lake Wellington and Lake Tyers. They reported that 'consumption or lung
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Tuberculosis
disease' was widely prevalent with many Aborigines dying and consequently
recommended to the government that the 'best medical talent procurable' be appointed to
investigate the disease and if possible determine how it could be mitigated (Curr &
LeSouef 1879).
The number of deaths from tuberculosis was lowest at Lake Tyers settlement
(9% of total) (Table 5.4). Only one death from tuberculosis, and very little sickness was
reported between 1876-85 (Bulmer 1880-81) on this settlement. After 1885 there were a
further 7 deaths reported from tuberculosis. The other settlements were not so fortunate.
At Lake Wellington, Hagenauer (1880-81) reported to the Board in 1880 that the state of
health among the Aborigines seemed to be good 'although one could never rely on it'. His
fears were realised because tuberculosis was to remain the principal cause of death on that
settlement despite the care provided by two medical practitioners from the nearby town of
Sale. The situation at the remaining stations in Victoria and South Australia was similar
with tuberculosis consistently being a major contributor to mortality.
5.4.3 Clinical Features
There are a handful of surviving reports that give reliable descriptions of the
clinical features of tuberculosis. During the period that Robinson was commandant of the
Flinders Island Aboriginal settlement, several autopsies were conducted by the medical
officers on the Aboriginal residents (Austin 1837; Walsh 1838). One report describing
progressive miliary tuberculosis with tuberculous ascites and body emaciation in an adult
male is given below: Table 5.5 summarises the remainder of the autopsies displaying
tuberculosis involvement, Appendix A contains the autopsy reports in full.
27 February 1838
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Tuberculosis
The body was quite emaciated prior to his dissolution and was in reality a
living skeleton. On opening the cavity of the thorax the lungs presented
chronic adhesions to the ribs, pericardium and sternum were for the greater
part solid and hepatised, particularly the upper lobe of the left lung, which
contained two or three large patches of a white caseous consistency. Both
lungs were thickly interspersed with small hard white lumps of a tuberculated
nature, although none of them had assumed a puriform state. The
pericardium was much enlarged and contained about six ounces of fluid.
The liver was of extraordinary size, was hard and adhered to the diaphragm.
On separating this connection a large ulcer was discovered on its upper
surface of a dirty gangrenous appearance; it contained a large quantity of
blood in a fluid state, was thickly covered with white hard small lumps
similar to those found in the lungs, which pervaded its internal structure also.
The whole peritoneal lining of the intestines exhibited the same tuberculated
appearance but much larger in size and containing a thick yellowish purulent
matter. The spleen was of natural size but hard and solid and on cutting into
exhibited the same tuberculous formation with the aforesaid viscera. The
peritoneal sack contained about four pints of water. The kidneys appeared
healthy.
(Walsh, M., in Robinson n.d.; Plomley 1987: 933)
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Tuberculosis
Table 5.5 Summary of autopsy reports 1837-1838 from Wybalenna Aboriginal settlement,
Flinders Island, involving tuberculosis (Robinson n.d; Plomley 1987: 927-937)
Date Sex Age Symptoms Diagnosis*
20- 8-37 Female Adult Adhesion of lungs to surrounding membrane and Miliary
ribs; extensive diffusion of tubercles externally tuberculosis
and internally of both lungs; liver enlarged with
small caseous foci; possible meningeal
involvement
30-12-37 Male Adult Adhesion of lungs to surrounding membrane; both Miliary
lungs indurated; diffusion of tubercles on external tuberculosis
and internal surface of lungs; extensive
dissemination of tubercles to liver and intestines.
12-5-38 Male Adult Extensive adhesion of lungs to surrounding Miliary
membrane and ribs; both lungs indurated and tuberculosis
dispersed with small tubercles; large purulent with possible
abscess on right lung; small intestines thickly cavitation of
coated with tubercles extending into peritoneum. right lung.
2-6-38 Female Adult Right lung extensively adhered to pleura; cavity of Pulmonary
thorax containing effusion of colourless serum tuberculosis
21-6-38 Female 2 Adhesions of lungs; both lungs hepatised and Miliary
interspersed externally and internally with small tuberculosis;
tubercles; left lung with three caseous cavitations; cavitating
liver and spleen indurated and interspersed with tuberculosis
tubercles; abscessing of pancreas.
2-7-38 Female 7 Adhesion of lungs to surrounding tissue; 2 to 3 Miliary
small suppurated lesions on lungs; liver enlarged tuberculosis
with extensive miliary involvement; spleen and
pancreas indurated, abscessed and covered with
small tubercles; intestines inflamed and
interspersed with tubercles
6-8-38 Male Adult Extensive hepatisation of lungs with a number of Cavitating
caseated cysts. tuberculosis
3-9-98 Male 3 Extensive lung adhesion to surrounding tissue; Miliary
both lungs hepatised and dispersed with tubercles; tuberculosis
left lung abscessed; spleen thickly dotted with
tubercles; liver enlarged.
29-10-38 Female 60 Adhesion of lungs to ribs, sternum, and Miliary
surrounding soft tissue; both lungs extensively tuberculosis,
hepatised with tubercles externally and internally; cavitating
large purulent cysts on both lungs; liver and spleen tuberculosis
extensively disseminated with tubercles; cause of of lungs.
death given as phthisis.
9-11-38 Female Adult Chronic adhesion of lungs to surrounding bone Pulmonary
and soft tissue; right lung tuberculous; left lung tuberculosis.
severely necrotised and purulent; cause of death
given as phthisis.
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Tuberculosis
17-12-38 Female Adult

Adhesion of lungs to surrounding tissue; both Miliary
lungs indurated and covered externally and tuberculosis
internally with small tubercles; internal tubercles
larger; adhesion of liver, external tubercles; spleen
enlarged and tuberculated externally and
internally; extensive dissemination of tubercles
along intestinal canal; cause of death given as
phthisis.
*Diagnoses taken from Plomley 1987: 927-937
In all cases but one the disease began as primary pulmonary tuberculosis,
exhibiting adhesions and well-developed external and internal granuloma of the lungs.
The exception was a seven year old female, whose lungs were described as 'healthy
except [for] a few adhesions of the left of a chronic nature with two or three small specks
on its posterior surface in an incipient state of suppuration' (Walsh 1838). Systemic
dissemination of the disease by haematogenous and/or lymphatic distribution to the
abdominal organs followed the primary infection in ten of the twelve cases. One of the
cases where this may not have happened was that of an 'aged' female who was suffering
concurrently from pneumonia and the another, a female, whose abdominal viscera were
described as 'natural' although the kidneys were large, but appeared healthy (Walsh 1838).
The organs infected were those favoured by miliary localisation, namely the liver and
spleen. Renal involvement, was, however, uncommon. Abnormal kidneys were noted in
only one case, that of a female whose kidneys were described as being 'quite flabby'
(Walsh 1838). Miliary dissemination of tubercle bacilli involved the intestines in four
cases and the pancreas in three.
Among the Ngarrindjeri in South Australia Taplin described the symptoms
and the course of the disease:
It also very often manifests itself in the form of tabes mesenterica about the
third or fourth year or even later. I have even known of a very bad case
occurring in a man of 25. This constitutional tendency often appears in the
form of induration and ulceration of the glands of the neck. Where it comes
out [like] this it is generally cured and the person becomes healthy afterwards.
But its most usual and most fatal form is that of tubercular consumption. Any
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Tuberculosis
accident to the chest seems to lead to the deposition of tubercle (Taplin

1876a).
5.4.4 Aboriginal Treatment
Little has been recorded on how traditional Aboriginal medical practices
perceived and coped with tuberculosis although they certainly were familiar with it. In
Victoria the Assistant Protector William Thomas reported that:
The blacks study much the colour of the spittle in those affected in the lungs,
and know well its stages. When the patient begins to expectorate blood, much
attention is paid him; should this increase, which is generally the case, the
doctors hold a consultation, and when once a consultation is held the doctors
will not allow the patient to take any more medicine from the whites. The
invalid is laid on his back and held firm by three or four blacks, whilst the
native doctor keeps continually pressing with his feet, and even jumping on
his belly. I need scarcely state that this cruel practice brings on premature
death (Thomas 1861-62).
Also in Victoria, Beveridge (1883) records Aboriginal people suffering from
pulmonary tuberculosis undergoing heat treatment:
The bath is constructed in a very similar manner to their cooking ovens, the
only real difference being simply that the hole for the bath is made
sufficiently large to contain the body of patient, and the glowing bottom of the
hole is covered to the depth of a foot and a half with boughs which had
previously been made damp, instead of a thin sprinkling of moist, grass, as is
the case when cooking. When the hole has been sufficiently heated the ashes,
etc., are scraped out and the damp green boughs nicely spread, upon which
the patient is carefully placed. He is then covered all over by an opossum
cloak, with the exception of his face, which is left bare. Then all over the
cloak earth is spread of a thickness capable of retaining the steam without
weighing too heavily upon the patient. To attain the former and obviate the
latter the finest earth that can be procured is used - that is, in the absence of
sand, sand in all cases being preferred when obtainable. During the progress
of the bath that perspiration exudes from the face in great globules, and the
hair becomes quite wet from the same cause.
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Tuberculosis
5.5 Discussion
The first recorded indication of tuberculosis among Aboriginal people comes
in 1824, after thirty-six years of European colonisation. Tuberculosis may not have been
able to spread into the Aboriginal populations away from main European settlements in
an extensive way during this period because of their mobility and infrequent contact with
the colonists. Humans are the major reservoir of the disease and infection is primarily
from human to human often requiring prolonged exposure to the bacilli before symptoms
are noticed. It has been described as a 'family' disease (Meyer, E.A. 1974: 126) often
acquired after long and close contact with an active case.
Although there was contact between Europeans and Aboriginal populations
during this time (Blainey 1982c: 3-48, 1987:413-443: Clark 1981) it is doubtful whether
it would have been sufficiently close to allow for the infection of many individuals. We
have no record that it did. Other predisposing factors in the development of the disease in
a community are a nutritionally poor diet, unsanitary living conditions, other acute and
chronic respiratory infections, and the reduced efficiency of the immune system in
individuals. While these factors were certainly present in the Aboriginal populations who
lived in the vicinity of the first European settlements (see Chapter Six) and received the
initial biological impact of colonisation, they were not factors affecting the majority of
the Aboriginal population in Southeast Australia at this time.
It was not until 1837, at Wybalenna on Flinders Island, and after 1850 on
mainland Southeast Australia, that tuberculosis began to be recorded as a major cause of
death among Aboriginal populations. Its increase was due mainly to interacting political,
social, and demographic factors affecting both the European and Aboriginal populations.
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Tuberculosis
The major factor in the increased prevalence of tuberculosis began when the
Aboriginal communities in Southeast Australia became increasingly more sedentary and
centralised. Government and missionary policies encouraged and sometimes forced
Aborigines to live in established settlements. In the early decades of the nineteenth
century the influence of humanitarians reached its peak and the British Government was
obliged to take steps to protect the rights and welfare of the indigenous peoples of its
colonies. In Australia this caused a dilemma for the Colonial Governments. The 1830s
and 1840s were periods of rapid European expansion across the southern part of the
continent, often resulting in conflicts with Aboriginal people over land occupation. The
official good intentions of the colonial governments and the concerns of the settlers were
often in acute opposition (Foxcroft 1941: 22-28). The answer found to this dilemma was
to establish government funded stations and missionary settlements where the Aboriginal
people could be confined and controlled.
By the mid-1870s, 18 Aboriginal settlements had been established in Victoria
and South Australia; most were administered and largely financed by missionary
societies, and two in Victoria were exclusively under the control of the Aboriginal
Protection Board, established in 1869 to provide for the protection and management of
the Aboriginal natives of Victoria (Barwick 1971; Summers 1986: 304-307). A census of
Aboriginal people both 'black' and 'mixed blood' taken in 1877 for the Aboriginal
Protection Board revealed that almost half (46%) of the estimated Aboriginal population
of 1,067 in Victoria were living on government stations and missions (BPA 1878;
Barwick 1971). In 1876 South Australia enumerated an Aboriginal population of 3,953
(many of whom lived in the more arid regions of the colony) of whom 5.3% were living
in the environs of Adelaide, on the four mission settlements, and in the settled counties
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Tuberculosis
near to government aid distribution points (South Australian Government Gazette 1879:
797).
The Wybalenna Aboriginal settlement on Flinders Island was among the first
of several of its kind in Australia established for the purpose of confining the Aboriginal
people. The primary objective of the Government in establishing the settlement was the
removal of the Aborigines from the mainland of Tasmania where their presence clashed
with the interests of the European settlers. A secondary objective, which was to become
commonplace in future settlements, was the Europeanization of the Aborigines once they
were confined. It was the intention of the Government to replace the traditional culture
and society of the Tasmanian Aborigines with that of a peasant society, as self-sufficient
as could be managed by the European commandants. Descriptions of the living
conditions endured by the Aboriginal inmates of the settlement (Ryan 1836) reveal they
were required to live a style of life totally which was totally foreign to them, and which
caused nutritional, medical, and psychological problems. They resided in cottages and
huts, inadequately maintained and frequently cold, damp and poorly ventilated; they
occupied a permanent settlement with inadequate and polluted water supply; far from
their homelands and often living side by side with traditional enemies.
Their diet was varied. The colonial government made attempts to supply the
settlement with rations but these were often late in arriving (Reynolds 1995: 175).
Reynolds (1995: 175-6), however, notes that the Aborigines on the settlement were better
provided for than the colony’s other welfare recipients. The expenditure on government
rations to the Aborigines was higher than that going to the colony’s paupers, convicts, and
destitute (Reynolds 1995: 175). In the early days of the settlement mutton birds (Puffinus
169
Tuberculosis
tenuirostris), which migrated annually to the island, were a valuable source of fresh meat
for the Aborigines but these were seasonal (Ryan 1996: 186). Although there is no
comparative study of the other nineteenth century Aboriginal settlements on the
mainland, it seems likely that Wybalenna was the best equipped and most heavily funded
of all. But given the degree of poverty on the mainland settlements this may be an
overstatement (Reynolds 1995: 176). Other respiratory infections were common
(Plomley 1987:915-937; and see Chapter Six). The lifestyle led on the island was highly
conducive to the development of tuberculosis as a major cause of morbidity and
mortality.
From the descriptions of the post-mortem examinations conducted by the
settlement's medical officers between 1835 and 1838 (Austin 1837; Walsh 1838; Plomley
1987: appendix II), miliary dissemination developed in most cases of tuberculosis leading
to death. The presence of small caseous tubercles, of effusion in the pleural, pericardial
and peritoneal cavities, together with adhesions described in the reports is characteristic
of this form of the condition. Extensive necrosis indicative of a long standing infection
was not common. There is no description of brain or meningeal pathology. This may be
because the skull was not opened. One might have expected evidence of tubercular
meningitis, which may have been the immediate cause of death (von Lichtenberg 1989:
377-378) in some of the subjects examined and others who were not subjected to post-
mortem examination. In these cases a reactivation of pre-existing tuberculosis seems
unlikely. Chronic pulmonary tuberculosis leads to the formation of cavities in the lungs,
which often become calcified. There is no reference to hard calcification in the autopsy
reports, or to cavities with thickened walls, which one would have expected in cases of
chronic pulmonary tuberculosis.
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Tuberculosis
A second factor contributing to the increase of tuberculosis among the
Aboriginal populations of mainland southeast Australia was the discovery of gold in 1851
in New South Wales. In the following ten years, 'the golden decade' (Moony 1987: 104),
Victoria's population increased from 77,000 to 539,000 and that of New South Wales
from 179,000 to 351,000 (Caldwell 1987). They comprised people from all strata of life,
and all economic circumstances. They often became wanderers, crowding on to the gold
fields while there were payable seams, then moving on to the next after each worked out.
Most of the immigrants were in the 25 to 35 year age-group.
While it may have been a 'golden decade' for the economy of Victoria and
New South Wales, it was a bleak period for those on the goldfields in regard to infectious
diseases. Dysentery and typhoid fever were the major diseases on the gold fields,
claiming many lives (Gandevia 1960: 757), but the demographic change brought with it
acute forms of tuberculosis at a growing incidence. In the period from 1 July 1855 to 30
June 1856 phthisis and scrofula accounted for 8.1% of all deaths in the European
population; by the end of 1856, the proportion of deaths from these diseases had more
than doubled, accounting for 18.0% of the total deaths in Victoria (Registrar General
1861, 1856). Doctor W.L. Richardson (1869), who was a physician practising at the
Ballarat District Hospital near to the largest gold fields in Australia during the gold rush
period commented that:
Tubercular pulmonary consumption presents frequently; it certainly has

become more frequent within the memory of the writer.
A third factor following the gold rush was the arrival of convalescent
tuberculosis sufferers to Australia. During the first half of the nineteenth century it was
generally believed by the English medical profession that a long sea voyage in the clear
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Tuberculosis
air of the oceans to a place with a mild and unchanging climate was of great therapeutic
value to sufferers of pulmonary tuberculosis (Dubos & Dubos 1953: 26; Ruddock 1873:
93-100). This supposition was also partly based on the belief that vomiting as a result of
sea-sickness helped the consumptive patient (Charlwood 1981:175). There was also little
or no suspicion that tuberculosis was communicable (Johnston 1993: 1061-1062;
Ruddock 1873: 26-44) and quite often the tubercular emigrants were not separated from
other healthy passengers. Many, therefore, would have passed on their infection to others
within the crowded confines of below-deck accommodation. Shipping companies catered
for those sufferers of tuberculosis wishing to migrate to Australia, offering them special
facilities on ships specially fitted out for convalescents. The Atlantic great circle route,
passing well south of the Cape of Good Hope and then east at latitudes 40o or 50o across
the Indian Ocean to Australia was especially recommended by medical practitioners and
favoured by the sufferers (Dubos & Dubos 1953: 26-27; Proust 1991b: 8). Doctor S.
Dugan Bird, who came to Australia himself suffering from pulmonary tuberculosis, was a
great proponent of the custom and wrote a book encouraging suffers in Britain to
emigrate (Bird 1863). He advised that the best time to leave England was in October and
November, leaving the northern winter behind and to arrive in Melbourne, as the
preferred destination, where the sufferer could soon look forward to complete recovery
(ibid: 83-89).
The hypothesis behind this conviction was, however, unsupported by any
scientific evidence. It arose from the cognizance that the disease was common in
England, which had a large and growing population living in densely packed industrial
cities and towns. Australia was known for its comparatively lower prevalence of
tuberculosis, its smaller population, less industrial pollution, and warmer climate (Dubos
& Dubos 1953: 26-27; Proust 1991b: 8). All these were thought by some medical
authorities to be factors leading to the cure of the disease. The opposite opinion was also
172
Tuberculosis
held by other medical practitioners (Thomas 1870; Proust 1991c: 234) and as early as
1830 it was noted that the change to a warmer climate was not necessarily a guaranteed
cure. Writing from Australia, McLeod observed:
Consumption of the lung/Phthisis Pulmonalis is much more frequent than

from the mildness of the climate might be expected, and more in advanced
life suffer from this disease than in England. It is remarked that in people
who arrive in this Colony labouring under this Complaint, it runs a much
more rapid course, than it is observed to do, in colder climates (McLeod
1830).
Nevertheless, many 'consumptives' fled England choosing to emigrate to
Australia to effect a last resort cure. By 1860 a growing number were making the trip; no
doubt the decision was made more enticing after 1851 by the prospect of finding gold
(Proust 1991b: 8). In a five and a half year period from 1865 to 1870, within the city of
Melbourne and its environs, over two thousand deaths from phthisis were recorded;
86.3% of these deaths were those of immigrants. Not only did the influx of tuberculous
immigrants increase the population of Victoria, they added substantially to the increased
mortality from the disease in the colony, and were the vectors for the disease which then
enabled it to become more firmly established in Australia and produce indigenous cases
(Cleland 1938: 257). As a result the mortality rate from pulmonary tuberculosis in
Victoria increased to 138 per 100,000 in 1880 from a rate of 115 per 100,000 population
for the period between 1864 and 1871 (Proust 1991b: 10).
The change in lifestyle and living conditions of the Aboriginal people, the
increasing European population, and the influx of infectious sufferers, were favourable to
the spread of tuberculosis among the Aboriginal populations. A pathogenic process
leading to active tuberculosis in individuals would have been further enhanced by poor
host resistance to infection. Many of the Aboriginal people living on settlements and in
pastoral regions had, for many years, been living in poor nutritional and contaminated
173
Tuberculosis
environments, suffering from a range of chronic and acute infections. Together with
alcohol and tobacco addiction, the inexorable result in many would be an impaired
immunological system resulting in less resistance to the pathogenic impact of tubercle
bacilli infection.
Once established, tuberculosis became, and continued to be, the leading cause
of death among Aboriginal people. Records of Aboriginal mortality from government
and mission settlements in Victoria and South Australia between 1876 and 1900 show
tuberculosis as the cause of 20% of all recorded deaths (Chapter 8). While this figure
indicates tuberculosis as a major cause of death among the Aborigines it possibly
understates the true impact of the disease on the Aboriginal populations and that the
mortality rate of infected individuals was higher. Misdiagnosis of the symptoms
presenting at time of death and secondary symptoms, particularly of respiratory
disturbance, would disguise and underlying chronic state of tuberculosis. For example,
many of the causes of death listed in the registers are given as 'lung disease', 'congestion
of the lungs', or 'inflammation of the lungs'. These symptomatic states may have been
misdiagnosed or may in fact be secondary conditions (pneumonia, bronchitis, influenza)
in individuals suffering from chronic tuberculosis.
Another factor in the underestimation of the deaths from tuberculosis is that
the Aboriginal people who lived permanently or temporarily off the settlements, or who
died away from the settlements, are largely unrecorded. An unknown number of these
latter cases would have had periods of exposure to other tuberculosis sufferers when they
spent time living on the settlements (Taplin 1876b). Others, who knew the seriousness of
their symptoms and were aware of approaching death, left the establishments in order to
die in their own home lands. Their numbers remain unknown.
174
Tuberculosis
Taplin (1876a) considered that fifty per cent of Aboriginal deaths among the
Ngarrindjeri of the Lower Murray River district of South Australia, between 1859 and
1869, were from tuberculosis. A similar situation was observed on settlements in
Gippsland region of Victoria in 1879. After visiting Ramahyuck and Lake Tyers
settlements in May of that year, Curr and Le Souef, members of the Aboriginal Protection
Board, reported:
We observed, however, with deep regret, that consumption, or lung disease,

here as elsewhere, was very prevalent, and the natives are rapidly decreasing
in numbers; few of those born on the stations seem likely to attain the age of
thirty years. The disease is always, sooner or later, fatal, and it has been for
many years a terrible scourge among the blacks, thousands having no doubt
died from its effects in the last thirty years. The complaint was most likely
engendered in the first instance by an entire change of life, consequent on
coming into contact with the whites (Curr & Le Souef 1879).
The first of these factors resulted in a general increase in the European
population and a subsequent increase in the prevalence and mortality from tuberculosis
among them; the third resulted in changes in social and living conditions of the
Aboriginal population leading to more exposure to the pathogen and lowered
immunological protection.
5.6 Conclusion
Tuberculosis probably arrived in Australia in 1788 with the members of the
First Fleet. Deaths from the disease were recorded among the colonists before the
subsequent arrival of further fleets. It is uncertain, however, how soon after the arrival of
Europeans the disease spread to the Aboriginal population.
175
Tuberculosis
Little is known about tuberculosis among Aborigines in the early years
following the colonisation of Australia. The first medically identified cases of the disease
were diagnosed as a result of autopsies on Aboriginal people interned at Wybalenna
settlement on Flinders Island in 1837 and 1838. These cases displayed extensive miliary
dissemination and were most likely the primary cause of death among the residents.
In the second half of the 19th century tuberculosis became well established
and was a major cause of mortality among the Aboriginal communities of southeast
Australia. Mortality records on Aboriginal settlements between 1859 and 1900 reveal
19.9% of all deaths attributable to tuberculosis in its several forms. A higher mortality
from the disease should be expected due to misdiagnosis of symptoms at death and
unrecorded Aboriginal deaths.
The change of lifestyle and living conditions predisposed the Aboriginal
people of mainland southeast Australia to increasing infection from tuberculosis. Adding
further to the increase of the disease was the rising European population and the
increasing incidence of the disease among the European population.
176
CHAPTER SIX
Acute Respiratory Diseases
6.1 Introduction
This chapter is concerned with respiratory diseases during the early contact
and diffusion stage (stage II) of the medical model. It focuses particularly on influenza
and pneumonia, as the most common respiratory diseases that have at one time or another
caused severe morbidity and/or mortality among indigenous populations. Other
respiratory diseases such as bronchitis, pertussis (whooping cough), and the common cold
are covered to a lesser degree. A further examination of acute respiratory diseases among
Aboriginal communities during the settlement stage (stage III) is covered in Chapter
Eight.
Although respiratory diseases were readily recognized as such by nineteenth
century medical practitioners, diagnosis was often not specific. Several disorders were,
however recognized. For example, influenza, pneumonia, and bronchitis were known to
be separate but often related disorders recognized by their differing clinical signs and
epidemiological circumstances. But in many cases, death or illness was ascribed in a

general way to 'congestion of the lungs', 'inflammation of the lungs' or 'lung disease'.
Given this ambiguity in diagnosis I have combined the numerous diseases and signs
affecting the respiratory system that were seen among the Aboriginal populations under
the ICD classification of diseases of the respiratory system. Because influenza and its
companion pneumonia were common in the nineteenth century and often reported in the
medical literature I have paid special attention to these diseases.
The most common respiratory infection carried from Europe to the New
World and Pacific was influenza. Influenza may have been the first epidemic disease
causing high mortality to be introduced into the New World by European colonists. An
outbreak of what was probably swine influenza emanating from the Spanish settlement of
La Isabela on Santo Domingo in 1493-94 has been blamed for the disappearance of the
indigenous populations of the Antilles (Guerra 1988: 305). Accounts of the outbreak
describe an acute infectious disease that was extremely contagious, with a very short
incubation period, affecting simultaneously a large population, and having the signs of a
high fever, prostration, and inflicting excessive mortality (Guerra 1988:316). A Spanish
observer recorded that 'so many Indians died that they could not be counted ... all through
the land the Indians lay dead everywhere (cited in Stannard 1992: 69). Influenza
epidemics and associated respiratory complications among the American Indians became
common during New World colonial expansion. Such outbreaks were responsible for
many deaths in the Southwest of North America (Dobyns 1983: 264; Thornton et al.
1992: 191; Upham 1992: 227); the Northeast (Cook 1973; Carlson et al. 1992: 149) the
St. Lawrence Valley (Dobyns 1992: 218), and New Spain during the seventeenth century
(Reff 1992: 268); on the Northwest coast in the early nineteenth century (Boyd 1992:
249); among the Chumash in the eighteenth and nineteenth century (Walker & Johnson
1992: 130-33); and among the Aleut of Alaska from the early days of contact (Thornton
et al. 1992: 128). Following the first epidemic, a second outbreak in 1539 of what was
possibly influenza spread among the northern Andes and into populations further inland
(Cook, S.F. 1992: 211). Further epidemics of influenza and other introduced maladies
caused severe population loss among the Inca (estimated to be around nine million) in the
sixteenth century (Thornton et al. 1992: 87-91).
Epidemics of influenza and secondary pneumonia occurred in the Pacific
Islands following European contact. Influenza was first reported in Tahiti in 1772
followed by Fiji in 1792, Samoa in 1830, the Cook Islands in 1837 and New Zealand in
1838 (Lange 1984: 325, 1988; Marshall 1993: 486; McArthur 1967). Severe epidemics
177
resulting in high mortality were recorded throughout the Pacific from the 1830s to the end
of the nineteenth century and after (Marshall 1993: 486).
6.2 Biology of influenza and pneumonia
Influenza is one of the most common diseases that infect humans. It is a
highly contagious and acute viral disease which has had a long history of association with
humans and appears regularly throughout the world in epidemic forms (Stuart-Harris &
Schild 1976:112; Crosby 1993b: 807). The clinical manifestation of symptoms differ.
Several host factors such as age, immunological status (i.e. prior exposure to a similar
viral subtype) and physiological state may influence the severity of the diseases
syndrome.
In its mildest form infection by the virus may result in an asymptomatic
condition or may produce mild symptoms such as fever or cold. More serious forms,
often occurring among the very young and the aged, may cause an acute, prostrating
febrile illness with a sudden onset of a range of symptoms including a sore throat, cough,
coryza, chills, headache, weakness, and myalgia. Infection may be accompanied by

undifferentiated acute respiratory complications, viral pneumonia, bronchitis and the
common cold. Gastrointestinal manifestations presenting as nausea, vomiting, diarrhoea,
prolonged fever, and convulsions may occur in children (Benenson 1990:224).
During epidemics the disease is often severe in very young or elderly victims,
or in victims with pre-existing underlying conditions. The latter include victims with
immunocompromised conditions caused by underlying chronic diseases such as
tuberculosis, cardiovascular disorders, other respiratory disorders such as chronic
bronchitis, asthma, emphysema, renal or metabolic disorders, anaemia, nutritional
178
deficiencies (starvation and alcoholism), age, a history of inflammation, inadequate
therapy, and iatrogenic insult (Beneson 1990: 224; Crosby 1993b: 807; Stuart-Harris &
Schild 1976: 97). Many of these medical states were common among post-contact
Aboriginal populations in various degrees of chronicity last century.
The causative agents for influenza are three myxoviruses, influenza viruses A,
B, and C. The most common, and the one that is the cause of the modern epidemics and
pandemics, is the A virus which exists in a number of sub-types or strains which usually
do not induce cross-immunity to each other. Type B has been associated with wide-
spread epidemics and type C with sporadic and localised minor outbreaks (Beneson 1990:
224). The antigenic shift of the influenza A virus leads to the emergence of new sub-
types that cause the regular outbreaks of new epidemics and pandemics of influenza.
Airborne spread of the virus is the predominant mode of transmission but the virus can
spread through direct contact, usually hands or fingers, by droplet dissemination. The
spread of the disease often occurs in the winter months and people living in crowded and
enclosed spaces are more susceptible to invasion by the virus (Beneson 1990: 224;
Stuart-Harris & Schild 1976: 29-35).
6.3 Influenza and pneumonia in the European population of Southeast Australia

In the examination of historical documents, single cases of influenza are often
difficult to resolve and differentiate from other respiratory complications like the
common cold, particularly when the symptoms are mild. But when a sudden outbreak of
the symptoms occurs within and/or between different communities it is almost always an
influenza virus (Crosby 1993b: 807). In many such cases, influenza virus infection often
leads to secondary, and more life threatening, complications of pneumonia. In

documenting the history of influenza and pneumonia in Australia Cumpston (1989: 319-
179
20) showed that the incidence of pneumonia among the European population was closely
associated with the epidemics of influenza. Secondary pneumonia complications
involving inflammation and destruction of alveolar tissue are often the major cause of
death during influenza epidemics.
There are no extant records referring to cases of influenza, an influenza-like
disease, or pneumonia in the historical literature during the first thirty-two years of
colonial settlement in Southeast Australia. The first recorded incident was an epidemic of
influenza which occurred in New South Wales in 1820 and may have persisted within the
colony until 1826 (Cumpston 1989:313). After the first recorded appearance, the
nineteenth century epidemic events of influenza in Australia have in the main paralleled
the pandemics of the northern hemisphere (Cumpston 1919: 2; 1989: 313). Table 6.1
shows the relationship between nineteenth century world pandemics of influenza and
subsequent epidemics and localised events of excessive morbidity and mortality in
Southeast Australia.
180
Table 6.1 Pandemics and periods of epidemic and unusually high

morbidity from influenza in Australia (after Beveridge 1977; Crosby
1993b; Cumpston 1989; Lancaster 1953; Warburton 1973).
Pandemics Australian Epidemics

N.S.W. Vic. S.A. Tas.
1800-02
1820
1826
1830-33
1836-39 1836-38 1837-38 1838 1838
1844-45 1844-45
1847-48 1847-48 1847-48 1847-48 1847-48
1850-52 1852 1852
1857-60 1860 1860 1860 1860
1873-75 1875 1875 1875
1885 1885 1885 1885
1889-91 1890-91 1890-91 1890-91 1890-91
1894-95 1894-95 1894-95
1898-99 1898-99 1898-99 1898-99
Apart from localised epidemics in 1820 and 1826 in New South Wales, in
Victoria and South Australia in 1845-46, and the non-appearance of the disease during the
pandemic of 1830-33, the epidemics of influenza in Southeast Australia have paralleled
that of the pandemics of the northern hemisphere (Cumpston 1919: 2; 1989: 313).
There are just a handful of extant references that document the first influenza
epidemic in 1820 and these were written at various times after the event. The Deputy
Inspector of Military Hospitals, Dr. D. McLeod, referred to the epidemic when he replied
to a set of questions posed by the Royal College of Physicians:
In July and August, 1820, an Epidemic Catarrh prevailed throughout the

Colony; occasional cases of it had been appearing from the beginning of the
Year, but most Families began at this time to suffer severely, there being
hardly a House that had not cases of more or less danger. It proved chiefly
fatal to infancy and old age; the symptoms of this Complaint were common
Cold, Cough, pains in the forehead, sneezing, Soreness and Spasms in the
Chest, copious discharge of mucous [sic] of various Colours from
consistencies from the Lungs (McLeod 1830)
181
The epidemic was considered serious enough to be recorded in the
'Chronological Table of Remarkable Events' of the Australian Almanac of Sydney:
An epidemical catarrh prevailed throughout the Colony about this period

Many families suffered severely from this strange complaint. The symptoms
of this disease were unaccountably varied. In many instances it appeared in a
hectic cough, accompanied by violent spasms. In others, it produced,
independent of the violent cough, a severe affection in the ear, with pus
occasioned by internal inflammation. Some cases were visited with external
eruptions, accompanied with extreme debility, and intense pain. The
complaint was general. Many of the inhabitants were consigned to the grave
in a few days, from the violence and fury of the attack; and some few, to this
day, have the remains of this visitation still as a painful companion. Great
numbers of the poor Aborigines fell victims to this novel and severe
distemper (Australian Almanac of Sydney 1832: 245).
Writing some six or seven years after the event Cunningham made a brief
reference to the epidemic and listed some of the more prominent symptoms:
An epidemic influenza carried off a number of the old Europeans some years
ago [1820], and also not a few of the aborigines, while many of our younger
individuals occasionally feel the effects of it to this day. It appeared at the
time, or immediately in the rear, of a hot northern wind, the symptoms being
violent headaches, cough, sneezing, and inflamed eyes; with a quick pulse,
and other general febrile concomitants (Cunningham 1827).
After the first epidemic subsided the infection may have persisted in the
colony at a low level of morbidity. Although there is little evidence for this in the records
of the colonists the second surgeon aboard the French ship La Coquille, which visited
Port Jackson between January and March 1824, recorded that:
The sailors of our crew, during this long stay presented only a numerous
series of catarrhal complaints, ephemeral inflammatory fevers, colds in the
head, illnesses neither interesting nor serious (Royle 1973: 951).
A second epidemic of influenza struck the colony in November of 1825 and
lasted into the next year (Cumpston 1989: 313). There is little evidence of the morbidity
and mortality upon the European populations from the subsequent epidemics up to 1890
182
other than to say that they were substantially higher than normal (Cumpston 1989: 314).
The 1860 and 1885 epidemics were general throughout the Southeast Australian colonies
and beyond (Table 6.1). The 1860 epidemic was called 'Fog Fever' in Victoria where 'the
cases were very numerous, some very severe in nature - whole families being affected'
(Jay cited in Cumpston 1989: 313).
The epidemic for which there are estimates of mortality is the 1890-91 event.
Table 6.2 shows the mortality rate per 100,000 population in the Southeast colonies from
influenza and pneumonia in 1890-91.
Table 6.2 Mortality rates from 1890-91 influenza

epidemic (deaths from pneumonia included) (after
Cumpston 1989:3i5-317).
Colony Mortality Rate

(per 100,000)
New South Wales 87
Victoria 98
South Australia 84
Tasmania 80
This epidemic was severe in terms of the mortality and morbidity it inflicted
upon the European population. Curson (1985: 125) has estimated that in Sydney there
were 100,000 cases of influenza making approximately 25 to 26% of the city's population
infected by the disease. The mortality rate from influenza alone was 61 per 100,000
population for 1891.
6.4 Influenza and pneumonia among the Aboriginal populations - source material
183
Evidence on influenza among the Aboriginal people begins with the first
epidemic of 1820 in New South Wales. This epidemic was a local event in New South
Wales and was not connected with a pandemic. Observations made by a 'Medical
Gentleman' in a letter to the Sydney Gazette describe the effects of the epidemic. Brief as
it is, this description of the 1820 epidemic among the Aboriginal people reveals the
severity of the symptoms and the Aboriginal response to the disease which was new to
them. It is worth quoting at length. After giving an account of his own experience with
the disease and that of his family he goes on to state that the Aboriginal populations of the
interior of the colony suffered excessively from the same infection:
which had produced a great mortality; and the many young stout [emphasis in
the original] and robust people among them had become its victims, during
the winter. In one severe instance a father, a very stout man, not exceeding
forty years of age, with the mother and two daughters, and the infant of one of
them, had all been carried off within the space of a month, leaving but one
alive, a male about three years old, very distressed, until taken into protection
by a European inhabitant of the settlement. Some cases ... appeared to ... have
terminated in inflammation of the lungs; and that they had for the most part
quitted the thinly wooded and more open tracts of the interior, and be taken
themselves to the sea-coast, and brush and broken country, where were
quantities of honey, and where they would undoubtedly remain until the
return of summer. That these people should suffer intensely under every such
contagion is not to be wondered at, when their state of privation from all
comforts of life is considered; and that when prevented by bodily ailment
from seeking their precarious means of sustenance, they are likely to become
victims to famine, as unhappily from distemper ('Medical Gentleman' 1820).
There are no further records of this epidemic among the Aboriginal
communities of New South Wales and we are left wondering about the severity of the
diseases and its demographic and social effects upon them.
The second epidemic of influenza spread through the European population of
the colony in 1826 (Cumpston 1989: 313). There is little known of its effects upon the
European population and it went largely unrecorded among the Aboriginal population.
184
Influenza and whooping cough associated with an outbreak of measles was reported
among Aboriginal populations in the Port Macquarie region in 1835 (Threlkeld 1835).
After these early reports the records on subsequent influenza epidemics and
accounts of acute respiratory disease allow a better insight into the effects influenza and
pneumonia in particular had among the Aboriginal people.
6.4.1 Influenza and acute respiratory disease among Tasmanian Aboriginal people
1831-67.
In May 1831 an epidemic of influenza, or a disease resembling influenza,
broke out among Aboriginal people who were taken from the mainland of Tasmania to
the small settlement on Gun Carriage Island. Gun Carriage Island is part of the Furneaux
Group of islands in Bass Strait and was the last temporary settlement before the
establishment of the major Aboriginal settlement on Flinders Island (Plomley 1987). On
March 20 of that year, prior to their arrival on the island, a young female died. Archibald
Maclachlan, a convict surgeon, submitted the following report on her death:
Died at eleven o'clock am, Mary, a native child aged six years, having been
afflicted with catarrh for some length of time, and from these last few days
past, from fresh exposure to cold, she was seized with acute inflammation of
the lungs which terminated her existence (Plomley 1966: 328).
By the end of March the epidemic had spread. Several were reported to be ill
and by late April two more had died, an adult male and adult female. On May 2
Robinson reported that fifteen Aboriginal people at the settlement were in 'a sickly state'
and later that month Maclachlan reported that 'catarrhal fever' was taking its course
among all the Aboriginal people (Plomley 1966: 329; 1987: 35, 938). The population on
Gun Carriage Island at this time was about fifty, including several women who had been
185
living with European sealers until the settlement was established. Maclachlan blamed the
outbreak of the disease on the 'bleakness of this place and the want of proper habitation'
(Plomley 1966: 456).
It is quite likely that this outbreak was associated with the 1830-33 world
pandemic (Table 6.1) although there are no records of major outbreaks among the
European population (Cumpston 1989: 313). If so, the virus may have been introduced
by one of the sealing ships which frequented Bass Strait although by then large scale
commercial sealing had ceased and only local sealers remained (Ryan 1996: 66-67). The
epidemic ran its course among the Aboriginal people and by November when the
settlement was eventually moved to Wybalenna on Flinders Island, 8 had died (Plomley
1987: 938).
Wybalenna functioned as a place of incarceration of the Tasmanian
Aborigines from 1833 to 1847. The colonial government sought to solve the problem it
had with the Aboriginal population (Reynolds 1995) by removing them from the main
island of Tasmania and isolated them on Flinders Island. From the beginning of the
settlement on the island the, commandant (Darling) impressed on the Aboriginal people
the need to eat European food in the European manner. The change from their traditional
diet was drastic. Their daily diet consisted largely of the colonial rations of salt meat and
flour substituted by local food sources collected from the land or obtained by hunting.
They had to learn new methods of cooking, boiling and baking, the new food with
unfamiliar European utensils (Plomley 1987: 72-73). Dampers made from the flour,
stews made from the salted meat with cabbage and turnips, and tea were the staple diet
(Ryan 1996: 186) Arrangements for supplying the settlement were often unsatisfactory,
with food running short, largely due to the irregular arrival of shipping at the island and
the colonial administration (Plomley 1987: 79). The Aboriginal people often had to leave
186
the settlement and live on what ever they could obtain in the bush. Game animals quickly
became scarce and on several occasions the annual arrival of mutton birds (Puffinus
tenuirostris) to the island averted a more serious food crisis (Plomley 1987: 66, 79; Ryan
1996:186).
Water for the Wybalenna had to be obtained from brackish lagoons and
brought to the settlement in containers. A fresh water creek near to the settlement ran
only in the rainy season. No attempts were made by Robinson or the other commandants
of the settlement to dam the creek to create an annual source of fresh water (Ryan 1996:
186). In 1835 the combined European and Aboriginal population was more than 150,
putting a serious strain on water resources (Plomley 1987: 92-94).
Prior to Robinson's arrival at Wybalenna in 1835 the houses or huts offered to
the Aborigines were neither warm nor comfortable (Plomley 1987: 91). In the early
period of the settlements on Flinders Island huts were made from bush materials collected
by the Aboriginal people. They were simple A-frame constructions expected to house six
persons but were unsuitable as a permanent structure against the cold westerly prevailing
winds of Bass Strait. Robinson attempted to improve the living conditions first by
repositioning the doorways so the winds did not blow directly into the huts. Later he built
brick houses with grass-thatched roofs in an L-shaped block of 20 dwellings which were
to be the permanent accommodation for the Aboriginal residents until their removal from
Flinders Island in 1847 (Plomley 1987: 92). Each dwelling had one room with two beds
for four people (Ryan 1996: 191). The dwellings later became infested by vermin
(Plomley 1966: 932; Ryan 1996: 186). In the last years of the settlement the living
conditions experienced by the Aboriginal residents had seriously deteriorated largely due
to neglect by Dr Jeanneret, commandant of the settlement from June 1842 to early 1844
187
and again in 1846, and a severe reduction in financial commitment by the colonial
government (Ryan 1996: 196).
An indication of the poor conditions at Wybalenna comes from a petition
written in February 1846. Signed by eight Aboriginal residents, it was forwarded to
Queen Victoria through the Secretary of State for the Colonies:
Dr Jeanneret kept plenty of pigs in our village which used to run into our
houses and eat up our bread from the fires and take away our flour bags in
their mouths also to break into our gardens and destroy our potatoes and
cabbage...Our houses were let fall down and they were never cleaned but were
covered with vermin and not white-washed. We were often without clothes
except a very little one and Dr Jeanneret did not care to mind us when we
were sick until we were very bad. Eleven of us died when he was here. He
put many of us into jail for talking to him because we would not be his slaves.
He kept from us our rations when he pleased and sometimes gave us bad
rations of tea and tobacco (Plomley 1987: 148-9; Reynolds 1995: 7-9).
In 1847 Wybalenna was finally closed and the Aboriginal survivors moved to
Oyster Cove on the main island of Tasmania.
Although the medical and mortality records at Wybalenna are inconsistent
(Plomley 1987: 916) they reveal a high level of acute respiratory diseases among the
residents. . Table 6.3 displays the number of deaths at Wybalenna and their recorded
causes with special attention to acute respiratory diseases.
Acute respiratory diseases (n = 33) accounted for 26% of the total recorded
deaths. This figure should, however, be seen as a minimum because of the high number
of deaths for which no cause was given (n = 64). The 18 deaths recorded as pneumonia
all occurred within the first 6 years of the settlement. This may indicate the decline of
188
this disease as a major cause of morbidity and mortality. Within the first 6 years of the
settlement 111 or 87.4% deaths occurred causing a severe population loss from an
estimated original population of 150 in 1833.
A number of individual cases of acute pneumonia leading to death were
documented by Dr Allen in 1837 (Allen 1837; Plomley 1987: 923-924). Two have been
selected in order to indicate the severity of symptoms suffered. Both show severe
inflammation, adhesion and destruction of lung tissue, oedema in the alveolar spaces, and
hepatization. A diagnosis of severe pneumococcal pneumonia is consistent with the
recorded signs.
Table 6.3 Total recorded deaths and causes from acute respiratory diseases at Wybalenna
Aboriginal settlement 1833 to 1847 (after Plomley 1987: 939-944).
Year No. of Pneumonia Influenza Other Other No cause

deaths ARD Causes recorded
1833 31 - - - - 31
1834 9 - - - - 9
1835 14 11 - - 3 -
1836 4 - - - 1 3
1837 29 3 - - 8 18
1838 14 4 - - 10 -
1839 8 - 8 - - -
1840 3 - - 1 1 1
1841 3 - - 1 - 2
1842 3 - - - 3 -
1843 1 - - - 1 -
1844 1 - - - 1 -
1845 2 - - - 2 -
1846 1 - - 1 - -
1847 4 - - 4 - -
Total 127 18 8 7 30 64
189
Case 1 is a 3 year old child seen by Allen and described as 'of spare habit of
body with a large abdomen large joints small unshapely limbs head disproportionably
large, with a pustular eruption over the scalp.
2nd day - Febrile symptoms increased with hurried respiration, and small
quick pulse.
3rd day - Pulse small and quick, dry hot skin, tongue furred, cough
accompanied with a glary [sic] expectoration which formed thick dark crusts
on the lips, a wheezing noise in the chest as if the breath was passing through
a fluid, a peculiar motion in the abdomen on inspiration and expiration as if
respiration was carried on in and not in the chest in which latter [sic] there
was very little motion. Comatose.
4th Day - Pulse small and quick. Thirst, will take nothing but water. Skin dry
and shrivelled, difficult respiration, troublesome cough.
5th Day - Great difficulty of breathing; towards evening convulsions set in
accompanied with dilation of the pupils; greatly emaciated; lingered until the
morning of the seventh day when the respiration having become very
laborious died.
Post mortem examination - The lungs and pleura were highly inflamed,
extensive adhesions had formed between them in several places, the parts
were joined together by thick layers of coagulable lymph, there was a
considerable quantity of a serous fluid in the cavity of the thorax. The air
cells [sic] were filled with a glary serum. The diaphragm was also inflamed.
The abdominal viscera were healthy.
Case 2 was a 26 year old male who initially complained of a pain behind the
ear which impaired his hearing. Allen noted an accelerated pulse, disinclination to move
about, a tendency to sleep, a clean tongue, and hot dry skin.
2nd day - Skin cool but dry, pulse not so full but rather quicker than
yesterday, inclination to sleep continues, the pain has shifted half way down
his neck, loss of appetite, tongue furred.
3rd day - Skin dry and hot, pulse small and quick, dry cough, difficult
respiration; the pain has shifted from his neck, it is now down in his chest.
4th day - Much the same as yesterday, cough increased with expectoration of
blood and mucus . Skin hot and rough, continually drinking cold water.
5th day - He seems very much relieved, skin moist, cough much easier, no
blood expectorated, the tendency to sleep has gone off, pulse soft and nearly
natural.
190
6th day - Improving fast. Pulses soft, skin moist, has been smoking this
morning which is a sign of favourable termination.
7th day - Improving rapidly.
8th day - Still improving.
9th day - He got up this morning and walked about and during the course of
the day he eat [sic] a large quantity of kangaroo meat and in the night was
taken ill again.
10th day - Complains of a pain in his left side, cough. Pulse small and quick,
skin dry and hot, considerable difficulty of breathing, prostration of strength.
11th day - The pain in his side still continues, febrile symptoms rather
increased, cough accompanied with a glary expectoration, difficult
respiration.
12th day - The difficulty of breathing much increased, he is now very much
emaciated, feeble quick pulse, dilation of the pupils, coma.
13th day - Greatly agitated, extreme difficulty of breathing, hot dry shrivelled
skin, lips and mouth thickly coated with the expectoration which flows from
his mouth and nose, in the evening he became convulsed and towards
morning he expired.
Post mortem examination - On cutting into the peritoneum a quantity of
serum escaped, the diaphragm and liver were inflamed and adhering firmly
together, on attempting to remove the latter which was indurated an of a dark
colour, it was easily torn. The spleen was indurated and thickly studded with
strumous tubercles. In the thorax - the pleura and pericardium contained a
large quantity of serum, the lungs and pleura were highly inflamed and
several extensive adhesions had formed, a layer of coagulable lymph of
considerable thickness in some places united the pleura which covers the
lungs to the pleura that lines the chest. The lungs were of a dark colour quite
inelastic and very much resembled indurated liver. The air cells were filled
with lymph and pus - there was several small tubercles interspersed through
the substance of the lungs, which contained a clot of hard dark blood, these
tumours were surrounded with a number of small blood vessels containing
dark blood, the heart was healthy.
Acute respiratory diseases were not confined to the epidemic events of
influenza at Wybalenna. Prior to the first recorded pandemic/epidemic event of influenza
in 1836-7, Allen (1837) reported that between 1834 and 1837, he had treated 230 cases of
new, or aggravated pneumonia at the settlement in a population that averaged 140
individuals. Out of the 140 estimated on the settlement, forty of them had not displayed
symptoms of pneumonia. That leaves, according to Allen, one hundred individuals who
191
presented 230 times with cases of pneumonia during the three year period leading up to
the first influenza epidemic. A further indication of the prevalence of severe pneumonia
comes from the records of death in 1835 (Plomley 1987: 941-941). Fourteen deaths were
recorded in that year (Table 5.3), 11 (79%) of which were recorded as due to pneumonia.
Of the remaining three deaths, two were recorded as 'anasurea' and one as phthisis. All
this strongly suggests that pneumonia became an acute and chronic disease among the
Aboriginal inhabitants of Wyballena soon after its establishment in 1831 and prior to the
first recorded epidemic of influenza in the colony (Cumpston 1989; and Table 6.1).
Influenza caused serious morbidity and mortality at the Flinders Island
settlement in 1837 during the course of the 1836-7 pandemic. On 16 January Robinson
reported to the Colonial Secretary that a 'direful epidemic the influenza' had swept
through the settlement. The Europeans were attacked by the virus but it was the
Aboriginal inhabitants who, according to Robinson, were the most severely affected.
There were 29 deaths recorded in the settlement for that year, an unusually high number.
For most no details of death were given, but for three adult females pneumonia was listed
as the cause of death, and four more died of the same causes in the following year
(Plomley 1987: 941).
Surgeon Walsh performed an autopsy on one, an adult female who died in
October 1837. The right lung revealed considerable empyema and the characteristic
consolidation of pneumonia:
On opening up the thorax the pleura was found considerably thickened and
highly vascular... a large quantity of thick brownish fluid spurted out, which
appeared to have occupied the greater part of the cavity... The right lung not
only adhered firmly to the ribs but also to all the neighbouring parts; it was of
a firm and solid consistency its cellular texture being quite obliterated... The
adhesions of the left lung were not extensive and it was on the whole healthy
in appearance (Walsh 1837).
192
A second wave occurred in 1839 when influenza again inflicted a severe
morbidity and mortality among the Wybalenna Aboriginal population (Table 6.3). A
week before his final departure from the settlement Superintendent Robinson wrote of the
epidemic:
I regret exceedingly to state that the influenza has already commenced its
ravages among the aborigines supposed to have been communicated by the
government vessels recently at this station. More than two-thirds of the
natives are now affected, several of whom are not expected to recover. The
aged and infants it is thought will suffer most although the worst cases at
present are among those who are the most hale and robust. This epidemic has
not confined its attacks to the natives, many of the whites being seriously
indisposed, though I do not anticipate any fatal results as regards them
(Plomley 1987: 785).
The two government vessels referred to by Robinson were the Vansittart and
the Eliza. Both vessels had previously been to Hobart where an epidemic of influenza
had been spreading among the European population for some months (Plomley 1987:
785). A second source of introduction may have been Robinson himself. He had
returned from Sydney in January 1839 immediately prior to the Wybalenna epidemic
suffering from influenza (Ryan 1996: 193).
George Robinson jnr., the son of the Commandant of the Flinders Island
settlement, began to record the epidemic among the Aboriginal people on the day his
father left to take up the position of Chief Protector of Aborigines on the mainland at Port
Phillip. The following are extracts from his journal (Robinson jnr. 1839). The first entry
begins on February 24 1839:
The Commandant left the settlement about mid day to proceed to Port Phillip
with several of the Aborigines, and as he proposed walking down to the Old
Settlement Mr Clark with myself accompanied him part of the way thither.
During our walk we met with several of the natives belonging to the
settlement proceeding to some of the others who were staying in the "bush"
with provision as we were informed they were in a bad state of health from
the influenza which had not long visited the settlement.
193
25 February...
The influenza to day shown itself to be very general amongst the natives who
had all or most of them encamped themselves in the "bushes" environing the
settlement.... Several of them were violently attacked with the epidemic.
27 February...
The influenza was spreading itself to a still more alarming extent among
them. The boat arrived near mid-night during a heavy gale of wind with the
sick people from Long Point.
28 February...
The native woman Semiramis died about break o'day. The rest of the natives
returned home from their "breakwinds" this morning, those most affected
with the influenza being brought in the truck by the others.
1 March...
On proceeding as usual to the square early in the morning I was greatly
surprised to hear that two of the natives, Phillip and George Robinson, had
died both about one time during the night.... A native child belonging to Sarah
died this afternoon. One of the native men "Billy" died in the early part of the
night.
2 March...
The natives still dangerously ill.
3 March...
About midday "Sabina" died and in the evening "Jane". Both the females had
been for several days in great suffering from the disease.
4 March...
Interred at the usual hour, viz four o'clock pm, two of the deceased natives
Sabina and "little Billy", and as rather a remarkable occurrence one of the sick
natives Queen Adelaide breathed her last as we were placing the corpses in
the coffins.
By March 6 Robinson jnr. was infected with influenza and soon after he
records the disease striking several members of his family, the staff, and convict labourers
of the settlement. The last reference to the disease in his journal is on March 14 when
Robinson jnr. records that he was still suffering. How long it lingered among the
Aboriginal population is unrecorded but by March 9 Robinson jnr. states that some of the
males had began to recover. According to his journal and the register of births and deaths
for the settlement eight of the Aboriginal people (3 males, 4 females, and a child) died of
influenza during the epidemic (Plomley 1987: 942). The real total is almost certainly
194
much higher as many of the Aboriginal people had no faith in the efficacy of European
medicines, and to escape the sickness, left the major settlement to live in the surrounding
bush during the period of the epidemic. Their suffering was probably made greater by
Robinson jnr. and his staff withdrawing rations, in particular freshly killed mutton, from
the Aboriginal people during their illness:
In consequence of the general prevalence of the present epidemic among the

natives it becomes necessary to restrict them from the use of animal food for
some time. I have therefore to direct that there be no issue of fresh meat
made to them till further notice, but in lieu of which let them have an
additional ration of the tea and sugar for dinner (cited in Plomley 1987: 787).
In August 1847 Wybalenna was abandoned. Two weeks before they left the
settlement the influenza pandemic of 1847-48 reached them. It lasted ten or twelve days
on the settlement and there was one more death reported as a result of the disease
(Plomley 1987: 162). The remaining Aboriginal people, now numbering 47, (original
population in 1831 was 150) were transported back to the Tasmanian mainland to the
Oyster Cove settlement, an abandoned penal station (Ryan 1996: 205), located at the
northern end of D'Entrecasteaux Channel (Figure 6.2).
Living conditions were worse at Oyster Cove than they had been at
Wybalenna (Ryan 1996: 205-212). The station was built on the drainage plains of the
Great Oyster Bay and Little Oyster Bay rivers. The buildings were made of wood which
offered little protection from the cold southerly winds. The floors were mostly damp and
often flooded by excess water draining from the rivers. The station had originally been
built as a probation station and in 1843 used as a penal settlement but by 1847 it had been
abandoned because it did not meet convict health standards (Ryan 1996: 205). James
Bonwick described the station in 1859 as
195
...a miserable collection of huts and outbuildings ... profoundly dirty and
swarming with fleas ... in a ruinous condition, roofs not waterproof, windows
broken and furniture gone (Bonwick 1870: 276-85).
At the Oyster Cove settlement the Aboriginal population continued to suffer a
high level of morbidity principally from acute and chronic respiratory infections.
Mortality was persistently reducing their numbers until by the end of 1861 just two males
and six women remained. There was scant concern shown by the Tasmanian government
towards the Aboriginal people and little commitment was given to basic health care
(Ryan 1996: 205-214). While the Flinders Island settlement was functioning there had
always been a medical practitioner on staff to provide for the needs of the Aboriginal
people, although in the majority of cases he would have been of little use to them. At
Oyster Cove there was no resident doctor despite the well known poor state of health of
the Aboriginal residents (Plomley 1987: 186-7). William Smith, a surgeon from
Kingston, made periodic visits to the settlement between 1858 and 1869, summoned by
the superintendent when emergency cases occurred; and more regular visits were made
when outbreaks of influenza occurred on the settlement, particularly during the winter
months.
During these visits Smith recorded his diagnoses and recommended

treatments of the patients he examined in the settlement's visiting officers' book (Smith
1858-69). They appear in a chronological sequence according to the date of each of his
visits to the settlement but when separated and rearranged into a sequence for each of the
Aboriginal patients they reveal a progression of symptoms for each of the individuals
Smith examined.
Influenza and pneumonia were common diseases throughout the period of

Smith's visits. In the winter of 1860 Smith reported an epidemic of influenza on the
196
settlement with at least 8 of the 15 Aboriginal residents affected as well as the European
superintendent and his family. During the period of the epidemic from July to September
two females and two males died from symptoms suggestive of an infection of influenza
(Smith 1858-69; Plomley 1987: 945). This epidemic was most likely part of the 1857-60
world pandemic which was recorded during 1860 all the colonies of Southeast Australia
(Table 6.1).
I will use two individual cases to depict the recurring morbidity of these
diseases at Oyster Cove. Both cases are adult Aboriginal women whose symptoms were
recorded by Smith over a period of three years in the first case, and seven years in the
second. The previous medical histories of both cases are unknown but both women had
come to the Oyster Cove settlement from Flinders Island in 1847 where influenza,
pneumonia, bronchitis, and tuberculosis were major health problems (see above). It is
quite likely that both women had a long history of tobacco smoking and alcohol
consumption. Pre-existing chronic bronchitis and emphysema may also have been
present in both cases.
The first case is an elderly female, Sophie (Dray.dur.ic), c60 to 70 years of

age. In 1829-30 she was living on Bruny island approximately 50 Km east of Hobart.
She accompanied George Robinson on his first expedition around the island and was later
sent to Flinders Island in September 1833 (Plomley 1987: 798; Ryan 1996: 124, 131).
Smith records:
[23 Sep 1858]

Suffering from flu with swelling of the glands of the neck.
[25 Sep 1858]
Still some swelling of the glands of the neck but in other respects better.
[27 Sep 1858]
Appears much better.
[27 Aug 1860]
197
... affected by the influenza [localised epidemic]. [She] appears to me to be in

a depressed state and the physical powers lower than natural under the
circumstances. I have recommended beer daily with beef tea and mutton
broth and linseed tea as often as [she] can be induced to take it.
[29 Aug 1860]
Sophie not so well, her cough is very troublesome and like many others, the
phlegm appears to accumulate in the air passages. The bowels are much
constipated. I have recommended Croton oil liniment to rub into the chest.
[1 Sep 1860]
Sophie is still complaining of her cough and has some pain in the epigastrium.
The conjunctiva of the eyes have a very yellow tinge.
[5 Sep 1860]
Sophie appeared somewhat better but still complained of cough, the Croton
Oil liniment has produced rather more eruption on the chest.
[21 Aug 1861]
... Sophie suffering from debility.
[25 Aug 1861]
Sophie has been poorly for several days and is apparently suffering from
Bronchitis and general disability being upwards of seventy years old. I have
recommended Brandy and Beer to be given at frequent intervals with as much
Beef Tea as she can be induced to take.
[27 Aug 1861]
Sophie is sitting out having an Airing in the sun which she seems to enjoy
much. Her breathing is still bad and there appears to be much mucus
accumulated in the air passage. She does not take to much nourishment as
she aught.
[29 Aug 1861]
Sophie died early this morning. Probably from exhaustion and the
accumulation of mucus on the air passages (Smith 1858-69).
The second case is an adult woman, Wapperty (or Wobberrertee), c1797-
1867. She was probably a Pyemmairrener born on the Northeast coast of Tasmania.
Little is known of her early life. As an adult she was abducted by sealers and lived on the
Bass Strait islands before being moved to the Flinders Island settlement in 1844 and
thence to Oyster Cove in 1847 (Horton 1994 vol. II: 1149; Plomley 1987: 833; Ryan
1996: 214):
[16 Jul 1860]

Wapperty not so well. Complaining of pain in the chest with cold chills.
[18 Jul 1860]
Wapperty somewhat better and is apparently free from pain.
[21 Jul 1860]
Wapperty more lively.
[14 Jul 1863]
198
Wapperty is suffering from influenza with pain on the left side attended with
some cough. I ordered a mustard plaister [sic] and mixture with taitan emetic
and compound camphor mixture.
[17 Jul 1863]
Wapperty is complaining of pain in the right side with difficult breathing and
symptoms of Bronchitis, to continue the mixture and have the taitan emetic
ointment rubbed into her chest and a blister on her right side.
[19 Jul 1863]
... the pain in the right side has left her, the cough somewhat better but the
tongue coated with thick brown fur. Pulse not so strong, her appetite is not
ample. To take Gin in linseed tea or milk if it be procured.
[21 Jul 1863]
... suffering symptoms of Bronchitis, in other respects better, the brown fur
has left the tongue the bowels are acted upon, she does not sleep very well.
To have Dovers Powder at bedtime in place of Gin, to have bottled porter
with egg and nutmeg.
[23 Jul 1863]
Wapperty is still suffering from Bronchitis. The bowels are regular, appetite
pretty good, breathing somewhat difficult. To continue the mixture and let
her have rum in linseed tea.
[25 Jul 1865]
Wapperty is in many respects better but the cough is still troublesome. The
Tartar Emilie has brought out a slight eruption on the chest, her appetite is
pretty good.
[27 Jul 1865]
Wapperty appears greatly improved and the breathing seems natural. Her
appetite is very good. She is allowed beer daily which is recommended to
continue.
[22 Jul 1865]
Wapperty is complaining of pain in the stomach.
[29 Jul 1865]
... complains of cough.
[24 Jun 1867]
[Wapperty sent to hospital suffering from dysentery]
[29 Jul 1867]
[Wapperty recovered]
[8 Aug 1867]
Wapperty suffering from Catarrh and debility, respiration difficult.
[9 Aug 1867]
Wapperty improved.
[11 Aug 1867]
Wapperty does not appear well, pulse weak and pain.
[12 Aug 1867]
[Wapperty died]
During the periods leading up to their death both women suffered repeatedly
from acute respiratory tract infections. No post mortem examinations were recorded for
these women but the cause of death given for Sophie in the settlement's records was
199
'congestion of the lungs', and for Wapperty 'catarrh debility' (Plomley 1987: 945). While
the official records giving causes of death among Aboriginal residents on settlements can
be vague (Chapter 8) there appears little doubt that the deaths of these two individuals are
closely related to the respiratory disorders they had.
6.4.2 Influenza among the Aboriginal population of Port Phillip, 1839
The 1836-39 influenza world pandemic reached the mainland Aboriginal
population in 1839. In that year the disease caused serious morbidity and mortality
among the European and Aboriginal population of Victoria. The first signs of the disease
began to be noted early in the year and by July and August it reached a peak prevailing
throughout the European population of the colony. In a report to the Royal College of
Physicians, the Deputy Inspector of Hospitals stated that hardly a household had escaped
the disease:
It proved chiefly fatal to infancy and old age; the symptoms of this Complaint
were common Cold, Cough, pains in the forehead, sneezing, Soreness and
Spasms in the Chest, copious discharge of numerous Colours and various
consistencies from the Lungs (McLeod 1830: 375).
The Sub-Protector of Aborigines, William Thomas, had just arrived in
Melbourne and one of his first encounters with Australian Aboriginal people was with the
Boonwurrung and Woiworung on 17th and 18th of January. He noted in his journal:
Saw several blacks. The inhabitants of Melbourne say that they are about
returning to the settlement, having left it on account of the influenza that
prevailed. The natives considered that the whites brought the disorder
(Thomas 1839a).
200
Some four weeks later Thomas noted in his journal that a family group of
four, all suffering from influenza, were the first to come into the settlement for aid
(Thomas 1839).
During February and March 1839 much larger numbers began to arrive in
Melbourne. They came from the outlying regions to the north, south east, and south
west. The reason for their going to the European settlement was seemingly to meet the
newly appointed Chief Protector of Aborigines, George Robinson (Robinson 1839a).
Robinson arrived in Melbourne by the government cutter Vansittart on 27th February and
by this time four hundred Aboriginal people had gathered in a large encampment on the
Yarra River opposite the main European settlement. On the very day of his arrival
Robinson reports he was suddenly attacked with influenza symptoms and was so severely
incapacitated that he was unable to perform his duties for several days (Robinson 1839b).
By the last week in March 1839, five hundred Aboriginal people had gathered
in Melbourne to meet Chief Protector Robinson and his assistants (Robinson 1839b). It
soon became apparent that many were suffering from influenza. Sub-Protector Thomas
reported in his journal that he, in company with Chief Protector Robinson, visited the
Aboriginal encampment on 5th May and found a scene 'truly appalling' (Thomas 1839a).
There was little that Robinson could do. The Protectorate had limited financial reserves
and no medicinal resources of its own to dispense among the Aboriginal communities.
Repeated requests by Robinson for extra financial support were more often than not
denied by Governor Gipps. The protectors could do no more than distribute just four
blankets, which they took from their own beds, among the Aboriginal people who were
sick.
201
On his return to the European settlement Robinson immediately instructed Dr.
P. Cussen, the assistant surgeon for the colony, to go to the encampment and give what
aid he could (Cussen 1839a). Cussen visited the encampment the next day and witnessed
what he called 'a most distressing scene of disease, destitution and misery' (Cussen
1839a). According to his report he found the Aboriginal people displaying the symptoms
of 'dysentery', accompanied with 'typhus fever of the worst description', 'rheumatism', and
in many the symptoms of chronic syphilis. The prevailing influenza epidemic which
Cussen referred to as 'acute catarrh' had already had a serious effect on the group gathered
on the banks of the Yarra River with six of them having died within the four days
preceding Cussen's visit; and many more were expected to die within the next days
(Cussen 1839a).
The Port Phillip Gazette (1839) expressed its serious concern, not particularly
about the well-being of Aboriginal people, but of the threat of influenza being further
disseminated into the European population. It warned its readers that it was well known
that influenza was epidemic and the Aboriginal people should be removed as quickly as
possible. It further advised:
... all mothers to be careful of allowing their children to be taken in the

direction of the native camps, the slightest attack of the influenza is sufficient
to carry off an infant in a few hours ( Port Phillip Gazette 1839)
Across Port Philip Bay the situation was similar among the Wathaurong
(Addis 1839). In August Sub-Protector Sievwright requested Assistant Colonial Surgeon
for the Geelong district, Dr. J. Clerk, to attend an individual who was suffering severely
from influenza with secondary lung complications. Clerk's response succinctly reveals
the plight of the Wathaurong in particular, and the Aboriginal population of the Port
202
Phillip colony in general, as well as the inadequacies of the Protectorate, and helplessness
of the medical establishment to render assistance:
In compliance with your [Sievwright's] request of yesterday, I visited the

native black man and found him dangerously ill with inflammation of the
pleura occasioned by exposure to the cold.
I bled and prescribed for him accordingly but fear that medicine can produce
little effect on him or any of the Aborigines whilst they are suffered to
continue in their present exposed, helpless, and miserable state, destitute
(when sickness attacks them) both of shelter and clothing and other
necessaries for their comforts. It cannot under these circumstances be
supposed that medicine can do much good.... Several to my knowledge this
season have been carried off by inflammation of the chest (Clerk 1839).
By September the epidemic had began to subside among the European
population of Melbourne but was still prevailing among the Aboriginal communities.
Assistant Protector Thomas (1839b) reported to his superior in September that many
Woiworung living along the Yarra River were 'labouring under affections of the chest'.
The number of Aboriginal people at Melbourne began to fall at the end of
April when groups started returning to their homelands. By October 1839 most of the
visitors had left Melbourne and there were less than fifty remaining; the majority of these
were reported to be from the local region (Thomas 1839b).
6.4.3 Influenza and acute respiratory disease among Victorian Aboriginal

populations 1845- 90.
An epidemic of influenza, restricted to the colonies of Victoria (Port Phillip)
and South Australia, occurred between 1844-45. Although its origin is unclear, it was
likely to have been introduced by ship and begun as an infection among the European
populations of the two colonies reaching a level of excessive morbidity towards the end
203
of 1845 (Cumpston 1989:313). Robinson (1845) reported that few families living in
Melbourne escaped infection, and out of a population of 12,000 at least two thirds had
suffered attacks of influenza.
The Aboriginal people, according to Robinson, were the greatest sufferers,
especially those living in the interior of the colony. At the Goulburn River Aboriginal
station morbidity was high among the Taungurong with 'upwards of one hundred'
reported to be affected and at least one death occurring for 1845 (Robinson 1845). A
similar situation occurred among the Gunditjmara at the Mount Rouse Aboriginal station
in the west of the colony. During the last three months of 1845 sixty-five individuals
were treated most of whom presented with 'influenza and diarrhoea with occasional
dysenteric symptoms' (Robinson 1845). No deaths were recorded among those living on
the station.
Cumpston (1989: 313) documents the next pandemic/epidemic of influenza
beginning in November 1851. It prevailed extensively throughout Victoria during the
following three months and continued to exist in other settlements of the continent
throughout 1852 and into 1853. The epidemic coincided with the beginning of the gold
rush period which attracted thousands of seekers from Europe, Asia, and America. As
stated previously the population of Victoria increased three-fold and that of New South
Wales doubled during the ten year period between 1851 and 1861 (Molony 1987: 104).
Few records of the effects of this epidemic upon the Aboriginal population have survived.
The source of much of the early information on the Aboriginal people of Victoria had
ceased when the Aboriginal Protectorate was abolished at the end of 1849. We can,
however, assume with reasonable confidence that the morbidity was severe among
Aboriginal people. The great influx of gold seekers to the newly established gold fields
and with it the pervasion of legal and illegal liquor outlets made it easier for Aboriginal
204
people to obtain alcohol, much of which was of dubious quality. Thomas (1852), the
former Assistant Protector, wrote that:
The present condition of the Aborigines have no way improved but lamentably
deteriorated, the discovery of Gold has greatly affected their moral condition, at all
events those who locate these colonies or make transient visits to them...the
consequence is that their frames are enervated in the absence of regular exercise and
their blood corrupted through continued dissipation, so much so, that when seized
with a violent cold inflammation follows so rapid [sic] that it is impossible in most
cases to save them; the old and middle aged do not die in any proportion to the
young, who, do not live out half of their days.
In 1861, following another pandemic/epidemic of influenza Thomas (1861-
62) reported to the Aboriginal Protection Board on the mortality from respiratory
disorders:
I may state that eight-tenths of the mortality among the aborigines of Victoria
arises through intemperance, bringing on pulmonary disorders, pleurisy,
pneumonia, disorders of the chest, consumption, & c., which carries them off
so speedily that the ablest medical treatment when available seldom save
them. I may safely state, that when their respiratory organs are once affected,
recovery becomes hopeless.
The second half of the nineteenth century saw much of the Aboriginal people
of Southeast Australia centralised on mission and government settlements. Acute
respiratory disorders were regularly reported on all these settlements (Appendix B). A
discussion on the respiratory diseases among the Aboriginal communities on these
settlements between 1876 and 1900 is contained in Chapter Eight which covers Stage III
of the medical model (Table 2.2). It is, however, worthwhile giving a brief outline of
respiratory diseases in the decade leading up to the settlement stage of the model.
Medical reports from the rural settlements of Coranderrk and Lake Condah
reveal respiratory and possible respiratory disorders as recurring causes of morbidity. Dr.
205
L. Gibson made regular and special visits to the Government settlement of Coranderrk
between 1865 and 1875 and reported his diagnoses and treatments to the Aboriginal
Protection Board (Gibson 1869-75). Over the eleven-year period of his visits, Gibson's
medical reports record periods of excessive morbidity from a possible outbreak of
influenza in 1867; whooping cough (pertussis) in 1868; and influenza in 1873 (Table
6.4). The periods of high influenza morbidity were most likely localised outbreaks as
they do not parallel the sequence of pandemics/epidemics of Southeast Australia (Table
6.1).
Gibson diagnosed the epidemic in April and May 1867 as 'intermittent fever',
a common medical term of the day often given to the febrile symptoms of malaria (Farr
1854). It is unlikely, however, that this was the disease causing the symptoms.
Nineteenth century cases of malaria among Aboriginal populations have been restricted to
the north coast of Australia and there is no evidence for appearance of the disease in
Southeast Australia (Basedow 1932: 10; Cleland 1928; Cumpston 1989: 330).
206
Table 6.4 Periods of excessive morbidity from respiratory and possible

respiratory disease on Coranderrk Aboriginal settlement between 1865 & 1875
(Gibson 1869-75).
Date of No. of No. with Percent Remarks
Visit Inmates Respiratory
Disorders
1867
21 Apr. 105 7 6.7 'Intermittent fever'.
Several others recovering.
14 May - 16 - Many leaving due to
epidemic.
8 Aug. 78 5 6.4 'Influenza'.
1868
5 Dec. 74 - - Whooping-cough attacking all
children & most adults.
29 Dec. 65 - - Whooping-cough still
present but incidence abating.
1873
16 Jun. 125 11 8.8 'Influenza'.
26 Jun. 129 13 10.1 Nine children & four adults
infected.
The term 'intermittent fever' together with 'fog fever' were occasionally used
as euphemisms for the various nineteenth century epidemics of influenza (Cumpston
1989: 331). By his November (1867) visit the symptoms had ceased and Gibson
described the general state of health of the settlement as 'good' with just three cases of
illness out of a population of seventy-six. The symptoms presented in both Aboriginal
males and females between two years of age to adults, and the superintendent of the
settlement and his children. In May of that year Gibson administered treatment to 16
(c.12%) of the residents but many others had left the settlement to escape the epidemic.
Against these periods of high morbidity was a backdrop of periodic influenza cases of
lower incidence and severity occurring mainly in the colder months of the year.
Morbidity from respiratory diseases at Lake Condah settlement during the
years 1886 to 1890 was higher than previous years. The superintendent of the settlement,
207
J.H. Stahle reported in 1886 an epidemic of whooping-cough followed two years later by
a severe attack of influenza in the spring and autumn. Initially the epidemic caused only
the confinement of people to their homes but in 1889-90 it became a serious health
problem:
We had several deaths during the first half of the year, and the latter half was
not better as regards the health of the people, for influenza visited the station
and was very severe on the poor blacks, all of whom were attacked and will
probably not feel much better until the warm weather sets in again (Stahle
1890).
The records of mortality from the settlement reveal nine deaths of a total of
twenty-five during the period 1886 to 1890 that could be attributed to infectious
respiratory diseases (Appendix B).
6.4.4 Influenza and acute respiratory disease among South Australian Aboriginal
populations.
The first reliable records of influenza or acute respiratory diseases among the
Aboriginal people of South Australia do not appear until 1850, fourteen years after the
colony of South Australia was established. There is no evidence regarding the effect of
the pandemics of 1838 and 1845-47, nor of the local epidemic of 1845. Little knowledge
of the health of the Kaurna, the Ngarrindjeri and the Peramantgk, the populations closest
to the European settlements is available in this period. In 1844 the Protector of
Aborigines, Dr. Matthew Moorhouse, reported to the Governor of the colony on the state
of the Aboriginal population (Moorhouse 1844: 358). He included a brief account of the
diseases suffered by them, listing venereal diseases and tuberculosis as the main diseases
and concluded that they were:
subject to those [diseases] common to the human race, as inflammation and

its consequences... (Moorhouse 1844: 358).
208
Moorhouse's reference to diseases was vague and whether or not he was making a
reference to influenza epidemics (Cumpston 1989: 313) is uncertain.
By 1850 acute respiratory diseases were becoming a serious source of
morbidity and mortality. In a quarterly report to the Governor, Moorhouse reported on an
epidemic which was most likely influenza with cases of secondary pneumonia:
I regret to have to remark, that the epidemic characterised by inflammation of

the lungs, continues to afflict the natives ... The deaths of three children and
three adults have been recorded by me... I have little doubt that many more
have died in the scrub, whose deaths will remain unknown to me for months,
if not altogether. The aborigines ... appear to have an instinctive knowledge
of the approach of death, and a desire to let the breath of life depart at or
about the place where it was first inhaled (Moorhouse 1850: 611).
In this instance Moorhouse may be referring to a local remnant of the major epidemic of
1847-48 in the eastern colonies.
Beginning in 1843 and continuing into the next decade, a regular migrational
trend developed when the Ngarrindjeri from the lower Murray River and Coorong and the
Meru from the eastern river region of the Colony began to gather in Adelaide (Moorhouse
1843a). They displaced the remnants of the local Kaurna and established encampments
on the banks of the Torrens River with numbers often exceeding seventy or eighty
individuals (Moorhouse 1843b; 1853). They became a common sight to the residents of
Adelaide staying each year for most of the winter months. Exposure to the cold, poor
nutrition, inadequate sanitary conditions, and alcohol abuse made them extremely
susceptible to infectious disease. After several years a concerned citizen wrote to the
South Australian Register:
It is painful to every one who comes into contact with the natives to witness
the dreadful colds with which they are nearly all afflicted in such a winter as
the present. The severity of such complaints among them is no doubt chiefly
owing to the want of shelter from the inclemency of the weather. Would it be
209
too much for our Government to provide them, out of our abundance, with a
building which would afford them some more substantial shelter than their
wretched "wurlies"? Their rude wants would require nothing elegant or costly
(South Australian Register 1855).
In 1852 the gold rush in the eastern colonies created a shortage of European
labour on the rural properties and Aboriginal people were required by the settlers to assist
with the crops. As a consequence, many of the Ngarrindjeri and Meru moved to the
agricultural districts where good wages and ample food supplies were offered for their
labour. A much larger number than usual came to the city late in the year. Moorhouse
reported:
In November, the City of Adelaide was visited by upwards of three hundred

natives; Encounter Bay, Lake Alexandrina, and Murray River tribes, all met
by appointment. The Lake Alexandrina tribe undertook to reap about ninety
acres of crop... They would have done more, but the influenza was raging at
the time, and the whole becoming more or less affected by it, ceased their
reaping, and returned to their own district (Moorhouse 1853b)
The influenza epidemic had already reached the Ngarrindjeri before their
arrival in Adelaide. Sub-Protector Mason reported to Moorhouse in July 1852 from
Wellington on the lower Murray:
I am sorry to report that a great amount of sickness prevails among the natives
at the present time, many are suffering from complaints of the chest, and
rheumatism. In such cases of sickness amongst them, they are generally
treated with kindness by the settlers (Moorhouse 1852).
West of Adelaide on Eyre Peninsula, the Nawu who occupied most of the
south and west of the peninsula were suffering the effects of the epidemic in 1852 and
1853. Archdeacon Hale informed Moorhouse:
In reporting upon the state of this Institution for the past four months, the
subject which, on account of its importance first demands our attention, is the
great extent to which sickness and mortality have prevailed amongst the
inmates during this period (Moorhouse 1853b).
210
It is not clear from Hale's report what the cause of the mortality was but a
later report by him, which includes a brief autopsy report, alludes to an epidemic of acute
respiratory disease:
I am again under the necessity of referring ... to the frequent instances of

mortality amongst our inmates. We had no less than three deaths since he
date of my last report. In the last case a post mortem examination was made
by our medical attendant, Dr. Lawson. He found the lungs to be extensively
diseased; one lobe having a very large ulcer upon it and the other lobe being
in a highly inflamed state (Adelaide Observer 1853)
The pandemic of 1850-52 affected the colonies of New South Wales and
Victoria (Table 6.1) but appears not to have influenced the morbidity or mortality of the
South Australian colonists. The origin of the above outbreak of influenza among the
Ngarrindjeri and Meru living in Adelaide is then somewhat of a mystery. The best way to
account for it is to assume that there was a low level of prevalence for the disease among
the colonial population of Adelaide and the disease was transferred to the Aboriginal
people where it developed a more serious morbidity.
Between the pandemic/epidemic events of 1852-53 and 1885 localised
epidemics of influenza and respiratory disease recurred among the Aboriginal

communities of South Australia. Acute respiratory disease continued to be a cause of
high morbidity and mortality among the Nawu living both on and off the Poonindie
settlement. In 1857, Octavius Hammond, a qualified medical practitioner, who succeeded
Hale as superintendent reported that 'bronchitis' and 'pleurisy' were among the most
commonly developed diseases (Hammond 1857). He observed the severe effects of the
disease in the rapid onset of symptoms and little resistance offered by the patients. He
further stated:
211
While speaking on this subject, however, it should be borne in mind, that

there has existed a similar state of disease and death among the natives in the
bush, in this neighbourhood, in a proportion, probably equal to that
experienced at Poonindie (Hammond 1857).
The 1860 pandemic saw the return of influenza universally across Southeast
Australia. It was reported to be causing excessive morbidity and mortality, this time
mainly among the Ngarrindjeri. George Taplin, from the Point McLeay settlement,
informed the Aborigine's Friends Association that:
The suffering of the natives from cold have been very great. The country
from which they used to get their opossum-skins for rugs being nearly taken
up, they are dependent on blankets for protection from cold. But it
unfortunately happens that the blankets supplied by Government are not
distributed when winter sets in. Had this been done, many who have this
winter fallen victims to influenza might have survived (Taplin 1868).
The excessive morbidity and mortality among the Ngarrindjeri, implied by
Taplin, was observed by an anonymous settler living on the Coorong. He informed the
Weekly Chronicle that 'a great many died from the influenza', during the winter months of
1860, 'generally brought on from being warmly clad one day and being in a state of nudity
the next' (South Australian Weekly Chronicle 1861)
By the mid 1860s respiratory disease among the Aboriginal people of South
Australia was common and wide-spread. Reports of morbidity and mortality from
respiratory infections in between the influenza epidemics of 1860 and 1885 come from
several observers: Sub-Protector Buttfield noticed 'catarrhal affection' among Narangga
on northern Yorke Peninsula in July 1866 (Buttfield 1866). Elderly Narangga suffering
from acute respiratory disease would regularly go to the Point Pearce settlement to obtain
treatment, and after many deaths from 'inflammation of the lungs' on the mission, several,
212
children were taken by their parents to live away from the settlement and avoid the
continuing infection (Scott 1867). George Taplin noted among the inmates of Point
McLeay in 1868 that, 'We have lost that very troublesome visitor the hooping [sic] cough
which only carried off three or four children altho [sic] so many suffered with it' (Taplin
1868). In 1878 Hamilton reported that the Aboriginal people throughout the colony were
'exceedingly susceptible to colds, which often settle on their lungs (Hamilton 1879). The
South Australian Government Gazette (1875, 1879) listed respiratory diseases (influenza,
whooping cough, and 'inflammation of the lungs') as the highest cause of mortality after
tuberculosis in the official returns of the causes of death in 1875 and 1879. The returns of
sick Aboriginal people under treatment in the Adelaide Hospital and among the Buandig
in the south east of the colony during 1874-76 show recurring cases of bronchitis,
pneumonia, influenza, catarrh, and 'pleuritis' (South Australian Government Gazette
1874, 1875, 1876).
In 1874-76 acute respiratory diseases inflicted excessive morbidity and
mortality. The respiratory infections accompanied a major epidemic of measles which
spread throughout Southeast Australia (See Chapter Seven). Sub-Protector Hamilton
reported a 'great deal of sickness' among the Ngarrindjeri on the south coast in February
1874; chiefly influenza accompanied by scarlet fever and rheumatism. In the north of the
colony Buttfield (1874) reported high morbidity, though few deaths, from influenza.
While acute respiratory diseases were becoming established in the settled
southern and western regions of the colony, a localised epidemic began among the
Aboriginal populations in the north. A boom in colonial expansion in South Australia
began in 1869 into areas specially selected for their suitability to cultivation (Williams
1969: 26). The spread of settlement north along the Flinders Ranges brought the
Europeans into closer contact with the Banggarla, Kuyani, and Adnyamathanha. In May
213
and June of 1870 unusual heavy rainfall fell along the Flinders Ranges. In a six week
period the rainfall was measured at ten inches (250 mm), almost the average annual
amount. Sub-Protector Buttfield, responsible to the Commissioner of Crown lands for the
welfare of the Aboriginal people in the Northern Districts, recorded an epidemic of what
was most likely influenza among the Kuyani and Adnyamathanha around Blinman in
June:
Owing to the heavy rainfall ... travelling has been quite impracticable during
the month of May. My time has, however, been fully occupied for the cold
and wet has increase the number of patients. Coughs, colds, sore throats have
been very prevalent. I have three cases under treatment of a more serious
nature - haemoorhage [sic] of the lungs (Buttfield 1870a).
The three 'haemoorhage' cases may have been pulmonary tuberculosis.
Buttfield had been confined to the settlement and ration station at Blinman
during the rains and had little or no contact with the people living away from Blinman
and was unable to report on their condition. Two months later, however, another report
by Buttfield reveals that the morbidity from respiratory diseases had increased:
Owing to the extreme inclemency of the weather my sick list was

considerably augmented during June. The Aborigines suffering from Catarrh
and other disorders. Scarcely a day passed without bringing some poor
creature seeking for relief (Buttfield 1870b).
By the end of the year the epidemic had waned and Buttfield reported in May
1871 that 'there has been less sickness during the past three months than at any similar
period during my residence here' (Buttfield 1871a). During the remainder of 1871
Buttfield visited an area of the Flinders Ranges to the north and east of Blinman and had
found the people in a satisfactory condition with only a few cases of sickness (Buttfield
1871b; 1872).
214
The continuing trend of improving health and the drop in morbidity from
respiratory diseases reflected in Buttfield's reports was attributed to the high rainfall in
1870. Buttfield (1871b) reported that the rain had promoted growth of plant and animal
food sources which had enabled the people to move away from the European settlements
and ration depots into the countryside. This in turn might have helped them to throw off
some of the less serious infections, and while being dispersed and not living in crowded
damp conditions near colonial settlements, enabled them to avoid further infection.
In 1885 the disease was again reported in the northern regions of the colony,
this time among the Dieri. It claimed several living on the Killalpaninna Mission
settlement and an unknown number living in the Lake Eyre and Coopers Creek region
(Stevens 1994: 112).
Of the remaining nineteenth century influenza epidemics the most serious was
the one that appeared in the last decade. It was reported to have come from Melbourne in
March 1890 (Cumpston 1989: 331) and spread rapidly in all directions when it reached
Adelaide. Forty-eight deaths from influenza were registered among the 320,000
European population of the colony during the 1890 epidemic. The epidemic may have
lingered among the Aboriginal populations in the north of the colony until 1893. Sub-
protector Beasley (1893) reported influenza spreading among the populations following
along the Transcontinental railway line to the Coopers Creek region, and among the
Banggarla and Nukunu north-west of Port Augusta. The extent of morbidity and
mortality from the disease is unknown as most cases were not seen by the sub-protector
and most deaths went unreported.
215
It should be noted that Aboriginal populations continued to suffer high
morbidity and mortality form influenza epidemics elsewhere in Australia and into the
twentieth century. The most severe episode was the 1918-1919 Spanish Influenza
pandemic. This pandemic cause 12,167 recorded deaths in Australia. In Queensland
1,030 died of which 315 (30.6%) were Aboriginal (Briscoe 1996: 1). The real figure is
almost certainly much higher than this because many Aboriginal deaths, particularly in
isolated regions, went unrecorded (Briscoe 1996: 7-9). Because few records of
Aboriginal deaths were taken little is known of the impact of the pandemic on Aboriginal
populations elsewhere although high morbidity and mortality would be expected. More
than 60 years after the pandemic it was still remembered by Aboriginal groups. In 1982
Professor McBryde was shown an area of sand dunes south of Lake Eyre by an Arabana
elder, who knew it as a place where many of his people who had died 'of the `flu' in 1918
and 1919 were buried (McBryde pers. com.).
6. 5 Discussion
The introduction into colonial Australia of pathogens causing acute
respiratory diseases had a long-lasting and severe effect upon the Aboriginal population
of the continent. The first recorded cases of influenza reaching the Aboriginal people of
Southeast Australia are in 1820 during the period of the first pandemic to reach Australia.
Was this then the first appearance of transcontinental respiratory disease to involve the
Australian Aboriginal population?
Although we cannot be entirely certain that there were no outbreaks of
influenza in Southeast Australia prior to 1820 (for example there is no record of the 1800
world pandemic reaching Australia) its apparent absence during the initial years of
colonial settlement can be accounted for epidemiologically (Young 1979: 207). The
216
colony of New South Wales was isolated geographically and temporally from the major
Old World sources of infection. Outbreaks of influenza, which were common enough
aboard ships leaving from England, often flared up in the initial days following departure
but in most cases were self limiting, failing to survive the long sea journey to Australia
(Cumpston 1919). Even after calling in to ports where influenza was endemic en-route to
the colony, the disease often burnt out before arrival at Sydney (Cumpston 1919). If the
disease did persist onboard and was to reach the colony its progress would then have been
impeded by the small and dispersed nature of the settlements in New South Wales, and
the low proportion of susceptible children in the colony's population (Curson 1985: 9).
Nevertheless, infections of influenza may have resulted prior to 1820, but if they did they
were most likely to have been localised and self-limiting and so of minor impact on the
colony in general.
A similar set of epidemiological circumstances applies to the Aboriginal
people. Prior to 1820 many Aboriginal populations living along the south-eastern and
southern coast had had contact with the sealing and whaling fleets as early as 1798.
Large-scale commercial sealing operations quickly developed, particularly among the
Bass Strait islands and the southern coastline. Kidnapping of women by the sealers for
sexual purposes and to assist in the capturing of seals was a common practice which
lasted into the 1840s when the industry declined (Ryan 1996: 66-72). There are no
records from this period of influenza, or any other respiratory diseases, affecting the
Aboriginal people who came into contact with the sealers (and perhaps little reason to
expect such documentary evidence as many of the sealers were illiterate and those who
did leave diaries were more concerned with the commercial aspects of the industry and
had little concern about the health of the Aboriginal people). Nevertheless, the means and
opportunity of passing on influenza did exist with contact between the Ngarrindjeri and
217
the sealing ships (for example I have discussed the likelihood of venereal disease being
introduced to the Ngarrindjeri this way).
The pandemics/epidemics of influenza occurring among the European
colonies of Southeast Australia were largely paralleled among Aboriginal communities.
Table 6.5 shows the temporal relationship of periods of excessive morbidity and mortality
from influenza and secondary respiratory infections among Aboriginal communities and
their relationship with world pandemics and localised epidemics among the European
population. The six nineteenth century influenza pandemics that reached Australia all
had an effect upon Aboriginal communities of Southeast Australia. Preceding the first
pandemic and following the second and fifth were four localised epidemics that spread
through the European communities and into the Aboriginal communities. This table does
not, however, detail the full extent of influenza throughout the Aboriginal communities in
each of the colonies. There can be few doubts that many of the outbreaks either went
unrecorded or those recorded events have not survived or are not included in historical
archives. Nevertheless, what evidence is available shows a strong correlation between
pandemics of influenza and outbreaks among Aboriginal communities.
218
Table 6.5 Evidence of influenza epidemics among Aboriginal populations in Southeast Australia
showing their relationship to Pandemics and localised epidemics.
Year Pandemic/epidemic Colony/region Remarks

1820 localised epidemic New South Wales Probable high morbidity &
mortality
1826 localised epidemic New South Wales Effect unknown
1831 Pandemic Gun Carriage Is. (Tas)
1836-38 Pandemic Victoria, Flinders Is. High morbidity & mortality;
acute respiratory diseases
common on Flinders Is.
1845 localised epidemic Victoria, South Australia? High morbidity & mortality;
acute respiratory diseases
becoming established
1847 Pandemic Flinders Is., Oyster Cove High morbidity & mortality
(Tas);
1852 Pandemic Victoria, South Australia High morbidity & mortality
1860 Pandemic Oyster Cove (Tas), South High morbidity & mortality
Australia
1870 Localised epidemic Northern South Australia High morbidity & mortality
1874-76 Pandemic Northern South Australia High morbidity & mortality
1890-91 Pandemic Northern South Australia High morbidity & mortality
Little can be said of the first recorded influenza epidemics in the 1820s. From
the handful of extant records it can be assumed with some confidence that influenza
reached the Aboriginal people in Southeast Australia during the 1820 pandemic. The full
epidemiological impact and spatial diffusion of this epidemic is, however, unknown. It
went largely unrecorded among both the European population of eastern Australia and the
Aboriginal populations of the southeast region. Many of the Aboriginal populations who
would have suffered the impact of the disease were beyond the colonial frontiers and so
beyond the cognizance of the colonists. The description of the clinical symptoms of this
disease, its selective and sometimes swift mortality, and the wide-spread morbidity that is
inferred by the few recorders is consistent with those of an epidemic of influenza or
influenza-like disease in a population not previously exposed to the virus (Cook 1973,
1992; Carlson et al. 1992; Dobyns 1983, 1992; Guerra 1988; Lange 1984; Marshall 1993;
McArthur 1967; McNeill 1976:195; Walker & Johnson 1992:131-133).
219
Influenza probably became endemic among the Aboriginal populations of
Tasmania sometime in the 1830s and on mainland Southeast Australia between the
decades 1840 and 1850. This period saw four pandemics reach Australia and at least one
localised epidemic in the southern colonies. The 1836-38 pandemic began the
establishment of influenza. This epidemic shows a pattern of first establishing a foothold
among European colonists before spreading to Aboriginal people living in the immediate
vicinity of the main colonial settlements and then possibly spreading out into the inland
populations. It was first recorded in Sydney during October and November 1836 where
the fatality among European hospital cases was 14.3% (Cumpston 1989: 313). It then
moved south to Tasmania (Van Diemens Land) and Port Phillip probably by sea.
Cumpston (1989: 313) states that the epidemic reached South Australia in 1838. There is,
however, no evidence of it crossing to the Kaurna from the settlement of Adelaide until
some eight years after the colony had been established.
The Woiworung, Boonwurrung, Taungurong, and the Wathaurong in the
districts surrounding the Port Philip settlement were the first Aboriginal people to suffer
the effects of influenza in the newly established Victorian colony. The large and
conspicuous gatherings on the Yarra River which began in February and March 1839 had
been unwelcome to the Government and by the European community as a whole. Their
meeting with Chief Protector Robinson and his sub-protectors achieved little in the way
of conciliation, and misunderstanding between the two cultures continued. For the large
assemblage gathered together in such numbers on the edge of a European settlement,
itself battling a severe epidemic of influenza, the meeting had other serious consequences.
Many of them were infected by influenza and an unknown number of them died. While
the number of deaths cannot be calculated, it is reasonable to assume that there was a
substantial mortality from influenza among them while they were in Melbourne. Their
situation there was worsened by the unavailability of the natural food resources of the
220
region which had been present in pre-European times but was now either severely
depleted or denied to them by European land-holders. Possibly adding further to their
susceptibility to influenza was the high prevalence of chronic and severe syphilis
symptoms which affected both sexes and all ages. Severely suppressed immune systems
could not function efficiently to adequately counter the invasion of the influenza virus.
Many of those who were among the first groups to leave Melbourne were in
all probability still suffering from influenza and were contagious. Did they then take the
infection back with them to their own homelands and further disseminate the disease? If
influenza did indeed spread among the Aboriginal people living inland and far away from
the main settlement of Melbourne, it went unrecorded and we have no knowledge of its
impact. It would appear, however, that by the early 1840s it was absent among
populations living away from the main European settlements. Chief Protector Robinson
made extensive tours of the central and western districts of the colony in 1840 and 1841,
contacting large groups of Aboriginal people (Presland 1977a, 1977b, 1980). He saw
several with possible syphilis but makes no mention of active cases of influenza.
Although he noted a sharp decline in numbers among some of the Aboriginal populations
he considered it to have been from a disease or diseases which had occurred 'about the
time when the first white men came', probably in 1834 (Presland 1977b: 48). Dr. Watton,
who was in charge of the Mount Rouse Aboriginal station in western Victoria, records no
occurrence of influenza or pneumonia among the Gunditjmara or surrounding populations
between January and November 1840 (Watton 1840). In 1842 Watton examined thirty-
three patients between October and December and found only one, a thirty-year old male,
suffering from a respiratory disorder which he diagnosed as bronchitis (Watton 1842).
Again in 1842 Campbell, the medical officer for the Goulburn River region, stated in his
monthly report of the Aboriginal station that 'very few cases [of disease] of any
importance had occurred among the Aborigines' (Campbell 1842). Two years later, in his
221
1844 annual report for the Loddon River Aboriginal Station, Sub-Protector Parker made
no reference to influenza or the state of health of the Jardwadjali under his supervision. A
total of 316 people had visited his station during that year with an average daily presence
of sixty-two (Parker 1845).
The lack of documentation on influenza among the inland populations of
Southeast Australia until 1845 should not be seen as evidence for its total absence. The
highly contagious nature of the disease and a period of communicability ranging from
three to seven days makes influenza an efficient traveller among humans moving from
one place to another. There is then a high chance that it accompanied the many infected
Aboriginal people leaving Melbourne to their homelands and disseminated further. The
documentation does, however, suggest that if the epidemic did disseminate inland of
Melbourne it had burnt itself out by 1840.
Soon after the colony of South Australia was proclaimed in August 1836 a
pandemic of influenza was swept through the eastern colonies. Nothing is known of its
impact on the Kaurna living along the coastal plains of Gulf St. Vincent. The initial
founding colonists had come by sea from Britain and had no contact with the eastern
colonies, so in all probability were free of the disease when they arrived. Cumpston
(1989) and Warburton (1973) record local epidemics of influenza among the colonists in
1838, two years after the settlement and later in 1844-45. The reference by Moorhouse
(1844: 358) to 'inflammation and its consequences' coincides with the second outbreak
and may be the first evidence of acute respiratory disease among the Aboriginal people of
South Australia. There is, however, no evidence that the epidemic inflicted the excessive
morbidity which it had done among the Aboriginal people of the Port Phillip Colony. A
clearer picture emerges during the 1850s. Social conditions arising from contact with
European colonists would have aided the dissemination of influenza. Large groups of
222
Ngarrindjeri and Meru were annually moving out of their homelands to live in temporary
camps along the banks of the Torrens River in Adelaide. Moorhouse (1854) estimated a
group of over seventy, mainly Meru, in July 1854. They usually arrived in Adelaide at the
beginning of winter and departed in the spring. By spending the winter months in
Adelaide the Ngarrindjeri and Meru faced serious hazards that affected their health,
impaired the function of immune responses, and increased their susceptibility to acute
respiratory diseases. Alcohol and tobacco became newly desired commodities and each
was readily obtained from the European community by cash payment to the publicans or
by the prostitution of women. Addiction to both drugs, particularly alcohol, was
widespread (Moorhouse 1854).
Little food was available to those in the encampments and the level of
nutrition was poor. Although the government later set up food and ration depots away
from Adelaide, very little was done in the way of supplying food to the encampments.
The colonial government was put under pressure by residents of Adelaide to remove the
groups from the Torrens and from the township. In their daily travel from one part of the
township to another, the residents of Adelaide came face to face with the disease and
squalor of the encampments and were often confronted by Ngarrindjeri or Meru men
demanding money or women soliciting for alcohol, tobacco, or tea (Dowling 1990: 173-
176; Summers 1986: 295-296). The epidemiological effects of these regular visits to
Adelaide for the Ngarrindjeri and Meru was an annual exposure to respiratory infections
which they often took with them when they left Adelaide and returned to their homelands.
Influenza infections became an annual experience for them often having fatal results.
Influenza infection reached the populations west and north of Adelaide
through the process of colonial expansion. During the 1850s and 1860s influenza was
recorded among the Nawu and Banggarla of Eyre Peninsula and the Narangga of Yorke
223
Peninsula. Later during the 1870s as the colonial frontiers were pushing further north the
Kuyani and Adnyamathanha in the mid-north regions became exposed. The construction
of a railway line linking Peterborough on the edge of the wheat-lands to the mines at
Broken Hill took influenza further to the north and west to infect the Dieri and
Yawarawarka in 1891.
In many cases influenza reached into Aboriginal populations that had already
been exposed to foreign pathogens and whose social structures were beginning to feel the
impact from British colonisation. Aboriginal people already, immunologically
compromised with acute chronic diseases, particularly syphilis and tuberculosis would
have had suppressed immune systems further weakened by nutritional deficiencies
experienced as a result of colonisation. They would have been highly susceptible to
influenza, particularly at the times when the disease became epidemic and would have
had little resistance to the progress of the disease leading to secondary bacterial
pneumonia. In turn, pneumonia, often as a secondary complication of influenza, became
a major morbidity and mortality problem. Among the Aboriginal people living at
Wybalenna on Flinders Island and later at Oyster Cove on mainland Tasmania, respiratory
disease displayed a long standing chronicity in some and in others it severe manifestations
that lead to death within 3 weeks (Plomley 1987:915-942; Smith 1858-69).
The morbidity pattern of respiratory disease, changed from initial epidemics
of influenza and pneumonia with few infections between epidemic periods, to a
background of infection particularly on sedentary populations, interspersed with
epidemics affecting both the Aboriginal and the European populations.
6.6 Conclusion
224
The history and pattern of epidemics of influenza among the European
population in Australia has paralleled that of the northern hemisphere. Influenza
outbreaks among the Aboriginal population paralleled that of the rest of the Australian
population. Documentation of the severity of influenza among the Aboriginal population
for most of the pandemics that reached Southeast Australia in the nineteenth century is
missing, and little more can be said about them other than that the morbidity and
mortality was severe in each case; probably equal to, or more than that among the non-
Aboriginal population. The epidemics of 1839 and 1847 were notably severe, particularly
in 1839 among the Tasmanians incarcerated on Flinders Island and among the
populations in southern and central Victoria.
The documentary evidence reveals that Aboriginal populations suffered
excessive morbidity and mortality when initially exposed to the influenza virus. The
changing style of life in residential communities such as the large gatherings in
Melbourne and Adelaide, and the incarceration of Tasmanians on Flinders Island and at
Oyster Cove favoured the spread of respiratory diseases. Infection rates by the influenza
virus increased and facilitated a rapid build-up of case-to-case transmission which
resulted in explosive epidemics and a persistence of virus between major outbreaks.
By the 1850s the pattern of acute respiratory disease, particularly influenza
and pneumonia as endemic diseases had become established in the Aboriginal
populations of Southeast Australia. The diseases were regularly reported by medical and
non-medical observers during inter-pandemic periods. While there were epidemic years
with excessive morbidity and mortality, influenza and secondary respiratory
complications became ever-present. It would probably be correct to state that every year,
since its first introduction into Aboriginal populations, could be termed an influenza year.
225
CHAPTER SEVEN
Measles
7.1 Introduction
This chapter discusses the final of the major epidemic diseases responsible for
excessive morbidity and mortality among the Aboriginal people of Southeast Australia
during the nineteenth century. Like smallpox, measles has been one of the most
devastating of the transoceanic diseases; it became a major cause of 'demographic
disasters' in virgin soil populations throughout the world (McNeill 1976: 194). During
the European colonial expansion into the western hemisphere and Pacific beginning in the
sixteenth century, measles was responsible for excessive mortality among the Native
Americans (Boyd 1990: 138; Cook 1973; Crosby 1972; Dobyns 1983; Reff 1992; Stodder
& Martin 1992), and the Pacific Islanders (Cliff & Haggett 1985; McArthur 1967).
McNeill (1976: 194) states that when measles swept through Mexico and Peru in 1530-
31:
Deaths were frequent, as is to be expected when such a disease encounters a

virgin soil population dense enough to keep the chain of infection going.
Four centuries later measles reached the Fijian Islands. During the first four
to six months of 1875 it was estimated to have killed between 27,000 to 40,000 people
comprising 20 to 30% of the population (Cliff & Haggett 1985: 35). Earlier, in 1848,
measles killed 40,000 (c.26% of the population) in Hawaii (Kim-Farley 1993: 874).
From the early 1830s when the first measles outbreaks were recorded in
Australia, the disease occurred in regular epidemic events throughout the nineteenth
century among the European population (Cumpston 1989: 305). Focusing on stage II
Measles
(early contact and diffusion) of the medical model (Table 2.1) the historical evidence for
measles in the Aboriginal population of Southeast Australia will be examined.
7.2 Biology of Measles

Measles is a highly communicable, common, and acute systemic disease,
principally of children. It is caused by the rubeola virus which today has a world wide
distribution. Humans are the only reservoir for the virus, which means that a continual
chain of infection must be maintained for the disease to spread and the virus to remain
within a population. The virus is spread by contact with secretions from the nose and
throat by airborne droplets or by direct contact with an infected individual. The virus can
also be transmitted by contaminated articles such as clothing and blankets.
Measles commonly presents an initial fever followed by Koplik's spots on the
buccul mucosa combined with a dry cough, coryza, and conjunctivitis. A second
exanthematous phase is characterized by a spreading maculopapular rash beginning
behind the ears and continuing down the face and body, reaching the feet in 2 to 3 days.
The period of infectivity is from two days before the onset of the prodromal phase of the
disease to four days after the appearance of the rash. The disease is usually benign and
self-limiting in children but can have serious effects in the immunosuppressed, where
nutrition and hygiene tend to be poor, and where there is a lack of supportive care. Post
measles pneumonia (caused by the virus or by secondary bacterial infection), encephalitis,
and otitis media causing deafness can occur as secondary symptoms, particularly during
epidemics. Severe diarrhoea can follow as a complication of measles infection, and is
often the main cause of measles-associated mortality (Benenson 1990: 269-271; Kim-
Farley 1993: 873; Merlin et al. 1994: 342-343; Morley 1980: 121-126).
226
Measles
7.3 Measles among the European population of Southeast Australia
Table 7.1 lists the occurrences of recorded measles epidemics among the
European population in the colonies of Southeast Australia during the nineteenth century.
Table 7.1 Nineteenth century epidemic years of

measles in the European population of Southeast
Australia by colonies (Cumpston 1989; Donovan
1970).
N.S.W. Vic. Tas. S.A.

1834 - 1835 -
- 1853-54 1854 -
1860 1860 1861 1861-62
1867 1866-67 - 1868
1874-75 1874-75 1874-75 1875
1880-81 1880 1881 1881
1883-84 1884 1885 1884
1888 - - -
1893 1893 1893 1893
1898 1898 1898 1898
The date of first entry of measles into Australia is not entirely clear.
Cumpston (1989: 305) states that measles was unknown in the colonies until 1842 when
two deaths were reported in Tasmania But a disease resembling measles had previously
been reported in the Illawarra district, south of Sydney in 1832. According to Donovan
(1970: 5) measles was first introduced into New South Wales by infectious patients
arriving in Sydney on board the David Scott in October 1834. It was diagnosed by
military surgeons when an epidemic broke out in Sydney and the outlying areas. Measles
was further diagnosed in Tasmania during January 1835 where it also became epidemic.
The same disease was most likely carried to the South Island of New Zealand resulting in
the first epidemic among the Maoris (Curson 1985: 13-14; Donovan 1970: 5-10).
227
Measles
Measles was a common traveller aboard ships departing Britain, particularly
amongst small children. The arrival of large numbers of free immigrant families to
Australia after 1838 increased the presence of measles among the Sydney population
(Curson 1985: 14) and the other colonies. It became established when it was reintroduced
into Victoria by the ship Persian in 1850 becoming epidemic there and in Tasmania in
1853-54. The disease reached New South Wales in 1853, and South Australia in 1859.
From then regular epidemics occurred among the colonies interspersed with years of low
incidence.
Table 7.2 shows the official mortality figures from measles for the two major
epidemics in Victoria and South Australia in 1874-75 and 1893.
Table 7.2 Mortality from major epidemics of measles in European

population of Victoria and South Australia 1874-75 & 1893 (Statistical
Register of Victoria 1876, 1894; Statistical Register of South Australia
1876, 1894)
Year Measles Total deaths %

deaths
Victoria
1874 256 12222 2.1
1875 1541 15287 10.1
1893 659 16508 4.0
South Australia
1874 280 3434 8.2
1875 75 4136 1.8
1893 261 4520 5.8
The most severe mortality occurred in the epidemic of 1874-75. It affected all
the colonies in Southeast Australia (Cumpston 1989: 305) and was carried by seas from
Sydney to Fiji (Cliff & Haggett 1985). It is not known exactly when measles became truly
228
Measles
endemic in Australia (the nineteenth century epidemics may well have been
reintroductions of the pathogen); but the regularity of the epidemics since 1875 (Table
7.1) fit the well established pattern of measles in a population able to sustain its
endemicity.
7.4 Measles among the Aboriginal population - source material
There are few historical accounts of measles among the Aboriginal people for
the first half of the nineteenth century. The first record of the disease among the
Aboriginal population is from the Reverend Threlkeld at Lake Macquarie Mission
(Newcastle) in 1835. Its origin was most likely the 1834 outbreak in Sydney. In his
Annual Report the Reverend Threlkeld (1835) commented on its presence:
During the present year the Measles have been very prevalent among the
Aborigines, and have carried off many of the natives, from whom Mrs.
Threlkeld and our nine children caught the complaint and were laid up at one
time.
The epidemic was not confined to the Aboriginal people living on the
settlement. Threlkeld's report alludes to high mortality from measles and respiratory
disorders causing extreme mortality among inland populations, probably the Biripi,
Worimi, and Geawegal:
...the Measles, the Hooping cough, and the Influenza, have stretched the
Black victims in hundreds on the earth, until, in some places, scarcely a Tribe
can be found. Of one large Tribe in the Interior, four years since, there were
164 persons, there are now only three individuals alive.
Threlkeld's observations of population loss following the measles epidemic
are supported by official returns of Aboriginal people enumerated at annual distributions

of Government issued blankets. Table 7.3 shows a sharp fall of 511 (24%) in the
229
Measles
enumerated population of the settled districts of New South Wales between 1835 and
1837.
Table 7.3 Official returns of estimated number of Aboriginal people in

the settled districts of New South Wales between 1835 and 1837
enumerated during government blanket distributions.
Year Male Female Total % Decrease

1835 1195 898 2093
1836 952 630 1582 24.4
1837 930 601 1531 3.2
From Threlkeld's report it is unclear whether measles or influenza was the
main cause of mortality. However, in January 1836 Charles Darwin, on the return voyage
of H.M.S. Beagle, visited the colony of New South Wales and travelled inland into the
Great Dividing Range as far as Bathurst. He commented on the mortality of measles
among the Aboriginal population:
This decrease no doubt, must be partly owing to the introduction of spirits, to

European diseases (even the milder ones of which, such as the measles, prove
very destructive (Darwin 1889: 520)
Threlkeld's missionary attempts had to be eventually abandoned due to the
steadily falling population in the district, and by 1841 the mission closed. While neither
measles, nor indeed whooping cough and influenza, can be held entirely responsible for
such a population loss (Aboriginal deaths had also resulted from acts of aggression by
European colonists) it was probably a major factor. Threlkeld (1835) was of the opinion
that many had died from the 'Act of God' during the measles epidemic.
The 1853-4 epidemic was restricted mainly to Victoria and Tasmania and
little is known of its effects on Aboriginal populations in those colonies. There is,
230
Measles
however, evidence of measles breaking out among Aboriginal people in South Australia.
In August 1854 Surgeon Clindening reported on an outbreak of measles among
Aboriginal employees at the Encounter Bay Fishery on Fleurieu Peninsula. It caused the
death of at least one Aboriginal worker and probably infected more:
The natives will not take medicine, and I have no doubt, from exposure to the
inclemency of the weather, there will be great sufferers [sic] from the disease
(Clindening 1854).
Clindening observed the same disease among European settlers on the
peninsula, although no deaths were reported among them. If the outbreak was indeed
measles it was in what was otherwise a non-epidemic period for South Australia and was
most likely a localised event; the infection arriving by sea from ports in either Victoria or
Tasmania.
Two outbreaks of measles causing severe mortality were reported among the
Ngunawal people of the southern highlands in what is now the Australian Capital
Territory, in 1858 and 1862 (Schumack 1927: 9, 1977: 51). There was no recorded
epidemic in the surrounding European population of New South Wales during the 1850s
but there was one among the European population in Victoria in 1853-54 (Table 7.1). If
the 1858 outbreak among the Ngunawal was measles it may have came from the south in
Victoria along with the annual movement of Aboriginal groups to the highlands to collect
aestivating moths (Flood 1980, 1983: 202-4). Large groups of Aboriginal people
gathering in the highlands were recorded until 1890,almost 60 years after the first arrival
of Europeans (Flood 1980: 68-69). Alternatively it may have been a localised epidemic
originating from the European settlers. The second outbreak in 1862 was most likely
associated with the general epidemic in New South Wales and Victoria.
231
Measles
During the Tasmanian epidemic in 1860 Surgeon Smith reported one woman
transferred from the Oyster Cove Aboriginal settlement to Hobart under treatment for
measles (Smith 1858-69). She survived the infection and was returned to the settlement
seven weeks later. This is the only mention of measles by Smith who attended the
inmates of the settlement for a period of ten years. During 1860 four deaths were
recorded, none were from primary measles infection or secondary complications.
Although the Oyster Cove people were subject to many ailments, measles was never
reported to be a serious cause of morbidity.
The 1867-68 measles epidemic was widespread throughout Victoria. Surgeon
Gibson administered to the Aboriginal people living on the Coranderrk settlement
between 1865 to 1875. He mistakenly reported the epidemic as 'intermittent fever', a
contemporary medical term for recurrent fevers and chills associated with malaria
(Morgan 1987). The disease was affecting the Aboriginal residents, the superintendent,
and his family (Gibson 1869-75). In March he noted seven out of 105 suffering while
several others were recovering from the infection. He returned in April and reported one
death, a male 22 years of age, and a further sixteen under treatment; four were adults, five
were in their teens, and the remainder ranged between two and ten years of age. Many
were leaving the settlement to avoid the epidemic. By June the general health of the
residents had improved with only four convalescing and by August the epidemic had
burnt itself out. There is no evidence to the fate of those who left the settlement during
the height of the epidemic and the presence of measles among Aboriginal people living
off the settlements.
The evidence for the 1874-75 measles epidemic is more substantial in terms
of its occurrence among the Aboriginal people. This epidemic was one of the more
severe episodes of measles in the nineteenth century, occurring throughout the European
232
Measles
settled regions of Southeast Australia. Table 7.4 shows the crude mortality rate of four
nineteenth century epidemics including 1874-75 and an interepidemic period for which
there is information available in South Australia.
Table 7.4 Crude mortality rate from measles in the European

population of South Australia for which there is information
(Cumpston 1927:223).
Year Mortality Rate

Per 100,000
Males Females
1874 144 136
1881 26 25
1882 6 1
1884 49 41
1893 74 74
The epidemic was also severe among the Aboriginal populations of southeast
Australia. Figure 7.1 depicts the extent of reported cases of measles infection discussed
below. The epidemic extended into several of the mission settlements causing high
morbidity among European and Aboriginal residents alike and in some cases exceedingly
high mortality among Aboriginal people. Other Aboriginal settlements experienced high
morbidity but recorded few deaths. Some regional centres of Aboriginal population and
settlements escaped the epidemic completely.
The first reports of the epidemic among Aboriginal people began in Victoria.
On 20th December 1873 Surgeon Gibson noted an 'eruptive disease' among Aboriginal
people on the Coranderrk settlement. He had not seen any Aboriginal people displaying
the primary stages of clinical symptoms but only the 'marks left on a few cases' (Gibson
1869-75). He diagnosed it as a species of Papulae viccae, and reported that there was no
233
Measles
danger from it. Whether these were the first cases of measles and Gibson was mistaken
in his diagnosis will remain unknown, but by 20th February the following year measles
was spreading through the community on the settlement; 15 cases were treated out of a
population of 142. By 20th March, apart from a few of the elderly people, who may have
developed immunity in a previous epidemic, all of the 142 residents had been attacked by
the disease. Gibson noted that none of the cases was severe and with a little care he
anticipated a satisfactory result (Gibson 1869-75).
Gibson's optimistic prognosis was grossly incorrect. By the end of 1875
measles had caused extreme morbidity and excessive mortality among the Aboriginal
residents. So high was the mortality that it came to the notice of the Victorian
Parliament. The report to the Legislative Assembly by the Colony's Chief Medical
Officer is worthy of repeating at some length:
... in 1875, with a population of about 150 people, 31 deaths took place - one
out of every five human beings in one year perishing from disease. This
awful mortality was doubtless exceptional, an epidemic of measles having
been prevalent in the early part of the year; but this epidemic prevailed all
over the colony, causing a considerable increase in the general mortality; yet
when the mortality of the whole colony, about 17 per 1,000 is compared with
that of [the Aboriginal residents of] Coranderrk, the discrepancy is appalling,
the latter amounting to 193 per 1,000, or in other words, for every person out
of the general population who died, 11 deaths occurred at Coranderrk
(McCrea 1879-80).
McCrea's assessment of the crude mortality rate at 193 per 1,000 is based on
all the recorded deaths on Coranderrk settlement for 1875 and from a population which
he estimates at 150. His estimate was close. An examination of the settlement's register
of births, deaths, and marriages (Massola 1975) shows 27 deaths that could be attributed
to the measles epidemic. Seven deaths were from measles directly, eleven caused by
pleuro-pneumonia, and four others caused by respiratory disorders and dysentery. Three
other deaths of children under one year old were given as 'thrush', a possible misdiagnosis
234
Measles
for the prodromal stage of measles ; and another, a two year old male given as 'disease of
the ear affecting the brain', was possibly post measles otitis media developing into
encephalitis. The population of the settlement just prior to and during the epidemic was
142, counted during Gibson's visits. The crude death rate from measles at Coranderrk
would then be 190 per 1,000.
Other settlements in Victoria were affected by the epidemic although not to
the same extent as Coranderrk. On 9th December 1874 Surgeon Brewer (1875) reported
an 'exanthematous disease' causing some illness and sore throats at Lake Condah
settlement. He reported the disease as scarlet fever. After his visit most of the children of
the settlement were attacked by measles together with the superintendent's own children.
The disease was seen as mild, causing no great stress to the Aboriginal children. By 3rd
January, however, measles had spread to most of the population (numbering c.86) with
twenty-four showing the signs.
I found nearly all the adults down with the measles. They were much more
severely affected than the children had been - two had severe pneumonia,
three severe bronchitis, two diarrhoea, one constantly recurring haemorrhage
from the nose, one woman just recovered from confinement had severe
bronchitis. (Brewer 1875).
The children, who had initially been infected, had recovered with just two in a
low febrile condition with pneumonia. The remainder of the establishment Brewer found
in bed or lying around in various symptomatic stages. Three deaths were recorded by
Brewer; two elderly females, one of whom died from post measles complications after
recovery from the initial infection, and a fourteen year old. A fourth death was later
recorded in official mortality statistics of the Aborigines Protection Board (APB 1876).
All other victims gradually recovered. By the end of April the disease had passed Lake
Condah settlement.
235
Measles
On Framlingham settlement Surgeon Jamieson (1875) reported measles
affecting approximately 20 out of a population of 58. The disease had been brought to
the settlement by returning Aboriginal males who had been working in the immediate
district where measles was prevalent among the European population. By 30th April
Jamieson reported all residents had recovered from their symptoms. No further cases
were reported.
Table 7.5 shows the Aboriginal mortality statistics from measles or post
measles complications during this epidemic which were reported to the Victorian
Parliament by the Aborigines Protection Board. The deaths were all recorded on
Aboriginal settlements and do not include Aboriginal people who may have died away
from the settlement, for example, when fleeing from the epidemic; nor are those who
were attached to European rural properties or residences included.
Table 7.5 Number of Aboriginal deaths on Victorian Aboriginal

settlements attributable to the 1874-75 measles epidemic.
Settlement Deaths Approximate %

attributed average
to measles population
Coranderrk 27 142 19.0
Lake Condah 4 86 4.7
Framlingham 6 58 10.3
Lake Hindmarsh 16 78 20.6
Lake Wellington 0 68 0
Lake Tyers 0 73 0
A differential rate of death from measles ranging from 0% to 20% is revealed
in the above table. The two Gippsland settlements of Lake Wellington and Lake Tyers
(Fig 7.1), located on the east coast, escaped the epidemic with no reported deaths
236
Measles
although the surrounding European population was affected. Separation of the Aboriginal
residents from the European population, particularly during the period of the epidemic,
most likely saved these two settlements from infection. Reverend Hagenauer,
superintendent of Lake Wellington, reported:
Different diseases have been about in the district, such as scarlet fever and
measles, and not one of our natives have had them though the measles were
within two miles of the place (Hagenauer 1877).
The settlements to the west were, however, involved in the epidemic with
varying degrees of mortality reported. A similar spatial pattern of differential mortality
during measles epidemics occurred during the epidemic of 1867 among the European
population of Sydney (Curson 1985: 62-66) and in the islands of Fiji in 1875 (Cliff &
Haggatt 1985).
Following the outbreaks in Victoria, measles appeared among the Aboriginal
people in South Australia (Fig 7.1). In the northern districts, along the Flinders Ranges,
the Sub-Protector of Aborigines reported from Blinman of the epidemic among the
Adnyamathanha and Kuyani in February 1875:
I am sorry to record the fact that in common with the settlers here and
elsewhere the Aborigines have suffered extensively from measles. At the
Sliding Rock [near Beltana] during one of my visits I found many suffering
and instructed Mr. Powell the surgeon to attend to those in the neighbourhood
of the mine professionally. Two of the Blacks - a man and woman have died
in this neighbourhood [Blinman] and I have been informed that several aged
Blacks at Beltana and at Numdowadana succumbed to the disorder named
(Buttfield 1875).
The epidemic had probably been present among the Adnyamathanha and
Kuyani since at least December (Hamilton 1876). The epidemic first appeared among the
Europeans in the Flinders Ranges and afterwards spread among the Adnyamathanha and
Kuyani who suffered severely (Hamilton 1876).
237
Measles
The epidemic was then reported to have moved into the western districts of
the colony. Traditional ceremonial and trading routes linked the two regions (McBryde
1987) and most likely facilitated the spread of the epidemic. Hamilton reported that
information passed to him indicated that measles made its first appearance among the
Banggaria of the Gawler Ranges and from there spread west along the coast among the
Nawu and Wirangu near the Venus Bay, Streaky Bay, and Fowlers Bay settlements and to
southern Eyre Peninsula where it infected almost all the residents living on Poonindie
mission. One resident of Fowlers Bay wrote to Protector Hamilton:
The epidemic (measles) carried away some twenty old and young. It first
made its appearance at Streaky Bay, and I hear, was brought there from
Adelaide by Europeans. Some of the Fowlers Bay natives were there at the
time, and caught it, bringing the disease here, and that I feel sure, was caught
from the blacks (Hamilton 1876).
Measles was also reported among the Buandig at Guichen Bay in the colony's
southeast. Police Trooper Morris reported to Protector Hamilton:
There has been much sickness among them than usual, owing to the
prevailing epidemic, measles and scarlatina; but they have all without
exception got over it favourably; it has necessitated me issuing them extra
blankets and medical comforts. The two deaths which have occurred here
have been caused by disease of the lungs, by which they all seem more or less
affected (Hamilton 1876).
Little could be done for those infected. Protector Hamilton supplied the
Aboriginal depots in the infected areas with 'medicines specially prepared, and medical
comforts' (Hamilton 1876) but with little effect. Some accepted the limited treatment and
help from those Europeans settlers who offered it to them; but in many cases the
Aboriginal people refused treatment, preferring their own traditional healers and methods.
238
Measles
Only one was treated for measles in the Adelaide Hospital in 1875, a one year old female
who was admitted for treatment on 30 November (SA Government Gazette 1875; 1876).
The measles epidemic bypassed the Point McLeay Aboriginal Mission on the
Lower Murray River, and the Nukunu living in the Port Augusta region at the head of
Spencer Gulf. Taplin (1876), writing from Point McLeay in January 1876 after the
epidemic had subsided stated:
We never had the measles on the Station at all altho [sic] settlers had them
within two miles of us and they raged violently at Milang and Meningie.
Altho a large number of natives were gathered in camps at a sheep shearing
and some of them, mostly half castes had measles, yet they did not spread
generally. This is surprising since absolutely no care was taken to prevent
infection.
In his half-yearly report on the Aboriginal people at Port Augusta, Police Sergeant
O'Shanahan stated quite specifically that they had 'not suffered in any way from measles'
(Hamilton 1876).
The failure of the epidemic to affect the Point McLeay settlement and the
Aboriginal population of Port Augusta, even though no measures were taken to prevent
infection, may indicate that many had been exposed to the virus during an earlier outbreak
and had gained immunity to the present epidemic. The epidemics of 1861-62 and 1868
which reached South Australia may then have been the source of original exposure and
protection from the 1874-75 epidemic. Although there is little evidence to support this
Taplin (1876), in the same report does state that measles had been 'very prevalent' at some
time in the past.
Although most sources reporting on measles indicate severe morbidity and
many deaths, there are few statistics available giving a more precise indication of the
239
Measles
degree of mortality. Hamilton (1876) reported an exceptionally high death rate among
Aboriginal people in the colony for 1875. Out of 140 deaths recorded from all districts,
55 (39.3%) were attributed directly to the measles epidemic. On Poonindie Mission 75
cases of measles were reported with 10 deaths (a case fatality rate of 13.3) in a population
of approximately 90 (Brock & Kartinyeri 1989); at Fowlers Bay 20 people, both old and
young, died (Hamilton 1876). These figures can only be accepted as an approximate at
best, as many other deaths would have gone unnoticed and unrecorded, particularly in the
Flinders Ranges among the Adnyamathanha and Kuyani, and in the western districts of
the colony among the Banggarla and Nawu. No evidence is available for the desert
regions of the colony further north and west of established European settlement.
There were five succeeding epidemics of measles in Southeast Australia
during the nineteenth century. Apart from just a handful of reports mentioning measles
there is little other evidence of the disease affecting the Aboriginal people. In 1887 at
Lake Wellington Aboriginal Settlement, Hagenauer (1887) reported one case of measles
which did not spread to the rest of the community. During the epidemic period of 1893-
94, measles was reported among the populations (possibly the Bundjalung and
Gumbainggiron) on the north coast of New South Wales:
There are now fifty Aborigines in residence at the [Aboriginal] "Home" near
Grafton. The health generally has been good during the year. Measles and
influenza went through the settlement, but all the patients recovered, though
several died of the same complaints in camps in other parts of the Clarence
district (Frosby 1893).
Measles accompanied by respiratory disease was also reported in the New
South Wales southern highlands at Tumut (Frosby 1893) and on the Point McLeay
Aboriginal mission, South Australia in 1894:
240
Measles
The epidemics of influenza and measles have been prevalent at the [Point
McLeay] station, and this cause may have attributed, to a certain degree the
comparatively heavy mortality over the year (South Australian Register
1894).
The extent of mortality from these epidemics is unclear. There were 19
deaths recorded among the Aboriginal people in the South Australian colony for 1894; 7
children, 2 youths, and 10 elderly. Eight of these appear on the register of births and
deaths for Point McLeay Mission and 1 for Point Pearce Mission, but measles as a cause
of death was not attributed to any.
The last epidemic of the nineteenth century reached the Arabana in South
Australia's north in 1898. This was probably their first exposure to measles. The Sub-
protector of Aborigines, F.J. Gillen, described the epidemic:
The general health of the Aborigines was good until the month of December,
when measles, first appearing at Oodnadatta, rapidly spread through the
tribes, causing much suffering and a number of deaths, chiefly among the old
people. Only such deaths as have occurred at or near, the depots have been
recorded, and it is therefore reasonable to suppose that the mortality in outside
districts, where the aborigines have no opportunity of getting medical
treatment or advice, was much heavier. The disease, which is often
complicated by pleurisy, is still raging, and will doubtless spread from tribe to
tribe throughout the continent. Where the sufferers have access to a
waterhole their favourite method of treatment is to plunge into the water for
the purpose of cooling their bodies, and this very often proves fatal (Gillen
1898).
Although this last epidemic in the nineteenth century occurred in the
European populations in all the colonies of Southeast Australia, the extent of its presence
among other Aboriginal population centres is unknown. The records of death from
Aboriginal settlements in Victoria and South Australia record no mortality from measles,
nor do they report its presence among the residents. It would appear that the settlement
Aboriginal population in those two colonies escaped the epidemic for that year.
241
Measles
It should be noted, however, that the 1898 measles epidemic was not the last
among Aboriginal populations. Although outside the temporal and geographical scope of
this study, reference should be made to two further epidemics which occurred among
Aboriginal populations in the desert regions of central Australia in 1948 and 1956.
During this time the Pitjantjatjara an Yanykunytjatjara populations were experiencing a
period of intensifying colonisation from missionaries, mining companies, and pastoral
activities (Goodall 1994: 57). At Ernabella in 1948 over 300 were suffering severe
febrile symptoms and acute pneumonia after being infected with measles virus. Goodall
(1994: 75, note 16) suggests a conservative estimate of between 25 and 33% mortality
among the two populations with all ages being affected. The second epidemic in 1956
affected mainly children under the age of 9 years presumably with no acquired immunity
to the virus. The 1948 epidemic was then most likely the first exposure these people had
to measles.
7.5 Discussion
Little of substance can be said on the extent of Aboriginal mortality due to
measles epidemics prior to 1874-75. The historical documentation presented above

shows that the disease was present among the Aboriginal populations in Southeast
Australia during the three major epidemic periods of 1835, 1853-54, and 1867.
Just what the levels of morbidity and mortality were, and the extent of their
spatial distribution in these early epidemics is a matter of conjecture. Most of the
Aboriginal deaths from measles went unrecorded or unnoticed by European observers and
only indirect and anecdotal evidence survives. During the 1834-35 epidemic some
impression of the extent of mortality can be reckoned from reports concerning population
loss in the settled districts between Sydney and Newcastle (Lake Macquarie). The
242
Measles
Reverend Threlkeld noticed a sharp decline in the number of Aboriginal people he was
able to contact after the epidemic:
During the present year [1837] I have attempted to carry into effect the plan
contemplated...of endeavouring to meet the Aborigines in the neighbouring
districts; but the numbers are now so very much reduced, that it is almost
impossible to form any settled plan to assemble them at any given time or
place. Sometimes two or three are seen, at most, half a dozen...
Although such a severe population loss could have been caused by many
factors other than measles it comes at a time immediately following an epidemic. In a
population that had no previous experience with measles and no herd immunity to it, high
morbidity and high mortality are to be expected (Cliff & Haggett 1985; McNeill 1976;
Neel et al. 1970: 418). In this early stage of colonisation (Stage II of the medical model,
Table 2.2) the Aboriginal populations of Southeast Australia had not been fully
institutionalised and confined to designated settlements. Traditional lifestyles and
economies were still present among many groups living away from major European
centres and beyond the frontiers of colonial settlement. While these groups could not
maintain measles endemically, they may have facilitated a chain of infection enabling
dissemination of measles and the relocation of epidemic centres throughout regions
beyond the European frontiers.
It is also quite likely that differential disease experience occurred, with some
receiving the full force of the epidemic and others escaping the infection entirely.
Linguistic and socio-cultural differences between groups would have acted as permeable
or inviolable barriers restricting the spatial dissemination of the virus. Physical obstacles
such as rivers, lakes, and mountain ranges would also have affected the spread of the
disease, again acting as barriers slowing, shaping or even stopping the process of
diffusion. Those groups that escaped one epidemic would then, however, have been
equally susceptible to the next. Whatever the case may have been, it would be expected
243
Measles
that the dissemination of the epidemic was wide and severe population loss would have
been experienced in the regions affected by the first three major epidemics leading up to
1874-75.
By the second half of the nineteenth century, Aboriginal population centres
were not large enough, or closely associated enough, to keep the measles chain of
infection going, enabling it to spread throughout most of Southeast Australia and remain
endemic. However, during at least the 1875 epidemic the Aboriginal population did not
need to be large enough to sustain an epidemic. The chain of infection was easily
supported by the European population which, with its high numbers of immunologically
susceptible, maintained the active disease at low incidence levels peaking periodically
into epidemics. It is safe to assume then that because of the highly communicable nature
of the virus and the associations between Europeans and Aboriginal people, the virus
would have crossed repeatedly from the former population to the latter. It is most likely
that the disease spread in this way throughout the Aboriginal populations of Southeast
Australia.
For the 1874-75 epidemic, local death at a local rates on Aboriginal
settlements in Victoria and South Australia can be estimated. Table 7.6 compares the
Australian estimates of crude death rate (CDR) with those from Methodist Church centres
in Fiji (Cliff & Haggett 1985) for 1875. The Fijian epidemic can be considered a trans-
Pacific extension of the 1874-75 epidemic experience in Southeast Australia. While the
crude death rates for Australian Aboriginal people are in most cases lower than those in
Fiji they share a similar pattern of widely varying mortality between one population
centre and another.
244
Measles
Table 7.6 Estimated crude death rates

(CDR) from 1874-75 measles epidemic
among Fijians (after Cliff & Haggett 1985)
and Aboriginal Australians.
Centre CDR n
Australia
Coranderrk 190 27
Lake Condah 47 4
Framlingham 103 6
Ebenezer 205 16
Poonindie 111 10
Point McLeay 0 0
Fiji
Totoyo 137 75
Komo 192 20
Matuku 229 162
Lakemba 258 210
Moala 259 205
Fulaga 342 107
Kabara 363 107
Moce 383 59
Namuka 435 54
Oneata 755 120
There are two significant epidemiological points to consider arising from the
figures of Table 7.6. The first is that the crude death rates among the local Fijian
populations are generally all higher than those of the Australian Aboriginal populations.
The exceptions are Coranderrk (CDR 190) and Ebenezer (CDR 205) which have higher
crude death rates than those of Totoya (CDR 137) and Komo (CDR 192).
Two explanations may be offered for this. Firstly, the local populations are
smaller for Australia and the crude death rates may be influenced by a small sample size.
If this were the case, however, it would be expected that the bias would show random
death rates both above and below that of Fiji. This does not occur.
245
Measles
A second explanation, and one which goes towards addressing the former
problem, is that the low crude death rates among the Australian Aboriginal population
when compared to the Fijian samples reflect the true nature of the epidemic. Prior to this
epidemic, Aboriginal people in Victoria and South Australia had been exposed to three
previous epidemics (see Table 7.1); twenty years, fifteen years, and eight to ten years
before. An unknown number of Aboriginal people living through the 1874-75 epidemic
had presumably been infected in one of the previous epidemics, survived, developed
immunity to the virus, and so did not fall to the disease on its return in 1874-75. A small
herd-immunity to the disease would have then existed. This was not the case for Fiji in
1875. This epidemic was the first experience the Fijians had with measles. Measles had
spread from Australia into the Pacific in 1854 when it reached Tahiti and the Cook
Islands (probably from an American ship on her way from Newcastle in New South
Wales), but it did not reach Fiji (Cliff & Haggett 1985). The Fijians can be considered an
island population with no herd-immunity to measles in 1874-75, whereas in Australia for
the same period there was at least some degree, albeit unknown, of herd-immunity to the
virus. The differences in the crude death rates between the two shown in Table 7.6 then
are explained.
This explanation then raises further questions. If, as I think we can safely
assume, there was no endemic measles in Australia prior to European settlement, and if
the first recorded epidemic in 1834 was the initial exposure to the virus for the Aboriginal
population, was the crude death rate in 1834 much higher than in 1874-75; and was it as
high as seen for some areas in Fiji? There are of course no solid answers to these
questions, but we can speculate by epidemiological inference, in this case the subsequent
measles epidemics in Fiji. When a second epidemic of measles was introduced into Fiji
in 1903 there was a much reduced mortality. Although there are no official records on the
timing or extent of this epidemic, the estimated number of deaths was between 1,800 and
246
Measles
2,000 (Cliff & Haggett 1985: 40; McArthur 1967: 32). Based on a higher than average
crude death rate for all deaths for Fiji in 1903, McArthur (1967: 32) estimates the crude
death rate from measles for that year at approximately twenty per thousand. The reason
for this much reduced figure can be explained by a higher herd-immunity at the time of
the population's second exposure to the virus. The majority of the population who
survived the first epidemic would have acquired an immunological protection from the
virus and would have escaped the symptoms of the disease. The section of the population
at risk to measles in 1903 comprised those born after the 1875 epidemic, that is those
under the age of twenty-seven. A substantially reduced number of susceptible individuals
would then account for the reduced crude death rate. There is of course nothing new in
this. It follows the well-known epidemiological pattern of measles epidemics occurring
throughout the world and their effect among virgin-soil populations (Adels & Gajdusek
1963; Black 1966; Neel et al. 1970).
We can then, I believe, assume by analogy with Fiji that the initial epidemics
of measles among the Aboriginal people of Southeast Australia were responsible for a
much higher crude death rate than those calculated for the 1874-75 epidemic. This
assumption can be strengthened further if we take into consideration the supportive care
available to the Aboriginal people living on missionary and government settlements
during the 1874-75 epidemic, and the lack of it among those infected in previous
epidemics. Whether one dies from measles largely depends on the availability of
supportive care and the quality of hygiene and nutrition that is maintained throughout the
course of the primary and secondary illnesses (Cohen 1989: 54). It is therefore important
that the ill person receives care from those not infected or not immobilised from the
disease. In a virgin-soil population with all susceptible to the infection, typically, many
individuals of all ages are sick at once, and there is often no-one to provide for the basic
needs (food, water, comfort) of the sick or attend to basic hygiene. Such a situation was
247
Measles
almost certainly the case among Aboriginal groups living beyond the European frontiers
when they experienced the first epidemics of measles. The mortality from measles would
thus have been reduced by the supportive care offered to the Aboriginal people living on
settlements during the 1874-75 epidemic by those who were not incapacitated by the
diseases. The crude death rates from the 1874-75 epidemic are then from localised
populations who have developed a measure of herd-immunity to the disease and who had
access to supportive care, food, water during the epidemic; all of which would have
reduced mortality from measles.
The second epidemiological point involving the local level crude death rates
presented in Table 7.6 is their irregularity, and by inference, the irregularity of the attack
rates of the virus. A number of factors operating in conjunction are responsible. Unlike
the influenza virus which undergoes regular and major genetic changes the measles virus
is a stable myxovirus (Neel et al. 1970: 118). Therefore on the basis of present
virological knowledge we can accept that the measles virus attacking a population centre
during an epidemic is genetically the same as that which attacks another centre. The
same can be said for epidemics several decades apart. For the same reason lifelong
immunity to the virus is gained after the first infection. Further, the virus has a simple
transmission mechanism. It is transmitted primarily from one human to another and
requires no intermediate host or vector to intercede. Attack rates then depend on the
amount of exposure each individual has to the virus and on their personal immunological
immunity to the virus.
The mortality rate is also dependent upon the ability of the immune system to
fight the virus effectively. Those with impaired immune systems due to other infectious
agents, particularly chronic infections such as syphilis or tuberculosis, lose the ability to
combat the virus effectively and are prone to more severe and debilitating primary
248
Measles
symptoms. These same individuals are more susceptible to post-measles secondary
invasion by other pathogens. Further to this, as we have seen, the irregular pattern of
crude death rates also relate to the effectiveness of local supportive health care available
during an attack.
7.6 Conclusion
The history of measles in Australia can be seen as a series of recurring
epidemic events beginning in 1834. Although there is little evidence available regarding
the morbidity or mortality among the Aboriginal populations during the epidemics before
1874-75, there is evidence to suggest a similar pattern in the timing and periodicy of
measles epidemics between the Aboriginal population and the European population in
Southeast Australia. Excessive morbidity and mortality during these early epidemics on
immunologically vulnerable Aboriginal populations could be expected. The few
surviving reports referring to these early epidemics suggest that this is the case.
The 1874-75 epidemic in Southeast Australia was a part of a world pandemic
of measles. Records of this epidemic provide the best evidence regarding the morbidity
and mortality of measles among the Aboriginal populations. Historical accounts show
that this epidemic spread throughout many Aboriginal population centres living both on,
and away from, established settlements in Victoria and South Australia. The hardest hit
settlements in terms of mortality caused by the disease were Lake Hindmarsh which lost
20.6% of its population and Coranderrk which lost 19%. Other population centres were
bypassed by the epidemic. The settlements of Lake Wellington and Lake Tyers on the
east coast of Victoria, Point McLeay in South Australia, and the population living in the
European town of Port Augusta escaped the epidemic with no recorded morbidity or
mortality.
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Measles
The crude death rates from the 1874-75 epidemic, while indicating excessive
mortality from measles, are much less than those from Fiji for the same epidemic. The
experience of previous epidemics among the Australian Aboriginal population providing
a substantial number of immunologically protected, can account for the lower mortality in
Southeast Australia and in turn suggests greater severity of the earlier epidemics.
It cannot be ascertained whether measles became endemic among any of the
Aboriginal population centres of Southeast Australia during the nineteenth century,

although it is unlikely because of their small numbers and relative isolation from the main
European centres.
After the 1874-75 epidemic records from Aboriginal settlements suggest that
measles was no longer a major lethal disease among the Aboriginal population of
Southeast Australia. An exception was the 1898 epidemic which penetrated into the
Arabana regions of South Australia's north following pastoral expansion. This was the
last epidemic of the nineteenth century seriously to affect an Aboriginal population.
250
CHAPTER EIGHT
Diseases on Aboriginal Settlements 1876 to 1900
8.1 Introduction
The previous chapters were concerned with stage two of the medical model
(see Table 2.2) which dealt with the early years of contact between European and
Aboriginal people and the diffusion of epidemic diseases among the latter populations in
their traditional regions. This chapter will now consider stage three (settlement and
acculturation) of the medical model.
The primary aim is to identify and compare the principal disease states
causing mortality among the Aboriginal people living in settlements in Southeast
Australia. The period concerned will be from 1876 to 1900 when a high proportion of the
Aboriginal people of Southeast Australia were living on missionary and government
organized settlements (Barwick 1971: 288: Broome 1995: 139; Christie 1979: 199;
Jenkin 1976: 179-80; Smith 1980). Following the theme of previous chapters the focus
will be placed on infectious and respiratory diseases.
Using the surviving records of births, deaths, and marriages kept by the
administrators of six settlements in Victoria (Framlingham, Lake Condah, Lake
Wellington, Lake Tyers, Coranderrk, and Lake Hindmarsh) and two in South Australia
(Point McLeay and Point Pearce) causes of deaths will be extracted, collated and
examined.
A further aim of this chapter is assess the health status of the Aboriginal
populations living on the settlements. Infant mortality ratios calculated from the mortality
records will be used as indicators of general health. Comparisons with other nineteenth
Diseases on Aboriginal Settlements 1876-1900
and twentieth century indigenous and colonial populations throughout the world will be
made.
The processes of nineteenth century institutionalization of Aboriginal people,
the development of settlements controlled by missionary bodies and colonial governments
through Aboriginal protection boards, and the subsequent acculturation of the Aboriginal
people of Southeast Australia have been the subject of previous discussions (Attwood
1989; Barwick 1971, 1972; Brock 1985, 1993, 1995; Christie 1979; Corris 1968;
Foxcroft 1941; Gale & Brookman 1975; Jenkin 1979; Long 1970; Massola 1970, 1975;
Rowley 1970; Woolmington 1973; Yarwood & Knowling 1982). They need not be
repeated in detail here other than to discuss factors relevant to the themes of this thesis,
especially those predisposing the Aboriginal people to disease.
The settlements, established to contain and confine Aboriginal people, were
often established on land not immediately required or wanted by Europeans and out of the
way of main European settlements (Summers 1986: 305). Although in many cases the
land was unsuitable for agriculture, the managing authorities and the colonial
governments expected the settlements to become largely self-supporting; efficient in
growing crops and grazing sheep and cattle for their own consumption to supplement the
government rations, thereby reducing the Government's financial commitment (Long
1970: 15).
The result was that food shortages were common (Barwick 1972; Jenkin
1976, 1979). Barwick (1972), discussing the mission settlements in Victoria, states that
before the food ration was doubled in 1875 the men who were able to work subsisted on 5
pounds of flour, 1 pound of sugar, and 2 ounces of tea per week, while others had to do
with even less. By the last quarter of the nineteenth century, traditional game species had
252
became scarce around the settlements and could no longer be relied on as satisfactory
supplement for the inadequate rations. The able bodied men often had to disperse
seasonally to find paid work in order to buy food as well as providing capital for the
development of their settlement. Barwick (1972: 29) describes the meat ration provided
to the Aboriginal people on Corandederrk settlement as meagre and always causing
discontent among the residents.
...from 1871 'regular workers' were allotted one pound of meat per day and
other men half that amount. From 1875 to 1877 all adults were entitled to six
pounds per week with half rations for children, but for the next five years the
Board expected residents to purchase meat, increasing wages on a sliding
scale according to numbers of dependents, and gave rations only to the aged
and ill.
This economic measure imposed by the settlement supervisors was the cause of real
hardship for the residents, reducing their ability to purchase other necessities.
Although living conditions varied between the settlements and over the time
of their operation, funding by the responsible missionary bodies and government agencies
was almost always inadequate and failed to maintain long-term satisfactory housing and
conditions (Barwick 1972; Jenkin 1976, 1979; McCrea 1879). Some Aboriginal families
had huts or cottages. They were often of one or two rooms, and while adequate for a
childless couple they were often inadequate when family size increased with surviving
children (Brock 1993: 18) or when required for accommodation of extended family
groups. The Aboriginal occupants were frequently required to meet the costs of
maintenance themselves and with limited financial resources, maintenance requirements
were often neglected (Barwick 1972). Not all those who lived on settlements had huts or
cottages. Children often slept and ate communally in classrooms and dormitories
(McCrea 1879). Single males and females were often required to sleep in segregated
dormitories. Even by 1876, despite the passing of several years after their establishment,
253
some settlements could only offer bark shelters which the Aboriginal people constructed
themselves (Jenkin 1976: 180). In 1876 the Chief Medical Officer of Victoria reported
after a visit to Coranderrk which at that time had 32 huts:
The huts of the natives are built on a street which runs nearly north and south
across the face of the slope, instead of up and down it, the natural advantage
of the fall of the ground for drainage being thus lost... The construction of the
huts is, in a sanitary point of view, the worst possible; the walls are of slab,
paling, or bark, mostly the latter, with openings in them so numerous that they
may fitly be compared to bird cages. The roofs are almost always bark, with
openings nearly as numerous as in the walls; some of the natives have
endeavoured by paper and bags to cover the chinks and openings in the walls
and roofs, but in most cases with little effect. The floors are of clay, and are
damp even at this the driest season of the year, whilst in the winter the natives
complain that the water rises to the surface of the floors after every shower of
rain. In wretched hovels like these it is no wonder the mortality is excessive
(McCrea 1879-80).
The sanitary and human waste disposal facilities on the settlement were
reported to be little better:
There are few closets of a common description, covering mere holes in the
ground, scattered about irregularly over the establishment, insufficient in
number for the wants and decency of the population [approximately 150].
Even these are not always used, the Superintendent stating that at night the
children and some of the adults pass their excrement in the water channels in
the street opposite their huts (McCrea 1879-80).
Few if any of the settlements had a resident doctor and medical needs were
either met by the superintendent or by local medical practitioners who were called on to
attend ill Aborigines. Lack of sufficient money often severely reduced the number of
times doctors were called to the settlements. Phillip Pepper, writing his family's history
centred on Lake Wellington and Lake Tyers settlements, remarks:
Once the reserves were established it became obvious that doctors would have
to be called in and the managers were authorised to seek medical assistance if
required. Over the years their accounts were often questioned and the
254
managers were told to find out from the doctors exactly what services they
had rendered. As a result some doctors reduced their fees and many did not
charge for visits (Pepper & De Arago 1985).
Despite the willingness of some doctors to forego full fees for their
attendance, the Aboriginal Protection Board of Victoria saw the costs of medical
assistance as too high. In 1886 they advised settlement managers that they could not call
a doctor without due authority, unless the patient in their opinion was going to die
(Pepper & De Arago 1985: 203; BPA 185-86). The result was that the limited medical
care made available to the Aboriginal inhabitants could not meet their increasing health
needs. Alcohol and tobacco consumption was high throughout the settlements adding
further to the health hazards faced by the Aboriginal people.
While these conditions may be considered to be extreme they were common
throughout the settlements in various degrees of severity for much of the last quarter of
the nineteenth century. The state of the settlements in Southeast Australia during the
nineteenth century and living conditions on them can be summarised as:
 Often small settlements (with the exception of Point McLeay)
 Located on poor land, often infertile for exotic crops, often badly drained
 Poor facilities to deal with health problems
 Few of the staff were properly trained to deal with a different culture
 Poorly constructed and maintained houses - often cold in winters and hot in summers;
unsuitable for Aboriginal lifestyles
 Few services provided - fresh water and sanitation were minimal or entirely lacking
 Diet nutritionally inadequate
 Communal eating causing cross-infection.
255
(Barwick 1972; Brock 1993: 48; Broome 1982; Jenkin 1976, 1979, Long 1970: 15-23;
Massola 1970; Pepper & De Arago 1985).
In attempts to convert the Aboriginal people to Christianity on the settlements
traditional cultural practices were actively discouraged by settlement superintendents.
The erosion of long-existing social structures by the frequent deaths, and the mixing of
different socio-linguistic groups within the confines of the settlements caused further
anxiety to many residents. Against this backdrop was the persistence of introduced
infectious diseases and nutritional disorders many of which had become endemic.
8.2 Source materials
Records of Aboriginal births, deaths and marriages during the last quarter of
the nineteenth century (1876 to 1900) were examined from eight Aboriginal settlements -
six in Victoria and two in South Australia (Figure 8.1, Plate 8.1).
The period 1876 to 1900 was selected for examination of stage three of the
medical model for a number of reasons. The period 1876 to 1900 saw a high proportion
of the surviving Aboriginal population of Southeast Australia institutionalised on
settlements. In 1876, 46% of the Victorian Aboriginal people enumerated in that year's
census lived on the six settlements to be examined below (Broome 1995: 139; VPP 1877-
78). By 1901, at the end of the period of examination, the figure had increased to 65% of
the enumerated population (BPA 1901).
The proportion of the Aboriginal population in South Australia
institutionalised during the period of concern is difficult to quantify from official census
256
statistics mainly due to the difficulties encountered by census official in reaching and
counting the Aboriginal populations, particularly in the northern and western regions of
the colony. In 1875-76 George Taplin, the superintendent of Point McLeay, completed a
census of Narrindjeri showing 511 living on the lower Murray River, Lakes Alexandrina
and Albert, and the Coorong (Hamilton 1876; Taplin 1876a). The Point McLeay
settlement on Lake Alexandrina had a population of 135, or 26%, of the Narrindjeri. By
1896 the average population of the settlement and its nearby out-station 'The Needles',
was 234 with few of the Narrindjeri living continuously on traditional lands (South
Australian Register 1896). The Point Pearce settlement on Yorke Peninsula averaged 52
residents in 1878 (Hamilton 1879). The Aboriginal population on the peninsula was not
enumerated in the 1876 census, but a figure of 439 was given for the Western District
Pastoral Region (South Australian Government Gazette 1877a: 798). Many of these lived
far from the influence of the Point Pearce settlement. By 1890, despite severe
depopulation of the Western District, the population of the settlement was still roughly
the same at 56 residents (Sutton 1890). The number of Aboriginal people living in the
colony's northern and eastern pastoral regions was calculated in the 1876 census to be
approximately 3,500 (South Australian Government Gazette 1877a). Distance would
have precluded all but a few of these people having contact with the two settlements of
Point McLeay and Point Pearce. Throughout the remainder of the nineteenth century the
colonial governments maintained their policies of moving Aboriginal people (sometimes
by force) on to settlements and the numbers living traditional lifestyles were steadily
reduced (Barwick 1971: 288-290; Broome 1982: 73; Corris 1968; Foxcroft 1941; Long
1970; Saggers & Gray 1991: 69; Yarwood & Knowling 1982:162-3).
With many of the Aboriginal people living on settlements enumeration and
the recording of vital statistics became more precise. It was from the beginning of this
period that the most accurate official nineteenth century records of Aboriginal mortality
257
and birth were kept (Barwick 1971: 302). Each of the settlements examined was required
by the colonial government to keep a register of births, deaths and marriages and to
furnish quarterly and annual reports of the same. These records are today available from
several sources. Massola (1970 & 1975) collected and published a list of births and
deaths for Victorian Aboriginal settlements drawing on their original registers of births,
deaths and marriages from the institutions and from those included in the quarterly and
annual reports of the Aborigines Protection Board presented to the Victorian Parliament.
The records of deaths from Lake Condah, Lake Wellington (Ramahyuck), Lake
Hindmarsh (Ebenezer), and Coranderrk cover the full period 1876-1900. Records from
the Victorian Government's Framlingham station cover the period 1876-1883. The
original records of births, deaths, and marriages for Point McLeay mission station are
housed in the State Library of South Australia and extracts of these together with extracts
of the register from Point Pearce mission (Gale n.d.) are available in the library of the
Australian Institute for Aboriginal and Torres Strait Islander Studies, Canberra. The
original registers of births, deaths and marriages from Lake Tyers, held in a private
collection, were made available for this study. Table 8.1 lists the selected settlements, the
respective temporal distribution of mortality data, and the abbreviations used for each
below.
258
Table 8.1 Aboriginal settlements in Victoria and South Australia

for which there are reliable nineteenth century mortality data.
Aboriginal settlement Abbreviation Time

period
Victoria
Framlingham FRM 1876-1883
Lake Condah LCD 1876-1900
Lake Wellington (Ramahyuck)` LWL 1876-1900
Lake Tyers LTY 1876-1900
Coranderrk CRD 1876-1900
Lake Hindmarsh (Ebenezer) LHD 1876-1900
South Australia
Point McLeay PMC 1876-1883
1888-1900
Point Pearce PPR 1880-1900
A total of 714 Aboriginal deaths were identified and extracted for the period
(Table 8.2). For a detailed listing of each settlement see Appendix B.
Table 8.2 Number of deaths recorded on selected

Aboriginal settlements in Southeast Australia for period
1876-1900.
Settlement Number of
deaths recorded
Victoria
Framlingham 18
Lake Condah 96
Lake Wellington (Ramahyuck) 89
Lake Tyers 93
Coranderrk 71
Lake Hindmarsh (Ebenezer) 82
South Australia
Point McLeay 223
Point Pearce 42
Total 714
259
8.2.1 Nature of the data
Deaths were recorded by the various superintendents of the settlements and
medical practitioners who had diagnosed either the cause of their death or the major
clinical signs leading up to death. The individuals whose deaths were recorded had for
some period of their lives lived on designated settlements under the control of colonial
governments or missionary bodies (Plate 8.2). There is little doubt, however, that many
individuals living and dying in the last quarter of the nineteenth century never became
fully institutionalised. The Aboriginal populations of central and northern South
Australia were among the last to move from their own lands onto settlements, many
during the twentieth century (Brock 1995: 220). Others in both South Australia and
Victoria lived on the settlements for only short periods during the year, coming and going
largely at will (Brock 1995; Broome 1995; Jenkin 1979). The demographic
circumstances of these people are lost to historical record. Others spent only limited
times away from the settlements, working for European employers on a seasonal round
(Broome 1982: 73, 1995: 139). The sample used in this study therefore does not take into
account Aboriginal deaths that occurred off the selected settlements and which were not
recorded in the death registers. Nevertheless, because of the temporal range used (25
years) it takes into account over 700 deaths of Aboriginal people who lived most of their
lives on the settlements or closely attached to them, and so provides a statistically useful
sample.
The sample under consideration comprises residents of eight localised
settlements, each with fluctuating numbers caused by migration on and off the settlements
and between them. Individuals in this sample were exposed to chronic disease and poor
nutrition. It should also be noted that the twenty-five year period (1876-1900) under
examination does not cover the complete life-spans of all individuals. Many individuals
whose deaths are recorded in the time period would have been born and lived a greater or
260
lesser part of their lives outside the period (before 1876). The same goes for those who
were born within the period but whose deaths are not considered as they died after the
period ended (after 1900). Others in the sample would, however, have lived and died
(before the age of 25 years) within the 1876-1900 period.
After the 'Aborigines Act of 1886' the population structure changed on
Victorian settlements. The Act differentiated the Aboriginal populations throughout the
colony into 'full bloods' and 'half-castes'. Those determined as 'full bloods', 'half-castes'
over 34 years of age and their 'half-caste' wives and children were allowed to remain on
the settlements supported by missionary and government funding. 'Half-castes' under the
age of 34 years were either forced to move into the general community or required special
licences to reside on the settlements. The Act caused great distress among the Aboriginal
population, isolating individuals and splitting families. It resulted in settlement
populations being reduced and the communities losing many of their young adults up to
the age of 34 years. For instance, the population of Framlingham fell from 94 to 35 (a
reduction of 63%) after the Act while that of Coranderrk fell from 120 to 60 (a reduction
of 50%) (Broome 1995: 139-140).
Such a sample would have inherent problems in some forms of demographic
analysis (e.g. life tables) yet the causes of death derived from it and analysed in the form
of ratios and rates, can prove extremely useful in making assessments of the principal
diseases occurring among the inhabitants of the settlements.
8.3 Methods of analysis
The sex and age at death of each individual death were noted where recorded.
It was often the case, however, that the sex of the individual went unrecorded in the
261
registers. When this occurred, sex could sometimes be determined by the European name
given. If no name, or an Aboriginal name only were recorded, the sex of the individual
remains undetermined. In the entries where age at death was not recorded attempts were
made to trace the individual back through the register of births. This proved difficult for
a number of reasons. Many deaths with no recorded age also had no recorded names,
making a check of birth impossible. European names were sometimes untraceable
because the same name was given to more than one child. Finally, many of those who
had their deaths recorded did not have their births recorded. In some cases, however,
where age was not given in the records the individual could be assigned an age range
based on the recorded cause of death. For example, 'old age', or 'senile decline' as causes
of death were allocated to the 15+ age range. This method reduced redundancy. Of the
714 individual deaths extracted, 632 (88.5%) had sex, and cause of death recorded.
Table 8.3 displays a breakdown of the data.
Table 8.3 Breakdown of data set - extracted from records of

Aboriginal deaths between 1876-1900 on selected settlements in
No. Per cent

Sexed, aged, cause of death 632 88.5
Unsexed 45 6.3
Unaged 18 2.5
Unaged & unsexed 1 0.1
Sexed, aged, no cause of death 14 2
Sexed, unaged, no cause of death 1 0.1
Unsexed, aged, no cause of death 3 0.4
Total 714
Where the cause of death was given for an individual it was noted and
grouped according to the International Classification of Diseases (ICD.9.CM 1991).
262
Particular attention was needed when ascribing causes of mortality given in the registers
to a particular ICD group, but in most cases (81%) the recorded disease was unambiguous
and classifiable according to specific groups. The Nosological index of 1863 (Morgan
1987) was used as a guide when specific diseases were given more than one name (e.g.
'phthisis', and 'consumption' were listed as tuberculosis). In the other remaining cases,
however, the recorded cause could only be classified under symptoms, signs, and ill-
defined conditions (ICD 780-799). For example, 'senility', 'general decay', and 'old age',
given as causes of death are closely linked to the longevity of the individual, and while
contributing to death, cannot be ascribed as the cause. Likewise, causes such as 'weakly
child', 'general debility', and 'decline' which are ambiguous were included in the ill-
defined category. In all 121 (19%) of all the causes of death had to be ascribed to the ill-
defined category making it statistically the third highest cause of death.
Table 8.4 lists the ICD to which the recorded causes of death have been
assigned and the abbreviations used for the purpose of this analysis. A detailed
breakdown of each cause of death and the ICD category in which it was placed is in
Appendix B.
263
Table 8.4 International Classification of Diseases categories and

abbreviations used (ICD.9.CM 1991).
Abbreviation ICD Diseases

used Group
RES 460-519 Diseases of the respiratory system
INF 001-139 Infectious and parasitic diseases
CIR 390-459 Diseases of the circulatory system
DIG 520-529 Diseases of the digestive system
NEO 140-289 Neoplasms
INJ 800-999 Injury and poisoning
GEN 580-629 Diseases of the genitourinary system
PRG 630-676 Complications of pregnancy, childbirth,
and the puerperium
END 240-279 Endocrine, nutritional, and metabolic
diseases and immunity disorders
NER 320-389 Diseases of the nervous system and
sense organs
PER 760-779 Certain conditions originating in the
perinatal period
ILL 780-799 Symptoms, signs, and ill-defined
conditions
Before the causes of death from the eight settlements were combined the
frequency of each ICD category was compared to detect any differences in their
occurrence. A multi-variate statistical technique, correspondence analysis (CA), was
chosen to compare the frequency of each of the ICD groups in each of the settlements. A
null hypothesis proposed that there was no difference between the settlements in the
frequency of reporting of the various causes of death. In other words, all the settlements
were expected to show a similar pattern of causes of death throughout the twenty-five
year period, 1876 to 1900.
Correspondence analysis is particularly suited to the analysis of tables
expressed as raw counts (in this case the number of times each disease group was
reported as a cause of death) where some of the objects (settlements) have a greater
abundance than others. In Appendix B it can be seen that the counts of different disease
groups vary considerably within each settlement and also between each settlement. There
264
are quite a number of very small or zero counts and some large ones. Correspondence
analysis is designed to cope with such a data set and gets rid of any general factor of
abundance of counts (Wright 1992, 1994).
Figure 8.2 displays the relationship of ICD disease groups. There are five
groups - respiratory diseases (RES), infectious diseases (INF), circulatory disorders
(CIR), neoplasms (NEO), injuries (INJ), and nervous system disorders (NER), forming a
cluster around the centre of the two axes. As will be shown below respiratory diseases
and infectious diseases are the most commonly reported groups on all settlements (Table
8.5, see also Appendix A). In correspondence analysis the nearer any variable is towards
the centre of the territorial map the less it contributes towards the overall differences
between the objects (Wright 1992, 1994). The clustering around the centre of the
territorial map (particularly that of respiratory and infectious diseases) can be interpreted
as a comparable pattern of reporting for each group of diseases throughout the settlements
with neither group contributing greatly towards the overall differences between the
settlements.
The remaining ICD groups are scattered along the first two principal axes
indicating higher differences in frequency of reporting. At first sight this distribution
seems at odds with the null hypothesis and might suggest that combining these groups
would introduce a bias coming from one or more of the settlements. However, as will be
265
Figure 8.2 Relationship of ICD categories reported as causes of death according to their
occurrences on Aboriginal settlements with respect to the first two component axes of
correspondence analysis.
CAx2
DIG 3 21%
2.5 END
2
1.5
CIR 1 GEN
0.5
NEO
CAx1
0
INF 51%
-2 -1 PER
RES-0.5 0 1 2 3 4 5
INJ NER
-1
-1.5
-2 PRG
-2.5
RES = Diseases of the respiratory system; INF = Infectious and parasitic diseases; CIR = Diseases
of the circulatory system; DIG = Diseases of the digestive system; NEO = Neoplasms; INJ = Injury;
GEN = Diseases of the genitourinary system; PRG = Complications of pregnancy, childbirth &
puerperium; END = Endocrine, nutritional and metabolic diseases; NER = Diseases of the nervous
system; PER = Conditions originating in the perinatal period; ILL = Ill defined conditions.
266
shown below (Table 8.5, also see Appendix B), these groups have low frequencies of
reporting on all the settlements and would therefore contribute little to the combined rate
of reporting. The null hypothesis stating that there is no difference in the frequency of the
various causes of death among the settlements can be supported at least for the two major
disease groups - infectious and respiratory. These groups will be the major focus of the
following discussion.
8.3.1 Proportional Mortality Ratios (PMR)
In order to ascertain the major diseases and their impact on the Aboriginal
residents of the settlements for the period 1876-1900 proportional mortality ratios (PMR)
have been calculated for age ranges 0-4, 5-14, and over 15 years of age. Proportional
mortality is calculated:
Number of deaths from a particular

disease per region per time
____________________________ x100
Total number of deaths per
region per time
The PMR does not directly measure the risk or the probability of a person in a
population dying from a specific disease. Rather, it is a measure of the relative
importance of a particular disease within a population over a period of time (Lilienfeld &
Lilienfeld 1980: 74).
267
8.4 Results and discussion
An overview of the principal mortality ratios of ICD disease categories and
the major causes of death is given first. This is followed by an analysis of the principal
causes by age ranges 0 to 4 years, 5 to 14 years, and 15+ years.
Table 8.5 Proportional mortality ratios

(PMR) for disease categories on selected
Aboriginal settlements in Southeast
Australia 1876-1900.
Group n PMR
INF 238 32.4
RES 143 20.3
CIR 19 2.7
DIG 41 5.8
END 15 2.1
GEN 2 0.3
INJ 16 2.3
NEO 16 2.3
NER 36 5.1
PER 9 1.2
PRG 4 0.6
ILL 175 24.9
Total 714
Inf = Infectious and parasitic diseases; Res = Diseases of the

respiratory system; Cir = Diseases of the circulatory system; Dig =
Diseases of the digestive system; End = Endocrine, nutritional and
metabolic diseases; Gen = Diseases of the genitourinary system; Inj =
Injury; Neo = Neoplasms; Ner = Diseases of the nervous system; Per
= Conditions originating in the perinatal period; Prg = Complications
of pregnancy, childbirth & puerperium; Ill = Ill defined conditions.
Table 8.5 shows the proportional mortality ratios (PMR) of disease categories
for all age ranges combined from the Aboriginal settlements.
Figure 8.3 shows the same principal mortality ratios of the disease categories
in order of their relative frequencies.
268
Figure 8.3 Proportional mortality ratios of ICD categories in

their relative order on Aboriginal settlements in Victoria and
South Australia 1876-1900.
35
30
25
20
PMR
15
10
0
Inf Res Dig Ner Cir Neo Inj End Per Prg Gen Ill
Disease Group
Inf = Infectious and parasitic diseases; Res = Diseases of the

respiratory system; Cir = Diseases of the circulatory system; Dig =
Diseases of the digestive system; End = Endocrine, nutritional and
metabolic diseases; Gen = Diseases of the genitourinary system; Inj =
Injury; Neo = Neoplasms; Ner = Diseases of the nervous system; Per
= Conditions originating in the perinatal period; Prg = Complications
of pregnancy, childbirth & puerperium; Ill = Ill defined conditions.
Infectious diseases (PMR 32.4) and respiratory diseases (PMR 20.3) stand out
from all others as the two major causes of mortality among the Aboriginal residents of the
settlements. Apart from the ill defined category of diseases (PMR 24.9) all other
identified disease groups have a PMR of less than 6 and were of substantially lesser
importance as causes of mortality.
Two hundred and twenty eight deaths were recorded for the infectious disease
category (INF) (Table 8.6).
269
Table 8.6 Frequency (%) of diseases in the infectious

disease category (INF) recorded as causes of death.
Disease n %
Tuberculosis 143 62.4
Diarrhoea/dysentery 45 19.7
Hydatids 13 5.7
Measles 6 2.6
Unspecified fevers 6 2.6
Others 15 7.0
Total 228
Tuberculosis infection was by far the commonest recorded cause of death
(62.4%, n = 143) followed by diarrhoea & dysentery (19.7%, n = 45). Only 6 deaths were
recorded from measles throughout the settlements for the period 1876-1900 (see below),
which contrasts sharply with the previous mortality from this disease (Chapter 7).
One hundred and forty three deaths were recorded from respiratory diseases
(RES) (Table 8.7)
Table 8.7 Frequency (%) of diseases in the respiratory disease

category (RES) recorded as causes of death.
Disease n %
Bronchitis 53 37.3
'Inflammation of the lungs' 24 16.9
Pneumonia 23 16.1
'Congestion of the lungs' 6 4.2
Whooping cough (pertussis) 15 10.6
Influenza 11 7.7
'lung disease' 6 4.2
Other 5 3.5
Total 143
270
Bronchitis (37.3%, n = 53) was the major recorded cause of death in this
category. It should be noted that the cause of death 'inflammation of the lungs' may be
referring to pneumonia (Morgan 1987: 27) in which case it would make the frequency of
this cause of death 32.4% (n = 47). Pneumonia would then be the second most common
cause of death from respiratory system disorders. The term 'congestion of the lungs' is
less clear in its meaning. It could refer to chronic passive congestion of the lungs
resulting from the failure of the left ventricle (Mergner & Trump 1988:254) in which case
the primary cause of death would be from a cardiac disorder. On the other hand, the term
could indicate a non-specific infection or disorder of the lungs causing a build up
pulmonary fluid. The term 'lung disease' is also unclear and could refer to any number of
specific disorders of the lungs.
Table 8.8 displays the total number of deaths and proportional mortality ratios
of each category of disease by age ranges. Of the 714 deaths recorded, 18 lacked
information on age at death sufficiently specific for categorization into age groups.
The ill-defined category represents 24% of the reported deaths. It is due to
the vagaries of reporting the cause of death mainly during the periods of early childhood
and later adulthood (Appendix B) rather than to any specific non-identified condition or
conditions. It is included in the denominator for the following analysis therefore making
the defined causes of death 76% of the total data set.
271
Table 8.8 Numbers of deaths and principal mortality ratios for age ranges 0 to 4, 5 to 14,
and 15+ years for Aboriginal settlements in Southeast Australia 1876-1900
0-4 5 - 14 15+ Total

n PMR n PMR n PMR n PMR
INF 59 25.1 54 54.0 121 33.7 234 33.6

RES 66 28.0 13 13.0 59 16.4 138 19.8
CIR 2 0.8 0 0 17 4.7 19 2.7
DIG 4 1.7 10 10.0 27 7.5 41 5.9
END 13 5.5 1 1.0 1 0.2 15 2.1
GEN 0 0.0 0 0 2 0.5 2 0.3
INJ 4 1.7 4 4.0 8 2.2 16 2.3
NEO 1 0.4 2 2.0 13 3.6 16 2.3
NER 14 5.9 6 6.0 15 4.1 35 5.0
PER 9 3.8 0 0 0 0.0 9 1.3
PRG 0 0.0 0 0 4 1.1 4 0.6
ILL 64 27.1 10 10.0 93 25.8 167 24.0
236 100 360 696
Inf = Infectious and parasitic diseases; Res = Diseases of the respiratory system; Cir =
Diseases of the circulatory system; Dig = Diseases of the digestive system; End = Endocrine,
nutritional and metabolic diseases; Gen = Diseases of the genitourinary system; Inj = Injury;
Neo = Neoplasms; Ner = Diseases of the nervous system; Per = Conditions originating in the
perinatal period; Prg = Complications of pregnancy, childbirth & puerperium; Ill = Ill
defined conditions.
The following discussion will centre on an examination of the causes of death
in the three age ranges 0 -4 years, 5 - 14 years and 15+ years (Figure 8. 4).
272
Figure 8.4 Total recorded deaths (%) by age ranges for

Aboriginal settlements in Southeast Australia.
60.0
15+ years
50.0
40.0 0 to 4 years
%
30.0
20.0 51.7
5 to 14 years
34
10.0
14.4
0.0
Infectious and respiratory diseases were the major causes of disease in all age
ranges, having a combined PMR of over 50, and will be the main focus of discussion.
8.4.1 Age range 0 to 4 years
One third of all deaths (33.5%, n =-236) were recorded for this age range
(Figure 8.3). Infectious diseases (PMR 25.1; n = 59) and respiratory diseases (PMR 28.0;
n = 66) were the major causes of death in the age range. There is no significant difference
between these two groups (x2 =0.392, p = 0.531, 1df).
273
8.4.1.2 Infectious Diseases
Diarrhoea and dysentery
Diarrhoea and dysentery are terms often used synonymously to distinguish
between two clinical syndromes of diverse aetiology (Sommers 1980: 526). Diarrhoea is
associated with the abnormal frequency, urgency, and liquidity of faecal discharges often
accompanied by vomiting and fever. Dysentery refers to various disorders marked by
intestinal inflammation and attended by abdominal cramps, tenesmus, and frequent stools
containing blood and mucus (Benenson 1990: 129; Sommers 1980: 526). The two
clinical syndromes often present simultaneously in individuals infected with enteric
pathogens, or the symptoms can range from a mild, transient diarrhoea to full-blown
dysentery. In general use of the terms, dysentery usually refers to diarrhoea with
abdominal cramping and tenesmus (von Lichtenberg 1989: 355).
The two syndromes are discussed together here because of their frequent
diagnostic confusion by pre-twentieth century medical practitioners. In reviewing the
history of diarrhoeal diseases in Australia, Cumpston (1989: 224-5) points out that no
precise opinion as to the nature of each of the syndromes can be formed.
Both terms were used loosely in nineteenth century Australian medical
literature and official nomenclature to cover either or both sets of clinical syndromes,
particularly when seen in infants. Both syndromes were recorded in the European
populations of Southeast Australia soon after colonisation and were described as
attacking all ages, but having a high mortality rate among infants (Cumpston 1989: 224-
5).
274
The pathogenic micro-organisms responsible for the syndromes are numerous
(Benenson 1990: 129-138; DuPont 1994: 678; Marcy 1976: 892-978; Mata 1980: 4;
Sack: 1980:53-66; Sommers 1980: 526). Bacillary dysentery is the most frequent form
among humans today and was most likely among the Aboriginal people living on
settlements. Enteropathic Escherichia coli, Shigella, Salmonella, and Staphylococcus are
commonly implicated and there is little reason to doubt their presence among the
European and Aboriginal populations of nineteenth century Australia (Cumpston 1989:
224-225). Cumpston states there is little evidence for amoebic dysentery in Australia last
century.
Table 8.9 is an extract from the mortality records showing the reported
distribution of diarrhoea and dysentery reported as causes of death.
What is immediately noticeable in Table 8.9 is the large proportion of deaths
under 3 years of age from diarrhoea and dysentery. This age group was responsible for
81% of all deaths reported as diarrhoea and dysentery. It is quite likely that the two
syndromes were responsible for more infant deaths when other causes are taken into
consideration. The term 'teething' was given as a cause of death in 19 cases of children
between the ages of 0 and 1 years. What this term implies when it is given as a cause of
death is unclear and hence I have placed it in the ill-defined category (Appendix B), but it
may be a euphemism for diarrhoeal symptoms accompanying tooth eruption. If so, then
up to 87% of deaths from diarrhoea and dysentery would come from this age range.
The high number of deaths in the under 3 age range is typical of diarrhoeal
diseases (Marcy 1976: 892; Mata 1980:11). Epidemiologically, both syndromes are
common amongst infants and very young children, particularly those living in
underdeveloped countries (DuPont 1994: 677; Marcy 1976: 892; Rubin & Farber 1988:
275
666; Sommers 1980: 540-1). Despite the improvements in public health in recent
decades, most children are still expected to suffer attacks of diarrhoeal diseases (Mata
1980:3) and
Table 8.9 Reported occurrence of diarrhoea and dysentery

as causes of death on Aboriginal settlements in Southeast
Australia 1876-1900.
Settlement Year Sex Age

Diarrhoea
Coranderrk 1889 Female 1
Female 2
1890 Female 7
1893 Female 0
Point McLeay 1876 Male 0
1877 Male 2
Female 0
1878 Male 2
Female 0
Female 0
Male 1
1880 Female 0
1882 Female 1
Female 2
Female 0
1883 Male 1
Unknown 0
1888 Female Unknown
Female Unknown
1892 Male 1
1895 Male 18
1896 Male 0
Female 0
1897 Female 0
Dysentery
Lake Condah 1877 Male 17
Lake Tyers 1881 Male 2
Lake Hindmarsh 1891 Female 1
Point McLeay 1880 Female 1
Female 0
1882 Male 30
1890 Female 0
1893 Male 0
1894 Male 65
Female 1
1899 Female 0
276
1900 Female 1
many in the world today live through a substantial risk of acquiring a fatal infection
(Marcy 1976: 892; Hardy 1956). Living conditions that are characterised by a lack of
plentiful clean water, inadequate sewerage, poor food and personal hygiene, poor
nutrition, and inadequate health care are favourable to the spread of infectious enteric
microorganisms. Infants usually acquire E. coli during the first days of life by ingesting
maternal organisms at birth and later in life from the hands of other infants, toddlers, and
elder carriers, who may be symptomatic or asymptomatic, and are shedding the bacteria
(Marcy 1976:905). The young are susceptible to the symptoms when loss of maternal
antibody protection occurs after breast feeding ceases and before contact with the various
bacteria has generated a sufficient level of self protection (Marcy 1976: 904).
The distribution of deaths throughout the period 1876 to 1900 is suggestive of
endemicity of the pathogens. The highest number of deaths in any one year was 4 in 1878
at Point McLeay, which regularly had the largest population of all the settlements; the
remaining deaths occurring at levels of 1 or 2 per year. If living conditions allow bacteria
to become locally endemic, a high morbidity and mortality can be expected in the early
years of life. But when an enteric infectious organism becomes endemic a degree of
antigenic homogeneity can develop among the strains, particularly E. coli and Shigella
sp., in turn leading to a more efficient immune response by the host with increased age.
This leads to lower morbidity and less mortality after the initial years of life.
There is little other evidence in the historical literature from which an
assessment of the overall prevalence of diarrhoeal diseases can be made. From the causes
of death, particularly in those under three years of age, and the conditions under which the
277
Aboriginal people lived on the settlements (Barwick 1972, Jenkin 1976, 1979; McCrea
1879) we can assume that it was high and that most children acquired an infection at least
once during their life. If infections led to chronic or repeated acute diarrhoeal illness it
would have had an adverse effect on the growth of the children and contribute to further
malnutrition. DuPont (1994: 678) has estimated that there is a 20 to 60% decrease in the
caloric intake during a bout of diarrhoea, depending on the severity and the length of the
symptoms. Mata (1983: 13) identifies a protein-losing enteropathy occurring in diarrhoea
due to tissue-invading bacteria and viruses.
Chronic diarrhoea in children is a contributing factor in marasmus and
kwashiorkor, particularly during the first two years when weaning occurs (Mata 1983:
13). There were 9 causes of death given as marasmus at Point McLeay (Appendix B);
eight were in children under 3 years of age and a further case in a 60 year old female. The
age range and the prominence of children (89%) are similar to those whose deaths were
recorded as diarrhoea and dysentery. These individuals may therefore have suffered from
chronic diarrhoeal infection prior to death causing a deficiency in food absorption leading
to prolonged protein-energy malnutrition (PEM).
It appears then that a high number of childhood diarrhoeal diseases infections
can be inferred as a character of life on Aboriginal settlements. In many cases it was a
principal cause of death. In other cases chronic or repeated diarrhoeal infection would
have led to anorexia and weakened the immune response, exposing the young to a further
threat from other infections. Diarrhoea and dysentery would thus have been common
underlying conditions predisposing to death from other causes.
Other infectious diseases
278
Table 8.10 lists all other infectious diseases reported in this age range less
diarrhoea and dysentery.
Table 8.10 Infectious diseases less diarrhoea

and dysentery reported as causes of death in
age range 0-4 years.
Reported cause of n %1
death
Tuberculosis 8 9.6
Measles 4 4.9
Thrush 4 4.9
Hydatids 1 1.2
Scarlet fever 1 1.2
Low fever 1 1.2
Total 19
(Ill defined causes 64 77.1)
1 Includes the ill defined category in the denominator
Because of the large number (n = 64) in the ill defined category it is difficult
to make strong inferences from this table. It can be assumed with some safety, however,
that for most of the diseases the figures represent a minimum number of the total causes
of death. The 8 cases of tuberculosis can, I believe, be certainly seen as a minimum
number when its generality in the Aboriginal populations prior to 1876 (Chapter 5) and its
frequency or reporting in later age ranges (see below) is taken into consideration.
The four deaths from measles may, however, reflect a more reliable
frequency. Three of the deaths reported, 1 at Point McLeay in 1893 and 2 at Lake
Wellington in 1894, were during an epidemic period among the European populations
(Chapter 7). The last death was at Lake Tyers in 1900. Its relative absence among the
Aboriginal people can be explained, however, by their isolation from the main European
population centres. The missionaries and superintendents of the settlements made
279
concerted efforts to restrict contact between the Aboriginal inmates and the nearby
European townships. Their reasons were not so much to do with protecting the
Aboriginal people from infectious diseases but rather to regulate their movements,
Christianise them and shield them from what they saw as moral corruptness within
European society (Broome 1982: 69-86; Saggers & Gray 1991:69). Their efforts were
encouraged by the colonial governments who saw institutionalisation and isolation as a
major step in controlling the Aboriginal people. While their efforts at isolation were not
always successful and contact between the two groups continued it was much reduced
compared with earlier years. The result was to shield the inmates of the settlements to a
large degree from localised outbreaks of measles which regularly arose in the European
population. There were five major epidemics of measles in the European population
between 1876 and 1900 (Chapter Seven, Table 7.1); the latter two in 1884 and 1893 had
high cause-specific mortality rates of 41-49 per 100,000 and 74 per 100,000 respectively.
As discussed in Chapter Seven there is little evidence of these epidemics among the
Aboriginal people living on settlements in Southeast Australia.
Thrush was reported in what would appear as a localised outbreak at Point
McLeay in 1893 (Appendix A). Thrush (or candidiasis) is usually a benign condition
presenting in the oral cavities during the first weeks of life. The disease can become life-
threatening under two situations. In children, who are immunosuppressed by other
infections or under antibiotic therapy. The former would most likely have been the cause
in these children. In such a situation candidiasis can cause severe and fatal disseminated
infection involving almost all tissues, with the kidneys, liver, spleen, heart, and brain
often implicated (Miller 1976: 638, 641).
The reporting of this disease as a cause of death in such temporal and spatial
isolation is odd when it is considered that candidiasis is common in newborn infants and
280
that the causative organism Candida sp. is part of the normal human flora. The reason for
the outbreak may lie in the varying pathogenicity of the species or strains of Candida
concerned. It is usually Candida albicans but several other species can be implicated.
The degree of pathogenicity depends on the toxin produced by the organism and can vary
between each strain (Benenson 1990:72-73; Miller 1976: 638). Another alternative that
should be considered is that of misdiagnosis. Candidiasis can be confused with other oral
and disseminated infections particularly when only clinical diagnosis is available.
Herpesvirus and coxsackie virus lesions in infants with disseminated infection may
appear clinically similar to those with sepsis due to other organisms (Miller 1976: 643).
Post natal infection with Treponema pallidum cannot be ruled out as a contributing factor.
8.4.1.3 Respiratory diseases
With a PMR of 28.0 respiratory diseases were the second most definable
disease group recorded as cause of death in age range 0 to 4 years. Table 8.11 lists the
causes of death from respiratory diseases.
Table 8.11 Respiratory diseases reported as causes of death

in age range 0-4 years.
Reported cause of death n %1

Bronchitis 29 22.3
Whooping cough (pertussis) 14 10.8
Pneumonia 10 7.8
Influenza 6 4.6
'Inflammation of lungs' 3 2.3
'Congestion of lungs' 2 1.5
'Lung disease' 2 1.5
Total 66
(Ill defined causes 64 49)
281
Bronchitis
Bronchitis (n = 29, 22.3%) was the outstanding disorder amongst respiratory
diseases. Age distribution of deaths from bronchitis among the Aboriginal settlements is
compared with the European population of Victoria for the years of 1876, 1880, 1890,
and 1900 in Figure 8.5. Both curves show similar high frequencies of death during early
childhood and late adulthood with a long period of low frequency during the intervening
years. The peaks during middle adulthood displayed by the Aboriginal curve do not
indicate a high mortality from bronchitis when compared with the European population,
but rather reflect a much smaller sample size.
Figure 8.5 Age distribution of deaths from bronchitis, among Aboriginal

populations living on settlements in Southeast Australia 1876 to 1900 compared to
European population of Victoria for the years 1876, 1880, 1890 & 1900.
45
40
Aborigines
35
30 Europeans Vic.
25
%
20
15
10
5
0
0 5 10 15 20 25 30 35 40 45 50 55 60 > 60
Age
Rubin and Farber (1988: 584) define bronchitis as the hyperplasia and
hypertrophy of the bronchial mucous glands and an increased production of mucus in the
282
bronchial passages. The principal clinical sign of bronchitis is a persistent productive
cough, often more severe in the winter months. Acute respiratory failure can occur in
advanced cases leading to insufficient oxygenation of the blood (hypoxaemia) and
ventricular failure. Chronic bronchitis can often be an underlying factor for a number of
degenerative disorders. Because of retained mucous secretions, individuals with chronic
bronchitis are at an increased risk of bacterial infections of the lungs, particularly
pneumonia. Further, the risk of lung cancer and cardiovascular disease is increased by
chronic bronchitis. As such, the significance of bronchitis in its effects upon the mortality
experience of a community is often unrealized because of its contributory role in the
deaths formally attributed to other causes (Young 1979: 320).
Three important causative factors have emerged in the development of the
condition: infection, tobacco inhalation, and atmospheric pollution (Benenson 1990: 367-
8; Cotran et al. 1989: 771-3; Thurlbeck & Miller 1988: 585-591). Episodes of bronchitis
ranging from mild to severe symptoms can be initiated by pathogenic invasion
particularly from Haemophilus influenzae and Streptococcus pneumoniae. Symptoms
resulting from these bacterial invasions may also be associated with concurrent viral
infection of the respiratory tract or with chronic exposure to atmospheric pollutants
(Rubin & Farber 1988: 584). Age is a significant factor in infectious bronchitis (Cotran et
al. 1989: 772). Figure 8.5 shows a high frequency of deaths from bronchitis among both
Aboriginal and European children, particularly during the first year of life and then a
levelling out at age three years.
During the first year of life children are particularly susceptible to bronchial
disturbances initiated by bacterial or viral infection. Predisposing factors for acute and
life-threatening symptoms for these early ages would include the unfavourable
socioeconomic circumstances and poor nutrition experienced by most Aboriginal people
283
on the settlements. A further predisposing factor would have been the dwellings which
were often over crowded, dusty in summer and damp during the winter (Barwick 1972;
Jenkin 1979: 222; McCrea 1879-80). Passive tobacco smoke inhalation would have been
common among new born and young Aboriginal children, further promoting the onset of
bronchitis.
Whooping cough (pertussis)
Whooping cough (n = 14, 10.8%) was the second major cause of death from
respiratory disease. Whooping cough is an acute bacterial disease common to children 0
to 5 years of age worldwide, regardless of climate, or geographic location. The causative
agent is Bordetella pertussis. Infection is primarily by direct contact with airborne
discharges from respiratory mucous membranes of infected persons (Benenson 1990:
318-319). The disease would have been readily recognised in the nineteenth century.
Observable symptoms begin with a catarrhal phase which gradually develops into severe
paroxysms characterised by repeated violent coughing. Each series of coughs continues
without intervening inhalations and is followed by the characteristic high pitch inspiratory
whoop from which the diseases gets its common name. The paroxysmal stage can last for
1 to 2 months or longer with as many as 50 coughing episodes per day (Benenson 1990:
319; Connor & Gibson 1988: 364-365). Immunity is often conferred after the first
infection by B. pertussis but second attacks can occur. Compromised immune systems
can assist subsequent infections in infants and initial infections in adolescents and adults
(Benenson 1990: 321).
Whooping cough deaths were confined to the 0 to 4 years age range with the
exception of one 8 year old male. This is the common pattern of mortality from the
disease with death rates highest in children up to the age of 5 years (Connor & Gibson
1988: 365). Of the deaths within the 0 to 4 years age range 8 (57.1%) were in the first
284
year of life; 3 (21.4%); in two year olds; and 1 in a three year old. There was no sex
difference.
Other respiratory diseases
Pneumonia was recorded as a cause of death in 10 cases (Table 8.8). If the
term 'inflammation of the lungs' is referring to the same disorder (Morgan 1987) then
another three cases can be added giving pneumonia a similar ranking to whooping cough.
The low reported frequency of influenza is most likely a misrepresentation of the real
threat this disease had to the Aboriginal infants and children due to the reporting of other
symptoms. Infection by the virus can cause a range of secondary conditions that if left
untreated can be life threatening. They include viral and bacterial pneumonia, bronchitis,
the common cold, gastrointestinal manifestations presenting as nausea, vomiting,
diarrhoea, prolonged fever, and convulsions (Benenson 1990: 224). It is quite likely that
much of the mortality from respiratory causes was precipitated by an influenza virus
infection.
8.4.2 Age range 5 to 14 years
One hundred deaths (14.4% of the total) were recorded in this age range
(Table 8.5). Infectious diseases (PMR 54.0, n = 54) and respiratory diseases (PMR 13.0,
n = 13) were the leading causes of death. Combined, they accounted for 67% of all the
deaths in this age range.
8.4.2.1 Infectious disease
Table 8.12 shows the number of deaths from infectious disease for age range
5 to 14 years.
285
Table 8.12 Causes of death from infectious diseases in age

range 5 to 14 years.

Intermittent fever 2 3.7
Fever 1 1.9
Rheumatic fever 1 1.9
Enteric fever 1 1.9
Diarrhoea 2 3.7
Hydatids 2 3.7
Total 44
(Ill defined) (10) (18.5)
Tuberculosis
Tuberculosis (n =35, 64.8%) was the major infectious disease responsible for
mortality in this age range accounting for 35% of all deaths. Table 8.13 shows the
number of male and female deaths reported from tuberculosis in the 5 to 14 years age
range.
Table 8.13 Number of deaths from

tuberculosis in age range 5 to 14 years.
Age Male Female

5 2 2
6 2 1
7 0 0
8 0 1
9 0 0
10 0 4
11 1 3
12 0 8
13 3 3
14 1 4
Total 9 26
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Female deaths (n =26) were significantly more than male deaths (n =9) (x2 =
8.26, p = 0.004, 1df).
The age and sex of a tuberculosis infected individual have a strong influence
over the outcome of the disease. The main age periods of high susceptibility are during
infancy, puberty, and old age. The specificity of tuberculosis mortality for each of the
sexes also varies. In youth and early adulthood females suffer from a heavier mortality
than males (as seen above). This trend can reverse itself in later adulthood, with males
suffering a higher mortality. The onset of menarche and higher rates of mortality from
tuberculosis in young women are linked (Johnston 1993: 1060) although the reasons are
not fully understood. The metabolic changes during menarche increase the body’s need
for protein and this in turn may reduce the efficiency of the immune system. Its response
to new mycobacterial infection, or a present latent infection, would then be less effective,
resulting in the onset of acute clinical symptoms of tuberculosis.
Another factor that could be influential in the deaths of females from
tuberculosis is the differing daily lifestyle of males and females of this age range. Both
sexes spent much of their day in classrooms under instruction by the missionaries
(Massola 1970, 1975). Crowded classrooms can be fertile breeding grounds for
tuberculosis if one individual is infected and capable of spreading the mycobacteria.
Evidence of this can be seen of the sporadic epidemic outbreaks of tuberculosis in school
children in western countries this century (Proust 1991a: 227-230) where the disease is
not a major cause of morbidity. In such cases both sexes would be equally exposed to the
infection. Out of the class rooms, however, the young females were often required to
spend much of their time indoors learning domestic skills while young males spent time
out of doors learning labouring and agricultural skills (Jenkin 1979: 97-111; Masssola
287
1970, 1975) . The young females would then have more daily contact with tuberculosis
sufferers in confined spaces and would be more exposed to infection.
Table 8.14 shows the frequency of respiratory diseases recorded as a cause of
death.
Table 8.14 Causes of death from respiratory diseases in age

range 5 to 14 years.

Pneumonia 5 21.7
'Pulmonary' 1 4.3
'Inflammation of lung' 2 8.6
'Congestion of the lungs' 1 4.3
'Lung disease' 1 4.3
Whooping cough 1 4.3
Bronchitis 2 8.6
Total 13
(Ill defined 10 43.5)
Pneumonia with 5 deaths (or 7 if 'inflammation of the lungs' is grouped with
it) is the major cause of mortality in this age range. The small number of deaths in this
category precludes any meaningful analysis or statements other than to note the total of
deaths (n = 13) attributed to respiratory disorders. The highest levels of mortality from
the majority of respiratory diseases are usually during infancy, early childhood and the
aging (Benenson 1990: 330). The low level (PMR 13, n = 13) of these diseases in the 5
to 14 years age range is therefore not unusual . Low socioeconomic circumstances and/or
underlying medical conditions can promote this disorder to life threatening situations in
the young (Benenson 1990: 330).
288
8.4.2.3 Digestive system diseases
Diseases of the digestive system had a PMR of 10.0 (n = 10) in this age range.
Peritonitis was given as the cause in 5 cases; 3 females and 2 males aged between 5 and 9
years. Other causes of death in this category were given as bowel, stomach and liver
disorders.
Peritonitis (inflammation of the peritoneum) is a serious, life-threatening
disorder. The most effective treatment is surgery. Peritonitis is most commonly caused
by perforation of the abdominal viscus leading to bacterial invasion of the peritoneum.
An escape of bile from a ruptured gall bladder can also initiate inflammation. A primary
form of peritonitis is caused by toxins from the blood stream entering the peritoneum.
Common primary disorders leading to peritonitis are peptic ulcer, inflamed appendix,
colonic diverticulum, and strangulation of the bowel. Tuberculosis infection may also be
involved (Rubin & Farber 1988: 717-718). For nineteenth century medical practitioners
it was readily diagnosed by the sudden onset of abdominal pain in the area of initial
invasion becoming general as inflammation spreads, and a characteristic abdominal
rigidness caused by contraction of abdominal muscles (Dayal & DeLellis 1989: 905;
Rubin & Farber 1988: 717-718). The likely causes of the disorder among the 5 children
would have been a ruptured appendix or an underlying tuberculosis infection.
8.4.3 Age range 15+ years
Three hundred and sixty deaths (51.7% of total deaths) were recorded in this
age range (Table 8.5). Infectious diseases had a PMR of 33.7 (n = 121) and respiratory
diseases a PMR of 16.4 (n = 59). Combined they account for 50% of the total deaths in
289
this age range. The next highest category was digestive system diseases with a PMR of
7.5 (n = 27). The remaining disease categories had PMRs of 4.7 or less. The ill defined
category (n = 93) had a PMR of 25.8. This was mainly due to the reporting of 70 deaths
given as either 'senile decay', 'old age', or 'general decay'.
8.4.3.1 Infectious diseases
Table 8.15 shows the frequency of infectious diseases reported as causes of
death.
Table 8.15 Causes of death from infectious diseases in age

range 15+ years.

Hydatids 10 4.7
Dysentery 4 1.9
Diarrhoea 1 0.5
Enteritis 4 1.9
Measles 2 0.9
Scarlatina 1 0.5
Typhoid 2 0.9
Total 121
(Ill defined) (93) (43.4)
Tuberculosis
Tuberculosis (n = 97, 45.3%) was the outstanding cause of death in the
infectious disease category. Overall it accounted for 27% of all deaths in this age range.
Table 8.16 compares the reported causes of death from tuberculosis infection for the 15+
age range in age increments of 10 years for each sex. .
290
Table 8.16 Recorded cases of tuberculosis deaths in age range

15+ years where both age and sex were recorded.
Age Males Females

n % n %
15-24 18 41.9 19 38.0
25-34 9 20.9 14 28.0
35-44 6 14.0 6 12.0
45-54 6 14.0 6 12.0
55+ 4 9.3 5 10.0
43 50
There is no significant difference between males and females (X2 = 0.5268, p

= 0.4679) for the age range.. What is noticeable is that for both sexes the majority of
deaths from tuberculosis occurred before the age of 35 years (males 62.8% and females
66%). After 35 years of age the number of deaths from tuberculosis falls. Age has a
strong influence in the final outcome following infection by M. tuberculosis. Infancy and
puberty are typically periods of low resistance and high susceptibility to tuberculosis.
The lowest mortality rates usually occur after 3 years old and before the age of 15 years in
both males and females. The risk of developing life threatening symptoms of the disease
increases again among adolescents and young adults (Benenson 1990: 460; Dubos &
Dubos 1953: 194; Johnston 1993: 1066). This can result either from reactivated
symptoms of long latent infections or primary exposure to the pathogen (Benenson 1990:
460; Connor & Gibson 1988: 395). Among the Aboriginal populations on the settlements
the high mortality from the disease in early adulthood is typical of endemic tuberculosis,
ineffectively treated.
Hydatids
Hydatid disease (echinococcosis) as a cause of death was reported 10 times
(5.0%) in the 15+ age range (Table 8.17). (Three other cases; a 4 year old male, 10 year
291
old female and a 13 year old female were reported). The cases occurred throughout 6 of
the 8 settlements. Coranderrk settlement recorded the most deaths with 5 (38%) cases, 4
of which occurred in a 3 year period between 1879 and 1881. Because of the small
number or reported cases no age/sex pattern can be statistically determined but in the 15+
age range male deaths (n = 7) outnumbered female deaths (n = 3). Among the European
population males were more susceptible to hydatids than females (Thomas 1884: 150-
168) most likely due to more males than females being employed in rural activities.
Table 8.17 Reported occurrence of hydatids as a cause of death

on Aboriginal settlements in Southeast Australia 1876-1900.
Settlement Year Sex Age

Framlingham 1879 Male 50
Lake Wellington 1884 Female 45
1885 Female 10
Coranderrk 1879 Male 45
1879 Female 26
1880 Male 35
1881 Male 50
1900 Male 56
Lake Hindmarsh 1879 Male 32
Point McLeay 1880 Male 32
1891 Female 27
1892 Male 4
Point Pearce 1883 Female 13
Hydatids had most likely become common among the Aboriginal populations
of the Southeast by the early 1860s (Hudson 1861: 75). Probably the first reference to
hydatids disease among the Aboriginal populations of the Southeast comes from Hudson
(1861: 75) who carried out a post mortem on an Aboriginal male and identified hydatid
cysts. Hudson states that the male had been 'living in the bush' and had eaten under-
cooked 'diseased mutton' given to him on the sheep stations. Another early reference to
hydatids among Aboriginal populations comes from Point McLeay in 1876. Taplin
292
(1876a), reviewing the diseases he had observed among the Ngarrindjeri during the
previous 18 years, lists 'hydatids in the liver' as one of the diseases they were subjected to.
He did not record any deaths from hydatids during this period.
From the second half on the nineteenth century hydatid disease had become a
serious disease among the European populations of Victoria and South Australia. During
the period 1861 to 1880, 584 deaths (mean death rate per annum 16.23 per 1,000) were
recorded in Victoria from hydatids. In South Australia between 1865 and 1880 the mean
death rate per annum was 15.16 per 1,000 (Thomas 1894: 150, 167).
Hydatid disease is a zoonotic infection of humans occurring mainly in rural
areas. Although no organ is exempt, the disease causes cyst formation mainly in the liver
and lungs and less frequently in the kidneys, spleen, bone, and central nervous system
(Stevenson & Hughes 1980: 40; Thomas 1884). Echinococcus granulosus (a dog
tapeworm) was most likely the causative agent of the disease on the settlements. Today it
is the most common cause of hydatid infection in rural communities of Southeast
Australia. E. granulosus occurs where dogs are used to muster grazing animals,
particularly sheep, and where they have an intimate contact with humans. These
conditions were common to most of the Aboriginal settlements where attempts at self-
sufficiency were made by grazing sheep and cattle on lands adjacent to living areas. Dogs
were popular both as working animals and as pets on the Aboriginal settlements (Gibson
1869-75; Plate 8.1).
The major life cycle of the tapeworm is dog-sheep-dog. Transmission to
humans is usually by hand to mouth transfer of the mature tapeworm’s eggs from dog
faeces. Exposure occurs in handling infected dogs and objects soiled by dog faeces.
Exposure can also occur through contaminated food and water (Benenson 1990:149).
293
Another life cycle occurs in endemic Australian mammals of dingo-wallaby-dingo
(Stevenson & Hughes 1980: 40) which may have involved different variants of E.
granulosus (Thompson & Kumaratilake 1982: 16).
Although 13 deaths from hydatid disease were recorded on the settlements
during the period the real extent of morbidity and mortality is unclear because of the
difficulties involved in diagnosis last century. There is no record of post mortems.
Diagnosis of hydatids would have involved an assessment of the clinical symptoms, most
likely by tactile detection of cysts lying close to the body surface, and by fragmenting cyst
portions, particularly those occurring in the peritoneal cavity, lung or intestinal tract,
being coughed up, vomited or passed in the faeces (Thomas 1894): If hydatid disease was
not diagnosed by these means other causes of death would have been recorded. Causes of
death such as 'tumified liver', 'enlarged liver', 'liver disease’, 'lung disease', or those
involving the brain may in reality be related to advanced hydatids infection. Thus
hydatids may have been directly or indirectly responsible for a greater number of deaths
than is reflected in the settlements’ records of death.
Enteric fever (typhoid)
There were 2 causes of death listed as typhoid and 4 listed as enteritis or
enteric fever in this age range (Table 8.15), and 1 cause of enteritis listed for the 5 to 14
years age range (Table 8.18).
294
Table 8.18 Causes of death in 15+ age range possibly attributed to typhoid.
Settlement Year Sex Age Cause of death

Lake Hindmarsh 1877 Female 16 Enteritis
Lake Condah 1877 Male 30 Typhoid Fever
Point McLeay 1878 Female 15 Enteritis
1880 Female 12 Enteric Fever
1880 Male 40 Enteric Fever
Point Pearce 1891 Male 16 Typhoid
There was considerable confusion over the diagnosis of typhoid in nineteenth
century Australia (Cumpston 1989: 230). Typhoid is easily confused with other diseases
displaying a febrile onset; for example, hepatitis, tuberculosis, typhus (LeBaron & Taylor
1993: 1073). Typhoid (or enteric fever, enteritis) has been present in Australia since the
arrival of the First Fleet but did not become a major medical problem until after 1850
when the gold fields were opened and a massive increase in population ensued
(Cumpston 1989: 230). From then until 1890 typhoid was responsible for high death
rates among the Europeans of between 30 and 80 per 100,000. Deaths were highest
between the ages 15 and 44 years. A gradual decline in the incidence of the disease then
occurred in the eastern colonies (Cumpston 1989: 230). The disease almost certainly did
not exist among the Aboriginal population of Australia prior to 1788. Its history among
the Aboriginal people during the colonial period is largely unknown but the deaths
reported on the settlements suggest that a typhoid-like disease was present among them
although at a minor level.
Table 8.19 shows the frequency of respiratory system diseases reported as
causes of death.
295
Table 8.19 Causes of death from respiratory diseases in age

range 15+ years.
Recorded cause of death n %1

Bronchitis 22 14.5
Inflammation of lungs 18 11.8
Pneumonia 7 4.6
'Lung disease/complications' 4 2.6
Congestion of lungs 3 2.0
Influenza 2 1.3
Pleurisy 1 0.7
Laryngitis 1 0.7
Asthma 1 0.7
Total 59
(Ill defined causes) (93) (61.2)
Bronchitis
Bronchitis (n = 22; 14.5%) was the second most recorded cause of death from
respiratory disorders if 'inflammation of the lungs' and pneumonia are grouped as the
most recorded cause. There was no difference between male (n = 11) and female (n = 11)
frequencies. Table 8. 20 displays a breakdown of deaths in 10 year age increments.
Table 8.20 Breakdown by age of recorded

deaths from bronchitis (male and female) in
age range 15+ years.
Age n %
15 - 24 0 0
25 - 34 2 9.1
35 - 44 2 9.1
45 - 54 6 27.3
55 - 64 3 13.6
65 - 74 6 27.3
75+ 3 13.6
Total 22 100
A sharp increase of deaths from bronchitis from age 45 years and onwards is
noticeable. Nineteen deaths or 81.8% occurred after this age. This trend is quite likely to
have been a result of chronic bronchitis due to many years of tobacco smoking. The most
296
important factor in the development of chronic bronchitis in later adulthood is the practice
of tobacco smoking. The mortality rate from bronchitis is significantly higher in tobacco
smokers than in non smokers (Rubin & Farber 1988: 584). In recent years 90% or more
of all cases of chronic bronchitis have been found to occur in smokers; the frequency of
the symptoms in chronic smokers is more than 25%, in moderate smokers 10 to 15%, and
in non-smokers it is less than 5% (Rubin & Farber 1988: 584).
The European colonists smoked a lot of tobacco, often seeing it as a necessity
of the hard life in the colonies rather than as a luxury. Contact with Europeans introduced
Aboriginal people to tobacco and smoking quickly became a particularly common
practice among most communities (Bulmer 1876; Mason 1859; Saggers & Gray 1991:
86-88). A currency of addiction was created from tobacco. The colonial governments
provided Aboriginal people with regular weekly or monthly rations of tobacco, often
giving extra proportions to the elderly or sick. The substance was further bartered or
bought from European traders. Pastoralists often used tobacco rather than money as an
enticement to Aboriginal people to work for them.
Tobacco was easily obtained on the settlements and addiction was widespread
among both males and females. It took the place of indigenous narcotics such as pituri
(Duboisia hopwoodii) which had in the past been traded through the extensive trade and
exchange networks (McBryde 1987; Watson 1983) and which now no longer operated.
On Lake Tyers settlement in 1878 there were sixty people (many of them elderly women),
out of just over one hundred residents who were addicted to tobacco (Bulmer 1876). The
manager of the settlement, Rev. J. Bulmer, allowed a three-monthly ration of 30 lbs (14
kg) a month for the whole settlement which he rationed out at no more than two 'figs' per
week. He could not get them to abstain from smoking tobacco. Tobacco was seen by
297
many Aboriginal people as the only drug in the British pharmacopoeia that was of any
use. Opium was also smoked by some (Bulmer 1879).
The third aetiological factor in the development of bronchitis is atmospheric
pollution, particularly from industrial sources. The precise agent or agents in atmospheric
pollution remain uncertain but high levels of sulphur (as SO2 and H2SO4) in the air may
be responsible for initiating the symptoms of chronic bronchitis (Rubin & Farber 1988:
584). It would be expected that this factor played a minor role in the development of
bronchial disabilities among the Aboriginal communities concerned in this study.
Nevertheless, domestic fire-places have been associated with high levels of bronchitis.
Ashley (1967) examined the distribution of bronchitis in 83 county boroughs of England
and Wales and found that pollutants derived from domestic fire-places rather than
industrial sources were primarily indicated in the aetiology. Poorly ventilated dwellings
were common on the Aboriginal settlements and smoke from internal domestic fires may
have played a part in the development of chronic bronchitis among the residents.
Pneumonia/Inflammation of lungs
Pneumonia (n = 7; 4.6%) and 'inflammation of the lungs' (n = 18; 11.8%)
taken jointly accounted for 25 (16.4%) of recorded respiratory disease deaths. As
discussed above and in Chapter 6 high levels of mortality from respiratory diseases are
common in the ageing. Pneumonia is often a secondary complication of other disorders,
particularly influenza infections and is often aggravated by chronic tobacco inhalation and
alcohol consumption (Thurlbeck & Miller 1988: 567-569). Both were common habits
among Aboriginal populations (Bulmer 1876; Cannon 1988: 64; Lewis 1992: 152-156;
Mason 1859). Even with modern treatment case fatality rates among patients with
substantial underlying disease can reach 20 to 40% (Benenson 1990: 330). Among the
Aboriginal people on the settlements, however, the case fatality would be expected to be
298
much higher when the lack of effective treatment of the disease and the socioeconomic
circumstances are taken into consideration. The high mortality from pneumonia here can
be seen as a continuation of this disease among adult Aboriginal people living on the
settlements which began during the incarceration of Tasmanians on Flinders Island
(Wybalenna) between 1831 and 1847 and later at Oyster Cove (Plomley 1987:915-942;
Smith 1858-69).
8.4.3.3 Digestive system diseases
Table 8.21 lists diseases of the digestive system (PMR 7.5; n = 27) recorded
as causes of death.
Table 8.21 Causes of death from digestive system diseases

in age range 15+ years.

Liver disorders 9 7.5
Bowel disorders 7 5.8
Peritonitis 3 2.5
'Chronic disease of stomach' 5 4.5
Hepatitis 1 0.8
Gastric Fever 1 0.8
Dyspepsia 1 0.8
Total 27
(Ill defined causes) (93) (61.2)
It is difficult to make any substantial statement regarding this disease group
other than to recognise that disorders of the liver and disorders of the bowels are the two
most prominent recorded causes of death. Disorders of the liver included 'cirosis [sic] of
liver', 'enlargement of liver', 'liver inflammation', 'tumefied liver', 'liver complaint', and
'disease of liver'. Although the liver is vulnerable to a wide range of metabolic,
circulatory, toxic, microbial, and neoplastic insults (Cotran et al. 1989: 915) the recorded
299
causes, together with one cause of death named as 'hepatitis', may suggest the presence of
acute viral hepatitis A (HAV). Hepatitis has been recognised by medical practitioners
and observers for millennia and was usually associated with jaundice (Rubin & Farber
1988: 739). This latter term, however, does not appear in the Aboriginal mortality
records although the reason for this may be that it is less visible in darker-skinned people.
Acute viral hepatitis usually causes inflammation and necrosis of the liver to which the
above terms may apply. If so the disease was probably hepatitis A. HAV is spread from
person to person by the faecal oral route usually by oral ingestion of contaminated water
or food supplies. With the poor sanitation and hygiene conditions of the Aboriginal
settlements HAV would most likely be the most common form of hepatitis. Its low
frequency as a cause of death is most likely due to the fact that HAV never pursues a
chronic course, there is no carrier state, and infection provides lifelong immunity (Rubin
& Farber 1988: 739).
There were 6 causes of death recorded as 'inflammation of the bowels'. The
term is ambiguous but may be referring to what is recognised today as nonspecific
inflammatory bowel disease. The aetiology of this disease category is uncertain but
ulcerative colitis and Crohn's disease (regional enteritis) have been implicated as either
two separate entities or opposite ends of a single inflammatory spectrum (Dayal &
DeLellis 1989: 868; Rubin & Farber 1988: 692).
8.4.4 Less frequent causes
This section will briefly cover the remaining disease categories not discussed
above. Because of their low PMRs and consequent lesser importance to Aboriginal
mortality they will be discussed in overview and not according to age range.
300
The less frequent conditions recorded as causes of death were diseases of the
digestive (PMR 5.9), nervous system (PMR 5.0), circulatory system (PMR 2.7), perinatal
conditions (PMR 1.3), injuries and poisonings (PMR 2.3), neoplasms (PMR 2.3),
endocrine system (PMR 2.1) complications of pregnancy (PMR 0.6), and diseases of the
genitourinary system (PMR 0.3). As shown by their respective principal mortality ratios
these categories were of less importance than infectious and respiratory system diseases
and did not pose serious mortality and health problems to the Aboriginal inhabitants of
the settlements.
Forty-one deaths were recorded from digestive system disorders. This group
included abnormal conditions of the mouth, stomach, peritoneum, bowels, and liver.
Diseases of the nervous system were reported in 38 deaths. They included a broad range
of disorders and symptoms - disorders of brain tissue, hydrocephalus, meningitis,
paralysis, convulsions and fits. Heart disorders accounted for 19 deaths. Sixteen deaths
from injury included drowning, suffocation, sunstroke, falls, burns and gunshot wounds.
Fifteen cases of marasmus were reported; 5 from Lake Hindmarsh and 10
from Point McLeay. All but one case, a 64 year old female, were of children under 9
years of age. The link between marasmus and diarrhoeal disorders has been discussed
above and it is possible that these deaths may have been due a chronic diarrhoeal state.
Their recording on just two of the settlements is most likely due to the different
diagnostic or recording practices rather than a differential occurrence. 'Cancers' and
'tumours' were recorded in 13 cases. The bladder, tongue, intestines, chest, leg, and
unspecified regions of the body were given as sites. Perinatal and pregnancy
complications, and disorders of the genitourinary system accounted for 11, 4, and 2
deaths respectively.
301
No reliable epidemiological inferences can be drawn from these disease
groups other than to note their presence and their respective principal mortality ratios.
The two with the highest PMRs, digestive system diseases (6.4), and nervous system
diseases (6.0), each represent less than two deaths per year over the 25 year period for
each of the eight settlements; the others even less. Whilst there would have been more
than the occasional error in their diagnosis as a cause of death, their universally low
reporting in the eight settlements strongly indicates that these causes of death were
overshadowed by infectious and respiratory system diseases.
Two final references to infectious diseases are needed. The first is the
infrequent reporting of scarlet fever (scarlatina) among the settlements. Two deaths due
to ‘sraclatina’ were reported, one in a 45 year old (sex not recorded) and the other in a 2
year old female. The low frequency of recorded deaths from this disease reflects the
pattern in the general population of Southeast Australia for the period. In both Victoria
and South Australia scarlet fever had its highest recorded death rate in 1876; (280 per
100,000 for Victoria and 112 per 100,000 for South Australia) and throughout the
remainder of the century it was in a steady decline with localised minor epidemic
occurrences (Cumpston 1989: 301). The disease was thus never a major threat to the
Aboriginal settlements.
Finally, there was one reported death from congenital syphilis. Syphilis had
been one of the major causes of morbidity and mortality among Aboriginal people since
the arrival of European colonists (Chapter Four). There are frequent references to the
disease in the historical literature from all three mainland colonies in Southeast Australia.
The majority of these references are to the disease existing in Aboriginal populations
living in regions bordering the European settlement frontiers. Syphilis had been reported
as a cause of death on at least one of the settlements prior to 1876. In 1876, J. Green, the
302
former manager of the Coranderrk settlement, reported that during the first 14 years after
its establishment there were approximately 51 deaths in total:
Fifteen of those who died came to the station sick with a complication of
diseases, principally pleuro [sic] and syphilis. Four died of old age, two were
killed, and one drowned, and several others (29) were born while their
mothers were suffering from the effects of syphilis (four at the very least), in
all twenty-six (26), leaving twenty five (25) to have died of diseases that
could be in any way ascribed to the climate at Coranderrk. And eleven (11)
of the twenty-five were the children of syphilitic parents; they died of
"pleuro", the other deaths were principally of low fever... nearly all the
aborigines, old and young, when they first came to settle at Coranderrk, were
suffering in some way or other from syphilitic disease... (Green 1877-78).
While similar situations probably existed on other settlements prior to 1876
there are no further records of death from syphilis on the settlements in Southeast
Australia apart from the one incident above. This does not however mean that it was
entirely absent. The case of congenital syphilis indicates that at least the mother of the
child had the disease. Congenital syphilis in newborn infants and acquired tertiary
syphilis in adults may have gone unnoticed or unrecorded if more recognisable disorders,
or other secondary causes could be diagnosed as cause of death. Treponemal infection
could then have been an underlying foundation predisposing for other and more fatal
infections.
8.5 Infant mortality

So far the emphasis of this chapter has been on the identification and
discussion of the principal diseases causing mortality among the Aboriginal populations
of the settlements. An assessment will now be made of the general state of health of
these populations. This will be done by way of calculating infant mortality rates (deaths
in the first year of life)
303
8.5.1 Method
Infant mortality (deaths in the first year of life) has provided a common way
of measuring the health, health services, and social progress of populations. This is
largely because the baby, in its first year of life, is at a critical stage of disease risk and is
entirely dependent on the care of others and their ability to provide a healthy and safe
environment (Cox 1976:110). It follows then that measurements of death during this
period of life will be an assessment of the general health state of the community
concerned. This measurement does, however, have limitations in that it assumes that the
period of greatest danger for children is only in the first year and that it is the same for
each community examined.
Infant mortality for Aboriginal and non-Aboriginal populations were

calculated as:
Deaths under age one for period

____________________________ X 1000
Live births during period
In addition to the infant mortality rates a rate ratio was calculated to show the
differential between Aboriginal and non-Aboriginal infant mortality.
The differential rate ratio was calculated as:
Non-Aboriginal infant mortality

_______________________
Aboriginal infant mortality
The Aboriginal and non-Aboriginal infant mortality rates and differential rate
ratios were compared with corresponding twentieth century rates.
304
8.5.2 Results and discussion
305
Table 8.22 displays the infant mortality rate of Aboriginal people living on
the settlements in the period compared with other pre-twentieth and twentieth century
world populations.
Table 8.22 Infant mortality rates of Aboriginal people living on settlements in Victoria and
South Australia 1876-1900 compared with selected pre-20th and 20th century populations.
Population Period IMR Reference

(deaths
per
1000)
pre 20th Century
Aboriginal settlements This study
Victoria & South Australia 1876-1900 184
Non-Aboriginal Victoria 1876-1900 119 Statistical Register of
Victoria 1876-1900
Non-Aboriginal South 1876-1900 118 Statistical Register of South
Australia Australia 1876-1900
Six London Parishes 1690s 185 Landers 1990
London 1870-1879 152 Stockwell 1993

English towns 1870-1879 174 "
East Prussia 1876-1895 220 Vogele 1994
West Prussia 1876-1895 230 "
20th Century
South Australian Aborigines 1986-1988 20 Thomson & Briscoe 1991
Queensland Aborigines "
(settlement communities) 1972-1988 44
Northern Territory Aborigines 1972-1988 49 "
Central Australian Aborigines 1980-1982 56 "
Australia 1986-1988 9 "
Papua New Guinea 1946 251 van de Kaa 1967
1980 78 (m) Bakker 1983
66 (f)
Irian Jaya before 1921 202 Groenewegen & van de Kaa
1965
Islands Papua New Guinea 1949-1952 189 Scragg 1969
1962-1967 49
Japan 1924 166 Louden 1991
U.S. 1990 10 Stockwell 1993
Northern Europe 1990 10 "
Ethiopia, Guinea, Mali, Sierra "
Leone >150
306
The Aboriginal infant mortality rate of 184 deaths per 1000 is higher (1.5-1.6)
than both the non-Aboriginal Victorian and South Australian rates. In comparison with
the Victorian and South Australian non-Aboriginal populations the rate reveals that sixty-
five more Aboriginal infant deaths occurred for every 1000 live births. However, when
compared with other communities, for example, 17th century London, 19th century
Prussia, Irian Jaya (West Irian) before 1920, and mid 20th century Papua New Guinea
islands, the Aboriginal infant mortality is not especially high. The infant mortality rate
indicates that the Aboriginal people on the settlements were less healthy than the non-
Aboriginal Victorians and South Australians but healthier than say the West Irian
communities under Dutch colonial rule. The infants and children of West Irian had to
cope with similar introduced diseases but had an added risk with a high infection rate
from naturally occurring malaria. Thomson (1990: 7; 1991: 235) has pointed out a
similar pattern in the levels of 20th century Aboriginal infant mortality which show rates
approximately three to four times higher than other Australians but relatively low
compared to some European, Asian and Pacific populations.
The high infant mortality among the Aboriginal children is not fully
explainable with the absence of health records of the Aboriginal people living on the
settlements. These do not exist in any comprehensive form. But among the prime
contenders for the extension of mortality, and by nature morbidity, into early childhood is
a combination of malnutrition and diarrhoeal infection.
There is little to be gained in attempting to reach a reliable assessment of the
nutrient value of the foods consumed by the Aboriginal people on the settlements last
century. Little quantitative data is available in the historic records and that which does
occur is vague and often unreliable. Even recent attempts at quantifying and assessing the
daily nutrient intake of contemporary Aboriginal communities over varying periods have
307
been beset with problems of methodology and inaccuracies. What meaningful
assessments have been made are of an indirect nature usually centred on comparative
measures of growth and weight retardation among children and adults (e.g. Cheek et al.
1989; Cameron and Debelle 1986; Gracey et al. 1983; Gracey and Sullivan 1987; Kamien
1976; Kirke 1969; Maxwell & Elliot 1969; Roberts et al. 1988). What such studies have
unanimously determined is that Aboriginal nutrition is substantially below that of the
European communities throughout Australia and Aboriginal children suffer from growth
retardation and high rates of infection and intestinal parasites (Thomson 1982).
On the nineteenth century settlements the Aboriginal people were almost
totally reliant upon government issued food which was controlled by the supervisor or
missionary in charge of each settlement. Flour, sugar, tea, rice, and tobacco were the
mainstays of the daily diet, providing bulk but little protein. The meat, mainly beef and
lamb, which was supplied to the settlements by private contractors was often of poor
quality, principally bone, and was sometimes diverted by the supplier for sale elsewhere
(Murray 1898). The cultural practice of sharing food among those not eligible under
government legislation to receive rations further reduced the available intake (Murray
1898). In the early years of each settlement the Aboriginal people could supplement the
government diet with endemic foods collected form available lands surrounding the
settlement. But as the land was taken up by Europeans for grazing, the endemic food
sources rapidly declined and became unavailable to the majority of the settlement
residents. The result was a nutritionally poor diet, high in bulk, high in refined
carbohydrates, and low in protein, fibre and essential fatty acids.
Much of the diarrhoea and dysentery recorded as cause of death in the first
two years of life (Table 8.9) on the settlements quite likely occurred during the weaning
period of the Aboriginal children. A trend showing substantial mortality in the first year
308
of life and extending into the early childhood period is demonstrative of the weaning
process taking place in an undernourished environment (Winikof 1980:117). Little,
however, is known about the weaning practices on the settlements. There is no evidence
available to indicate at what ages children were weaned, how this may have differed over
time or between settlements, how much influence the European supervisors and medical
practitioners had in the process, nor what cultural beliefs were involved. But whatever
the case, the Aboriginal children living on the settlements were subjected to an extended
period of health risk that was largely, if not wholly, due to poorer nutrition and living
standards.
Table 8.23 shows the relative difference (Aboriginal IMR / European IMR)
between nineteenth and twentieth century Aboriginal and European infant mortality rates.
Table 8.23 Infant mortality rates and differential rate ratios between nineteenth
and twentieth century non-Aboriginal and Aboriginal populations (Statistical
Register of Victoria 1876-1900; Statistical Register of South Australia 1876-
1900; Thomson & Briscoe 1991).
Population Period IMR Differential

rate ratio
19th Century
Non-Aboriginal Victoria 1876-1900 119
Non-Aboriginal South Australia 1876-1900 118
Aboriginal Settlements 1876-1900 184 1.5-1.6
20th Century
Australia 1986-1988 9
South Australian Aborigines 1986-1988 20 2.2
Queensland Aborigines 1972-1988 44 4.9
(settlement communities)
Northern Territory Aborigines 1972-1988 49 5.4
Central Australia Aborigines 1980-1982 56 6.2
309
The Aboriginal infant mortality rate shows a substantial improvement from
the last quarter of the 19th century to a corresponding period in the 20th century. The rate
shows a nine-fold improvement over the period from 1876-1900 (184) to that of South
Australia for 1986-1988 (20). Comparative rates from Aboriginal settlements in
Queensland for the period 1972-1988 show a more than four-fold improvement over the
nineteenth century settlements of Victoria and South Australia (184 to 44). Infant
mortality for the European population also showed improvement but at a much higher
level. Comparison of the nineteenth century rates of 119 and 118 for non-Aboriginal
Victoria and South Australia respectively and the rate of 9 for Australia in 1986-1988
shows a thirteen-fold improvement.
The differential ratios between the infant mortality rates reveal that while the
general health of the two populations has improved from the nineteenth to the twentieth
century the improvement has been much stronger in the European populations.
Calculations on recent data confirm this trend.. Thomson (1990,1991) and Thomson &
Briscoe (1991) have shown that Aboriginal people are the least healthy identifiable sub-
population in Australia, with death rates two to four times higher than the total Australian
population. What the above infant mortality rates reveal is that this has been the case for
at least the last 125 years (and probably longer). Despite the many attempts by state and
commonwealth governments to improve the health status of the Aboriginal people the
health differential between the two populations has widened.
8.6 Conclusions
Infectious diseases and respiratory diseases were the major disease categories
recorded as cause of death among the Aboriginal populations living on settlements.
Together they accounted for just over one half (53.4%) of the total deaths on the 8
310
stations between 1876 and 1900. For the three age ranges combined infectious diseases
had a PMR of 33.6 and respiratory diseases a PMR of 19.8. There were no significant
differences between these two groups in the 0 to 4 years age group but in the two later age
ranges, 5 to 14 years and 15+ years, the infectious disease category (PMR 54 & PMR
33.7 respectively) was responsible for more deaths.
The major causes of death were from tuberculosis, bronchitis, pneumonia,
diarrhoea and dysentery all of which were endemic on the 8 settlements.
The major disease in the infectious disease category was tuberculosis. It was
responsible for 35.0% of all deaths in the 5 to 14 years age range and 26.7% in the 15+
age range. In the 5 to 14 years group female deaths from tuberculosis outnumbered the
males by almost 3 to 1. The higher mortality in females may be a result of their suspected
increased susceptibility to the development of life-threatening symptoms of the disease
during the onset of menarche and/or to an increased period of exposure to other sufferers.
There was no sex differential in mortality from tuberculosis in the 15+ years group but
most of the deaths occurred before 35 years of age.
Diarrhoea and dysentery were major causes of death in the 0 to 4 years age
range particularly among infants and young children between 0 and 2 years of age The
living conditions on the settlements characterised by a lack of a plentiful supply of clean
water, inadequate sewerage, poor food and personal hygiene, poor levels of nutrition, and
inadequate health care were the factors largely responsible.
Bronchitis and whooping cough were the main respiratory diseases among the
0 to 4 years age range. Bronchitis deaths showed a typical pattern of high mortality
during the first 2 years of life, levelling off during childhood and early adulthood, then
311
climbing to high frequencies after 45 years of age. In the 0 to 4 years age range deaths
from bronchitis were more common during the first year of life. Predisposing factors for
acute and life-threatening symptoms for these early ages would include the unfavourable
socioeconomic circumstances and poor nutrition experienced by most Aboriginal people
on the settlements. A further predisposing factor would have been the dwellings which
were often dusty in summer and damp during the winter. Passive tobacco smoke
inhalation would have been common among new born and young Aboriginal children,
further promoting the onset of bronchitis. A sharp increase in deaths from bronchitis
occurred after age 45. This trend is quite likely to have been a result of chronic bronchitis
due to many years of tobacco smoking.
Pneumonia and inflammation of the lungs caused deaths in all age ranges but
showed a pattern of increasing mortality in the 15+ years age range. Pneumonia was most
probably a secondary complication of other disorders, particularly influenza infections
aggravated by chronic tobacco inhalation and alcohol consumption both of which were
common on the Aboriginal settlements.
Deaths from hydatid disease occurred in 6 of the 8 settlements. Ages of death
ranged from 4 years to 56 years in both sexes with no discernible age/sex pattern
emerging.
The environment in which the Aboriginal people lived and their particular
socio-economic circumstances played a great part in the continued presence of the
pathogens causing these diseases and their ability to move from one host to another. The
confined living conditions in poorly ventilated, and often damp, houses favoured the
transmission of tuberculosis. The same living spaces and the widespread practice of
smoking tobacco facilitated bronchial infections. The poor sanitation and waste disposal
312
common to the settlements promoted enteric infection and was a strong factor in the high
rates of childhood mortality from diarrhoeal diseases.
On the other side of the coin the environment of the settlements protected the
Aboriginal inhabitants from other infectious agents. The five measles epidemics between
1880 and 1898 that spread through the European populations had little effect on the
settlements. The small populations and the geographic separation of the settlements from
larger European population centres, together with the cultural isolation of the Aboriginal
people acted as buffers, protecting the settlements
Infant mortality was high when compared to the non-Aboriginal populations
of Victoria and South Australia. This measurement reveals a substantial health
differential between Aboriginal and European populations. Aboriginal infant mortality
has improved into the latter quarter of the twentieth century but the corresponding
improvement in European infant mortality has been at a higher rate. The gap between the
health status of each has widened rather than narrowed over the last one hundred years.
313
Conclusions
CHAPTER NINE
Conclusions
This thesis has been the first attempt to investigate and assess the early post-
contact disease environment of Aboriginal people in Southeast Australia. While other
authors have approached this topic in various ways their combined works have
highlighted serious gaps in our knowledge of this part of our history. The central aim of
this thesis was to begin filling in those gaps.
A model of the changing medical circumstances in Aboriginal populations of
Southeast Australia has been presented beginning with the arrival of the First Fleet in
1788 and covering the colonial period to 1900.
The major elements of change to Aboriginal morbidity, mortality and
population decline were introduced epidemic diseases in the first stage of European
contact and chronic endemic diseases during the settlement phase.
The first of the major epidemic diseases to enter the Aboriginal population of
Southeast Australia was smallpox in 1789. Evidence for this epidemic suggests that it
was confined mainly to the eastern coastal regions. Two other epidemics of smallpox
have been recorded in 1828-31 and 1866. The three epidemics had little effect in terms of
morbidity and mortality among the European population but in the immunologically
unprepared Aboriginal populations it is reasonable to expect that 30% or more population
loss occurred in areas reached by each epidemic.

Conclusions
Sexually transmitted diseases, particularly syphilis, spread rapidly among the
Aboriginal populations following the establishments of the major European settlements
Sydney (1788), Melbourne (1835) and Adelaide (1836). A second source of introduction
was most likely from sealing and whaling crews visiting coastal South Australia
sometime after 1803. The fulminating symptoms and high mortality from syphilis were
commonly referred to in ethnohistorical texts. Supporting the written evidence is
osteological evidence of tertiary syphilis along the Murray River. The pattern of
infectivity and severity of syphilis seen in Southeast Australia is similar to other

continents where the disease has been introduced for the first time.
Tuberculosis probably accompanied the arrival of the First Fleet in 1788 but
little is known of it among the Aboriginal populations until the 1830s. The first
medically identified cases of tuberculosis were from autopsies conducted in 1837 at
Wybalenna Aboriginal settlement on Flinders Island. These cases showed extensive
pulmonary and systemic miliary dissemination. In the second half of the nineteenth
century tuberculosis became well established in Aboriginal populations. Mortality
records on Aboriginal settlements between 1859 and 1900 reveal 19.9% of recorded
deaths attributable to tuberculosis in its several forms. A higher mortality from the
disease should be expected due to misdiagnosis of symptoms at death and unrecorded
Aboriginal deaths. Changes in lifestyle and living conditions forced upon Aboriginal
people were largely responsible for the establishment of tuberculosis in the populations of
From 1836 influenza epidemics among the European population of Southeast
Australia paralleled that of the world pandemics. Epidemics among the Aboriginal
populations showed a similar occurrence. Little is known of the effects of early influenza
outbreaks but those of 1839 and 1847 were notably severe among the Aboriginal
313
Conclusions
Tasmanians on Flinders Island, and among the populations of southern and central
Victoria respectively. Documentary evidence shows that Aboriginal populations suffered
excessive morbidity and mortality when initially exposed to the influenza virus.
Changes in lifestyle and residential manner favoured a build up of case-to-
case transmission resulting in a persistence of influenza between major epidemic
episodes. By the 1850s influenza and pneumonia had become endemic in the Aboriginal
populations.
The 1874-75 measles epidemic in Southeast Australia was part of a world
pandemic. Records of this epidemic provide the best evidence regarding the morbidity
and mortality of measles among the Aboriginal populations. Population loss of up to
20% resulted on some of the settlements reached by the epidemic. Other population
centres escaped. Crude death rates up to 205 per 1000 population, while indicating
excessive mortality, were much less than those from the same epidemic in Fiji which
ranged from 137 to 755 per 1000 population. The experience of previous epidemics
between 1834 and 1868 providing a substantial number of immunologically protected,
can account for the differential in crude death rates. It cannot be ascertained when
measles became endemic among Aboriginal population centres during the nineteenth
century, but after the 1874-75 epidemic records indicate that measles was no longer a
major disease. An exception was the 1898 outbreak in northern South Australia. This
was the last epidemic of measles to seriously affect an Aboriginal population in the
nineteenth century.
During the final phase of contact in the colonial period infectious and
respiratory diseases were the major causes of death among Aboriginal residents on
settlements in Southeast Australia. Together they accounted for 53.4% of all recorded
314
Conclusions
deaths. Tuberculosis was the major cause, responsible for 35.0% of all deaths in the 5 to
14 years age range and 26.7% in the 15+ age range. A differential in mortality of 3 to 1
for females and males occurred in the age range 5 to 14 years. High susceptibility during
menarche and an increased period of exposure are suggested as reasons for the
differential. Diarrhoea and dysentery were major causes of death in the 0 to 4 years age
range. Settlement living conditions characterised by inadequate sewerage, lack of clean
water, poor nutrition levels and inadequate health care were factors largely responsible.
Bronchitis and whooping cough were the main respiratory diseases among the 0 to 4 years
age range. A sharp increase in deaths from bronchitis occurred after age 45.
Unfavourable socioeconomic circumstances, poor nutrition, active and passive tobacco
smoke inhalation are seen as strong predisposing factors. Pneumonia caused deaths in all
age ranges but showed a pattern of increasing mortality in 15+ age range. Chronic
tobacco inhalation and alcohol consumption were predisposing factors.
Comparison of infant mortality between Aboriginal and European populations
reveal a substantial health differential for the period 1876 to 1900. While both
populations’ health has improved, modern comparisons show that the gap between
European and Aboriginal health has widened.
An afterword
At the beginning of this thesis I characterised it as beginning an investigation
and assessment into the medical circumstances of Aboriginal populations following
colonisation. I consider that still to be the case as I see much more work remains to be
done on the subject. The obvious extension of this work would be into other regions of
the continent not covered here - for example, the west and southwest coastal regions of
315
Conclusions
Australia, inland desert regions, and the tropical north of the continent. These regions are
physically and climatically different from the Southeast and I would suspect the nature of
introduced diseases may be different to what has been described here.
Another expansion of this work would be to examine Aboriginal morbidity
and mortality on a more local scale. In many regions of the Southeast such a study would
be difficult due to lack of archival documentation, but the records from Tasmania may
have much to offer in this case. Although they are incomplete (what set of historical data
is ever complete?) the birth and mortality records from Gun Carriage Island, Wyballena,
The Lagoons, and Oyster Cove still require a detailed study. Most of these records have
been published as an appendix by Plomley (1987: 915-947) and others are stored in the
Archives Office of Tasmania in Hobart.
A further extension would be to examine the medical circumstances of the
indigenous populations of South Africa and New Guinea during their colonial periods.
316
Appendix A 1
Appendix A
Autopsy reports diagnosed as tuberculosis
Flinders Island Aboriginal Station
20 August 1837
Female adult
Having examined the body of the deceased ... I beg obedience to your directions to
forward for your information the opinion I have arrived at relative to the cause of her
death consequent upon the examination. The first that presented itself on examining the
chest of the deceased was the remains of a very extensive inflammation of the lungs
which must have been of some months standing. The left lobe was firmly adherent to the
investing membrane of the inner surface of the ribs, to the bag containing the heart with
tubercles in every direction throughout the substance of the lung. The principal valve of
the heart was partly cartilaginous (the effect perhaps of age). The right lobe had also
formed considerable adhesions but not so firmly as the left. The bag containing the heart
contained rather more than a healthy portion of fluid. The liver especially the right lobe
was considerably enlarged with small caseous spots impacted in several places throughout
its substance. The gall bladder considerably relaxed. The mucous membrane of the two
firsts of the small intestines presented in several places and inflammatory appearance, the
vessels being numerous and large. The rest of the abdominal viscera healthy. The brain
also healthy excepting rather a large quantity of fluid in the left ventricle. From these
appearances I beg to state I can arrive at no other opinion than that expressed in my
memorandum of the 16th inst that is that she died of typhus niction or low nervous fever.
(Austin, A. 1837 Robinson Papers, ML A7067: 149-150)
30 December 1837
Male adult
In the cavity of the thorax there was general adhesions of the lungs; they were dense and
heavy and covered externally with small hard tubercles, the same being found contained
in their internal structure. Of the abdomen - on opening this cavity it was found full of
water; the quantity was at least a gallon full. The surface of the small intestines and their
appendages were literally studded quite thick with small tubercles mostly of a yellowish
colour and containing pus. There were also a number of small patches of the same
intestines in a state o gangrene and encircled with these tubercles. The surface of the liver
also exhibited the same appearances. The spleen was considerably enlarged and of a
quite soft and friable substance.
(Walsh, M. 1837 Robinson Papers, ML A7068: 225)
27 February 1838
Male adult
The body was quite emaciated prior to his dissolution and was in reality a living skeleton.
On opening the cavity of the thorax the lungs presented chronic adhesions to the ribs,
pericardium and sternum were for the greater part solid and hepatised, particularly the
Appendix A 2
upper lobe of the left lung, which contained two or three large patches of a white caseous
consistence. Both lungs were thickly interspersed with small hard white lumps of a
tuberculated nature, although none of them had assumed a puriform state. The
pericardium was much enlarged and contained about six ounces of fluid.
The liver was of extraordinary size, was hard and adhered to the diaphragm. On
separating this connection a large ulcer was discovered on its upper surface of a dirty
gangrenous appearance; it contained a large quantity of blood in a fluid state, was thickly
covered with white hard small lumps similar to those found in the lungs, which pervaded
its internal structure also. The whole peritoneal lining of the intestines exhibited the same
tuberculated appearance but much larger in size and containing a thick yellowish purulent
matter. The spleen was of natural size but hard and solid and on cutting into exhibited the
same tuberculous formation with the aforesaid viscera. The peritoneal sack contained
about four pints of water. The kidneys appeared healthy.
(Walsh, M. 1838 Robinson Papers, ML A7069: 111-112)
12 May 1838
Male adult
The contents of the thorax formed one mass of compact chronic adhesions. The lungs
adhered to the ribs and all surrounding membranes; there was no trace of mediastinum
remaining. They were dense and heavy containing numerous hard small tubercles. The
right lung contained a large abscess filled with purulent matter. There were chronic
adhesions formed between the heart and pericardium.
In the abdominal cavity the liver of natural appearance. The gall bladder was much
distended with black bile resembling tar both as to colour and consistence, which deeply
stained the neighbouring parts. The spleen was remarkably small and firm. The kidneys
were natural. The folds of the mesentery and omentum with the peritoneal appendages of
the small intestines were thickly covered with round hard tubercles about the size of a pea
of a whitish colour.
2 June 1838
Female adult
In the cavity of the thorax was found an effusion of colourless serum (about two English
pints). The right lung adhered to the pleura but was otherwise pretty healthy. The left
formed one uniform mass of purulent matter scarcely holding together but breaking down
at the slightest touch, adhering to all the neighbouring parts; its anterior surface was
covered with a thick coat of coagulated lymph. The heart appeared healthy.
In the cavity of the abdomen there was also found an effusion of clear serum of about four
pints. The liver was of natural size but quite friable in substance and easily breaking
down under the finger. The gall bladder was much distended with a deep orange coloured
bile. The spleen also equally friable with the liver of the usual size. Nothing remarkable
appeared in the other viscera. This old woman absolutely refused medical interference.
Appendix A 3
21 June 1838
female two years of age
The lungs formed adhesions to the pleura, ribs, sternum, diaphragm and pericardium on
either side, were dense and hepatised, thickly interspersed with small white tubercles both
externally and internally. The left lung contained three large cysts filled with a pale
yellowish matter of a cheesy consistence.
The abdomen contained about a gallon of colourless serum. The liver was extremely
enlarged and indurated; was thickly dotted externally with small tubercles similar to those
found in the lungs; on cutting into [it] exhibited a dark yellowish colour. The bile was of
a lighter colour and thicker consistence than natural. The spleen was quite indurated of a
dark purple colour interspersed with large whitish tubercles which pervaded its entire
substance and exhibited a most curious and singular specimen of pathology. The
pancreas was also indurated and their posterior surface exhibited a large cyst of similar
appearance to that found in the left lung. The mesenteric glands were considerably
enlarged and indurated.
2 July 1838
Female seven years of age
The lungs were healthy except a few adhesions of the left of a chronic nature with two or
three small specks on its posterior surface in an incipient state of suppuration. Heart and
pericardium natural.
Liver much enlarged and considerably indurated and replete with tubercles on the external
surface as well as in its internal structure. Bile of a pale straw colour.
Spleen remarkably diseased being much indurated and covered with large tubercles of a
yellowish colour each surrounded with a bright scarlet circle or base on a dark purple
ground; about the centre was found a large superficial abscess of a vesicular nature of
about an inch in diameter filled with a viscid fluid of a yellowish green colour much
resembling bile in appearance. The pancreas were indurated and contained a few small
abscesses containing purulent matter. The intestines and appendages exhibited marks of
chronic inflammation and were thickly interspersed with small hard yellowish tubercles.
The mesenteric glands were much enlarged and indurated. There was an effusion of
colourless serum of about six ounces in the abdominal cavity.
6 August 1838
Male adult
The cavity of the abdomen contained about four pints of water. The liver appeared
healthy; on making an incision into it a number of tubercles were discovered. The gall
bladder was smaller than natural and contained a black and thickish fluid. Spleen natural
in external appearance but being divided was found tubercular. Pancreas natural.
Appendix A 4
In the cavity of the thorax was a serious effusion of about a pint, the whole contents of
which formed one lump of adhesion and firmly incorporated with the ribs sternum and
diaphragm. Both the lungs with the exception of a small portion of the upper and
posterior lobe of the right lung which was light and crepitus, were solid heavy and
hepatised, containing a number of cysts filled with a firm yellowish cheesy like substance.
The heart and its envelope were concealed in the substance of the left lung. The heart
was soft and flabby. The blood was quite fluid and the body and limbs flexible.
(Walsh, M. 1838 Robinson Papers, ML A7070: 183-184)
3 September 1838
Male three years of age
In the cavity of the abdomen there was an effusion of about one pint of serum. The
mesenteric glands were considerably enlarged, contained cysts filled with concrete
purulent matter. The liver was much enlarged and indurated. Contents of gall bladder
natural. Spleen indurated and thickly dotted with tubercles containing a bright yellowish
matter of a cheesy consistence. Pancreas indurated and partly in a semi-purulent state.
The contents of the thorax adhered closely together and to all the surrounding parts. The
right lung was externally hepatised, heavy and contained on division an extensive abscess
filled with pus. It exhibited also in its substance numerous tubercles in a state of
separation. The left lung was also much diseased, a small portion only of which was light
and crepitus, it exhibiting many tubercles in the same state as the former.
This child has been weakly these twelve months and although about three years old had
never been able to walk. The appetite was always considerable till within a few days of
its death, the belly relaxed and the breath at all times was highly offensive.
29 October 1838
Female adult
Cavity of the thorax - adhesion of the lungs with the ribs, sternum, mediastinum,
pericardium and diaphragm. Both lungs heavy [sic] hepatised and tuberculated
externally; exhibiting a similar appearance internally except being considerably larger,
forming cysts containing a thickish purulent like matter; only a small portion of the left
lung was crepitus.
Abdomen - liver covered with small whitish tubercles; also thickly interspersed with the
same internally but larger and of a yellowish colour. Spleen much enlarged, friable in
substance, full of large yellowish tubercles throughout its entire substance. There was
about two pints of serous effusion in the cavity of the peritoneum.
(Walsh, M. 1838 Robinson Papers, ML A7070: 315
Appendix A 5
9 November 1838
Female adult
General chronic adhesions of the lungs to all the surrounding parts; right lung
tuberculated but otherwise rather light and crepitus; the left lung formed one entire mass
of purulent matter. There was about three pints of serous effusion in the cavity of the
abdomen. The abdominal viscera were natural; the kidneys were remarkably large but
healthy.
17 December 1838
Female adult
Thorax. The lungs adhered to all the neighbouring parts being of a chronic description
and of long standing; were dense covered with small whitish tubercles externally and
thickly interspersed internally with the same but of a much larger size and in a state of
suppuration; only a small portion of the upper lobe of the right lung was crepitus. The
pericardium was full of water.
Abdomen. This cavity contained about a gallon of water. The liver formed adhesions to
the right side of long standing; was covered with small tubercles and was otherwise of
unnatural appearance. The bile was thickish of a dark brown colour. The spleen was
enlarged, of a dark purple colour, full of tubercles both externally and internally of a large
size than those of the liver or lungs. There was a firm adhesion of the upper surface of
the spleen to the stomach. The kidneys were quite flabby. The other viscera natural
except the appearance of tubercles all along the peritoneal adhesions of the intestinal
canal.
Appendix B 1
Appendix B - Recorded causes of death on Aboriginal settlements - 1876 to 1900

Settlement Date Sex Age Cause of Death ICD
Framlingham
Victoria 1876 ? 17 Consumption INF
1877 ? 45 Scarlatina INF
M 50 Hydatids INF
? 90 Senility ILL
1878 M 80 Senility ILL
M 80 Senility ILL
1879
1880 M ? Inflammation of lungs RES
M 40 Inflammation of lungs RES
F 8 Consumption INF
F 10 Inflammation of lungs RES
1881
1882 M 55 Enlargement of liver DIG
M 50 Disease of heart CIR
F 45 Enlargement of liver DIG
M 60 Enlargement of liver DIG
1883 ? 0 Inflammation of lungs RES
M 14 Chronic enlargement of the liver DIG
M 50 Phthisis INF
M 55 Phthisis INF
Lake Condah 1876 M 30 Inflammation of lungs RES

Victoria M 50 ? ILL
M 60 Old Age ILL
M 45 Consumption INF
1877 M 17 Chronic dysentery INF
F 40 Inflamation of bowels DIG
M 65 Old Age ILL
M 50 Paralysis NER
M 30 Typhoid Fever INF
1878 M 40 Inflammation of the lungs RES
M 45 Congestion of the lungs RES
1879 M 0 Suffocation INJ
1880 F 24 Consumption INF
M 5 Hydrocephalus NER
F 12 Consumption INF
F 2 Consumption INF
M 0 Haemorrhage PER
1881 M 0 Bronchitis RES
M 70 Inflammation of the lungs RES
F 18 Tuberculosis INF
F 50 General decay ILL
1882 M 0 Pneumonia RES
1883 F 0 Teething ILL
F 45 Peritonitis DIG
1884 M 75 Old age ILL
Appendix B 2

F 12 Congestion of the lungs RES
F 48 Asthma RES
F 1 Injury from fall INJ
M 0 Pneumonia RES
1885 F 1 Convulsions NER
F 1 Disease of throat and mouth ILL
M 60 Peritonitis DIG
1886 F 0 Whooping cough RES
M 2 Whooping cough RES
M 2 Pneumonia whooping cough RES
1887 M 26 Pleurisy and lung congestion RES
F 46 Chronic disease of liver DIG
1888 M 50 Peritonitis DIG
M 50 Chronic disease of stomach DIG
1889 F 0 Congestion of the lungs RES
F 3 Chronic bronchitis RES
F 12 Extensive burns INJ
M 0 Bronchitis RES
F 25 Phthisis INF
F 12 Phthisis INF
M 60 Disease of stomach DIG
M 22 Phthisis INF
F 54 Bronchitis RES
1890 M 90 Old age ILL
M 2 Chonic bronchitis RES
M 50 Phthisis INF
M 60 Congestion and bronchitis RES
1891 M 78 Heart disease CIR
F 0 Premature birth PER
F 45 Fatty degeneration of heart CIR
1892 M 24 Drowning INJ
1893 F 65 General decay ILL
M 56 Blood poisoning ILL
F 32 Bronchio-pneumonia RES
M 62 Dyspepsia DIG
1894 F 0 Exhaustion and intense heat ILL
M 70 General decay ILL
F 1 Pneumonia RES
1896 F 25 Phthisis INF
M 18 Phthisis INF
M 36 Laryngitis RES
Appendix B 3

F 1 Bronchitis RES
F 60 Phthisis INF
1897 F 15 Tubercular peritonitis INF
F 19 Phthisis pulmonatis INF
F 80 Senile decay ILL
M 5 Acute phthisis INF
F 12 Phthisis pulmonatis INF
M 18 Phthisis pulmonatis INF
1898 M 6 Tubercular peritonitis INF
F 23 Phthisis INF
F 11 Phthisis INF
F 12 Phthisis INF
M 7 Pneumonia RES
F 3 Phthisis INF
1899
1900 M 19 Tuberculosis INF
M 60 Peripheral neuritis NER
M 75 Cancer of the bladder NEO
Lake Wellington 1876 M 25 Abscess ILL

(Ramahyuck) ? 49 Disease of heart CIR
Victoria F 60 Old Age ILL
1877 ? 40 Consumption INF
M 1 Teething ILL
F 7 Peritonitis DIG
F 5 Peritonitis DIG
M 8 Whooping Cough RES
1878 M 16 Consumption INF
F 14 Lung disease RES
F 30 Abcess ILL
M 46 Brain fever NER
? 0 Teething ILL
F 70 Old age ILL
F 0 Teething IKLL
1880 F 58 Inflammation of the bowels DIG
F 45 Inflammation of the bowels DIG
M 54 Drowning INJ
1881 M 0 Weakly child ILL
? 70 Old age ILL
? 46 Inflammation of the lungs RES
F 29 Bursting blood vessel CIR
F 65 Old age ILL
Appendix B 4

1882 F 3 Lung disease RES
M 1 Bronchitis RES
M 54 Dropsy ILL
1883 F 19 Inflammation of the bowels DIG
F 0 Bronchitis RES
M 6 Consumption INF
F 1 Bronchitis RES
1884 M 27 Inflammation of lungs RES
M 56 Abscess ILL
F 5 Consumption INF
F 45 Hydatids INF
F 10 Inflammation of the bowels DIG
1885 F 10 Hydatids INF
M 1 Teething ILL
M 9 Pneumonia RES
M 3 Dropsy ILL
M 47 Spinal disease ILL
F 54 Inflammation of the lungs RES
M 0 Bronchitis RES
1887 M 56 Disease of heart CIR
F 16 Inflammation of heart CIR
F ? Teething ILL
1889 F 79 Old age ILL
1890 F 26 Spinal disease ILL
M 41 Phthisis INF
1891 M 59 Inflammation ILL
1892 M 1 Teething ILL
F ? Old age ILL
1893 M ? Old age ILL
1894 F 1 ? ILL
M 1 Measles INF
M 70 Old age ILL
F 0 Measles INF
F 2 Heart failure CIR
F ? Bronchitis RES
F ? Influenza RES
F ? Whooping cough RES
1895 F 42 Heart disease CIR
1896 F 0 Teething ILL
F 0 Teething ILL
Appendix B 5

M 1 Decline ILL
F 22 Fits ILL
F 2 Decline ILL
M 24 Inflammation of the bowels DIG
1897 F 22 Exhaustion PRG
1899 M 67 Cancer NEO
1900
Lake Tyers 1878 M 50 Hepatitis

Victoria F 70 General decay ILL
M 40 Gastric fever DIG
M 60 Cancer of the tounge NEO
1879 M 19 Inflammation of the lungs RES
1880
1881 M 2 Dysentery INF
M 14 Pneumonia RES
M 0 Bronchitis RES
1882 F 80 Senile decay ILL
F 1 Theething ILL
M 0 Erysipelas
M 50 Dropsy of the extremities ILL
M 86 Senile decay ILL
F 1 Bronchitis RES
1884 F 56 Tumified liver DIG
F 1 Bronchitis RES
F 5 Pneumonia RES
F 65 Inflammation of lungs RES
F 1 Teething ILL
M 45 Heart disease CIR
M 50 Inflammation of brain NER
F 19 Phthisis & spinal congestion INF
F 0 Premature birth NEO
F 65 Phthisis pulmonias INF
M 3 Scrofula & suppuration in joints INF
M 70 General debility ILL
1886 M 76 Senile decay ILL
M 50 Drowned INJ
F 1 Teething ILL
M 54 Cancer of the intestines NEO
1887 F 1 Thrush
M 1 General deility since birth ILL
Appendix B 6

M 16 Disease of brain, Amaurosis NER
F 3 Dysentery INF
F 0 Whooping cough RES
M 30 Hydatids of liver & Ascites INF
1888
1889 M 32 Pneumonia RES
F 1 Diarrhoea INF
M 0 Diarrhoea INF
F 0 Congenital syphilis
F 32 Phthisis INF
M 11 Cerebral tumor NER
1890 F 20 Chronic dysentery INF
F 25 Phthisis INF
M 0 Influenza RES
M 0 Influenza RES
M 1 Bronchitis RES
M 11 Injury to head & menengitis INJ
F 20 Cirrhosis of liver & dropsy DIG
M 3 Tabes mesentrica INF
1892 F 0 Bronchitis RES
1893 F 39 Laryngitis
F 39 Pneumonia following measles
F 0 Diarrhoea INF
M 30 Acute Phthisis following measles
F 0 Diarrhoea INF
1894 F 65 General debility following measles
1896 M 1 Influenza RES
1897
1898 M 1 Sunstroke INJ
F 7 Chorea, abcess on brain NER
1899 M 1 Diarrhoea & vomiting INF
F 60 Phthisis INF
F 57 Disease of brain, heart failure NER
M 22 Bursting of internal abcess ILL
M 46 Influenza & pneumonia RES
1900 M 4 Diarrhoea INF
M 6 Diarrhoea INF
F 76 Influenza, senile decay RES
Coranderrk 1878 M 21 Consumption INF

Appendix B 7

Victoria M 3 Consumption INF
M 5 Consumption INF
F 16 Softening of the brain NER
? 0 Low fever INF
M 45 Hydatids INF
F 5 Convulsions NER
M 0 Bronchitis RES
F 26 Hydatids INF
1880 F 0 Convulsions NER
F 13 Convulsions & dropsy NER
M 35 Hydatids & Phthisis INF
M 0 Bronchitis RES
M 50 Hydatids INF
M 13 Consumption & Dropsy INF
1882 F 0 Dentition ILL
M 1 Dentition ILL
F 7 Rheumatic fever INF
1883
F 60 Bronchitis RES
M 35 Gunshot wounds INJ
? 59 Paralysis NER
F 5 Consumption INF
F 0 Bronchitis RES
? 8 Burns INJ
M 75 Bronchitis RES
M 12 Bronchitis RES
1887 F 54 Dropsy ILL
1889 F 1 Diarrhoea INF
F 0 Bronchial-pneumonia RES
M 8 Acute rheumatism ILL
F 1 Diarrhoea INF
1890 F 7 Acute rheumatism ILL
F 7 Diarrhoea & exhaustion INF
M 70 Bronchitis RES
F 23 Influenza RES
Appendix B 8

F 0 Convulsion fits NER
M 0 Bronchitis RES
1893 F 51 Heart failure CIR
M 50 Spinal caries ILL
F 0 Diarrhoea INF
1894 M 70 Injury in fall INJ
1895 M 2 Bronchial pneumonia RES
1896 M ? Phthisis INF
F 70 General decay ILL
1897 F 3 Pneumonia RES
F 45 Septic poisoning ILL
F 50 Cancer NEO
F 58 Cancer NEO
1900 M 3 Measles INF
F 62 Pneumonia RES
M 56 Hydatids INF
Ebenezer 1876 F 40 Consumption INF

(Lake Hindmarsh) M 40 Heart Disease CIR
Victoria F 35 Consumption INF
M 10 Drowning INJ
F 10 Stomach Complaint DIG
M 0 Convulsions NER
M 65 Heart disease CIR
1877 F 16 Enteritis INF
F 70 Tumor NEO
F 1 General debility ILL
F 19 Dropsy ILL
M 32 Hydatids INF
M 13 Bronchitis RES
F 14 Dropsy ILL
M 70 Paralysis NER
1880 M 4 Marasmus END
M 1 Stomach complaint DIG
F 6 Consumption INF
? 100 Senile decay ILL
F 21 Drowning INJ
M 7 Marasmus END
Appendix B 9

? 36 Tumor NEO
? 3 Marasmus END
M 45 Disease of brain NER
F 1 Dentition ILL
F 45 Dropsy ILL
M 19 Fever ILL
F 0 Convulsions ILL
F 3 Congestion of brain NER
M 40 Liver complaint DIG
M 0 Convulsions ILL
F 1 Bronchitis RES
F 1 Dentition ILL
? 1 Dentition ILL
1884 F 60 Liver complaint DIG
F 0 Dentition ILL
M 3 Peritonitis DIG
M 0 Bronchitis RES
M 0 Dentition ILL
F 28 Fever INF
M 42 Lung disease RES
M 50 Tumor in chest NEO
M 80 Bronchitis RES
M 50 Bronchitis RES
M 65 Bronchitis RES
M 1 Dentition ILL
1888 M 65 Stomach complaint DIG
F 2 Marasmus END
1890 M 0 Congestion of stomach DIG
1891 F 80 Old age ILL
F 1 Dysentery INF
1892 M 1 Marasmus END
1893
1894
1895
1896 M 70 Cancer of leg and exhaustion NEO
Appendix B 10

M 6 Inflammation of stomach DIG
M 0 Bronchitis RES
M 20 Phthisis INF
1898
1899 F 0 Dentition ILL
1900
Point McLeay 1876 ? 75 Old age ILL

South Australia ? 0 Teething ILL
M 0 Diarrhoea INF
F 6 Marasmus NEO
? 60 Old age ILL
? 0 ? ILL
? 75 Old age ILL
1877 M 1 Atrophy ILL
? 65 Old age ILL
? 60 Heart disease CIR
M 0 Teething ILL
M 50 Stomach disease DIG
M 4 Pneumonia RES
M 24 Throat disease ILL
M 2 Diarrhoea INF
? 60 Consumption INF
M 60 Stomach disease DIG
M 60 ? ILL
F 0 Diarrhoea INF
? 65 Old age ILL
M 37 Bright's Disease GEN
F 8 ? ILL
1878 F 15 Enteritis INF
? 0 Dentition ILL
? 0 Atrophy ILL
M 1 Marasmus END
F 3 Pneumonia RES
M 1 Dropsy ILL
M 3 Pneumonia RES
M 2 Diarrhoea INF
F 2 Atrophy ILL
F 0 Bronchitis RES
F 0 Atrophy ILL
? ? Old age ILL
Appendix B 11

F 8 Malignant stomachitis ILL
F 0 Diarrhoea INF
F 0 Diarrhoea INF
M 1 Diarrhoea INF
1879 M 15 Shot INJ
M 60 Old age ILL
? 1 Marasmus END
F 2 Marasmus END
? 0 ? ILL
F 21 Puerperal Fever PRG
1880 F 11 Malignant stomachitis ILL
F 4 Pneumonia RES
F 12 Enteric fever INF
F 0 Diarrhoea INF
M 40 Enteric fever INF
M 32 Hydatids INF
M 60 Old age ILL
F 1 Dysentery INF
F 0 Dysentery INF
1881 M 9 Peritonitis DIG
M 50 Paralysis NER
F 12 Liver disease DIG
M 0 Infantile convulsions PER
F 9 Peritonitis DIG
1882 M 30 Acute Dysentery INF
M 30 Chronic bronchitis RES
M 1 Hydrocephalus NER
F 1 Diarrhoea INF
F 2 Chronic diarrhoea INF
F 45 Paralysis NER
M Acute pneumonia RES
M 11 Tabes mesenteric INF
F 0 Diarrhoea INF
1883 M 40 Epilepsy NER
M 1 Convulsions NER
M 6 Peritonitis DIG
M 1 Diarrhoea INF
? 0 Diarrhoea INF
1884
1885
Appendix B 12

1886
1887
F ? Diarrhoea INF
F ? Consumption INF
F ? Diarrhoea INF
M ? ? ILL
F ? Senile decay ILL
M ? Inflammation of brain NER
F 25 ? ILL
M ? ? ILL
M ? ? ILL
M ? ? ILL
1890 F ? Senile decay ILL
F 0 Dysentery INF
M 30 Accident INJ
F 0 ? ILL
1891 ? ? ? ILL
F 0 Teething ILL
M 0 Teething ILL
F 27 Hydatids INF
F ? ? ILL
F 21 Pueperal fever PRG
? 0 ? ILL
1892 F 2 Atrophy ILL
? 0 ? ILL
M 1 Diarrhoea INF
? 0 ? ILL
F 1 Marasmus END
? 2 Consumption INF
M 4 Hydatids INF
M 0 Infantile convulsions NER
M ? Heart disease CIR
F 1 Cerebral affliction NER
1893 M ? ? ILL
M ? Senile decay ILL
? 1 Bronchitis RES
? 75 Senile ILL
? 0 Premature birth PER
Appendix B 13

M 48 Bronchitis RES
M 70 Chronic bronchitis RES
F 1 Measles INF
M 0 Thrush INF
F 0 Thrush INF
F 1 Thrush INF
F 60 Bronchitis RES
? 0 Thrush INF
M 0 Dysentery INF
1894 M 65 Dysentery INF
F 50 Liver inflammation DIG
F 70 Inflammation of bowels DIG
F 12 Inflammation of brain NEO
F 1 Dysentery INF
? 12 Spinal disease ILL
1895 M 18 Diarrhoea INF
? 0 Premature birth PER
F 5 Intermittent fever INF
F 8 Intermittent fever INF
M 0 Meningitis NER
M 1 Meningitis NER
? 0 Marasmus END
? 0 Marasmus END
M 54 Bronchitis RES
M 1 Infammation of brain NER
1896 F 60 Marasmus END
M 0 Scrofula INF
M 0 Diarrhoea INF
F 0 Diarrhoea INF
M 4 Meningitis NER
F 0 ? ILL
M 1 Burns INJ
F 30 Heart disease CIR
F 30 Inflammation of bladder GEN
F 2 ? ILL
M 4 ? ILL
M 54 ? ILL
? 0 Marasmus END
M 8 Brain apoplexy NER
Appendix B 14

? 0 Marasmus END
F 0 Diarrhoea INF
F 40 Cancer NEO
F 64 Apoplexy NER
F 24 Consumption of bowels DIG
1898 F 0 Birth debility PER
F 0 Ulcerated throat DIG
F 1 Marasmus END
M 0 Premature birth PER
? 0 Birth debility PER
F 65 Acute bronchitis RES
F 0 Bronchitis RES
1899 M 14 ? ILL
F 1 ? ILL
F 50 Cancer NEO
? Stillborn PER
F 0 Dysentery INF
M 0 Debility PER
1900 F 1 Dysentery INF
F 0 Influenza RES
F 0 Influenza RES
M 0 Influenza RES
F 0 Teething ILL
M 1 Teething ILL
F 0 Influenza RES
M 54 Cancer NEO
Point Pearce 1880 M 34 Phthisis INF

South Australia M 19 Phthisis INF
F 50 Bronchitis RES
1881
M 28 Phthisis INF
F 1 Teething ILL
1883 F 13 Hydatids INF
F 40 Bronchitis RES
M 52 Lung complications RES
1884 M 51 Phthisis INF
M 0 Bronchitis RES
F 2 Bronchitis RES
F 22 Phthisis INF
1885 M 0 ? ILL
F 32 Confinement PRG
Appendix B 15

F 13 Phthisis INF
1886 F 0 ? ILL
F 27 Bronchitis RES
F 20 Phthisis INF
1888 M 0 ? ILL
M 50 Dropsy ILL
M ? ? ILL
M 16 Typhoid INF
F 62 Paralysis NER
F 6 Pulmonary RES
1892
1893 M 0 Heart complications CIR
F 6 Fever INF
F 0 Tubercular meningitis NER
1894 M 0 Whooping cough RES
1895
1896
1897
F 2 Scarlet fever INF
F 2 ? ILL
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"A Great Deal of Sickness"1

Introduced diseases among the Aboriginal People of

(Enya & Ryan 1987)

Palaeopathological studies have sought to build up a picture of Australian Aboriginal health

Go raibh míle maith agat.

1.2 Research to date 2

1.5 Significance of thesis 10

1.6 Sources and methods 11

1.6.1 Historical sources 11

1.6.2 Skeletal evidence 14

1.7 Origin of diseases 17

Chapter 2: Disease Environments and Epidemiological Considerations 18

2.2 A medical model for contact in Southeast Australia 19

2.3 Epidemiological considerations 22

2.3.1 Pre-contact disease 23

2.3.2 Post-contact epidemics 31

2.4 European and Aboriginal concepts of disease and curing 39

3.2 Biology of smallpox 48

3.3 Smallpox among the European population of Southeast Australia 51

3.4 Small pox among the Aboriginal populations - Source material 52

3.4.1 The first epidemic û 1789 54

3.4.2 The second epidemic - 1828-32 66

3.4.3 The third epidemic - 1866-67 83

Chapter 4: Sexually Transmitted Disease 98

4.2 Biology of sexually transmitted diseases 101

4.2.1 Syphilis 101

4.2.2 Gonorrhoea 103

4.4.1 At the frontiers 106

New South Wales 106

Victoria (Port Phillip) 109

South Australia 117

4.4.2 Beyond the frontiers 121

Historical Evidence 122

Osteological evidence 126

An early introduction into South Australia 138

4.5 Conclusion 139

5.1 Introduction 141

5.2 Biology of tuberculosis 142

5.3 Tuberculosis among the European population of Southeast Australia 149

5.4 Tuberculosis among the Aboriginal populations - source material 152

5.4.1 Early contact and diffusion (Stage II) 152

5.4.2 Settlement and acculturation (Stage III) 158

5.4.3 Clinical features 162

5.4.4 Aboriginal treatment 165

5.5 Discussion 165

5.6 Conclusion 174

Chapter 6: Acute respiratory diseases 176

6.1 Introduction 176

6.2 Biology of influenza & pneumonia 178

6.4 Influenza among the Aboriginal populations - source material 183

6.4.1 Influenza and acute respiratory disease among Tasmanian

6.4.3 Influenza and acute respiratory disease among Victorian Aboriginal

6.4.4 Influenza and acute respiratory disease among South Australian

6.5 Discussion 215

6.6 Conclusion 223

7.1 Introduction 225

7.2 Biology of measles 226

7.3 Measles among the European population of Southeast Australia 227

7.4 Measles among the Aboriginal population - source material 229