2.3 Epidemiological Considerations
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,
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.
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 distribution
Lower population density
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
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.
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
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
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
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
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.