Dissertationen zum Thema „Aboriginal Australians. Diseases“

"January 2003." Bibliography: 10.1-10.11 leaves. This thesis presents results from the Katherine Region Diabetic Retinopathy Study (1993-1996). These results provide the first detailed information on the basic epidemiology of diabetic retinopathy and impaired vision in an Aboriginal diabetic population.

Thesis (Ph.D.)--University of Melbourne, Dept. of Opthalmology, 2007.
Typescript. SAFE Strategy refers to Surgery for trichiasis, Antibiotics for active infection, Facial cleanliness and Environmental improvements. Includes bibliographical references (leaves 233-253). Also available electronically: http://eprints.unimelb.edu.au/archive/00003844.

[Truncated abstract] Indigenous Australians suffer cardiovascular disease (CVD) at a rate six times greater than the general population in Australia and while the incidence of CVD has been reduced dramatically amongst the majority of non-indigenous Australians and amongst Indigenous populations in other countries in the last 30 years, there has been little change in the figures for Aboriginal Australians, showing that heart health campaigns have little impact, for this group of people. Aims : The principal aims of this study were firstly, to determine and record the barriers to the development and delivery of CVD prevention programs amongst Indigenous Australians and secondly, to develop an alternative, effective and culturally sensitive method of delivering heart health messages. Methods and results : The study was qualitative research undertaken in three South-West towns of Western Australia where the incidence of CVD was high amongst the Aboriginal community members. The use of semi-formal interviews, informal individual consultation, observation, and focus groups were methods implemented to obtain information. The first phase of the research was to identify the barriers which affected the Aboriginal Health Workers’ ability to deliver specialist educational programs. Questionnaires and interviews with the Aboriginal Health Workers and other health professionals in the towns, and community focus groups were undertaken in this phase of the study. The second phase of the research was aimed at developing an alternative strategy for delivering heart health messages. The focus changed to adopt more traditional ways of passing on information in Indigenous communities. The idea of small gatherings of friends or family with a trusted community member presenting the health message was developed. The third phase of the research was to implement this new approach. Lay educators who had been identified within focus groups and by Aboriginal Health Workers were trained in each of the towns and a protocol involving discussions of health issues, viewing a video on CVD, produced by the National Heart Foundation, sharing in a ‘heart healthy’ lunch and partaking in a ‘heart health’ knowledge game which was developed specifically for the gatherings. Several of these gatherings were held in each of the towns and they became known as ‘HeartAware parties’.

The reading and school performance of Aboriginal and Torres Strait Islander (A & TSI) children has been reported to be poorer than that of the wider community. The known association between reading and vision formed the basis of the principal hypothesis tested in this thesis that the poor reading performance of these children has a visual basis. Two experiments made up the main study which examined the visual characteristics and reading performance of children attending two different urban schools; the Holy Rosary school, which catered for children from many ("mixed") cultural backgrounds and the St Francis school, whose students were predominantly of A & TSI culture. In experiment I, the visual characteristics of 41 A & TSI children (13 from the Holy Rosary school, 28 from the St Francis school), aged between 8 and 11 years were measured. In general, A & TSI children exhibited low hyperopic refractive errors and other optometric findings were similarly within normal limits. Agematched data for 13 A & TSI children from each of the two schools was also compared. Horizontal eye movement ability and reading comprehension skills were significantly poorer in the A & TSI children attending the "mixed" (Holy Rosary) school, while the perceptual skills of the A & TSI students attending the "A & TSI" (St Francis) school were significantly worse. The second experiment investigated the vision and reading performance of A & TSI and non-A & TSI children attending the same school. Age-matched data of 13 A & TSI and 13 non-A & TSI students were analysed. While the visual profiles of the A & TSI and non-A & TSI students were not significantly different, the reading accuracy and comprehension scores were significantly worse in the A & TSI children when compared with the non-A & TSI group. The results from both experiments are consistent with previous reports of poor reading performance in A & TSI children but argue against poor vision being the cause of this reduced reading performance. As an adjunct to this study, the Turtle chart, designed specifically for use with A & TSI children, was evaluated. The vision of 97 students, 60 A & TSI and 37 non-A & TSI students, aged between 6 and 12 years, was measured using both a standard Bailey-Lovie chart and a Turtle chart. The results obtained with the two charts were highly correlated, indicating that the Turtle chart is a culturally appropriate alternative for the measurement of vision in A & TSI children.

Undernutrition in prevalent in Aboriginal communities, in utero, infancy and childhood. It influences childhood morbidity and mortality and growth patterns. Undernutrition and poor socio-economic status also contribute to endemic and epidemic infectious disease, including scabies and streptococcal infection. It has been suggested that early undernutrition, and streptococcal and scabies infection are risk factors for renal disease, which is at epidemic levels and increasing. This thesis examines the prevalence of undernutrition in newborns and infants in an Aboriginal community over time, and its impact on childhood growth and child and adult renal markers. The association between skin lesions, streptococcal serology, post-streptococcal glomerulonephritis (PSGN) and renal markers as evaluated through a community wide screening program in 1992-1995 is also examined. Birthweights have increased since the 1960s, but they are still much lower than the non-Aboriginal values. Weights in infancy have decreased since the 1960s. At screening in childhood stunting was common, reflecting the presence of long-term poor nutrition in infancy. In both adults and children, birth weight and infant weights were negatively associated with albuminuria measured by the albumin to creatine ratio (ACR).

Thesis (Ph. D.)--University of Sydney, 2009.
Degree awarded 2009; thesis submitted 2008. Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Dept.of History, Faculty of Arts. Title from title screen (viewed 3 December, 2009). Includes graphs and tables. List of tables: leaf 9. List of illustrations: leaves 10-12. Includes bibliographical references. Also available in print form.

I commenced the Master of Philosophy in Applied Epidemiology (MAE) in February 2015. My field placements were shared between the Communicable Diseases Control Directorate, Public Health Division at the Western Australia Department of Health (CDCD) and the Telethon Kids Institute (TKI), both located in Perth. Two of the three projects that I completed at the CDCD involved a statewide protracted mumps outbreak that went on for the duration of my MAE and reached almost 900 cases. The epidemiology of this outbreak including a discussion about vaccination is presented in Chapter 1. This satisfies the outbreak investigation requirement of the MAE. Chapter 2 comprises a late draft manuscript that explores the vaccine effectiveness (VE) of the measles-mumps-rubella vaccine among paediatric cases during the mumps outbreak. I designed and carried out a matched case-control study using paediatric outbreak cases and controls from a population database. I measured VE using a conditional logistic regression model and compared it with the screening method. Both methods yielded a very low VE this population. This is likely due to a multitude of factors that are discussed in the chapter. My work at TKI involved a data analysis using linked-administrative data on a total population birth cohort involving all children born in Western Australia between 1996-2012. I explored the burden of hospital separations that resulted from otitis media (OM), the most common infectious disease in children, and a common related procedure, myringotomy with ventilation tube insertion (MVTI). I calculated the age-specific hospitalisation rates for OM and MVTI over the study years. The second part of this analysis involved investigating the maternal and infant risk factors and population attributable fractions for OM-related hospitalisation in early life. This work was important because of its implications for practice. All of this is presented in Chapter 3. Chapter 4 is an evaluation of SmartVax, a novel, real-time Adverse Events Following Immunisation (AEFI) surveillance system using SMS text messages to communicate directly with vaccinees after their vaccination. This was the third project that I completed at the CDCD. The chapter begins with a peer-reviewed publication, Continuous active surveillance of adverse events following immunisation using SMS technology, that describes the system and analyses data outputs for children <5 years from 2011-2015. I have included the publication first to provide a brief system overview including summarised surveillance data, to give context to the evaluation since SmartVax is a relatively new and developing system. The publication is followed by the formal evaluation. Finally, I include a summary of the teaching exercises that I was involved in during my MAE. The first was a “lesson from the field” where I prepared an exercise for my fellow scholars. The exercise was useful for me and the feedback from my colleagues was positive. The second was a collaborative teaching exercise about confounding that we taught to the first year MAE scholars on their last day of courseblock. These combined activities at both placements have enriched my understanding of epidemiology while working in health and research environments.

Until recently, there was no dementia screening tool for Indigenous Australians and a paucity of information on the extent of dementia in Indigenous Australians. This thesis describes the development and validation of a tool to assess cognitive impairment in remote Indigenous Australians with the primary purpose of determining the prevalence of dementia and other associated conditions in this population. The tool was reevaluated with the larger prevalence sample and a short version of the tool was developed and evaluated. The Kimberley Indigenous Cognitive Assessment (KICA) tool was validated with Indigenous Australians aged over 45 years from the Kimberley region of Western Australia (n=70). The results were later confirmed in a larger sample from the remote Kimberley (n=363), and an additional sample in rural and remote areas of the Northern Territory (n=47). The KICA results were compared to independent consensus diagnoses using DSM-IV and ICD-10. Interpreters were used whenever participants were not proficient in English. These data led to the determination of a cut-off score of 33/34 out of a possible total score of 39 for the cognitive component of the KICA (KICA-Cog), with a sensitivity of 0.93 and specificity of 0.95 and AUC of 0.98. The tool is now widely used within remote areas of Australia. A short version of the KICACog (sKICA-Cog) was developed and found to be a valid brief screening tool for dementia in the Kimberley population, and had a cut-off score of 20/21 out of a possible 25, with a sensitivity of 0.89, specificity of 0.95 and AUC of 0.98. The sKICA-Cog should be used in combination with the KICA cognitive informant questionnaire (KICA-IQ). The KICA-IQ cut-off score of 2/3 out of a possible 16 was determined, with a sensitivity of 0.76 and specificity of 0.84 and AUC of 0.91. Using the validated KICA, the prevalence of dementia and cognitive impairment not dementia (CIND) was determined in a semi-purposive sample consisting of 363 Indigenous Australians aged over 45 years from 6 Aboriginal communities and one town in the Kimberley region. Participants were screened with the full KICA and 165 participants had an independent specialist review with consensus diagnoses. The prevalence of dementia was 12.4%, 5.2 times greater than the Australian prevalence of 2.4%, after age adjustment. The prevalence of CIND was 8.0%. Characteristics associated with dementia included older age, male gender (OR 3.1, 95% CI 1.4, 6.8), no formal education (OR 2.7, 95% CI 1.1, 6.7), smoking (OR 4.5, 95% CI 1.1, 18.6), previous stroke (OR 17.9, 95% CI 5.9, 49.7), epilepsy (OR 33.5, 95% CI 4.8, 232.3) and head injury (OR 4.0, 95% CI 1.7, 9.4). Other factors associated with dementia included incontinence, falls and poor mobility. The KICA is a valid assessment tool for rural and remote Indigenous Australians. The prevalence of dementia amongst Indigenous Australians is substantially higher than generally found in non - Indigenous Australians and other populations in the developed and developing world.

Doctor of Philosophy(PhD)
Indigenous health is one of the most pressing issues confronting contemporary Australian society. In recent years government officials, medical practitioners, and media commentators have repeatedly drawn attention to the vast discrepancies in health outcomes between Indigenous and non-Indigenous Australians. However a comprehensive discussion of Aboriginal health is often hampered by a lack of historical analysis. Accordingly this thesis is a historical response to the current Aboriginal health crisis and examines the impact of colonisation on Aboriginal bodies in Queensland during the early to mid twentieth century. Drawing upon a wide range of archival sources, including government correspondence, medical records, personal diaries and letters, maps and photographs, I examine how the exclusion of Aboriginal people from white society contributed to the creation of racially segregated medical institutions. I examine four such government-run institutions, which catered for Aboriginal health and disease during the period 1900-1970. The four institutions I examine – Barambah Aboriginal Settlement, Peel Island Lazaret, Fantome Island lock hospital and Fantome Island leprosarium – constituted the essence of the Queensland Government’s Aboriginal health policies throughout this time period. The Queensland Government’s health policies and procedures signified more than a benevolent interest in Aboriginal health, and were linked with Aboriginal (racial) management strategies. Popular perceptions of Aborigines as immoral and diseased directly affected the nature and focus of government health services to Aboriginal people. In particular the Chief Protector of Aboriginals Office’s uneven allocation of resources to medical segregation facilities and disease controls, at the expense of other more pressing health issues, specifically nutrition, sanitation, and maternal and child health, materially contributed to Aboriginal ill health. This thesis explores the purpose and rationales, which informed the provision of health services to Aboriginal people. The Queensland Government officials responsible for Aboriginal health, unlike the medical authorities involved in the management of white health, did not labour under the task of ensuring the liberty of their subjects but rather were empowered to employ coercive technologies long since abandoned in the wider medical culture. This particularly evident in the Queensland Government’s unwillingness to relinquish or lessen its control over diseased Aboriginal bodies and the continuation of its Aboriginal-only medical isolation facilities in the second half of the twentieth century. At a time when medical professionals and government officials throughout Australia were almost universally renouncing institutional medical solutions in favour of more community-based approaches to ill health and diseases, the Queensland Government was pushing for the creation of new, and the continuation of existing, medical segregation facilities for Aboriginal patients. In Queensland the management of health involved inherently spatialised and racialised practices. However spaces of Aboriginal segregation did not arise out of an uncomplicated or consistent rationale of racial segregation. Rather the micro-histories of Fantome Island leprosarium, Peel Island Lazaret, Fantome Island lock hospital and Barambah Aboriginal Settlement demonstrate that competing logics of disease quarantine, reform, punishment and race management all influenced the ways in which the Government chose to categorise, situate and manage Aboriginal people (their bodies, health and diseases). Evidence that the enterprise of public health was, and still is, closely aligned with the governance of populations.

Chronic disease is the most significant contributor to the mortality gap between Australia’s First Nations people and the overall Australian population. This study explored chronic disease self-management and health literacy in First Nations adults living in remote Queensland. Key findings were poor communication by healthcare providers coupled with limited health literacy abilities of individuals were the major barriers to active engagement with managing chronic disease. Providing a supportive health literacy environment and the provision of appropriate health information delivered in a cultural safe way using clinical yarning, may assist with closing the gap in First Nations people.

The disparity in life expectancy between Indigenous and non-Indigenous populations, including within high-income countries, is driven by a heightened risk of cardio-metabolic diseases. The current study recruited independent panels of experts in Indigenous cardio-metabolic health from Australia, New Zealand and the United States, in order to establish local consensus opinion and initiate dialogue on appropriate prevention strategies. Therefore, a three-round Delphi process was used to consolidate and compare the opinions of 60 experts, 20 from each country. Round one, the experts were asked twelve open-ended questions across six domains: (i) prevention; (ii) consultation; (iii) educational resources; (iv) societal issues; (v) workforce issues; (vi) culture and family. Round two, the experts completed a structured questionnaire based on results from the first round, in which they ranked items according to their importance. Final round, the experts were asked to re-rank the same items after receiving summary feedback about the rank ordering from the previous round. Several themes emerged common to all three countries: (i) socio-economic and education inequalities should be addressed; (ii) educational, behaviour change and prevention strategies should address physical environmental determinants and be responsive to the local context, including being culturally appropriate; and (iii) cultural appropriateness can be achieved through consultation with Indigenous communities, cultural competency training, use of Indigenous health workers, and use of appropriate role models. These findings highlight several key priorities that can be used to initiate dialogue on appropriate prevention strategies. Such strategies should be contextualized to the local Indigenous populations.

Background: Evidence-based policy making (EBPM) has become an article of faith. While critiques have begun to emerge, they are predominately based on theory or opinion. This thesis uses the 2008 case study of tobacco control policy making for Indigenous Australians to analyse empirically the concept of EBPM. Research questions: (1) How, if at all, did the Government use evidence in Indigenous tobacco control policy making? (2) What were the facilitators of and barriers to the use of evidence? (3) Does the case study augment or challenge the apparent inviolability of EBPM? Methods: Data were collected through: (1) a review of primary documents largely obtained under the Freedom of Information Act 1982; and (2) interviews with senior politicians, senior bureaucrats, government advisors, Indigenous health advocates and academics. Results: Historically, Indigenous smoking was not problematised because Indigenous people faced other urgent health/social problems and smoking was considered a coping mechanism. High prevalence data acquired salience in 2007/08 in the context of a campaign to reduce disparities between Indigenous and non-Indigenous health outcomes. Ensuing policy proposals were based on recommendations from literature reviews, but evidence contained in those reviews was weak; notwithstanding this, the proposals were adopted. Historical experiences led policy makers to give special weight to proposals supported by Indigenous stakeholders. Moreover, the perceived urgency of the problem was cited to justify a trial-and-evaluate approach. Conclusion: While the policies were not based on quality evidence, their formulation/adoption was neither irrational nor reckless. Rather, the process was a justifiable response to a pressing problem affecting a population for which barriers existed to data collection, and historical experiences meant that evidence was not the only determinant of policy success. The thesis proposes a more nuanced appraoch to conceptualising EBPM wherein evidence is neither a necessary nor a sufficient condition for policy. The approach recognises that rigorous evidence is always desirable but that, where circumstances affect the ability of such research being conducted, consideration must be given to acting on the basis of other knowledge (e.g. expert opinion, small-scale studies). Such an approach is justifiable where: (1) inaction is likely to lead to new/continued harm; and (2) there is little/no prospect of the intervention causing additional harm. Under this approach, non-evidentiary considerations (e.g. community acceptability) must be taken into account.

Many researchers have recognized the value of investigating the history of race contact in Australia, but too few have sought to explain in detail why the Aboriginal population declined so much and so rapidly when colonization advanced across the continent. The central aim of this thesis is to identify and assess the impact of the major causes of Aboriginal population collapse in the Riverland (Murray River) region of South Australia. It is estimated that prior to 1800 the population density of the Riverland was between 0.3 and 0.5 km^ per person with a total population for the region of around 3000. In 1881 the South Australian State Census enumerated just 14 Aboriginal people for the Riverland region. The population collapse has been viewed in two stages. The first has been termed pathological contact and is considered to be the major cause of the collapse. Introduced venereal syphilis, gonorrhoea and smallpox spread ahead of the major European frontiers of South Australia causing extreme mortality among the Riverland Aborigines. The second stage began after European settlement of South Australia. Violent clashes were quick to erupt on the overland cattle route which linked the settlement of Adelaide with the Eastern settlements. The combined effect resulted in an increase in the mortality rate, a decrease in the fertility rate and social and economic disruption. The population was unable to recover.

This thesis has attempted to evaluate whether Australian Aboriginal mortality patterns are different from those exhibited by indigenous groups in other countries or by the general Australian population; and whether the high rate of coronary heart disease among Australian Aborigines is attributable to the underlying prevalence of specific lifestyle (risk) factors. At a macro-level, I have compared contemporary mortality patterns of and risk factor prevalence levels among Australian Aborigines and other indigenous groups. At a micro-level, I have made the same comparisons between Aborigines living in western New South Wales (especially those in Bourke) and other Australians. This study has made four important points regarding these issues. The first point is that although Australian Aborigines and other indigenous groups have similar patterns of high adult mortality, the relative importance of some more notable causes of death is strikingly different. The second point is that Aborigines have much higher total and age-specific death rates than other Australians, especially during adulthood and most notably from circulatory system diseases. The third point is that, compared with the general Australian population, Bourke Aborigines have much higher risk factor prevalence levels for a number of coronary heart disease risk factors. The fourth and final point is that Bourke Aboriginal risk factor prevalence levels tend to vary quite considerably by several demographic, environmental, and social-cultural conditions (risk markers) — more specifically, by age, location, employment status, and pay period. Overall, these findings suggest that the mortality pattern of Australian Aborigines is experienced by no other population; and that lifestyle factors, which are influenced by often uncontrollable conditions, can at least partially account for the observed high rate of coronary heart disease.

Previous 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 set in the intervening colonial period, our knowledge of Aboriginal health following European colonisation remains understudied. This thesis is a contribution to filling that gap through an examination of documentary and skeletal evidence in the changing bio-chemical situation experienced by Aboriginal populations of Southeast Australia from 1788 to 1900. This thesis examines one of the major biological components of this change – disease that were introduced unto 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. The 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 morbidity and mortality form the introduced diseases. The major epidemic diseases during the early stage were smallpox, syphilis, tuberculosis, influenza, and measles. Each of these diseases was 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 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.

In this thesis I examine aspects of disease, health and healing among the indigenous people in Western Australia and Queensland from 1900 to 1940. I argue that diseases have helped to shape and influence the interaction between the indigenous people and the various members of the settler community most concerned with them - government protectors, missionaries, pastoralists and health workers. In developing this argument I draw on the distinction made by Stephen J. Kunitz between the universalistic and particularistic approaches to historical epidemiology. Kunitz argues that the development of physiology and bacteriology transformed the practice of medicine by revealing universalistic 'natural histories' of diseases and their causative agents, but that this approach should be tempered by attention to the particular individual, cultural and institutional circumstances of disease occurrence. Diseases have a past, a present and a future of their own, and when considered within the context of human social history, are seen to be a powerful motivate force in human affairs. My approach involves examining the history of diseases, health and healing among the indigenous peoples using models of causation, some of which are biomedical, some are anthropological and others are demographic and epidemiological. There are differences between such models. The biomedical model is 'universalistic' and 'scientific', based on general principles subject to proof or denial through empirical research. In the same way, the demographic and epidemiological models are also universalistic. The anthropological model, however, is articularistic' in that each situation is unique and is explained by its history and internal dynamics, not by reference to general principles. The combination of the biomedical, demographic and epidemiological methods with those of social history allows an otherwise silent indigenous population to be brought into the historical narrative from which they would otherwise have been excluded. In Western Australia, contrary to previous thinking, the total number of Aborigines increased during the study period. In particular, the number of females and older males increased under the influence of protection laws. The increases contradict the popular belief that the indigenous populations were still in decline. However, the spread of disease and the growing population worsened the already poor personal and public hygiene practices, creating the mistaken impression that the indigenous populations were declining. Indeed, diseases such as leprosy, respiratory and sexually transmitted diseases had by the 1930s reached epidemic proportions, which suggested that the indigenous people were a dying race. The indigenous populations already contained some pathogenic infections prior to contact with Europeans. The Aborigines had developed a means, however rudimentary, of predicting how sick people reacted to an illness and of determining what the disease might be that healers treated. But following European contact, other diseases came from contact not only with Europeans but also with Asians, who introduced leprosy into mining camps and Kanakas, who introduced leprosy into the cane plantations and tuberculosis into the Cape York regions. Protection policies intensified the effects of the diseases. In Queensland, the government applied its protection policies with increasing vigour over the period, resulting in most Aborigines living on government ·relief depots, missions and reserves by the 1930s. Demographic analysis reveals that Queensland consistently overestimated its indigenous populations. Death, disease, health and heating among indigenous groups, therefore, came to have social and political dimensions which few, if any, people recognised at the time. In hindsight, however, we can appreciate that the assumption behind health programs was that the indigenous populations should be the passive, but grateful, recipients of welfare rather than historic actors in their own right. The consequences in terms of disease dynamics were profound. The associated practice of gathering together sick, infirm and infected people in 'disease compounds' created reservoirs of exotic diseases to infect newcomers with low immunity. The social consequences of weakened populations meant, in turn, higher numbers of inmates who succumbed to virulent infections. Even in the absence of 'disease compounds', overcrowding of depots and inadequate health services based mostly on religious compassion (on both mission and government compounds) were instruments in promoting increased infection. After 1920 professional services supervised by government protectors and health officials became the norm, but in general, Aborigines were not allowed access to normal hospital facilities. During epidemics, overcrowding of depots and settlements meant a greater susceptibility to respiratory and sexually transmitted diseases, which became endemic, as well as to other infections such as hookworm and leprosy.

Jennifer Carr worked with Aboriginal families with Machado-Joseph disease (MJD) in the Top End of Australia to co-design and pilot a physical activity and lifestyle program. The 'Staying Strong Toolbox' program significantly improved mobility, ataxia and quality of life, will be implemented in Australia and shared with families with MJD worldwide.

Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) are auto-immune conditions associated with prior exposure to Group A streptococcus (GAS). ARF is an acute condition associated with fever and joint, brain, skin and heart inflammation. RHD is its chronic sequela and is characterised by permanent heart valve damage which can, in turn, lead to heart failure and an increased risk of endocarditis and stroke. To avoid such complications interventions may be required to repair or replace damaged valves. ARF and RHD are preventable diseases rarely encountered in mainstream Australia. However, Aboriginal Australian and Torres Strait Islander peoples have amongst the highest reported rates of ARF/RHD in the world with significant morbidity and mortality. This thesis comprises complementary projects and articles that can inform the community and health service response to prevention, diagnosis and management of ARF/RHD with a particular focus on Indigenous Australians. Prevention: Three systematic reviews are presented that examine strategies to improve primary and secondary prevention of ARF/RHD. High quality studies are often lacking and much of the evidence informing strategies to prevent ARF/RHD is limited or absent. Available evidence indicates primordial prevention via improvements in social, economic and environmental conditions is key. While primary prevention may be achieved through improved diagnosis and early treatment of GAS pharyngitis, implementation can be difficult and research into the development of a GAS vaccine remains crucial. Effective secondary prevention of ARF/RHD is possible with long-acting benzathine penicillin (LAB). Nonetheless, delivery of LAB is highly variable and frequently poor. Further work is needed to enhance health care systems to maximize uptake of LAB and to identify more effective formulations or delivery devices for administration. Diagnosis: The utility of screening for RHD via echocardiography (heart ultrasound) to detect early disease is topical as this may facilitate early administration of secondary prophylaxis thereby limiting disease progression. A review of the feasibility of implementing RHD screening in Australia is presented and a number of limiting factors are highlighted. These include a lack of an agreed case definition and a limited understanding of the significance, natural history and potential treatment of early and subclinical RHD. Further, the delivery of secondary prevention is often suboptimal and the impact of additional cases on health services, and the psychosocial health of patients and families, can be substantial. The refinement of a screening-based case definition for RHD, and particularly the significance of minor heart valve abnormalities, was informed by the Rheumatic Fever Follow-up Study (RhFFUS). Children with prior Borderline RHD (defined under World Heart Federation (WHF) criteria) were up to nine times more likely to experience ARF compared with children with a normal echocardiogram. Their risk of having progressive valve damage was also significantly greater and 1 in 6 developed Definite RHD. In contrast, children with less severe valve abnormalities not satisfying criteria for Borderline RHD were at no greater risk of ARF or echocardiographic progression of valvular lesions. These results provide cogent evidence that, in some children, valvular changes consistent with Borderline RHD detected on screening echocardiograms represent the earliest stage of Definite RHD. Such children may benefit from secondary prophylaxis or enhanced surveillance through regular echocardiographic monitoring to assess for progression of disease. Moreover, these results lend support to the validity of WHF criteria that distinguish Borderline RHD from other minor echocardiographic changes, as it is only in the former group that there is a greater risk of ARF and valvular lesion progression. Nonetheless, the fact that individuals with minor echocardiographic changes not satisfying criteria for Borderline RHD still had an increased risk of developing Definite RHD suggests that such individuals should be initially monitored with echocardiography to ensure they do not progress. Management: The final component of this thesis comprises two papers that describe projects that were undertaken to inform potential improvements in the management of ARF/RHD. The first compared the quality of care provided to patients in the Kimberley and far north Queensland where differing models of care were operating. This highlighted more severe disease in the Kimberley and greater specialist follow-up and prescription and receipt of secondary prophylaxis in far north Queensland. This supported an association between far north Queensland's single-provider model of care and centralised RHD control programme and improved patient care, potentially fewer cases of severe disease, and reduced need for surgical and other interventions. Since this study was completed, a centralized RHD control and management programme has been implemented in the Kimberley. The second project related to the use of prophylactic antibiotics to prevent bacteremia, and potentially infective endocarditis (IE), in patients with RHD undergoing high-risk procedures. While this is recommended for Indigenous patients with RHD under Australian guidelines, American guidelines were recently amended to recommend prophylaxis only in people with prosthetic valves and not in those with "native-valve" RHD. A review of infective endocarditis cases in northern Australia was undertaken to determine whether native valve RHD was associated with an increased risk of IE. Results of this study showed that those with native valve RHD were at increased risk of IE (RR 58) compared to individuals without native valve RHD. Interestingly, the risk of IE in non-Indigenous patients with RHD was found to be 3.7 times higher than in Indigenous Australians with RHD. This study led to recommendations to broaden current Australian guidelines so as to offer prophylactic antibiotics to all persons with RHD undergoing procedures associated with a high risk of bacteraemia. In conclusion, this thesis provides a number of new insights to address existing knowledge gaps regarding prevention, diagnosis and management of ARF/RHD. It is hoped that continued work on developing a GAS vaccine will eventually deliver an effective and safe method of primary prevention. In the interim the continued focus on early and accurate diagnosis of ARF/RHD and best-practice management (particularly improving uptake of secondary prophylaxis) should be pursued. Overarching these health initiatives must be a commitment to improving the socioeconomic and environmental status of Aboriginal Australian and Torres Strait Islander peoples living in remote communities as a means of effecting ARF/RHD primordial prevention.