Academic literature on the topic 'Diabetes Australia Epidemiology'

Abstract Background Available data on the effects of heatwaves on hospitalizations for diabetes and the post-discharge status of diabetics are scarce. This study aimed to assess the effects of heatwaves on hospitalizations and post-discharge deaths for diabetes, and to identify the individual- and community-level characteristics [i.e. age, gender, Socio-economic Indexes for Areas (SEIFA), and normalized difference vegetation index (NDVI)] that modified heatwave effects. Methods Health data were extracted from a cohort study which included patients in Brisbane, Australia, who were hospitalized due to diabetes from 1st January 2005 to 31st December 2013, and died within 2 months after they were discharged. Data on community-level modifiers, including SEIFA and NDVI (i.e. urban vegetation), were obtained from Australian Bureau of Statistics and Australian Bureau of Meteorology, respectively. Case-crossover design was used to quantify the effects of heatwaves on hospitalizations and post-discharge deaths due to diabetes. Four heatwave definitions incorporating both intensity (i.e. 90th, 95th, 97th and 99th percentiles of mean temperature distribution) and duration (2 days), as well as excess heat factor (EHF), were used. A case-only design was adopted to identify the modifiers of heatwave effects. Results There were 10 542 hospitalizations for diabetes, and 513 patients died due to diabetes within 2 months after discharge. During low-intensity heatwave days (i.e. 90th percentile & 2 days), we did not observe a significant increase in hospitalizations for diabetes [9% at lag 0; 95% confidence interval (CI): –3%, 23%; P = 0.146], but we observed a significant increase in post-discharge deaths (46% at lag 2; 95% CI: 3%, 107%; P = 0.036). During middle-intensity heatwave days (i.e. 95th percentile & 2 days), hospitalizations for diabetes increased by 19% at lag 0 (95% CI: 2%, 39%; P = 0.026), and post-discharge deaths increased by 64% at lag 0 (95% CI: 6%, 154%; P = 0.027). During high-intensity heatwave days (i.e. 97th percentile & 2 days), hospitalizations for diabetes increased by 37% at lag 1 (95% CI: 11%, 69%; P = 0.004) and post-discharge deaths increased by 137% at lag 1 (95% CI: 39%, 303%; P = 0.002). When heatwave intensity increased to 99th percentile, we did not observe a significant increase in hospitalizations (–1% at lag 0; 95% CI: –38%, 59%; P = 0.870) or post-discharge deaths (79% at lag 0; 95% CI: –39%, 431%; P = 0.301). When we used EHF to define heatwaves, we observed significant increases of hospitalizations (7%; 95% CI: 1%, 15%; P = 0.039) and post-discharge deaths (68%, 95% CI: 10%, 158%; P = 0.017) during heatwave days, compared with non-heatwave days. Children and male diabetics were particularly vulnerable to heatwave effects, but we did not find any significant modification effect of SEIFA or NDVI on the associations of heatwaves with hospitalizations and post-discharge deaths due to diabetes. Conclusion Heatwaves may lead to hospitalizations of diabetics and their premature deaths. Heat-related diabetes burden in children may increase as climate warms and with increasing obesity rates in adolescents.

Melioidosis is a potentially fatal bacterial infection caused by the Gram-negative bacillus, Burkholderia pseudomallei following contact with a contaminated environmental source, normally soil or water in tropical and subtropical locations. The disease spectrum varies from rapidly progressive bacteraemic infection with or without pneumonia, to focal lesions in deep soft tissues and internal organs to superficial soft tissue infection and asymptomatic seroconversion with possible long-term dormancy. Most infections occur with a background of chronic illness such as diabetes, chronic kidney disease and alcoholic liver disease. Improvements in diagnosis, targeted antimicrobial treatment and long term follow up have improved clinical outcomes. Environmental controls following rare point source case clusters and heightened awareness of melioidosis appear to have reduced the disease burden in some parts of northern Australia. However, the impact of climate change on dispersal of environmental B. pseudomallei, and changing land use in tropical Australia is expected to change the epidemiology of melioidosis in future.

Melioidosis is endemic in the remote Katherine region of northern Australia. In a population with high rates of chronic disease, social inequities, and extreme remoteness, the impact of melioidosis is exacerbated by severe weather events and disproportionately affects First Nations Australians. All culture-confirmed melioidosis cases in the Katherine region of the Australian Top End between 1989–2021 were included in the study, and the clinical features and epidemiology were described. The diversity of Burkholderia pseudomallei strains in the region was investigated using genomic sequencing. From 1989–2021 there were 128 patients with melioidosis in the Katherine region. 96/128 (75%) patients were First Nations Australians, 72/128 (56%) were from a very remote region, 68/128 (53%) had diabetes, 57/128 (44%) had a history of hazardous alcohol consumption, and 11/128 (9%) died from melioidosis. There were 9 melioidosis cases attributable to the flooding of the Katherine River in January 1998; 7/9 flood-associated cases had cutaneous melioidosis, five of whom recalled an inoculating event injury sustained wading through flood waters or cleaning up after the flood. The 126 first-episode clinical B. pseudomallei isolates that underwent genomic sequencing belonged to 107 different sequence types and were highly diverse, reflecting the vast geographic area of the study region. In conclusion, melioidosis in the Katherine region disproportionately affects First Nations Australians with risk factors and is exacerbated by severe weather events. Diabetes management, public health intervention for hazardous alcohol consumption, provision of housing to address homelessness, and patient education on melioidosis prevention in First Nations languages should be prioritised.

SUMMARY Melioidosis, caused by the gram-negative saprophyte Burkholderia pseudomallei, is a disease of public health importance in southeast Asia and northern Australia that is associated with high case-fatality rates in animals and humans. It has the potential for epidemic spread to areas where it is not endemic, and sporadic case reports elsewhere in the world suggest that as-yet-unrecognized foci of infection may exist. Environmental determinants of this infection, apart from a close association with rainfall, are yet to be elucidated. The sequencing of the genome of a strain of B. pseudomallei has recently been completed and will help in the further identification of virulence factors. The presence of specific risk factors for infection, such as diabetes, suggests that functional neutrophil defects are important in the pathogenesis of melioidosis; other studies have defined virulence factors (including a type III secretion system) that allow evasion of killing mechanisms by phagocytes. There is a possible role for cell-mediated immunity, but repeated environmental exposure does not elicit protective humoral or cellular immunity. A vaccine is under development, but economic constraints may make vaccination an unrealistic option for many regions of endemicity. Disease manifestations are protean, and no inexpensive, practical, and accurate rapid diagnostic tests are commercially available; diagnosis relies on culture of the organism. Despite the introduction of ceftazidime- and carbapenem-based intravenous treatments, melioidosis is still associated with a significant mortality attributable to severe sepsis and its complications. A long course of oral eradication therapy is required to prevent relapse. Studies exploring the role of preventative measures, earlier clinical identification, and better management of severe sepsis are required to reduce the burden of this disease.

The aim of this doctoral thesis was to study the incidence, risk factors and outcomes of type 1 diabetes for children in South Australia, born from 1999-2013. The incidence of type 1 diabetes has doubled in the last four decades in many countries including Australia, and has substantial individual and economic consequences. Evidence from studies on type 1 diabetes aetiology and its implications is mixed. In this thesis, the linkage of multiple population-wide administrative data over 15 years, and use of rigorous epidemiological approaches has resulted in a better understanding of the risk factors and implications of type 1 diabetes. There are four studies in this doctoral thesis. In the first descriptive study, the incidence of type 1 diabetes was estimated by individual and area-level socioeconomic characteristics among children (aged ≤11 years) in South Australia, born from 2002-2013. Findings of the study showed that type 1 diabetes incidence rates differed depending on the measures of socioeconomic characteristics. Individual-level indicators showed higher type 1 diabetes incidence among more advantaged children, however, there was no clear area-level socioeconomic patterning of type 1 diabetes. Area-level measures of socioeconomic position are likely to have a greater risk of misclassification from true socioeconomic position, which suggests that the use of area-level measures may be misleading. Socioeconomic position is a major determinant of health and can modify the risk factors of type 1 diabetes. For example, as per hygiene hypothesis, the socioeconomically dis-advantaged children are less likely to have type 1 diabetes, which is supported by the findings of individual-level socioeconomic patterning of type1 diabetes in the first study. In addition, socioeconomically disadvantaged women are less likely to have a caesarean birth and more likely to smoke in pregnancy. I chose to study these two risk factors of type 1 diabetes because the evidence was inconsistent, and some studies had methodical limitations. Evidence about the effect of caesarean section on childhood type 1 diabetes is mixed; ranging from very small or no risk to 20-30% increased risk. A prevailing theory is that exposure to the gut and vaginal microbiota during a vaginal birth protects against type 1 diabetes. Therefore, in the second study, the impact of caesarean birth on childhood type 1 diabetes (aged ≤15 years) was estimated. This involved linking multiple administrative datasets of children in South Australia, born from 1999-2013. The question was extended to whether type 1 diabetes risk differed for children born by prelabour or intrapartum caesarean to further test the idea of microbiota exposure on type 1 diabetes. That is because children born by prelabour caesarean do not get exposure to maternal vaginal microbiota, and intrapartum caesarean births may have some exposure. Findings of the study obtained from Cox proportional hazard regression analysis showed a negligible 5% higher incidence (HR = 1.05, 95% CI 0.86-1.28) for caesarean births compared with normal vaginal delivery, with wide confidence intervals including the null. Contrary to the hypothesis of a higher type 1 diabetes risk for prelabor caesarean (because of non-exposure to maternal vaginal microbiota) type 1 diabetes risk for intrapartum caesarean was slightly higher (HR = 1.08, 95% CI 0.82-1.41) than prelabor caesarean (HR = 1.02, 95% CI 0.79-1.32). This negligible risk of type 1 diabetes for children who had caesarean birth, either prelabor or intrapartum, and the potential for unmeasured confounding suggested that birth method induced variation in neonatal microbiota might not be involved in modifying type 1 diabetes risk. Like caesarean section, maternal smoking in pregnancy is also a debated risk factor for childhood type 1 diabetes. Evidence about maternal smoking on childhood type 1 diabetes is inconsistent; studies have been small, and many did not adjust for important confounders or address missing data. In the third study of this doctoral thesis, the effect of maternal smoking in pregnancy on childhood type 1 diabetes was estimated using Cox proportional hazard regression analysis, once again by linking multiple administrative datasets of children in South Australia, born from 1999-2013. The analytical approach for this study ranged; from Cox proportional hazard analysis with adjustment for wide range of confounders using the SA ECDP linked data, involving multiple imputation for missing data; to conducting meta-analysis in order to get more precise estimate. But smoking is notoriously residually confounded, therefore, I made special efforts to investigate the possibility of residual confounding by using a negative control and E-value. The findings demonstrated that maternal smoking in pregnancy was associated with a 16% (HR 0.84, 95% CI 0.67, 1.08) lower childhood type 1 diabetes incidence, compared with unexposed children, which was also supported by the meta-analytic estimates of population-based cohort studies (HR 0.72, 95% CI 0.62, 0.82) and case-control studies (OR 0.71, 95% CI 0.55, 0.86). The negative control outcome and E-value analyses indicated the potential for residual confounding in the effect of maternal smoking on childhood type 1 diabetes. Triangulation of evidence from this study along with the results of similar population-based studies, suggested a small reduced risk of childhood type 1 diabetes for children exposed to maternal smoking in pregnancy. However, the mechanisms linking maternal smoking in pregnancy with childhood type 1 diabetes require further investigation. In the fourth study of this thesis, the impact of childhood type 1 diabetes on children’s educational outcomes in year/grade 5 at age ~10 were estimated, linking population-wide data of children in South Australia, born from 1999-2005. In this study, a doubly-robust analytical method called augmented inverse probability weighting (AIPW) was used to compute the average treatment effect of type 1 diabetes on children’s educational outcomes. AIPW gives an unbiased estimate if either the outcome model or the treatment model is correctly specified. The findings of this study demonstrated that children with type 1 diabetes are not disadvantaged in terms of educational outcomes in year 5, potentially reflecting improvement in type 1 diabetes management in Australia. In summary, the work in this doctoral thesis has demonstrated that type 1 diabetes incidence differed depending on the measure of socioeconomic position. The hygiene hypothesis was only supported by the individual-level socioeconomic pattering of type 1 diabetes incidence in South Australia. The involvement of birth method induced variation in neonatal microbiota in type 1 diabetes was not supported by the caesarean and childhood type 1 diabetes study. Despite the evidence of residual confounding in the estimate of maternal smoking in pregnancy on childhood type 1 diabetes, triangulation of the evidence suggested small reduced risk for children exposed to maternal smoking in pregnancy, but further research will be needed to understand the mechanism. The findings of similar educational outcomes for children with and without type 1 diabetes, highlighted the importance of improvements in diabetes management.
Thesis (Ph.D.) -- University of Adelaide, School of Public Health, 2020