Campylobacter is currently the most common cause of acute bacterial diarrhoea in Australia among all the notified enteric pathogens with more than 15,000 cases each year. The incidence of notified campylobacteriosis has steadily increased during the past 15 years from 67.0/100,000 population in 1991 to 121.4/100,000 in 2005, though the factors contributing to this increase had not been studied. Adjusting for under-reporting there are, at this point in time, an estimated 225,000 infections occurring each year in Australia, most of which are sporadic in nature. Much of our knowledge in Australia about risk factors for sporadic disease has been based on overseas literature. Prior to the studies undertaken in this thesis, the epidemiology of Campylobacter infection had not been thoroughly studied in Australia, nor had there been any national studies examining risk factors for locally-acquired infection. The broad aim of this thesis was to examine in depth the descriptive epidemiology of Campylobacter infection in Australia, explore the reasons for the sustained increase in incidence of infection and to identify the major risk factors for locally acquired infection using a multi-centre case-control study design. The descriptive study of the epidemiology of campylobacteriosis in Australia was based on Australian notifiable disease surveillance data collected over a 15-year period between 1991 and 2005. This study described the key epidemiological characteristics of this disease in Australia and identified some significant differences in incidence trends across states and territories and among different age groups which had not been previously reported. The study identified gaps in our knowledge of this disease in Australia and made recommendations for future research including the investigation of factors associated with the decline in incidence of infection among children aged 4 years and further studies to identify age and sex-specific risk factors for infection. The issue of seasonality, transmission routes and infection was addressed and areas for further research were specified including longitudinal studies at a regional level that incorporate a comparison of human, animal and environmental genotypes. This study also provided strong compelling evidence to support the hypothesis that the increase in notification rates in Australia during this period represented a real increase in the incidence of infection and that the main driving force behind this rise has been the ongoing increase in chicken consumption among the Australian public. The multi-centre case-control study, involving 1,714 participants 5 years of age, identified the major foodborne and non-foodborne risk factors for Campylobacter infection among the general population in Australia. This study confirmed that chicken meat is a major source of sporadic infection in this country and is responsible for almost one-third of all cases that occur in the Australian community each year. Other independent risk factors for sporadic infection in Australia included consumption of offal and ownership of domestic dogs or chickens aged 6 months. The Nagelkerke R² value of 16% for the final multivariable model indicated a considerable proportion of our case-patients had unexplained risk factors. The combined population attributable risk (PAR) estimate for the independent foodborne risk factors in this study was 31%, which is considerably less than the 75% to 80% of cases in the general population which are thought to be caused through foodborne transmission. Possible explanations for these results include the likelihood that a proportion of foodborne transmission in Australia occurs through food vehicles other than chicken due to cross-contamination from raw products, and the likelihood that much of the population attributable risk that is unaccountered for, may in fact be due to inherent limitations of study design resulting in systematic errors (information bias) and possibly reduced estimates of effect. The burden of illness among the general population in Australia attributable to different independent risk factors was estimated using a novel method developed specifically for this study. Briefly, community incidence data was coupled with PAR data from the case-control study and simulation techniques were used to: (i) estimate the number of infections attributable to specific risk factors, and (ii) derive credible intervals for these estimates by modeling the uncertainty in each variable component. This model of using case-control data in conjunction with pre-existing surveillance data provides researchers with a simple but robust tool for conducting source attribution studies on enteric pathogens. In conclusion, the studies undertaken in this thesis have made important contributions to our understanding of the epidemiology of sporadic Campylobacter infection in Australia.
| Identifer | oai:union.ndltd.org:ADTP/286523 |
| Creators | Russell Stafford |
| Source Sets | Australiasian Digital Theses Program |
| Detected Language | English |
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