Discussion
We found that there were substantial differences in the Gini coefficients across the four HIV/STIs and across the risk groups. The highest Gini coefficients were among heterosexual males and females for HIV or syphilis, suggesting these infections are concentrated among heterosexuals with higher infection risk scores. These risk scores were calculated using our machine learning based risk assessment tool, MySTIRisk, which considers a variety of factors such as age, gender, country of birth, sexual behaviour and history of previous STIs. Therefore, a higher risk score suggests a higher probability of acquiring HIV and STIs. In contrast, the Gini coefficients were lower among GBMSM, particularly for chlamydia or gonorrhoea, suggesting these infections are widely distributed throughout the GBMSM population. The significance of these findings is that for HIV and syphilis, the interventions will be most cost-effective if they are focused on small, high-risk groups of heterosexuals. In comparison, the interventions for GBMSM should involve the entire GBMSM community, particularly for chlamydia and gonorrhoea, where risk appears to play a minimal role in identifying those most at risk.
Our study demonstrated that Gini coefficients for syphilis and HIV were higher than those for chlamydia and gonorrhoea. In particular, the finding that syphilis demonstrated the highest disparity followed by gonorrhoea and chlamydia is consistent with another study conducted in the Netherlands.16 Specifically, higher Gini coefficients indicate that infections are more concentrated in a smaller group of individuals with higher risk scores. This finding implies that more targeted interventions are necessary for HIV and syphilis infection, while more widespread programmes would be suitable for chlamydia and gonorrhoea. Higher Gini coefficients among HIV and syphilis may be explained by the known fact that those infections are more concentrated among certain subpopulations such as men who have sex with men, and sex workers leading to a higher degree of inequality in terms of disease prevalence.23–25 It means that a relatively small proportion of people disproportionately affected by syphilis and HIV, can lead to higher Gini coefficients than more evenly distributed STIs such as gonorrhoea and chlamydia. Additionally, HIV and syphilis are more severe and chronic conditions with a social and cultural stigma attached to them, which can prevent the infected individuals from seeking the testing and treatment and may potentially lead to higher Gini coefficients.26–28
In another study, Gsteiger et al15 used population data in the UK to calculate the Gini coefficients to measure the distribution of chlamydia. The authors compared the Gini coefficients for STIs for two survey periods of Natsal-2 (1999–2001) and Natsal-3 (2010–2012) and found similar results for chlamydia with 0.30 (95% CI 0.12 to 0.50) in Natsal-2 and 0.33 (95% CI 0.18 to 0.49) in Natsal-3 among females. However, our study has a slightly higher Gini coefficient of 0.40 (95% CI 0.35 to 0.45) in women with chlamydia. First, the difference in study population could have contributed to the discrepancy. The Natsal studies employed general population data, whereas our study focused on data from a sexual health clinic. It is well known that individuals attending such clinics may have a higher risk profile for STIs than individuals from the community which can consequently influence the Gini coefficient. Second, our definition of the exposure variable differed from the Natsal studies. The latter used a single risk factor—the number of new opposite-sex partners in the previous year—while we adopted a broader approach. By employing machine-learning algorithms, we generated a composite risk score encompassing multiple exposure variables. This more comprehensive risk assessment likely impacted our Gini coefficient. Lastly, unlike the Natsal studies, which focused solely on heterosexual females, we included heterosexual, bisexual and women who have sex with women (WSW). Similarly, it is important to note that the Natsal studies provided limited analysis on subgroups for different age groups and population groups as it only included the opposite-sex contacts for sexual behaviour variables population because of a limited proportion of individuals having same-sex partner in the dataset.
Our finding that the Gini coefficients were significantly lower in GBMSM is consistent with a previous study.16 van Wees et al16 developed a risk score calculator using multivariable logistic regression for HIV/STIs and used this to calculate the Gini coefficients for chlamydia, gonorrhoea and syphilis during the period before PrEP(2009 to mid-2015) and after PrEP (mid-2015 to 2019) was introduced. This study examined the distribution of STIs among HIV-negative MSM in Amsterdam Cohort Studies and found a similar pattern to our study, but with a slightly higher Gini coefficients for gonorrhoea (0.46) and chlamydia (0.43) and lower Gini coefficient for syphilis (0.50). These higher Gini coefficients for chlamydia and gonorrhoea in the Netherlands study may be explained by the lower positivity of chlamydia and gonorrhoea in their dataset compared with our study (4.6% vs 8.8% for chlamydia and 5.1% vs 7.8% for gonorrhoea). However, the Gini coefficient for syphilis was lower in the Netherlands study despite the lower positivity (0.7% vs 1.9%). This variation may partly be explained by the difference in sampling frame as the study only included HIV-negative MSM while our study included all GBMSM, regardless of the HIV status and the difference in the nature of risk prediction tools in calculating infection risk scores. While direct comparisons are not currently available, variations in healthcare systems, sexual health education and societal attitudes towards GBMSM populations between different countries such as the Netherlands and Australia could potentially lead to differences in the distribution of STIs such as syphilis. Further research is required to confirm this.
Based on our findings, we propose the need for both targeted and widespread intervention strategies for the control of HIV/STIs. For HIV and syphilis, which show a high degree of concentration in individuals with higher risk scores, targeted interventions are essential. Such interventions can be integrated into existing services and may include initiatives focused on testing, treatment adherence and education about safe sex practices. For chlamydia and gonorrhoea, which have a more widespread distribution across the population, broader public health strategies are needed. These could include regular STI screening programmes, public awareness campaigns and improving access to treatment, which can be integrated into general healthcare services. The strategic integration of these interventions into existing public health programmes and policies could contribute significantly to the control of HIV/STIs.
To our knowledge, this is the first research from Australia to examine the distribution of four STIs across different risk populations (GBMSM, heterosexual men and women) and different age groups. The main strength of the study is the use of a composite risk score that was only available because of the extensive data on sexual risk from attendees at MSHC. This composite score was generated using a machine learning approach20 and is likely to be a better representation of overall risk than a single epidemiological measure.
This study has several limitations. First, the predictive criteria are based on the clients' self-reported information, which is subject to recall, non-response and social-desirability biases. However, there is no other way to collect risk information and we have previously shown that the self-interview method which we used is the least influenced by social-desirability bias.29 Second, the datasets only included MSHC clients, who are at higher risk than the general population that includes lower-risk individuals. This may lead to an underestimate of the Gini index because our dataset likely under-represents the lower-risk individuals. While our focus was on the disparities within the clinic population, we acknowledge that this may limit the generalisability of our findings to other populations or settings. Therefore, it is important for policymakers and public health officials to consider these limitations when applying our findings to their respective contexts. Caution must be applied when extrapolating these results to broader contexts, as different populations may present unique risk profiles. Further studies in diverse settings are necessary to validate and extend our findings. Third, our unit of analysis was client consultations, not individual clients. This means our study reflects the number of consultations rather than the number of unique individuals. This approach could potentially over-represent individuals who had multiple consultations, thereby skewing the positivity rates of STIs and creating potential bias in estimating Gini coefficients. Nevertheless, given our large sample size and our focus on internal population disparities, we believe this approach’s impact on our findings is minimal. Fourth, we only used data from 2015 to 2018 because in 2015 we moved from culture to nucleic acid amplification testing for gonorrhoea30 and this period was too brief to identify a changing trend in HIV/STIs in Australia. Fifth, although our dataset was large enough for machine learning training and testing, the number of HIV and syphilis-positive cases was notably low, which may affect MySTIRisk prediction risk scores and Gini coefficients. Sixth, as the PrEP uptake status was not included as a predictor, we were unable to examine the changes in Gini coefficients before and after PrEP utilisation. Seventh, for gonorrhoea and syphilis, we did not include the anatomical site of infection as a predictor, for which we could not identify the distributions of STIs at different anatomical sites. Looking forward, we propose several directions for future research that could address our study’s limitations and enrich our understanding of HIV/STI disparities. Longitudinal studies are crucial for capturing shifts in HIV/STI distribution over time and evaluating the impact of interventions like PrEP. Additionally, exploring STI distribution across various anatomical sites could offer insights for targeted prevention strategies.
While our current study explores disparities in the distribution of HIV/STIs, we have not distinguished between high-risk and low-risk individuals based on explicit thresholds; a more nuanced approach is planned for future research. In anticipation of these future investigations, we intend to define these thresholds and risk subgroups, balancing factors such as disease burden, healthcare capacity and government funding. Therefore, the objective of our ongoing research is to refine our existing findings, thereby guiding the development of HIV/STIs intervention strategies and policy.
In conclusion, our study demonstrates that disparities exist in the distribution of HIV/STIs among different population groups, with implications for policy and interventions. The higher concentration of HIV and syphilis among heterosexual men and women indicates the need to identify and target high-risk subsets with focused testing and treatment. In contrast, the widespread distribution of chlamydia and gonorrhoea among GBMSM reinforces implementing broader screening and prevention. Estimating Gini coefficients enables tailored, data-driven approaches to early HIV/STI testing and treatment for those most affected. Our findings highlight the potential of Gini coefficients to inform resource allocation and policies aimed at HIV/STI control through precision public health strategies.