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Background Clients diagnosed and treated for Chlamydia trachomatis are a recognised high-risk group for subsequent infection. An estimated 8% of clients treated for chlamydia at Cairns Sexual Health Service return for re-testing within the recommended 3e4-month period. There is no recall or reminder system in place. This study assesses the effectiveness of using short messaging service (SMS) reminders with and without incentive payments to increase re-testing rates. Methods Eligible consenting clients were randomly allocated to one of three groups. Group 1 (controls) received the standard advice from the clinician to return for re-testing in 3e4 months. Group 2 received the standard advice and an SMS reminder at 10e12 weeks post-treatment. Group 3 received the standard advice and the SMS reminder, which also offered an incentive payment on clinic attendance. Results 32 participants were recruited to groups 1 and 2 and 30 participants to group 3. 62 SMS reminders were sent with 13 (21.0%) reported as undelivered. Re-testing rates were 6.3%, 28.1% and 26.7% for groups 1, 2 and 3, respectively. Conclusion SMS reminders with or without an incentive payment increased re-testing rates in our clients who were diagnosed and treated for chlamydia. However, re-testing remained less than ideal, and the high rate of undelivered SMS reminders suggest that this intervention alone will not achieve desired re-testing rates and that a range of strategies will be required to increase re-testing in this population.

BackgroundSome human cancers demonstrate cellular hierarchies in which tumor-initiating cancer stem cells generate progeny cells with reduced tumorigenic potential. This cancer stem cell population is proposed to be a source of therapy-resistant and recurrent disease. Ewing sarcoma family tumors (ESFT) are highly aggressive cancers in which drug-resistant, relapsed disease remains a significant clinical problem. Recently, the cell surface protein CD133 was identified as a putative marker of tumor-initiating cells in ESFT. We evaluated ESFT tumors and cell lines to determine if high levels of CD133 are associated with drug resistance.MethodsExpression of the CD133-encoding PROM1 gene was determined by RT-PCR in ESFT tumors and cell lines. CD133 protein expression was assessed by western blot, FACS and/or immunostaining. Cell lines were FACS-sorted into CD133+ and CD133- fractions and proliferation, colony formation in soft agar, and in vivo tumorigenicity compared. Chemosensitivity was measured using MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxy-methoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assays.ResultsPROM1 expression was either absent or extremely low in most tumors. However, PROM1 was highly over-expressed in 4 of 48 cases. Two of the 4 patients with PROM1 over-expressing tumors rapidly succumbed to primary drug-resistant disease and two are long-term, event-free survivors. The expression of PROM1 in ESFT cell lines was similarly heterogeneous. The frequency of CD133+ cells ranged from 2-99% and, with one exception, no differences in the chemoresistance or tumorigenicity of CD133+ and CD133- cell fractions were detected. Importantly, however, the STA-ET-8.2 cell line was found to retain a cellular hierarchy in which relatively chemo-resistant, tumorigenic CD133+ cells gave rise to relatively chemo-sensitive, less tumorigenic, CD133- progeny.ConclusionsUp to 10% of ESFT express high levels of PROM1. In some tumors and cell lines the CD133+ fraction is relatively more drug-resistant, while in others there is no apparent difference between CD133+ and CD133- cells. These studies reveal heterogeneity in PROM1/CD133 expression in ESFT tumors and cell lines and confirm that high levels of PROM1 expression are, in at least some cases, associated with chemo-resistant disease. Further studies are required to elucidate the contribution of PROM1/CD133 expressing cells to therapeutic resistance in a large, prospective cohort of primary ESFT.

BackgroundLife expectancy has increased for newly diagnosed HIV patients since the inception of combination antiretroviral treatment (cART), but there remains a need to better understand the characteristics of long-term survival in HIV-positive patients. We examined long-term survival in HIV-positive patients receiving cART in the Australian HIV Observational Database (AHOD), to describe changes in mortality compared to the general population and to develop longer-term survival models.MethodsData were examined from 2,675 HIV-positive participants in AHOD who started cART. Standardised mortality ratios (SMR) were calculated by age, sex and calendar year across prognostic characteristics using Australian Bureau of Statistics national data as reference. SMRs were examined by years of duration of cART by CD4 and similarly by viral load. Survival was analysed using Cox-proportional hazards and parametric survival models.ResultsThe overall SMR for all-cause mortality was 3.5 (95% CI: 3.0–4.0). SMRs by CD4 count were 8.6 (95% CI: 7.2–10.2) for CD4<350 cells/µl; 2.1 (95% CI: 1.5–2.9) for CD4 = 350–499 cells/µl; and 1.5 (95% CI: 1.1–2.0) for CD4≥500 cells/µl. SMRs for patients with CD4 counts <350 cells/µL were much higher than for patients with higher CD4 counts across all durations of cART. SMRs for patients with viral loads greater than 400 copies/ml were much higher across all durations of cART. Multivariate models demonstrated improved survival associated with increased recent CD4, reduced recent viral load, younger patients, absence of HBVsAg-positive ever, year of HIV diagnosis and incidence of ADI. Parametric models showed a fairly constant mortality risk by year of cART up to 15 years of treatment.ConclusionObserved mortality remained fairly constant by duration of cART and was modelled accurately by accepted prognostic factors. These rates did not vary much by duration of treatment. Changes in mortality with age were similar to those in the Australian general population.

The availability of tailored resources may assist in improving partner notification for chlamydia.

ObjectiveTo estimate the rate of combination antiretroviral treatment change and factors associated with combination antiretroviral treatment change among patients recruited in the Australian HIV Observational Database (AHOD). MethodsAnalyses were based on patients in the AHOD who had commenced combination antiretroviral treatment after 1 January 1997. Combination antiretroviral treatment change was de®ned as the addition or change of at least one antiretroviral drug. A random-effect Poisson regression model was used to assess factors associated with increased rates of combination antiretroviral treatment change. ResultsA total of 596 patients in the AHOD were included in the analysis, with a median follow-up of 2.3 years. The overall rate of antiretroviral treatment change in this group was 0.45 combinations per year. In a multivariate analysis, a low CD4 count (, 200 cells/mL) at baseline was associated with an increased rate of treatment change [rate ratio (RR) 1.43; 95% con®dence interval (CI), 1.13, 1.80; P 0.003)]. Combinations including a nonnucleoside reverse transcriptase inhibitor were also associated with slower rates of change than treatment combinations including a protease inhibitor (RR 0.64, 95% CI, 0.51, 0.80, P , 0.001). ConclusionInitiating combination antiretroviral at a CD4 cell count , 200 cells/mL may be associated with poorer patient outcomes. However, the possibility that clinician or patient concerns about low immunological status led to faster rates of treatment change in this group cannot be discounted.

Micro-elimination of hepatitis C virus (HCV) infection through rapid uptake of government-funded direct-acting antiviral therapy within an Australian prison setting is demonstrated. During a 22-month period, 119 patients initiated treatment for chronic HCV infection, with HCV in-prison viremic prevalence declining from 12% to 1%.

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