No abstract

We speculate that a C. trachomatis infection control program based on early case identification and treatment interferes with the effects of immunity on population susceptibility to infection and that, in the absence of strategies to alter sexual networks, a vaccine will be needed to halt the spread of infection at the population level.

Despite having the largest NEP in North America, Vancouver has been experiencing an ongoing HIV epidemic. Whereas NEP are crucial for sterile syringe provision, they should be considered one component of a comprehensive programme including counselling, support and education.

No abstract

We found no evidence that this NEP is causally associated with HIV transmission. The observed association should not be cited as evidence that NEP may promote the spread of HIV. By attracting higher risk users, NEP may furnish a valuable opportunity to provide additional preventive/support services to these difficult-to-reach individuals.

Background Some screening and treatment programs implemented to control genital Chlamydia trachomatis infections and their complications have shown initial reductions in infection prevalence followed by rises to pre-program levels or higher. One hypothesis is that treatment shortens duration of infection, attenuates development of protective immunity and thereby increases risk of re-infection. Methods A literature review was undertaken to assess evidence supporting the concept of protective immunity, its characteristics and its laboratory correlates in human chlamydial infection. The discussion is organized around key questions formulated in preparation for the Chlamydia Immunology and Control Expert Advisory Meeting held by the Centers for Disease Control and Prevention in April, 2008. Results Definitive human studies are not available, but cross-sectional studies show chlamydia prevalence, organism load and concordance rates in couples decrease with age, and organism load is lower in those with repeat infections, supporting the concept of protective immunity. The protection appears partial and can be overcome upon re-exposure, similar to what is found in rodent models of genital infection. No data are available to define the duration of infection required to confer a degree of immunity or the time course of immunity following resolution of untreated infection. In longitudinal studies of African sex workers, a group presumed to have frequent and ongoing exposure to chlamydial infection, interferon gamma production by peripheral blood mononuclear cells in response to chlamydial heat shock protein 60 was associated with low risk of incident infection. In cross-sectional studies, relevant Th1 type responses are found in infected persons, paralleling the studies in animal models. Conclusions The data support the concept that some degree of protective immunity against re-infection develops following human genital infection, although it appears at best partial. It is likely that factors besides population levels of immunity contribute to trends in prevalence observed in screening and treatment programs. Future studies of protective immunity in humans will require longitudinal follow-up of individuals and populations, frequent biological and behavioral sampling and special cohorts to help control for exposure.

Are we losing ground in our efforts to control sexually transmitted Chlamydia trachomatis infection? Before we can answer this question, we must first consider recent trends in Chlamydia from around the world to establish a baseline for understanding the possible explanations underlying these data.

In the context of increasing Chlamydia infection rates, the reproductive complications of Chlamydia infection in women are declining overall. A recent increase in rates of ectopic pregnancies is cause for concern.