An important group of presentations today on STIs, a somewhat neglected area of discussion in HIV, despite evidence that people with higher rates of STIs are at increased risk of HIV and vice versa.
First presenter was Darren Russell from Australia presenting some background on the epidemiology of STIs. First and foremost, the point was made that, if you do not test for it, you will not find it and then you cannot treat it (much like the first 90 with HIV!) and that in contrast to HIV, testing, reporting and surveillance of STIs is inconsistent throughout the world, making STIs the “poor cousins“ of HIV. Given the international nature of the conference, epidemiological data from around the world was presented for STIs. One slide demonstrated that in the early 20th century, as many people died from syphilis as did from HIV/AIDS at the height of the epidemic in the USA. The incidence of syphilis from late last decade throughout the USA, Canada, Germany, Sweden, France, The United Kingdom and Australia was noted to have risen significantly in all countries and a special mention was made of the syphilis epidemic in Aboriginal and Torres Strait Islanders, a group in which we must try to do better if we are to close the gap. This presentation ended on a high note with a success – the roll out of the HPV vaccine and the dramatic decrease of genital warts in vaccinated Australian women and eventually men. I thought that ending on this information really served to demonstrate to the sexual health community what is really needed to stop epidemics – vaccine development.
Next Presenter was Scott McLelland from the United States who presented on STIs and susceptibility to infection. We have known for some time that STIs place people at risk of HIV and vice versa but elucidating exact mechanisms has been challenging and interventions have not been as successful as previously hypothesised. Yet more recent data has demonstrated significantly increased risk of HIV acquisition with HSV2, vaginal dysbiosis (bacterial vaginosis) and HPV due to the immune response. For example, the site of HSV lesions has been shown to have high numbers of CD4 T cells and dendritic cells as does HPV infected mucosa, providing increased target cells for HIV virus. How we use this information as a basis for further research, treatment and ultimately health policy remains to be seen.
Next was Connie Celum, also from the United States who presented on STIs in the era of TasP and PrEP. One of the first and very important points made was that there is no evidence to indicate decreased efficacy of PrEP in users who have an STI – demonstrated in both iPrEx and Partners PrEP studies. One caveat was that bacterial vaginosis may impact the efficacy of topical vaginal tenofovir. The possibility of PrEP programs actually leading to a long-term reduction in STIs was brought up and the role of regular STI screens as part of PrEP use as well as the potential for STI PEP using doxycycline, presented as part of the ipergay study at CROI in early 2017 were both put forward as mechanisms to reduce the burden of STIs in PrEP users. The model of STI testing, treatment and follow up was also addressed with reference to the Dean Street Express clinic in London with changes in service delivery proving effective in testing and treating more people in a shorter space of time and as mentioned previously – if you don’t test for it, you can’t treat it!
Last but not least was Cecile Bebear from France who gave a presentation called “should we fear antibiotic resistance for STIs?” with a focus on 4 bacterial STIs – Chlamydia trachomatis, Neisseria gonorrhoea, Treponema pallidum and Mycoplasma genitalium. For Chlamydia trachomatis, the concern for antimicrobial resistance (AMR) is low with the organism remaining sensitive to tetracyclines, macrolides and quinolones and only very rare cases of macrolide resistance being reported, so as Chlamydia trachomatis remains the most common bacterial STI, it also remains very easy to treat. Neisseria gonorrhoea is the complete opposite however, with resistance to almost every agent ever used against it since about the 1930s. First line treatment with combined antibiotics of two classes has held Neisseria gonorrhoea at bay, but for how long? Extended cephalosporin resistance rates in this organism, where there is resistance monitoring range from 0.1% to 30 % in various parts of the world (up to 5% in Australia). Azithromycin resistance ranges from 2-8% across the world, fluoroquinolone resistance 30%- 50% and tetracycline resistance more than 50%. New treatments are in development pipelines but the ideal way to tackle this organism would be through a vaccine. Syphilis remains relatively easy to treat with penicillin or doxycycline but does have a high prevalence of azithromycin resistance (84% in Australia). Finally, the new kid on the block, somewhat of a problem child, Mycoplasma genitalium, tetracyclines demonstrate poor levels of eradication but no resistance characterised, macrolide resistance is widespread, between 43% and 63% in Australia and there is acquired resistance to the agreed upon second line treatment moxifloxacin, ranging from 4.5% in the UK to 47% in Japan. Unfortunately, this problematic organism did not generate much discussion nor were potential third line agents for consensus discussed. Certainly more research needs to be done in regards to this organism and consistent guidelines on management are required.