ASHM Report Back

Clinical posts from members and guests of the Australasian Society for HIV, Viral Hepatitis and Sexual Health Medicine (ASHM) from various international medical and scientific conferences on HIV, AIDS, viral hepatitis, and sexual health.

Well I didn't think I'd be blogging on the penile microbiome, but Cindy Liu, Assistant Research Prof from George Washington Milken Institute School of Public Health gave such a fascinating talk on the role of the penile microbiome in relation to circumcision on acquisition of HIV that I wanted to at least highlight this research. It is of interest to my role as CNC of Victorian NPEP Service given that circumcision is taken into account when assessing HIV risk for men having insertive intercourse.. My understanding of why circumcision is protective has just increased. 

Firstly, microbiome throughout the body is being increasingly recognised in playing a role in certain diseases.

Circumcision is known to be protective against HIV acquisition for the following reasons:

1. Decrease in at-risk surface area i.e. epithelial lining of foreskin

2. Increase of keratinisation 

3. Change in the sub-preputial micro-environment 

4. Change in penile microbiome

The study involved taking a swab from the coronal sulcus at baseline and 12 months in 2 groups of men - those who were circumcised and those who were uncircumcised.

There was an increase in both the type and density of anaerobic bacteria in uncircumcised men, and a small increase in skin associated "good" bacteria. The anaerobic bacteria found were pro-inflammatory, therefore attracting cytokines to the area, activating HIV target cells, such as Langerhans cells and increasing risk of HIV acquisition.

That is it in a nutshell and I am looking forward to Cindy's next talk this afternoon on BV, a condition we know is characterised by proliferation of anaerobes, and HIV acquisition

 

M. genitalium was isolated 30 years ago.

The organism is difficult to culture, and NAAT is difficult to access.

Commercial NAAT point of care testing is around the corner, so diagnosis is about to become much more accessible.

It has taken longer to establish its role as a pathogen because it is more commonly asymptomatic.

No evidence to support screening, just test those who are symptomatic.

Prevalence is about 1-3% of men and women.

Has similar clinical features to chlamydia.

Increases the risk of tubal abort and PID 2-fold.

 

No cell wall so not sensitive to penicillin-like antibiotics.

There has been widespread use of azithromycin for NSU symptoms, so macrolide (azithromycin) resistance increasing and is now at 50%, however it remains the first-line recommendation.

Moxifloxacin looked promising but resistance to this is now at 15-25% and increasing, currently for second-line treatment.

Guidelines concentrate on urogenital infection and don’t cover rectal infection.

Pristinamycin currently is our only other option, reserved for third-line treatment.

Worldwide we are seeing increasing notifications for syphilis and gonorrhoea.

This is despite effective treatments for both, with the caveat that resistance is emerging for gonorrhoea.

Why is this happening? Various theories.

What can we do about it? Infectivity, number of susceptible contacts, duration of infectivity.

Infectivity - use of condoms with oral sex? Little else we can do to influence this.

Number of susceptible contacts (the rate of change of sexual partners) - vaccinations, chemoprophylaxis (doxycycline)? Again, little else we can do to affect this.

Duration of infectivity - early detection and treatment (sexual history, is your practice gay friendly, doing the right test, point of care testing), strengthening partner notification? Yes, these are within our ability to affect change.

Most STIs are diagnosed in primary care.

Testing rates in primary care are low.

90% of Australians visit their GP annually.

We have the opportunity to affect change.

Hepatitis C was first discovered in 1989.

Overall worldwide prevalence of 2.8%.

Most infections are acquired parenterally, with a significant amount of vertical transmission.

A large well powered study showed a very low sexual transmission rate among heterosexual monogamous relationships (0-0.6%/year, condoms not required but should be advised that they will reduce the risk).

What about MSM?

Hepatitis C incidence in HIV positive MSM has increased exponentially.

Risk factors are intravenous drug use, condomless anal sex independant of intravenous drug use, and syphilis infection independent of intravenous drug use.

There is also sexual transmission of hepatitis C in HIV negative MSM related to chemsex who are on PrEP.

More likely with rough sex and fisting.

Reinfection rates are common.

Screening is recommended annually in HIV positive individuals.

In HIV negative individuals we probably don’t need to screen for hepatitis C routinely, but should consider it in people on PrEP.

Rectal chlamydia is the most common STI in MSM.

Rectal chlamydia is more common than urethral.

Observational studies suggest doxycycline is more effective than azithromycin, but there is no evidence from RCTs

There is a move away from azithromycin to doxycycline.

 

There is much less evidence for mycoplasma genitalium.

M. genitalium was much more common in HIV positive men than HIV negative, accounting for 21% of symptomatic proctitis (as common as chlamydia) compared with 8% symptomatic proctitis in HIV negative MSM.

May be present in 4% asymptomatic MSM rectally.

M. genitalium is present in MSM and may be increasing.

Most are macrolide resistant.

Recommendations exist for urogenital infections, recommending azithromycin first-line, and moxifloxacin as second-line.

Until we have more evidence on how to treat rectal infections we will need to follow the recommendations for urogenital infection.

Third-line treatment is with pristinamycin.

There is a problem using monotherapy in these situations and we are likely to see resistance emerging.

Unfortunately synergy of pristinamycin with other antibiotics hasn’t been good.

Success rates using pristinamycin are about 85%.

RT @_afao: The flatter curve and a slower infection rate means a less stressed health care system, fewer hospital visits on any given day a…

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