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Why STI-induced infertility can also be a male problem.

2 Aug, 17 | by Leslie Goode, Blogmaster

Among long-term sequelae of STI that are asymptomatic and may consequently remain untreated are a number that affect men.  The condition of Chronic Pelvic Pain Syndrome (CPPS) has recently been discussed by Kenyon & Horner (STI), along with the feasibility of its treatment in the STI clinic (Crofts & Horner (STIs); Crofts & Horner (II) (STIs)).  But another important, and much dreaded, consequence of untreated STI in heterosexual men is infertility or sub-fertility.  It should not be forgotten that this is potentially a male problem – not just in the sense that it affects men, but because, in many cases, it is STI-induced damage to the genital tract of the male rather than the female partner that gives rise to the condition.

This male aspect of STI-induced infertility constitutes the topic of a recent review paper by Schuppe & Weidner (S&W).  A key finding cited (Schuppe & Hardt), apparently originating from work by same team of authors, is that a remarkable 25% of testicular biopsies obtained from infertile men reveal focal inflammatory reactions.  Of these, only 2% reported any previous episode of orchitis.  Yet, when it comes to determining the pathogens responsible for male infertility (which could be uropathogens as well as STI), current evidence allows us to draw few conclusions.  The same is true regarding the mechanisms by which these pathogens have an impact on male fertility.  Finally, it is not possible to  establish with any certainty the proportion of total cases of male infertility for which STI are responsible. Of course, where acute epididymitis is involved, there is evidence for azoospermia (c.10%) or oligospermia (c.30%).  Here the authors are reassuring as to the non-persistence of these effects (Pilatz & Linn). But where cases of STI are asymptomatic, they do not, of course, figure in information for ‘accessory gland infection’ as defined by WHO criteria.

Regarding the pathogens implicated, the investigations of the role of Mycoplasma genitalium (see Idahl & Fredland (STI)) and HPV viruses have produced conflicting results; Trichomas vaginalis has no significant effect.  As regards the mechanism, S&W consider evidence relating to reduced sperm motility, oxidative damage and immune-mediated infertility, but reach no very firm conclusions. As for the proportion of male infertility attributable to STI, the authors point to the variation in rates of infertility (between 9% in Germany and 30% in countries with less adequate healthcare) as offering some indicator.

Despite the inconclusiveness of these findings, the review has the merit of drawing attention to an aspect of STI that seems to receive relatively infrequent attention in these pages.  The authors recommend ‘systematic diagnostic evaluation and appropriate treatment’ where there is any suspicion of infectious disease.  However, they look forward to the day when the elucidation of mechanisms and the identification of biomarkers may enable more ‘conservative’ strategies of management.

Vertical HIV transmission may be influenced by complex synergies with other STI – such as Cytomegalovirus

26 Jul, 17 | by Leslie Goode, Blogmaster

The apparently greater susceptibility of sub-Saharan African women to HIV infection has led researchers to consider the various potential synergies between HIV and other genital infections (White & Glynn (STIs); Lurie & Matthews (STIs)) or conditions of the vaginal microbiome (The susceptibility of heterosexual sub-Saharan women (STI/blog)).  A recent study, Adachi & Nielson-Saines, brings this wider perspective to bear on mother-to-child transmission, casting some fresh light on the complex interrelation between the ‘vertical’ transmission of HIV and active and Cytomegalovirus (CMV) viruria.

The study is a late spin-off from HPTN-040 (reported in a 2012 paper by Nielson-Saines & Mofenson IN&M).  This compared the efficacy of different post-partum ART regimes for HIV infected children.  The original participants were c. 1,700, largely S. American women who presented in late pregnancy with HIV.  Matched urine specimens were available for 264 mother-child pairs.  Researchers returned to these specimens after the closure of the main trial in order to investigate through PCR testing the impact of CMV viral shedding on vertical transmission of Cytomegalovirus (CMV) and its concomitants.

The results were as follows.  Out of the 264 maternal urine samples 24 (9.2%) showed evidence of CMV shedding. Matching these maternal samples with infant samples revealed vertical CMV transmission in 10/264 cases.  Five of these were from among the 24 with maternal shedding (20.8%); five were from among the 240 without shedding (2.1%).  When the ratio of transmissions with shedding to transmissions without shedding was adjusted for mode of delivery, maternal gonorrhoea and maternal HIV viral load, it came out at 29.7%.   Women with CMV viral shedding also showed significantly higher odds of HIV transmission to their infants (aOR = 5.6%).

These findings are striking; but what is their relevance?  Maternal CMV shedding may indeed be a very good marker of vertical CMV and HIV transmission.  Presumably, however, health workers would give appropriate anti-retroviral therapy to 100% of infants at risk of HIV infection in any case – and anti-retroviral therapy has been shown to deal successfully with the CMV, without the need to give additional, and potentially toxic, drugs specifically for the CMV (Anfumborn & Tejiokern). So N&M’s research have little implications for management of these infections.

However, their importance may lie in showing how the problem of HIV – including vertically transmitted HIV – cannot be isolated from the wider problem of STI and sexual health in general. Maternal HIV may, for example, increase the likelihood of CMV transmission, and CMV infection of the infant may, in turn, lead to a more rapid progression of HIV.  Complex synergies with vertical HIV transmission may operate in the case of other STI as well – such as HSV-2 (Sivarajah & Tan (STIs)).  So the messages to take away may include not just ‘the necessity of controlling maternal HIV infection during pregnancy through cART’, but also the importance of STI control – above all through the promotion of practices of safe sex.


The challenges and achievements of conducting a multi-country qualitative study to explore the Bottlenecks to HIV care and treatment in sub-Saharan Africa

24 Jul, 17 | by lfountain

Blog post by Joyce Wamoyi1, Dominic Bukenya2, Robert Ssekubugu3, Alison Wringe4 and Jenny Renju4

  1. National Institute for Medical Research, Tanzania
  2. Medical Research Council, Uganda
  3. Rakai health Sciences Programme, Uganda
  4. London School of Hygiene and Tropical Medicine, UK

A newly published supplement to Sexually Transmitted Infections on the HIV Bottlenecks study presents the multiple tensions that exist between HIV programmes and the complex social realities that characterize the lives of PLHIV in seven health and demographic surveillance sites (HDSS) across sub Saharan Africa.


To tweet or not to tweet?

4 Jul, 17 | by Leslie Goode, Blogmaster

Blog post by Katy Turner (@katymeturner)

Who is responsible for tweet etiquette at conferences? Organisers? Presenters? Tweeters?

Conference organisers can certainly set the tone for an event with pronouncements like this one:

Tweet from Trish Groves (@trished)

Clear guide #ICTMC2017 on seeking permission to blog, tweet, take pics (I should’ve read this sooner)


This feels rather heavy handed and puts all the responsibility onto tweeters to “get permission” which rules out real time tweeting and could limit or even censor open discussion of ideas including the community outside conference attendees. I am going venture that the above was written by someone (or a committee of someones) who doesn’t “tweet”.

In our connected 21st century world, most conferences actively encourage tweeting. There are some excellent guidelines e.g. Ten Simple Rules of Live Tweeting at Scientific Conferences
( These are aimed at conference organisers e.g. choose a short hashtag (and check for unexpected clashes), publicise hashtag, encourage tweeting, use twitter to enable questions from outside and tweeters (mechanics of what to tween and how to tweet responsibly).

What about the presenters themselves? Conferences are exciting because they are a place to share new ideas with the other 3 people in the world similarly passionate about modelling sexually transmitted infections (or whatever floats your boat). Tweeting can widen and broaden the conversation and include people inside and beyond the conference. How can we continue to extend and diversify the conversation, whilst also protecting unpublished research and intellectual property?

Here are my top tips for presenters

1) Visual cues on all slides as tweetable or not

Presenters can indicate how much tweeting of their talk is acceptable. This doesn’t need to be onerous. I used the following stickers on all my slides when I had early unpublished results in a couple of slides that I didn’t want tweeted (FIgure 1). Simple to explain and use.

Figure 1 To tweet or not to tweet


2) Accurate informative reference information on all slides which include published data large enough to actually read

Ideally, references will be open access so tweeters can then help publicise the research by locating references and linking during the talk (I find this really useful as a twitter consumer) as well as linking to other relevant material the tweeter may be aware of.

3) Make slides tweet- (and audience-) friendly

Large, bold graphics and clear visual message make better tweets (and slides) than a table of numbers or list of bullet points.

If you have any other ideas for making tweeting work better for you during conference season we would like to hear from you.

Does it ever make sense to target HPV screening at HIV-infected individuals?

4 Jul, 17 | by Leslie Goode, Blogmaster

A number of recent studies have considered the case for HPV-related cancer prevention interventions that are targeted at specific populations. In the developed world, interventions of cervical screening and teenage vaccination aim to cover the female, or male and female, population (at a certain age) in order to prevent cervical cancer.  The question of more targeted interventions generally arises in relation to MSM – and especially HIV+ MSM – on account of their heightened risk of HPV-induced anal cancers.  There has been a marked rise in these cancers since the 1980s.  Unlike cervical cancers in heterosexual women (which decline with age), anal cancers are prevalent in MSM of all ages (Poynton & Grulich (STI)) – possibly reflecting higher rates of exposure through new partners.  Particularly high rates of anal cancer in older MSM living with HIV may be attributable to long-term immunologic defects in this population (van der Laar & Richel (STI)).  Elevated HPV rates have also been shown in sexual minority women (Reiter & McRee (STI)).  Of course, the problem of anal cancers in MSM could be resolved through vaccination of adolescent boys.  However, a recent UK study has investigated the feasibility of delivering a targeted HPV vaccination programme to adult MSM through STI clinics (Bayley & Soldan (STI)).

In developing countries, there could also be a case for targeting HPV screening – but for the prevention of cervical cancer in heterosexual women, rather anal cancer amongst MSM.  In most parts of sub-Saharan African, and other limited resource settings, neither cervical screening nor widespread adolescent vaccination have proved feasible, and rates of cervical cancer are relatively high (WJCO: Cervical Screening in Limited Resource Settings).  Here, Whitham & Kulasingam (W&K) have argued in a recent analysis of the evidence from six longitudinal studies undertaken in Senegal from 1994-2010, that some targeting of the available resources towards women who are HIV+ is justified given their considerably elevated levels of risk.  Like the HIV+ MSM in the studies mentioned above, HIV+ heterosexual women, according to W&K, have much higher rates of progression from HPV to high-grade squamous intraepithelial lesions (HSIL) (HR 2.55 times), as well as higher levels of progression from normal to HPV, and from normal to HSIL (respectively, HR 1.53 and 1.58). These rates corroborate the results of earlier studies (e.g. Mayaud & Lacey (STI)) that suggest high-risk HPV types and a tendency to HSIL in HIV+ in the older female population.

These findings prompt W&K to recommend, in the sub-Saharan setting, the policy of targeting of HPV vaccination to the HIV+ population recently proposed in the developed world for HIV+ MSM.  Unfortunately, various problems make such an intervention considerably less feasible in the case of sub-Saharan HIV+ women.  First, the sheer prevalence of HPV amongst the target population make HPV testing inefficient as a stand-alone screening strategy and tends to reduce its positive predictive value.  Second, the tests current in the West (cytology and Hybrid Capture 2) require laboratory equipment and technician expertise not likely to be available in Africa.  On the latter point, however, W&K note that the recently developed careHPV test may offer a more effective alternative to Visual Inspection with Acetic acid (VIA).

Can laboratory-guided treatment of gonorrhoea with ciprofloxacin help to stem the emergence of resistance to ceftiaxone?

28 Jun, 17 | by Leslie Goode, Blogmaster

With antimicrobial-resistant gonorrhoea now an urgent health threat, requiring improved antibiotic stewardship, one option frequently proposed is laboratory-guided recycling of older antibiotics (Lewis (STI); Ison & Unemo (STI); A new kind of treatment for gonorrhoea? (STI/blogs)).  Lewis (STI) alludes to the potential use of floroquinolone therapy – specifically in respect to the oropharyngx, which is the site at which treatment failure is most likely to occur.  Epidemiological typing to detect markers associated with antibiotic resistance makes this kind of intervention a real possibility (Graham & Jennison (STI).

Lao-tzu & Klausner (L&K) have recently reported a trial that claims to demonstrate the feasibility of just the kind of therapy envisaged by Lewis.  The researchers at University of California Los Angeles (UCLA) Health Clinical Microbiology Laboratory developed and implemented a molecular assay for the prediction of gonorrhoea (Ng) ciprofloxacin susceptibility.  Over the period from November 2015 to July 2016 all Ng positive specimens were subjected to the assay, and treatment recommendations issued on that basis.  In the final two months (June-July 2016) electronic reminder notifications were introduced – and it was only at that point that the intervention had any substantial impact on the treatment of patients.

Of the 176 infections detected, 121 (69%) were successfully genotyped.  Of the latter, 72 (60%) showed wild-type gyrA (the gene associated with antimicrobial resistance, 49 (40%) were mutant.  In the final successful two-month phase of assay implementation, this enabled 9 out of 11 (82%) of Ng infections to be treated with ciprofloxacin. The authors claim this shows the potential for laboratory-guided treatment of floroquinolones to limit recourse to ceftriaxone – and thereby slow the emergence of antibiotic resistant Ng.  Clearly, the trial needs to be run again, but this time using electronic reminder notifications from the start.

When it comes to the more specific issue of antimicrobial resistance to Ng at the oropharyngeal site, the results of the study are less promising. The proportion of gyrA mutant Ng infections did not vary significantly by site (pharyngeal 33%; rectal 45.7%; vaginal/cervical 57%; urine 39%); but of the 62 pharyngeal infections, most (40) could not be genotyped.  So laboratory-guided ciprofloxacin treatment would be of limited usefulness in key populations – such as MSM.




HPTN 071 attempts universal home-based HIV testing in sub-Saharan Africa: scaling the mountainous challenge of UNAIDS 90-90-90 target

9 Jun, 17 | by Leslie Goode, Blogmaster

Estimates of 96% for the preventative efficacy of ART against HIV transmission, reported in 2011 by Myron & Cohen (M&C), appeared at last to place long-term containment of the epidemic in our hands.  In the wake of this, UNAIDS: 90-90-90 proposed ambitious targets: 90% of those living with HIV to know their status; 90% of known HIV+ individuals to undergo ART initiation; 90% of ART initiated to achieve viral suppression.  Yet – for all the promise of known ART efficacy – the question remains how easy it will be to realize these targets in practice, especially in those settings (e.g. sub-Saharan Africa) where the impact of the epidemic is at its most severe.

Perhaps less easily than one might imagine, suggest Hayes & Fidler (H&F) – a first (one year in) report of results from HPTN-071.  This is a large cluster-randomized study of home-based HIV testing and treatment in 21 Zambian and S. African communities.  The results derive specifically from four of the seven ‘intervention’ communities situated in Zambia.  Of the c.100,000 consenting to the intervention, and visited by pairs of Community HIV Care Providers (CHiPs), 77% of men and 85% of women ended up knowing their status.  (The rest were presumably not reached, or refused testing.)  The estimated proportion of known HIV positive individuals who then went on to initiate ART was 42% within six months and 53% within 12 months.  Over the first year, the estimated overall percentage of HIV+ adults in the four communities who were on ART rose from 44% to 61%.  Obviously, these results reflect only the first year of the intervention, and CHiPs will revisit participants.  At this stage no estimate of the third UNAIDS target (viral suppression) is possible.  Nevertheless, the results reported by this paper give us a sense of the very considerable challenge that the achievement of the UNAIDS target represents in practice.  Among the difficulties, H&F refer specifically to the difficulty of accessing male participants at their homes, and the very slow rates of initiation to ART.

There are various ways of delivering testing.  Home-based testing has been trialled in populations that would otherwise be very difficult to access – e.g. in indigenous Amazonia (Ribeiro & Benzaken (STIs) (R&B); Benzaken & Peeling (STIs) (B&P).  In the case of HPTN-071, its attraction seems to be the possibility of most easily achieving quasi universal coverage.  At 90-90-90, achieved rates of viral suppression would be 73%; at 80-80-80, they would only be 43% – and the preventive efficacy of ART would be correspondingly reduced.  Yet even the latter target seems ambitious.  So far as the testing is concerned, however, the 90% is within reach – at least in Zambia.  The real challenge will be second (and probably also the third) stage of the cascade.  Other studies indicate that HPTN-071 is not unique in seeing large fall out at this point (see Schwartz & Baral (STIs)).  R&B and B&P point to further problem likely to arise at the stage of rolling out this kind of preventative ART intervention – namely that of maintaining the quality of POCT testing (Benzaken & Peeling (STIs)).


Sexually transmitted infections are amongst the fastest spreading high-incidence notifiable diseases in China

31 May, 17 | by Leslie Goode, Blogmaster

Sexually transmitted infections emerge from a recent epidemiological study as a particularly pressing concern for Chinese public health at the present time.  Yang & Li (Y&L) assess trends in incidence and mortality in 45 notifiable infectious diseases across China over the decade since the SARS tragedy in 2003 brought important changes in Chinese public health strategies (2003-2013). The main interest of the authors is to investigate the effectiveness of the new strategies.  But, for readers of this journal, what will be especially interesting about this study is the unique profile of three sexually transmitted – or potentially sexually transmitted – diseases: syphilis, HCV and HIV.

In terms of current incidence these three occupy 6th, 8th, and 15th place among the 45, with yearly incidence per 100,000 of, respectively, 20.75, 9.33, and 3.11.  In respect to mortality, HIV far outstrips all the others (even TB), with 48,199 deaths over the ten year period.  However, syphilis, HCV and HIV differ from other high-incidence diseases – hepatitis B, TB, mumps and bacterial dysentery (respectively, 2nd to 5th in the incidence table) – in that their year-on-year incidence is increasing, and at an impressive rate (estimated at a yearly 16.3%, 19.2% and 16.3% averaged over the decade).  These increases are unparalled except in the case of hand, foot and mouth.  The trend in STI incidence emerges particularly strongly against the background of overall trends in the other notifiable diseases. These have, on the whole, been towards stabilization in the latter half of the decade (2009-2013), following an earlier rise likely due in part to technological progress in laboratory detection and case identification (2003-2009).

This raises the questions whether, in the case of STIs, there are particular social factors at work.

For the authors of the study, syphilis, HCV and HIV fall into the category of those diseases whose recent spread can be attributed to the enormous demographic upheavals that have brought over 10% of the population from poor rural areas to the big urban centres in search of economic opportunities, and to ‘augmented human connectivity’.  As regards population mobility, the opinion of Y&L is corroborated by Chen & Tucker (STIs), and – in the case of MSM populations – by Yu & Shang (STIs).  Interestingly, Y&S identify a class of ‘recent migrants’ to the big cities, whose risk profile appears to differ very considerably from that of longer-term residents. Young FSM – many of them also recent migrants to urban centres – appear to represent another high-risk group (Zhang & Luchters (STIs)).  As for the related factor of ‘augmented human connectivity’, this has also been strongly corroborated (Tang & Tucker (STIs)).  Other studies, however, have traced regional outbreaks in these infections – syphilis, HCV and HIV – to causes that are less obviously linked to recent demographic change.  Zhang & Tang (STIs), for example, emphasize the part played in Guangxi by female sex workers who are patronized by older rural workers.  Epidemiological factors, especially over such a vast area, will obviously be complex and multifactorial.


Health vulnerability of peri-natally HIV-infected youth: a growing problem throughout the world

3 May, 17 | by Leslie Goode, Blogmaster

Mother-to-child, or ‘vertical’, transmission of HIV is not just a problem for developing countries; even in countries like the US and the UK, peri-natal transmission has probably not been eliminated.  But, with routine ‘opt-out’ ante-natal testing (BHIVA guidelines on HIV testing), cases are increasingly likely to involve births that have taken place overseas or before parental diagnosis (CHIVA guidelines on child testing) – cases that, for various reasons, may be difficult for health services to access (Editorial: ‘Don’t Forget the Children’ (STI)). Yet, even with such events becoming less frequent, and the increasing survival of peri-natally HIV-infected youth (PHIVY) beyond infancy, there remains the problem of managing those already infected, as they transition, in growing numbers, from childhood into adolescence and young adulthood. 

               Such problems are very considerable, according to Nailan & Ciaranello (N&C) – especially for adolescents (13-17yrs) and young adults (18-30yrs).  This recent study offers an analysis of data of PHIVY aged 7-30 years from two cohort studies in the US, the Pediatric HIV/AIDS Cohort Study (PHACS) and the International Maternal Pediatric Adolescent AIDS Clinical Trials study (IMPAACT).  As compared with the younger group (7-13 yrs), adolescents (13-18yrs) and young adults (18-30yrs) are likely to spend considerably more time with inadequate viral suppression (5% and 18% vs 2% with CD4 count <200/µL; 30% and 44% vs 22% with a viral load of 400 copies/mL), and to suffer correspondingly greater mortality (c.1 per 100 person-years amongst young adults) as well as HIV related events (c. 2 and 4 per 100 py. for CDC C and B category events amongst 18-30 yrs; c. 1 and 3 per 100 py. for CDC C and B category events amongst 13-18yrs).  The authors attribute inadequate viral suppression, and high mortality/morbidity, to poor adherence and retention in care. 

               The vulnerability of PHIVY as a group to poor health outcomes is not a problem unique to the US.  In the UK c.1,950 PHIVY are monitored through the Collaborative HIV Pediatric Study (CHIPS) cohort, and the data indicate comparable problems of inadequate viral suppression (around one in ten (CHIVA guidelines on transition)).  In some developing countries the health problems of this group are still more evident.  De Matos & dal Fabbro (STI), analysing the data for a cohort of 78 patients, aged 11-15 in 2009, from a municipality in Brazil, report five deaths, amongst other serious health events.  More generally, the UNAIDS 2016 Report (The ‘life-cycle’ approach (STI/blogs) points, in the case of sub-Saharan Africa, to the recent tripling in peri-natally infected 15-19 yr olds who now account for 40% of all HIV-infected 15-19 yr olds in the region.  Not only does poor adherence pose problems for PHIVY themselves; Nailan & Ciaranello also draw attention to the danger they represent for society at large, given rates of pregnancy and risky sex that appear no lower than in the general population, along with heightened transmission risk resulting from poor viral suppression, and, in some cases, emerging drug resistance.

Bacterial vaginosis-associated bacterium (Gardnerella) may after all have a role in the aetiology of non-gonococcal urethritis

28 Apr, 17 | by Leslie Goode, Blogmaster

The question of the aetiology of ‘non-gonococcal’ or ‘non-specific’ urethritis (NGU/NSU) has been a hot topic of debate in this journal and its predecessors since before 1951, when it was officially acknowledged in the Chief Medical Officer’s report as an independent category of infection (Oriel (STI)). More recently, a number of infectious agents have been recognized as potentially responsible (Hallen & Wallin (STIs); Moi & Moghaddam (STIs)).  But it would be misleading to suggest that, even today, the aetiological question has been altogether resolved.

The controversial hypothesis that bacterial vaginosis (BV) associated bacteria (i.e. Gardnerella) might have a role – proposed in 2001 in an STI editorial by a former editor (Shamanesh (STIs)) – seems to have raised its head once again in a recent animal-based study, Gilbert & Lewis (G&A). Results from studies that have tested for the presence of these – amongst other – bacterial agents seem not to have been particularly favourable to the hypothesis (Manhart & Fredericks (STI); Froelund & Jensen (STIs)).  It must be borne in mind, however, that ‘fastidious growth requirements make G. vaginalis unrecoverable, or at least unidentifiable, under conditions most often used by clinical microbiology labs for the culture and identification of potential uropathogens’ (G&A, p.11).

G&A hypothesize G. vaginalis operates indirectly in the case of NSU by triggering the emergence of Escherichia coli from reservoirs in the bladder of the pre-infected individual.  In this way repeated sexual contact could, they suggest, lead to recurrent UTI infections by an infection that is not itself sexually transmitted.  This theory of ‘covert pathogenesis’ is tested by exposing mice with latent E-coli infection – i.e. mice that had been transurethrally pre-infected but were now negative for bacteriuria – to repeated doses of G. vaginalis or Lactobacillus crispatus.  It was found that double exposure to G.v. triggered E-coli bacteriuria while exposure to L.c.  did not.  Furthermore, G.v. exposed mice had neutrophilic infiltrates, confirming the presence of active UTI.  In sacrificed mice, G.v. was also found to have induced bladder epithelial exfoliation and apoptosis in the bladder epithelium.

The theory of covert pathogenesis is intriguing – not least because it overrides any hard-and-fast distinction been sexually-related and non-sexually-related UTIs.  But, assuming it turns out to be correct, it also has practical implications.  The conventional paradigm assumes that the pathogen present at time of clinical presentation is the main driver of disease.  Given the alarming rise of multi-drug resistant E-coli, the authors point to the potential benefit of preventing UTI and sequelae (e.g. pyelonephritis) by targeting the organism that triggers the infection (i.e. G. vaginalis) rather than the pathogen that causes the symptoms.


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