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Non-specific urethritis

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.

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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