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.