Sir: We do not wish to perpetuate without good reason the correspondence on asymptomatic Chlamydia trachomatis-negative non-gonococcal urethritis (NGU). Both of us have said already all that we need to say on the subject. However, we feel that Colm O’Mahony, in his latest comments, oversteps the mark in two respects. First, in relation to Mycoplasma genitalium, he pours scorn on it being an ‘emerging pathogen’, at least on the speed of its emergence. He should be reminded that, following the discovery of the gonococcus by Neisser in 1879, it took about 10 years before it was accepted as a cause of urethritis in men, and, although gonococci were found in tubal pus in 1880, it took until the early years of the 20th century before Neisseria gonorrhoeae became recognized as the commonest cause of pelvic inflammatory disease (PID). Furthermore, the existence of chlamydial organisms had been recognized for 50 years before they were isolated in hen’s eggs in 1957 and eight years later in cell culture. The association with NGU came in the early 1970s and with PID in the late 1970s and beyond. In contrast, the existence of M. genitalium became first known when it was cultured in 1980 from men with NGU. Thereafter, progress was delayed because of the inability to isolate this microorganism, but the advent of the polymerase chain reaction brought about a change with reliable detection from 1992 onwards. As a consequence, a strong association with acute and chronic nonchlamydial NGU, with fulfilment of Koch’s postulates, was established by various studies from 1993 to the present time. In addition, M. genitalium was detected in the joint of a patient with Reiter’s disease, associated with cervicitis in 2003, with endometritis in 2002, and by serology with PID in 1984 and with tubal factor infertility in 2001. Much needs to be done, and it is certainly possible that eventually M. genitalium could prove to cause less disease than C. trachomatis. However, pop idols aside, in comparison with the speed with which the recognized aforementioned genital pathogens showed their colours, for a chrysalis that remained dormant for a dozen years, there seems to have been a quite rapid emergence of a multi-coloured M. genitalium butterfly. Second, concentrating entirely on the diagnosis of N. gonorrhoeae and C. trachomatis by nucleic acid amplification test, not attempting to explore C. trachomatis-negative NGU and ignoring the existence of M. genitalium may have deleterious implications for patients. The reason behind looking for another infectious agent in C. trachomatisnegative symptomatic NGU, which resulted in the discovery of M. genitalium, was that some cases of C. trachomatis-negative NGU responded to tetracycline therapy. Untreated M. genitalium infection may lead to chronic NGU and to some of the various conditions mentioned above. If organisms other than C. trachomatis are to be ignored, then at least treat non-chlamydial disease with a broadspectrum antibiotic. As for C. trachomatis-negative asymptomatic NGU, we realize that it is less likely to be associated with M. genitalium than is symptomatic NGU, and that, under some circumstances, not undertaking microscopy and ignoring the asymptomatic condition may be a reasonable thing to do. However, we believe that it is not only in the patient’s best interest but also in that of the public health that decisions regarding change of practice are evidence based. Knowing what causes the asymptomatic disease, if it can be called ‘disease’, and whether it is associated with disease in the partner(s) will be solved only by those who have the energy, resolve and resources to bother. Only then can properly informed decisions be made. David Taylor-Robinson and Patrick Horner Division of Medicine, Imperial College London, St Mary’s Hospital, London W2 1NY; Milne Sexual Health Centre, Bristol Royal Infirmary, Lower Maudlin Street, Bristol BS2 8HW, UK Correspondence to: Professor D Taylor-Robinson Email: dtr@vache99.freeserve.co.uk
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