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Investigating the microbial aetiology of pelvic inflammatory disease
  1. D Taylor-Robinson
  1. Division of Medicine, Imperial College London, St Mary’s Hospital, Paddington, London W2 1NY, UK; dtr{at}vache99.freeserve.co.uk

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    An effort to elucidate a subject which is laden with difficulties is noteworthy, so that it was interesting to read the report by Simms et al1 on the associations between Mycoplasma genitalium, Chlamydia trachomatis, and pelvic inflammatory disease (PID). The difficulties are at least threefold. Firstly, a diagnosis of PID based on symptoms and clinical signs, as in the study reported, is acknowledged, both generally and by the authors, to be imprecise. Clinical observations often do not tally with laparoscopic findings,2 laparoscopy being a fundamental diagnostic requirement in research investigations. Secondly, it is obvious that specimens cannot be taken from the inflamed site in question without laparoscopy. Indeed, it is axiomatic that this should be done if there is to be any chance of unravelling the microbial aetiology. Taking specimens from the cervix is very much second best as the results of microbiological testing may bear no relation to the pathological changes in the tubes. Thirdly, and no less relevant, is the question of an adequate control group. It seems that this should not comprise women undergoing tubal ligation. Although a source of normal tubes would seem sensible, the women were not in the same cohort as those with disease and, in any event, for comparative purposes specimens were taken from the cervix. Surely, an examination of specimens from women without symptoms and signs of PID but who were otherwise comparable to those who did have symptoms and signs would have been more appropriate? In future investigations, controls should be women within a laparoscopically based study who are found not to have PID on laparoscopy. Even then, the situation may be clouded because, in one study,3C trachomatis was detected as often in the tubes of women who did not have PID visually as in those of women who did. Certainly, however, finding M genitalium in the cervix of women with ill defined PID significantly more often than in the cervix of women who did not have PID and who, in other ways, appeared not to be comparable may mean nothing in relating M genitalium to tubal pathology. It is a far cry from unravelling the role of M genitalium in PID, despite some strong suggestions that it might be involved.4

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