Objective Assess risk factors for incident and endometrial Mycoplasma genitalium infection and determine if M. genitalium is associated with histological endometritis, an indicator of pelvic inflammatory disease.
Methods This study was a secondary data analysis within the T cell Response Against Chlamydia (TRAC) Study, a prospective evaluation of 246 women with or at risk for Chlamydia trachomatis from urban outpatient clinics, who were followed quarterly for 12 months. Risk factors for incident M. genitalium infection were determined by Cox regression. Relative risks were estimated by Poisson regression with robust error measurements for models examining the association between M. genitalium and endometritis (histological evidence of plasma cells in endometrial stroma and neutrophils in the endometrial epithelium) and for models examining risk factors for detection of endometrial M. genitalium infection.
Results M. genitalium prevalence was 16.7%, incidence was 25.3 per 100 person-years and 23% had repeated positive tests. Black race (non-black HRadj 0.4, 95% CI 0.2 to 0.9), less education (HRadj 2.4, 95% CI 1.2 to 5.1) and a new sexual partner (HRadj 3.1, 95% CI 1.7 to 5.4) were associated with incident M. genitalium. M. genitalium was associated with endometritis (RRadj 2.0, 95% CI 1.1 to 3.7). Trichomonas vaginalis (RRadj 2.0, 95% CI 1.2 to 3.4) and endometrial C. trachomatis (RRadj 1.7, 95% CI 1.1 to 2.8) were associated with endometrial M. genitalium.
Conclusions M. genitalium is prevalent in women at high risk for C. trachomatis, persists over multiple follow-up visits and is associated with histological endometritis. Studies are needed to determine if screening for M. genitalium will improve reproductive outcomes.
- Chlamydia trachomatis
- Mycoplasma genitalium
- sexually transmitted diseases, bacterial
- trichomonas vaginalis
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Handling editor Jonathan Ross
Contributors All authors were involved in the concept of this study. TD, HCW and SLH were involved in the design of the TRAC (parent) cohort and subsequent data collection. TD, HCW and SLH also assisted with data interpretation and manuscript revisions. BDT completed statistical analyses, interpreted the data and wrote the manuscript. CMO contributed to laboratory assays, data interpretation and manuscript revisions. XZ assisted with statistical analyses, data interpretation and manuscript revisions. DA contributed to the strain typing of MG samples, detection of drug resistance alleles and write-up for the methods and results. All authors approved the final version of this manuscript and agree to be accountable for all aspects of their contributions.
Funding This work was supported by the National Institute of Allergy and Infectious Diseases (grant numbers U19 AI084024 and R3 AI098660).
Competing interests SLH received funding from Becton Dickinson and Cepheid, which market products for the detection of STIs. All other authors have no conflicts to disclose.
Ethics approval University of Pittsburgh IRB (13-3074) and University of North Carolina IRB (MOD10010159-12/PRO10010159).
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement Any request for data should be made to TD, University of North Carolina Chapel Hill.
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