Mycoplasma genitalium: An Emerging Cause of Pelvic Inflammatory Disease

Mycoplasma genitaliumis a sexually transmitted pathogen that is increasingly identified among women with pelvic inflammatory disease (PID). AlthoughChlamydia trachomatisandNeisseria gonorrhoeaefrequently cause PID, up to 70% of cases have an unidentified etiology. This paper summarizes evidence linkingM. genitaliumto PID and its long-term reproductive sequelae. Several PCR studies have demonstrated thatM. genitaliumis associated with PID, independent of gonococcal and chlamydial infection. Most have been cross-sectional, although one prospective investigation suggested thatM. genitaliumwas associated with over a thirteenfold risk of endometritis. Further, a nested case-control posttermination study demonstrated a sixfold increased risk of PID amongM. genitaliumpositive patients. Whether or notM. genitaliumupper genital tract infection results in long-term reproductive morbidity is unclear, although tubal factor infertility patients have been found to have elevatedM. genitaliumantibodies. Several lines of evidence suggest thatM. genitaliumis likely resistant to many frequently used PID treatment regimens. Correspondingly,M. genitaliumhas been associated with treatment failure following cefoxitin and doxycycline treatment for clinically suspected PID. Collectively, strong evidence suggests thatM. genitaliumis associated with PID. Further study ofM. genitaliumupper genital tract infection diagnosis, treatment and long-term sequelae is warranted.

The Role ofChlamydia trachomatisPolymorphic Membrane Proteins in Inflammation and Sequelae among Women with Pelvic Inflammatory Disease

Chlamydia trachomatispolymorphic membrane proteins (Pmps) may increase genital tract inflammation and play a role in virulence. Antibody levels for PmpA, PmpD, and PmpI, measured in densitometric units, were assessed among a pilot sample of 40C. trachomatis-infected women with mild-to-moderate clinical PID. Women who expressed antibodies to PmpA were less likely to achieve pregnancy (40.0% versus 85.7%; ) and less likely to have a live birth (0.0% versus 80.0%; ) compared to women who did not express antibody to PmpA. Women who expressed antibodies to PmpI were more likely to have upper genital tract infection (61.5% versus 20.0%; ). However, seropositivity to PmpI and PmpD did not modify the risk of reproductive sequelae or inflammation. Seropositivity to chlamydial PmpA may represent a biomarker of increased risk of sequelae secondary to infection withC. trachomatis.