Abstract

Chlamydia trachomatis polymorphic 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 40 C. 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%; P = 0.042) and less likely to have a live birth (0.0% versus 80.0%; P = 0.005) 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%; P = 0.026). 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 with C. trachomatis.

Highlights

  • Chlamydia trachomatis is the most common bacterial sexually transmitted infection in the United States [1]

  • Seropositivity to chlamydial PmpA may represent a biomarker of increased risk of sequelae secondary to infection with C. trachomatis

  • C. trachomatis can ascend from the endocervix to the upper genital tract and cause pelvic inflammatory disease (PID) and serious reproductive morbidity including infertility and ectopic pregnancy [2]

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Summary

Introduction

Chlamydia trachomatis is the most common bacterial sexually transmitted infection in the United States [1]. C. trachomatis can ascend from the endocervix to the upper genital tract and cause pelvic inflammatory disease (PID) and serious reproductive morbidity including infertility and ectopic pregnancy [2]. Some women clear chlamydial infection without tissue damage, while in some cases C. trachomatis induces a chronic low-grade infection [3]. This may lead to persistent inflammation of the upper genital tract causing long-term reproductive sequelae. The pathogenesis of C. trachomatis disease is not well-understood, and pathogenspecific virulence factors that may contribute to variability in the course and outcome of infection have not been identified

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