Roles for Chlamydia trachomatis and Neisseria gonorrhoeae infections in pelvic inflammatory disease pathogenesis are well delineated; however, the etiologic contributions of herpes simplex virus type 2 (HSV-2) and Trichomonas vaginalis have been underexplored.
The goal of this study was to investigate the association between acute and plasma cell endometritis, fallopian tube obstruction, HSV-2 serology, and T. vaginalis infection.
The authors conducted a cross-sectional secondary analysis of 736 women at risk for bacterial sexually transmitted diseases that used endometrial biopsy data obtained at enrollment as well as hysterosalpingography results obtained 12 weeks after enrollment.
Women diagnosed with T. vaginalis at enrollment were more likely to have histologic evidence of acute endometritis. Both plasma cell and acute endometritis were significantly more common among women with positive serology HSV-2; furthermore, women coinfected with HSV-2 and C. trachomatis, N. gonorrhoeae, T. vaginalis, or bacterial vaginosis were much more likely to be diagnosed with acute endometritis than were women infected with HSV-2 or one of these pathogens alone. Among women with available HSV-2 serology and hysterosalpingogram results, HSV-2 was the only genital tract pathogen infection associated with fallopian tube obstruction.
Our analyses demonstrate that T. vaginalis infection and positive HSV-2 serology are associated with endometritis. Further work will be needed to determine the specific roles these pathogens may play in pelvic inflammatory disease pathogenesis.
Cross-sectional investigation of women at high risk for the acquisition of sexually transmitted diseases found that acute endometritis was more frequently detected among study participants with Trichomonas vaginalis infection, while both acute and plasma cell endometritis and fallopian tube blockage were significantly more common among those with positive HSV-2 serology.
From the *Department of Obstetrics, Gynecology, and Reproductive Sciences, the †Division of Molecular Diagnostics, and ‡Magee-Women’s Research Institute, University of Pittsburgh, Pittsburgh, Pennsylvania
The authors thank Christine M. Rullo and Lloyd Clarke for assistance in manuscript preparation.
This study was supported by the National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH [Bethesda, MD]) grants R01 AI41624 and 1 K23 AI064396-01 and the AIDS and Molecular Microbiology/Epidemiology Training Program, NIH (grant T32-AI07333 to TLC).
Correspondence: Thomas L. Cherpes, MD, Magee-Women’s Hospital, Room 3307, 300 Halket Street, Pittsburgh, PA 15213. E-mail: firstname.lastname@example.org
Received for publication December 25, 2005, and accepted February 23, 2006.