Pelvic inflammatory disease and infertility Original paper

What was reviewed?

This narrative clinical review discusses the pathogenesis, clinical evaluation, and management of pelvic inflammatory disease (PID) with a dedicated focus on fertility-related long-term sequelae. The article synthesizes current knowledge regarding PID’s microbial etiologies, diagnostic approaches, complications such as tubal infertility, and both medical and surgical management strategies. Special attention is given to the role of the microbiome in PID development and progression, particularly regarding upper genital tract infection by various microorganisms and their contribution to reproductive morbidity.

Who was reviewed?

The review synthesizes data and recommendations relevant to women of reproductive age who are at risk for, or have a history of, PID. It draws on evidence from studies involving women with clinically and laparoscopically diagnosed PID, women undergoing infertility evaluation, and specific population groups with higher reported PID incidence, such as those in developing nations and Indigenous Australian communities. The microbiological data reviewed come from studies isolating pathogens from women with PID and related infertility.

Most important findings

PID is a polymicrobial infection of the upper female genital tract, initiated by pathogens that disrupt the cervicovaginal barrier. Chlamydia trachomatis and Neisseria gonorrhoeae are implicated in 33–50% of cases, but other significant contributors include Mycoplasma genitalium, bacterial vaginosis-associated anaerobes, as well as respiratory and enteric organisms. The progressive ascent of these microbes, facilitated by alterations in the cervicovaginal microenvironment and host factors (e.g., menses, loss of mucus plug), leads to upper tract inflammation and damage. Despite adequate antimicrobial therapy, long-term sequelae are common: infertility (18%), ectopic pregnancy (0.6–2%), and chronic pelvic pain (30%). Tubal infertility, largely attributable to microbial damage and subsequent fibrosis or adhesions, is responsible for 25–35% of female infertility cases, with PID as the primary cause in over half. Notably, risk escalates with recurrent PID episodes and severity of tubal damage. The review underscores that even subclinical PID can have major reproductive consequences, and that the diversity of implicated microbes should be considered in diagnosis and management.

Key implications

For clinicians, this review emphasizes the importance of early suspicion, diagnosis, and treatment of PID to mitigate long-term reproductive sequelae, particularly tubal infertility. The polymicrobial nature of PID, including both classical sexually transmitted pathogens and diverse anaerobic and facultative organisms, highlights the need for comprehensive microbial assessment and broad-spectrum empirical therapy. The findings suggest that a history of PID should prompt early fertility evaluation and counseling, and that public health efforts in STI prevention and early intervention could substantially reduce infertility rates. From a microbiome perspective, the article reinforces the critical role of cervicovaginal microbial communities and their disruption in PID pathogenesis, supporting the inclusion of these microbial signatures in reproductive health databases for risk stratification and targeted interventions.