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Pelvic inflammatory disease: Pathogenesis, microbiology, and risk factors

Jonathan Ross, MD
Section Editor
Noreen A Hynes, MD, MPH, DTM&H
Deputy Editor
Allyson Bloom, MD


Pelvic inflammatory disease (PID) refers to acute infection of the upper genital tract structures in women, involving any or all of the uterus, oviducts, and ovaries; this is often accompanied by involvement of the neighboring pelvic organs. By convention, PID is initiated by a sexually transmitted agent, which ascends into the upper genital tract, distinguishing it from pelvic infections caused by trans-cervical medical procedures, pregnancy, and other primary abdominal processes that can extend to pelvic organs.

Overall, the prevalence of PID in the United States and many other resource-rich countries has decreased in the last decade [1,2]. In the United States, PID accounts for approximately 106,000 outpatient visits and 60,000 hospitalizations each year, and is a frequent cause for emergency department visits [1]. Each woman with PID costs around $2000 USD to treat, rising to $6000 if she develops chronic pelvic pain [3].

The pathogenesis and microbiology of PID as well as risk factors for PID will be reviewed here. The clinical features, diagnosis, treatment, and sequelae of this disorder are discussed separately. (See "Pelvic inflammatory disease: Clinical manifestations and diagnosis" and "Pelvic inflammatory disease: Treatment".)


The vaginal flora of most normal, healthy women includes a variety of potentially pathogenic bacteria [4]. Among these are species of streptococci, staphylococci, Enterobacteriaceae (most commonly Klebsiella spp, Escherichia coli, and Proteus spp), and a variety of anaerobes. Compared with the dominant, non-pathogenic, hydrogen peroxide-producing Lactobacillus species, these other organisms are present in low numbers, and ebb and flow under the influence of hormonal changes (eg, pregnancy, menstrual cycle), contraceptive method, sexual activity, and other as yet unknown forces.

The endocervical canal functions as a barrier protecting the normally sterile upper genital tract from the organisms of the dynamic vaginal ecosystem. Endocervical infection with sexually transmitted pathogens can disrupt this barrier. Disturbance of this barrier provides vaginal bacteria access to the upper genital organs, infecting the endometrium, then endosalpinx, ovarian cortex, pelvic peritoneum, and their underlying stroma. The resulting infection may be subclinical or manifest as the clinical entity of pelvic inflammatory disease (PID). The reasons why lower genital tract bacteria cause PID in some women but not others is not fully understood but may relate to genetic variations in immune response, estrogen levels affecting the viscosity of cervical mucus, and bacterial load [5,6].

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Literature review current through: Nov 2017. | This topic last updated: Oct 21, 2016.
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