Review: Look Beyond Gonorrhea, Chlamydia as Causes of Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is currently considered a clinical syndrome. It is diagnosed based on patient reports of pelvic or lower abdominal pain; tenderness of the cervix, adnexa or uterus on exam; and exclusion of other potential causes.

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These diagnostic criteria do not consider the severity of disease, require evaluation of adnexa versus endometrium or require identification of the causal agent(s), all of which contribute to the heterogeneity of the syndrome.

In The Journal of Infectious Diseases, Caroline Mitchell, MD, MPH, director of the Vulvovaginal Disorders Program in the Department of Obstetrics & Gynecology and researcher in the Vincent Center for Reproductive Biology at Massachusetts General Hospital, and colleagues explain why current guidelines for the diagnosis of PID are inadequate and review the latest data on the microbiology of the disease.

Limitations of the Clinical Criteria

Even the broad, nonspecific diagnostic criteria for PID do not capture everyone at risk of adverse outcomes:

• People with a uterus and cervix who do not report a clinical history of PID may have tubal scarring and other evidence of upper genital tract infection and inflammation
• Subclinical PID, the presence of endometritis in the absence of PID signs and symptoms, can be associated with Neisseria gonorrhoeae, Chlamydia trachomatis or bacterial vaginosis (BV) and can have adverse outcomes such as infertility

Overview of Etiologic Pathogens

Three general groups of pathogens have been isolated from the genital tract of patients with PID:

• Sexually transmitted organisms (N. gonorrhoeae, C. trachomatis, Mycoplasma genitalium and Trichomonas vaginalis)
• BV-associated bacteria (e.g., BVAB3, Prevotella bivia, Atopobium vaginae and Leptotrichia/Sneathia species)
• Gastrointestinal and respiratory bacteria (e.g., facultative anaerobes and aerobic bacteria such as Haemophilus influenzae, Escherichia coli and Bacteroides)

The presence of an organism does not imply it is the causal agent of PID, and co-occurrence of organisms from multiple groups can create a synergy that worsens the clinical course.

Latest Evidence About Etiologic Pathogens

The authors found evidence that:

• In about half of patients with PID, neither N. gonorrhoeae nor C. trachomatis can be detected, even with high-sensitivity tests
• BV-associated microbiota may be required for the acquisition of M. genitalium and its persistence in the upper genital tract
• The inflammatory changes that T. vaginalis elicits in the endometrium are indistinguishable from those of N. gonorrhoeae and C. trachomatis, suggesting the contribution of T. vaginalis to PID has been underappreciated
• A broad range of BV-associated bacteria seem to increase the risk of PID-associated endometritis

The Need to Improve Care

Serving as "a stark example of how women's health is undervalued and underresearched," there are prominent gaps in the understanding of the pathophysiology of PID and its devastating complications:

• Are differences in etiology tied to different risks of adverse outcomes?
• Could more precise identification of etiologic microbes and personalized treatment reduce the risk of sequelae?
• Does the presence of upper genital tract infection or the presence of endometritis or salpingitis predict a higher risk of sequelae?

Large, high-quality epidemiologic studies that follow participants longitudinally might lead to better screening, testing and evaluation algorithms that would bridge the gap between symptomatic cases and the full spectrum of disease.

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