Understanding pelvic inflammatory disease.

Chlamydia trachomatis

The most common STI-associated cause of PID globally. Often asymptomatic at the cervical level, allowing untreated infection to ascend silently. Chlamydia causes an intense inflammatory response in the fallopian tubes, leading to tubal scarring and damage. The intracellular lifecycle of chlamydia makes it particularly damaging: repeated cycles of infection and immune activation drive tissue destruction.

Haggerty et al., Am J Obstet Gynecol, 2010; den Hartog et al., Hum Reprod Update, 2006

Neisseria gonorrhoeae

Causes a more acute, symptomatic form of PID than chlamydia. Gonorrhoea produces enzymes that directly damage tubal epithelium and typically triggers a rapid inflammatory response with purulent discharge and more obvious symptoms. Growing antimicrobial resistance is a major concern worldwide, including in Australia.

Unemo et al., Lancet Infect Dis, 2017; Kirby Institute, 2024

Mycoplasma genitalium

An increasingly recognised cause of PID. M. genitalium is associated with endometritis, cervicitis, and tubal factor infertility. It is often resistant to first-line antibiotics (azithromycin), requiring resistance-guided therapy. Testing is now more widely available (NAAT testing), and Australian STI guidelines recommend testing in specific clinical scenarios.

Lis et al., Clin Infect Dis, 2015; Taylor-Robinson and Jensen, N Engl J Med, 2011

BV-associated organisms

Bacterial vaginosis (BV) organisms, including Gardnerella vaginalis, Atopobium vaginae, Prevotella species, and other anaerobes, are frequently isolated from the upper genital tract in women with PID. BV disrupts the normal vaginal microbiome, reducing protective lactobacilli and raising vaginal pH, which facilitates ascent of pathogenic bacteria. This is why metronidazole (which covers anaerobes) is included in PID treatment regimens.

Haggerty et al., J Infect Dis, 2004; Taylor et al., Sex Transm Infect, 2013

Brunham et al., N Engl J Med, 2015; Wiesenfeld et al., J Infect Dis, 2012

Subclinical (or “silent”) PID is more common than clinically apparent PID. Women have no classic symptoms of pain, fever, or discharge, yet histological examination reveals endometritis and/or salpingitis. Subclinical PID causes the same tubal scarring and fertility consequences as overt PID.

It is often discovered only during investigation for infertility, when tubal damage is found with no history of PID. Up to two-thirds of tubal factor infertility occurs in women with no prior PID diagnosis, suggesting that subclinical infection was responsible.

Wiesenfeld et al., Obstet Gynecol, 2005; Cates et al., Obstet Gynecol, 1990

Empiric treatment for PID should be initiated in any sexually active young woman or woman at risk for STIs who has pelvic or lower abdominal pain and in whom no other cause is identified, if one or more of the following are found on pelvic examination:

CDC STI Treatment Guidelines, 2021

Laparoscopy has historically been considered the gold standard for PID diagnosis, as it allows direct visualisation of tubal inflammation, adhesions, and pus. However, it is invasive, expensive, and impractical for routine use. It is not required for diagnosis and is reserved for diagnostic uncertainty, failed medical treatment, or suspected TOA requiring drainage.

Jacobson and Westrom, Am J Obstet Gynecol, 1969

The most important data on PID and fertility comes from Westrom’s landmark Swedish cohort study, which followed 1,844 women with laparoscopically confirmed PID and 657 control women over 25 years. This study established the dose-response relationship between PID episodes and infertility.

PID damages the fallopian tubes through inflammation and scarring. The delicate ciliated epithelium that lines the tubes and is essential for egg transport is destroyed by the inflammatory response. Adhesions form between the tube and surrounding structures, kinking or blocking the tube. In severe cases, the tube fills with fluid (hydrosalpinx) and becomes completely non-functional.

Tubal factor infertility accounts for approximately 25-35% of all female infertility. Of these cases, roughly half have no prior history of diagnosed PID, implicating subclinical infection as the cause.

Brunham et al., N Engl J Med, 2015; Practice Committee ASRM, 2012

Hydrosalpinx (a blocked, fluid-filled fallopian tube) is a consequence of PID that has particular significance for fertility treatment. The fluid from a hydrosalpinx can leak into the uterine cavity, creating a hostile environment for embryo implantation. In women undergoing IVF, the presence of a hydrosalpinx reduces implantation and pregnancy rates by approximately 50%.

Current evidence supports salpingectomy (removal of the affected tube) or proximal tubal occlusion before IVF in women with hydrosalpinx, as this improves pregnancy rates.

Johnson et al., Cochrane Database Syst Rev, 2010; Strandell et al., Hum Reprod, 1999

PID increases the risk of ectopic pregnancy (a pregnancy that implants outside the uterus, typically in the fallopian tube) by 6-10 times compared to women without PID. Tubal damage from inflammation creates an environment where a fertilised egg can become trapped in the tube. Ectopic pregnancy is a medical emergency that requires prompt treatment.

Hillis et al., N Engl J Med, 1997; Ankum et al., Fertil Steril, 1996

PID-related inflammation causes adhesions (bands of scar tissue) between pelvic organs, including the tubes, ovaries, uterus, bowel, and peritoneum. These adhesions can cause pain by restricting organ movement, pulling on sensitive structures, and trapping nerves. Dense adhesions, particularly those involving the bowel or cul-de-sac, can cause significant chronic pain.

Surgical adhesiolysis (cutting adhesions) can provide relief for some women, but adhesions frequently reform after surgery. The decision to operate must weigh the potential for pain relief against the risk of creating more adhesions.

Diamond and Freeman, Hum Reprod Update, 2001

In some women, the acute pain of PID triggers changes in the central nervous system that amplify pain signals. This process, called central sensitisation, means that pain continues or worsens even after the infection has cleared. The nervous system becomes “wound up,” responding to normal sensations as painful (allodynia) or amplifying mild discomfort into severe pain (hyperalgesia).

Central sensitisation explains why some women have chronic pelvic pain out of proportion to the structural damage visible on imaging. It also explains why purely surgical or antibiotic approaches may not resolve the pain.

Latthe et al., BMC Womens Health, 2006; Yong et al., J Pain Res, 2017

Chlamydia remains the most commonly notified STI in Australia, with the highest rates in women aged 15-29. Gonorrhoea notifications have increased significantly over the past decade, particularly in metropolitan areas and among heterosexual populations where previously it was predominantly seen in men who have sex with men.

Kirby Institute Annual Surveillance Report, 2024

Aboriginal and Torres Strait Islander Australians experience significantly higher rates of STIs, including:

These disparities reflect a complex interplay of factors including geographic remoteness, limited access to healthcare and STI testing, socioeconomic disadvantage, historical and ongoing systemic factors, and the self-reinforcing nature of high community prevalence. Addressing these disparities requires culturally safe health services, community-controlled health organisations, and targeted screening programmes.

Kirby Institute, 2024; Australian Institute of Health and Welfare, 2023

Antimicrobial resistance (AMR) in gonorrhoea is a major public health concern in Australia and globally. N. gonorrhoeae has progressively developed resistance to every class of antibiotic used to treat it. In Australia, the Australian Gonococcal Surveillance Programme monitors resistance patterns.

Current first-line treatment remains ceftriaxone, but reduced susceptibility has been reported. Dual therapy (ceftriaxone with azithromycin) was previously recommended but some guidelines now advise ceftriaxone monotherapy due to concerns about azithromycin resistance. Test of cure after gonorrhoea treatment is increasingly important.

AGSP Annual Report, 2024; WHO Global AMR Action Plan