Pelvic inflammatory disease

Pelvic Inflammatory Disease (PID)

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Key Point: PID is an ascending infection of the upper female genital tract (uterus, fallopian tubes, ovaries, and peritoneum). It is predominantly caused by Chlamydia trachomatis and Neisseria gonorrhoeae, with additional contribution from endogenous vaginal flora. Prompt treatment prevents long-term sequelae including tubal infertility, ectopic pregnancy, and chronic pelvic pain. A low threshold for diagnosis and empirical treatment is essential.

Introduction & Australian Epidemiology

PID affects approximately 1% of sexually active women of reproductive age annually in Australia. It is most common in women aged 15–25 years. The Kirby Institute Annual Surveillance Report consistently identifies chlamydia as the most notifiable STI in Australia, with highest rates in young women — the principal at-risk group for PID.

Approximately 10–15% of untreated chlamydial cervicitis and a higher proportion of untreated gonorrhoea ascend to cause PID. Each episode of PID roughly doubles the risk of subsequent ectopic pregnancy and tubal infertility. A single episode of PID results in tubal damage sufficient to cause infertility in approximately 10% of cases; this rises to ~40% after three or more episodes.

Aboriginal and Torres Strait Islander women have disproportionately higher rates of chlamydia, gonorrhoea, and PID, particularly in remote and very remote communities. The ongoing multi-jurisdictional syphilis outbreak since 2011 highlights the sustained burden of STIs in these communities.

Microbiology & Pathophysiology

PID is a polymicrobial infection in the majority of cases. The primary sexually transmitted pathogens initiate ascent through the cervix, disrupting the cervical mucus barrier, and facilitate superinfection by endogenous vaginal organisms.

Chlamydia trachomatis: Most common identifiable cause in Australia (detected in 30–50% of PID cases). Obligate intracellular organism — requires NAAT for detection. Causes a relatively insidious, less symptomatic presentation.
Neisseria gonorrhoeae: Detected in 10–20% of Australian PID cases; higher rates in Aboriginal and Torres Strait Islander communities and in the context of the ongoing gonorrhoea outbreak. Associated with more severe, acute PID.
Endogenous vaginal flora: Gardnerella vaginalis, anaerobes (Bacteroides, Prevotella), facultative gram-negative rods — involved in a large proportion, particularly in women with bacterial vaginosis.
Mycoplasma genitalium: Increasingly recognised as a significant cause — present in ~10–15% of PID. Associated with treatment failure if macrolide resistance not considered. NAAT testing now available in Australia.

PID typically begins as cervicitis, ascending to endometritis, salpingitis, and, if untreated, to tubo-ovarian abscess (TOA) or peritonitis. The host inflammatory response causes the tubal damage that underlies long-term sequelae — not the organism itself.

Clinical Presentation & Diagnostic Criteria

Clinical Features

PID diagnosis is predominantly clinical. No single symptom, sign, or laboratory result is sufficiently sensitive or specific. A low diagnostic threshold is warranted given the consequences of under-treatment.

Lower abdominal/pelvic pain: Bilateral > unilateral; onset typically within 2 weeks of menstruation; ranges from mild discomfort to severe pain.
Abnormal vaginal discharge: Increased volume, altered colour or odour; mucopurulent cervical discharge on speculum.
Cervical motion tenderness (CMT): Pain on lateral movement of the cervix — highly sensitive for PID when present with pelvic pain.
Adnexal tenderness: Bilateral or unilateral on bimanual examination.
Uterine tenderness: On bimanual palpation.
Fever: Temperature >38.3°C — present in minority; its absence does not exclude PID.
Abnormal uterine bleeding: Intermenstrual or post-coital bleeding.

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CDC/ASHM Minimum Diagnostic Criteria: Empirical treatment should be initiated in sexually active young women with uterine, adnexal, or cervical motion tenderness — in the absence of another cause for illness. Additional criteria (fever, elevated CRP/WCC, elevated ESR, mucopurulent cervicitis, positive NAAT for chlamydia/gonorrhoea) increase specificity.

Fitz-Hugh–Curtis Syndrome

Perihepatitis complicating PID — presents as right upper quadrant pain mimicking cholecystitis or pleurisy. Caused by C. trachomatis or N. gonorrhoeae spreading to the liver capsule via peritoneal fluid. Treat as PID.

Investigations

Investigations support the diagnosis but should not delay treatment initiation in clinically suspected PID.

Essential

Chlamydia & Gonorrhoea NAAT

Endocervical swab or first-void urine NAAT. High sensitivity for both organisms. A positive result confirms STI-associated PID and guides partner notification. Negative result does NOT exclude PID — empirical treatment should still be given if clinical criteria met.
Essential

Inflammatory Markers

FBC (leucocytosis), CRP (elevated in ~75% of PID), ESR. Elevated markers support diagnosis but are neither sensitive nor specific. Normal inflammatory markers do not exclude PID. Useful for monitoring treatment response.
Essential

Urine hCG (Pregnancy Test)

Mandatory in all women of reproductive age with pelvic pain — to exclude ectopic pregnancy (critical differential). PID treatment is modified in pregnancy; IUD removal must be discussed.
Essential

Pelvic Ultrasound (USS)

Transvaginal USS is preferred. In uncomplicated PID the USS may be normal. Indicated to exclude tubo-ovarian abscess (TOA), ovarian torsion, ectopic pregnancy, and appendicitis. TOA appears as a complex adnexal mass with internal echoes. CT or MRI if USS inconclusive.
Available

Mycoplasma genitalium NAAT

NAAT available through most Australian reference labs (e.g. Sullivan Nicolaides, Melbourne Pathology, VIDRL). Also includes macrolide resistance-associated mutation (MRAM) testing — critical for treatment selection given >50% macrolide resistance in Australia. Request this test routinely in suspected PID.
Available

Full STI Screen

Syphilis serology (RPR + TPPA), HIV Ag/Ab, hepatitis B serology. All patients with PID should receive a complete STI screen at diagnosis. Rectal and pharyngeal swabs for gonorrhoea NAAT if clinically indicated.
Available

Endometrial Biopsy / Laparoscopy

Laparoscopy is the gold standard for PID diagnosis (direct visualisation of fallopian tube erythema, oedema, purulent exudate) but is not routinely required. Endometrial biopsy showing plasma cell endometritis supports diagnosis histologically. Reserved for diagnostic uncertainty or failed treatment.

Severity Classification

MILD

Outpatient PID

Mild-moderate pelvic pain, no fever, no signs of peritonism, no TOA on USS. Tolerating oral medications. Sexually active woman meeting minimum diagnostic criteria.

Oral antibiotics; review in 48–72 hours

MODERATE

Inpatient PID

Fever >38.3°C, severe pain, uncertain diagnosis, failed outpatient treatment, unable to tolerate oral therapy, pregnancy, TOA (small, <9 cm), IUD in situ with severe disease.

IV antibiotics; admission; surgical review if TOA present

SEVERE

TOA / Peritonitis

Large TOA (>9 cm), ruptured TOA (peritonitis, haemodynamic instability), failed IV antibiotics for TOA after 72 hours, surgical emergency. Requires drainage ± surgery.

Surgical/interventional radiology; ICU if septic

Empirical Antimicrobial Therapy

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Gonorrhoea prevalence matters: In Australian settings with elevated gonorrhoea prevalence (remote communities, MSM contacts, overseas-acquired), ceftriaxone coverage is essential. In low-prevalence settings, regimens without cephalosporin may be used but clinical judgement is required.

Outpatient Regimen (Mild–Moderate PID)

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Ceftriaxone + Doxycycline + Metronidazole

ASHM first-line oral regimen — covers gonorrhoea, chlamydia, anaerobes

Ceftriaxone 500 mg IM or IV single dose (on day 1 only) — covers gonorrhoea

Doxycycline 100 mg orally BD for 14 days — covers chlamydia and M. genitalium (if susceptible)

Metronidazole 400 mg orally BD for 14 days — covers anaerobes and BV-associated organisms

Total Duration 14 days (doxycycline + metronidazole oral)

PBS Status ✓ All PBS Listed

Inpatient Regimen (Moderate–Severe PID / TOA)

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Ceftriaxone IV + Doxycycline + Metronidazole

ASHM first-line IV regimen

Ceftriaxone IV 1–2 g IV once daily

Doxycycline 100 mg IV/oral BD (oral preferred if tolerated — equivalent bioavailability)

Metronidazole 500 mg IV every 8–12 hours (or 400 mg oral BD if tolerating)

IV Duration Continue IV until clinically improving (>24–48 hours afebrile, pain improving). Then step down to oral doxycycline 100 mg BD + metronidazole 400 mg BD to complete 14 days total.

PBS Status ✓ All PBS Listed

Mycoplasma genitalium — Adjusted Therapy

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If M. genitalium detected: Check macrolide resistance-associated mutation (MRAM) result. If MRAM negative (macrolide-sensitive): add azithromycin 1 g stat + 500 mg daily for 3 days. If MRAM positive (macrolide-resistant): use moxifloxacin 400 mg orally daily for 14 days (specialist consultation recommended — quinolone resistance emerging). Doxycycline alone is insufficient for M. genitalium.

Penicillin Allergy / Alternative Regimens

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Azithromycin + Metronidazole (non-severe penicillin allergy, low gonorrhoea risk)

Alternative outpatient regimen

Azithromycin 1 g orally weekly for 2 weeks

Metronidazole 400 mg orally BD for 14 days

Limitation Does not cover gonorrhoea — only use if gonorrhoea excluded by NAAT and low epidemiological risk. Check M. genitalium MRAM if detected.

PBS Status ✓ PBS Listed

Monitoring Parameters

48–72 Hours

Mandatory clinical review for outpatient therapy. Assess symptom improvement, fever resolution, and examination findings. If no improvement or clinical deterioration: hospitalise, escalate to IV antibiotics, repeat USS to reassess for TOA. Review NAAT results.

Day 7

Review NAAT and M. genitalium results (including MRAM). Confirm partner notification has occurred. Assess adherence and tolerability. Adjust regimen if M. genitalium detected with macrolide resistance. Check STI screen results.

End of Treatment (Day 14)

Test of cure: repeat chlamydia/gonorrhoea NAAT 3–4 weeks after treatment completion (not earlier — dead organisms may cause false positive). Gonorrhoea test of cure recommended at 1–2 weeks if ceftriaxone not used. CRP/WCC if elevated at baseline.

3 Months

Repeat STI screen (reinfection common if partner not treated). Assess for chronic pelvic pain or symptoms of tubal pathology. Counsel on fertility implications and recommend gynaecology referral if planning pregnancy or concerns about tubal function.

Special Populations

🤰 Pregnancy

PID in pregnancy is uncommon but serious — associated with preterm labour, miscarriage, and intrauterine infection. Doxycycline and metronidazole (1st trimester) should be avoided.

Preferred regimen: Ceftriaxone 500 mg IM/IV + azithromycin 1 g oral weekly for 2 weeks. Metronidazole may be added after the 1st trimester.
IUD in situ: IUD removal is recommended if PID diagnosed in pregnancy — increased risk of miscarriage, but untreated PID carries greater risk.
Hospitalise: All pregnant women with PID should be hospitalised for IV antibiotics and monitoring.

👶 Adolescents

Adolescents (<20 years) are at highest risk for PID due to cervical ectropion facilitating STI acquisition. Young age is independently associated with worse tubal outcomes from PID.

Lower threshold: Initiate empirical treatment early — diagnostic delay has greater fertility consequences in young women with more reproductive years ahead.
Treatment: Standard adult regimens apply. Ensure chlamydia and gonorrhoea screening and partner notification.
Contraception counselling: Barrier contraception reduces STI risk — discuss alongside regular STI screening.

🛡️ HIV-Positive Women

HIV-positive women with PID tend to have more severe disease, higher rates of TOA, and may require more aggressive inpatient management. Immunosuppression correlates with disease severity.

Treatment regimen: Same as immunocompetent women; however, lower threshold for hospitalisation and IV antibiotics.
Drug interactions: Doxycycline and azithromycin may interact with antiretrovirals — review ART regimen. Metronidazole interacts with some protease inhibitors (monitor for nausea).
TOA: More common and often larger in HIV-positive women — monitor closely with serial imaging.

🫘 IUD in Situ

PID can develop in IUD users. Current evidence does not mandate IUD removal in mild-moderate PID that responds to antibiotics within 72 hours.

Mild PID responding to antibiotics: IUD may be retained — reassess at 72 hours. Remove IUD if no improvement or patient requests removal.
Severe PID or TOA: Remove IUD as part of management — retained foreign body impairs antibiotic efficacy.
Counselling: Discuss alternative contraception; new IUD can be inserted after treatment completion and confirmed cure.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander women experience a disproportionate burden of STIs and PID, particularly in remote and very remote communities where chlamydia and gonorrhoea prevalence is substantially higher than the general Australian population. The ongoing multi-jurisdictional syphilis outbreak further highlights the urgent need for culturally safe and comprehensive sexual health care in these communities.

High STI Prevalence

In remote communities, chlamydia prevalence in women of reproductive age may exceed 10–15%. Gonorrhoea and M. genitalium prevalence is also markedly elevated. Ceftriaxone coverage in empirical PID regimens is therefore strongly recommended in these settings regardless of NAAT availability.

Access to Diagnosis

Transvaginal USS and specialist gynaecology services may be unavailable in remote primary health care settings. Clinical diagnosis and empirical treatment should not be delayed while awaiting imaging or specialist review. Telehealth consultation with a sexual health physician or gynaecologist can assist.

Partner Notification

Partner notification in community settings requires culturally safe approaches. Aboriginal Health Workers and community nurses play a critical role in contact tracing. Contact tracing for gonorrhoea (a notifiable disease) is required under state/territory public health legislation — public health units can assist.

Treatment Completion

Fourteen-day oral regimens have poor adherence in remote settings. Consider directly observed therapy (DOT) or shorter, parenteral regimens where feasible. Ceftriaxone IM (single dose for gonorrhoea) + azithromycin 1 g stat reduces adherence burden. Return visits should be facilitated and supported.

Antibiotic Stewardship (ACSQHC NSQHS Standard 3)

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Targeted de-escalation: Initiate empirical broad-spectrum cover at diagnosis, then de-escalate once NAAT results are available. If gonorrhoea is excluded and M. genitalium is absent, streamline to doxycycline + metronidazole alone (no cephalosporin continuation required).

14-day duration is evidence-based: Shorter courses are associated with treatment failure and increased risk of long-term sequelae. Do not abbreviate treatment without clear evidence of clinical cure.
Test before treating M. genitalium: Empirical moxifloxacin should NOT be prescribed without confirmed M. genitalium detection and MRAM testing — quinolone resistance is increasing in Australia and will be worsened by empirical use.
Partner treatment: Epidemiological treatment of sexual partners is mandatory for confirmed chlamydia and gonorrhoea — reduces reinfection and interrupts transmission chains.
Gonorrhoea susceptibility monitoring: N. gonorrhoeae in Australia is monitored through the Australian Gonococcal Surveillance Programme (AGSP). Ceftriaxone resistance is currently rare but rising — report treatment failures.

Follow-Up, Prevention & Partner Notification

Partner Notification

All sexual partners from the preceding 60 days (or the most recent partner if the last contact was >60 days) should be contacted for STI screening and epidemiological treatment. Gonorrhoea and chlamydia are notifiable diseases in all Australian jurisdictions — the diagnosing clinician or laboratory must notify the relevant state/territory health authority.

Fertility Counselling

All women with PID should receive fertility counselling at the time of diagnosis and at follow-up. Tubal infertility and ectopic pregnancy are the primary long-term sequelae. Refer to a gynaecologist if the patient is planning pregnancy or experiences difficulty conceiving. Hysterosalpingography (HSG) or laparoscopy may be required to assess tubal patency.

Screening & Prevention

Annual chlamydia screening: Recommended for all sexually active women ≤25 years — reduces PID incidence by detecting and treating cervicitis before ascending infection occurs.
Barrier contraception: Condom use reduces STI transmission. Combined hormonal contraceptives (pill, patch, ring) do not protect against STIs but oral contraceptive pill use may reduce the risk of ascending PID by altering cervical mucus.
HPV vaccination: Reduces cervical cancer risk — recommend opportunistically for unvaccinated individuals presenting with STIs.

References

1Australasian Sexual Health Alliance (ASHA). Australian STI Management Guidelines — Pelvic Inflammatory Disease. 2023. Available at: https://sti.guidelines.org.au
2Ross J, Guaschino S, Cusini M, Jensen J. 2017 European International Union against Sexually Transmitted Infections (IUSTI) guideline for the management of pelvic inflammatory disease. Int J STD AIDS. 2018;29(2):108–114.
3Workowski KA, Bachmann LH, Chan PA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR Recomm Rep. 2021;70(4):1–187.
4Kirby Institute. HIV, viral hepatitis and sexually transmissible infections in Australia: Annual Surveillance Report 2023. Sydney: Kirby Institute, UNSW Sydney; 2023.
5Haggerty CL, Ness RB. Newest approaches to treatment of pelvic inflammatory disease: a review of recent randomized clinical trials. Clin Infect Dis. 2007;44(7):953–960.
6Australian Gonococcal Surveillance Programme (AGSP). Annual Report 2022. Sydney: Kirby Institute, UNSW Sydney; 2023.
7Vodstrcil LA, Plummer EL, Doyle M, et al. Combination therapy for Mycoplasma genitalium, and new evidence for spontaneous clearance of infection. J Infect Dis. 2019;219(12):2050–2056.
8Getman D, Jiang A, O'Donnell M, Cohen S. Mycoplasma genitalium prevalence, coinfection, and macrolide antibiotic resistance frequency in a multicenter clinical study cohort in the United States. J Clin Microbiol. 2016;54(9):2278–2283.
9Mitchell C, Prabhu M. Pelvic inflammatory disease: current concepts in pathogenesis, diagnosis and treatment. Infect Dis Clin North Am. 2013;27(4):793–809.
10Australian Commission on Safety and Quality in Health Care. NSQHS Standards — Antimicrobial Stewardship Standard. Sydney: ACSQHC; 2021.
11Cunningham FG, Leveno KJ, Bloom SL, et al. Williams Obstetrics, 25th ed. New York: McGraw-Hill; 2018. Chapter 65: Sexually Transmitted Infections.
12National Notifiable Diseases Surveillance System (NNDSS). Communicable Diseases Intelligence. Canberra: Australian Government Department of Health; 2023.