Clinical overview
Acute pelvic infection in the South African registrar's clinic almost always means pelvic inflammatory disease (PID): ascending infection of the upper genital tract from the cervix. PID is the single most under-diagnosed and over-treated condition in gynaecology — under-diagnosed in young women with subtle symptoms in whom we miss the diagnosis, then over-treated empirically in women with non-specific pain in whom we hand out antibiotics without good reason. Both errors have consequences: missed PID damages tubes and leads to infertility, ectopic pregnancy, and chronic pelvic pain (Chronic pelvic pain); over-treated PID misses an alternative diagnosis (appendicitis, ectopic, torsion, IBD) and exposes the patient to unnecessary antibiotics.
The chapter covers the spectrum from uncomplicated PID through tubo-ovarian abscess (TOA), endometritis (puerperal and post-instrumentation), pelvic peritonitis, and the related entities Bartholin's abscess and pyometra. We also cover the South African epidemiological context — high prevalence of chlamydia, gonorrhoea, Mycoplasma genitalium, and the substantial impact of HIV on presentation and management.
Core knowledge
Microbiology
PID is polymicrobial. The dominant pathogens in young, sexually active women in South Africa:
- Chlamydia trachomatis — commonest, often asymptomatic, accounts for ~30–40% of culturable PID.
- Neisseria gonorrhoeae — often more acute presentation.
- Mycoplasma genitalium — increasingly recognised, harder to detect (PCR), associated with macrolide resistance.
- Anaerobes — Bacteroides, Prevotella, Peptostreptococcus — common in TOA.
- Mycobacterium tuberculosis — important in SA; consider in chronic / recurrent presentations, especially with HIV.
- BV-associated organisms (Gardnerella, Atopobium) — disturb the cervical mucus barrier and facilitate ascent.
The "cervical barrier" — mucus plug, lactobacillus-dominated low pH — normally prevents ascent. Conditions that disrupt this barrier predispose: menses (loss of mucus plug), instrumentation (TOP, IUD insertion, hysteroscopy, D&C), bacterial vaginosis, HIV-related immune dysregulation.
Pathogenesis and staging
Ascending infection progresses from cervicitis and endometritis to salpingitis, pyosalpinx, TOA, and pelvic fluid.
Once organisms ascend through the cervical canal, they cause endometritis (often clinically silent), then salpingitis (the clinically dominant lesion), then potentially tubo-ovarian abscess and pelvic peritonitis. The Mahmood–Templeton anatomical staging (used at laparoscopy):
- Stage 1: mild — erythematous tubes, easily mobile.
- Stage 2: moderate — purulent exudate, tubes more rigid, may have peritoneal involvement.
- Stage 3: severe — pyosalpinx, TOA, dense adhesions.
- Stage 4: ruptured TOA, generalised peritonitis.
The 1990s Westrum and Eschenbach work established the long-term sequelae: tubal factor infertility (~10–20% after one episode, rising steeply with each subsequent episode), ectopic pregnancy (6-fold risk), chronic pelvic pain (~20%).
Fitz-Hugh-Curtis syndrome (perihepatitis) is upper-abdominal inflammation from transperitoneal/lymphatic spread of organisms (classically chlamydia) producing right upper quadrant pain and "violin-string" adhesions between liver capsule and abdominal wall — a clinical pearl that should not be forgotten because it mimics cholecystitis.
Bartholin's abscess
