Puerperal infection
Puerperal and postoperative infection: organisms, routes and group B streptococcus
Genital tract sepsis after birth or gynaecological surgery remains a leading cause of maternal death, especially where deliveries are unclean or abortions unsafe. CPSP asks which organism fits which picture, how infection reaches the uterus and the newborn, and the microbiology of group B streptococcus.
Puerperal sepsis: definition and risk
- Puerperal sepsis is infection of the genital tract from rupture of membranes or labour up to 42 days after delivery.
- Most infection ascends from the vagina through the cervix, so risk rises with: caesarean section (the strongest single factor), prolonged rupture of membranes, many vaginal examinations, prolonged labour, retained products, manual removal of placenta, anaemia, obesity and diabetes.
- Listeria is the exception: it reaches the placenta and fetus by the blood.
- The placental site is a large raw wound in a lochia-filled cavity, an excellent culture medium.
Organisms and their clinical clues
| Organism | Typical picture |
|---|---|
| Group A streptococcus (*S. pyogenes*) | Most dangerous: high fever, severe pain, rapid toxic shock within 1–2 days; lochia may not be offensive; carried in the throat or on the skin and spread by hands (the basis of handwashing in maternity care) |
| E. coli and other coliforms | Common cause of endometritis and urinary sepsis; endotoxic shock |
| Anaerobes (Bacteroides, peptostreptococci) | Foul-smelling lochia, mixed infection after caesarean or retained tissue |
| *Clostridium perfringens* | After unsafe abortion: gas in the myometrium, intravascular haemolysis (dark urine, bronze skin), shock. Large Gram-positive anaerobic bacilli with a double zone of haemolysis; alpha toxin is a lecithinase |
| *Staphylococcus aureus* | Wound infection and breast abscess; toxic shock syndrome |
| Group B streptococcus | Endometritis and maternal bacteraemia; neonatal sepsis |
| Chlamydia | Late, low-grade endometritis |
| *Ureaplasma*, *Mycoplasma* | Commonest in amniotic fluid infection; no cell wall |
- Spread beyond the uterus gives parametritis, pelvic abscess, peritonitis, septic pelvic thrombophlebitis and septic shock. Endotoxin (lipid A) triggers TNF, IL-1 and IL-6; shock that does not respond to fluids needs a vasopressor such as noradrenaline.
- Overzealous curettage of an infected uterus removes the basal endometrium, causing intrauterine adhesions (Asherman syndrome).
Chorioamnionitis
- Ascending infection after prolonged rupture of membranes: maternal fever, fetal tachycardia, uterine tenderness, offensive liquor. Usually polymicrobial.
- Neutrophil matrix metalloproteinases (MMP-8, MMP-9) digest amniotic collagen, causing preterm prelabour rupture.
- *Ureaplasma urealyticum* has no peptidoglycan cell wall: invisible on Gram stain and untouched by beta-lactams, so macrolides (erythromycin) are used after preterm rupture.
- The fetus aspirates infected liquor, giving pneumonia and early-onset sepsis.
Wound and other postoperative infections
- Wound infection (usually *S. aureus*) appears about day 4–7, more often in obese and diabetic women.
- Necrotising fasciitis: pain out of proportion to redness, dusky skin, crepitus, grey discharge. Type I is polymicrobial (after surgery in diabetics); type II is group A streptococcus.
- Toxic shock syndrome (staphylococcal TSST-1, also tampons and nasal packs): fever, sunburn-like rash with later desquamation, hypotension, multi-organ failure. A superantigen links MHC class II to the T-cell receptor beta chain outside the antigen groove, activating huge numbers of T cells and releasing cytokines.
- Pyelonephritis in pregnancy: progesterone dilates ureters and causes stasis; *E. coli* with P fimbriae (binding Gal-Gal) ascends to the kidney.
- Breast abscess: *S. aureus* from the baby's nose and mouth enters through cracked nipples; milk stasis allows abscess formation.
Group B streptococcus (*Streptococcus agalactiae*)
- Identification: Gram-positive cocci in chains, narrow beta-haemolysis, bacitracin resistant, CAMP test positive, hydrolyses hippurate, Lancefield group B.
- Virulence: a sialic acid-rich polysaccharide capsule blocks complement deposition and opsonisation. Maternal anti-capsule IgG crosses the placenta and protects; preterm babies get less.
- Carriage: about 1 in 4 women. The lower gut is the reservoir, colonising the vagina from the perineum, so screening swabs at 35–37 weeks take the lower vagina then the anorectum.
| Feature | Early-onset disease | Late-onset disease |
|---|---|---|
| Age | Under 7 days, mostly within 24 hours | 7–90 days |
| Source | Vertical, during labour | Mostly acquired after birth |
| Picture | Pneumonia, septicaemia | Meningitis |
| Prevented by intrapartum penicillin | Yes | No |
- Risk factors for early disease: preterm labour, membranes ruptured over 18 hours, intrapartum fever, GBS bacteriuria, previous affected baby.
- Neonatal meningitis organisms: GBS first, then *E. coli* K1 (polysialic acid capsule), then *Listeria*.
- Neonatal tetanus follows cutting the cord with an unsterile blade; maternal tetanus toxoid protects because antitoxin IgG crosses the placenta.
Remember Fever and shock within two days of delivery with little local sign: think group A streptococcus.
Exam trap Intrapartum antibiotics prevent early-onset, not late-onset, group B streptococcal disease.
Exam trap Ureaplasma will not respond to ampicillin; it has no cell wall.
Test yourself on this topic
5 of the 19 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Newborns are especially vulnerable to invasive group B streptococcal disease when the mother has low levels of type-specific antibody. Which bacterial component is the main virulence factor, and the target of that protective antibody?
Answer: Sialic acid-rich polysaccharide capsule
The capsular polysaccharide of GBS, of which there are ten serotypes (types Ia, Ib and II–IX), carries terminal sialic acid. Sialic acid mimics host cell surfaces and recruits factor H, inhibiting the alternative complement pathway and so blocking opsonisation and phagocytosis. Maternal IgG against the capsule crosses the placenta and protects the baby, which is why vaccines against capsular types are being developed. Lipopolysaccharide is found only in Gram-negative bacteria.
GBS capsule
- Polysaccharide capsule, 10 serotypes
- Sialic acid blocks complement
- Prevents opsonisation
- Maternal anti-capsule IgG protects
Remember Capsule plus sialic acid hides GBS from complement.
Exam trap M protein belongs to group A, not group B, streptococcus.
Why the other options are wrong
- Lipopolysaccharide of the outer membrane LPS is found in Gram-negative bacteria, not streptococci.
- Teichoic acid of the cell wall Teichoic acid is present but is not the main protective target.
- M protein on the fimbriae M protein is the key virulence factor of group A streptococcus.
- Pyrogenic exotoxin A Pyrogenic exotoxin A belongs to group A streptococcus.
A woman at 24 weeks develops fever, rigors and right loin pain; urine grows Escherichia coli. Most strains causing cystitis bind the bladder through mannose-sensitive fimbriae, but this strain has another adhesin that helps it ascend and attach to the renal tubules. Which adhesin is this?
Answer: P fimbriae (Gal-Gal binding)
Uropathogenic E. coli strains that cause pyelonephritis commonly carry P fimbriae, which bind galactose-galactose (globoside) glycolipids on the uroepithelium of the upper urinary tract and the kidney. Type 1 fimbriae bind mannose on bladder cells and are more linked to cystitis. In pregnancy, progesterone-induced dilatation of the ureters (more on the right) and urinary stasis make ascending infection more likely. K1 capsule is linked to neonatal meningitis.
P fimbriae
- Bind Gal-Gal glycolipids
- Linked to pyelonephritis
- Type 1 fimbriae: bladder
- Pregnancy: dilated ureters, stasis
Remember P for pyelonephritis.
Exam trap Asymptomatic bacteriuria in pregnancy is treated because it often progresses to pyelonephritis.
Why the other options are wrong
- K1 polysialic acid capsule K1 is linked to neonatal meningitis.
- Heat-labile enterotoxin (LT) Heat-labile toxin causes traveller's diarrhoea.
- Shiga-like toxin (verotoxin) Shiga-like toxin causes haemorrhagic colitis and HUS.
- Flagellar H antigen of motility H antigen is for motility and typing.
After preterm prelabour rupture of membranes at 29 weeks, a woman's amniotic fluid grows Ureaplasma urealyticum. Ampicillin alone would not be effective. Why?
Answer: The organism has no cell wall
Penicillins and cephalosporins act by inhibiting penicillin-binding proteins that build peptidoglycan. Mycoplasmas and ureaplasmas have no peptidoglycan cell wall, only a sterol-containing membrane, so beta-lactams have no target. Macrolides such as erythromycin or azithromycin, which block the 50S ribosome, are used, and erythromycin is the standard antibiotic after PPROM. Ampicillin crosses the placenta well, and urease has no effect on it.
Wall-less bacteria
- No peptidoglycan cell wall
- Beta-lactams have no target
- Use macrolides (50S)
- Erythromycin after PPROM
Remember No wall, no penicillin.
Exam trap Mycoplasma and Ureaplasma are not killed by any beta-lactam.
Why the other options are wrong
- The organism makes extended-spectrum beta-lactamase Resistance is due to lack of target, not beta-lactamase.
- Ampicillin does not cross the placenta Ampicillin crosses the placenta well.
- The organism lives only inside red cells Ureaplasma is not an intracellular red cell parasite.
- Ampicillin is inactivated by urease Urease does not inactivate penicillins.
Three weeks after delivery, a breastfeeding woman with cracked nipples has a hot, tender, fluctuant swelling in the upper outer quadrant of her right breast and a fever of 38.8 °C. Pus is aspirated. Which organism is most likely, and where does it usually come from?
Answer: Staphylococcus aureus from the baby's mouth
Lactational mastitis and breast abscess are usually caused by Staphylococcus aureus, including MRSA in some settings. The baby's nose and mouth are commonly colonised from the mother's skin and the hospital, and organisms enter through cracked nipples into milk that is not drained well. Milk stasis then allows infection to progress to an abscess. Tuberculous mastitis is chronic with sinuses, and Candida causes nipple pain without abscess.
Lactational breast abscess
- Organism: Staphylococcus aureus
- Source: baby's nose and mouth
- Entry through cracked nipples
- Milk stasis allows abscess
Remember Breast abscess in lactation: think Staph aureus.
Exam trap Breastfeeding from the affected side usually continues; drainage of milk helps healing.
Why the other options are wrong
- Streptococcus agalactiae from the mother's gut GBS is an uncommon cause of mastitis.
- Escherichia coli from the mother's perineum E. coli is not a usual cause of breast abscess.
- Mycobacterium tuberculosis from the lungs TB mastitis is chronic with sinuses, not acute.
- Candida albicans from the mother's vagina Candida causes painful nipples, not abscesses.
Screening for group B streptococcus at 35–37 weeks uses a swab of the lower vagina followed by the anorectum rather than a high vaginal or cervical swab. Why is the rectum included?
Answer: The gut is the main reservoir of the organism
Streptococcus agalactiae lives mainly in the lower gastrointestinal tract, and the vagina is colonised secondarily from the perineum. Colonisation is often intermittent, so sampling both the lower vagina and the anorectum, in a selective broth, greatly increases detection compared with a vaginal swab alone. About 20–25% of pregnant women carry it. Babies acquire it from the birth canal during labour or delivery, not from the rectum itself.
GBS carriage
- Reservoir: lower gut
- Vagina colonised from perineum
- Swab lower vagina + anorectum
- Carried by about 1 in 4 women
Remember GBS lives in the gut; swab low and rectal.
Exam trap A high vaginal swab misses many GBS carriers.
Why the other options are wrong
- Rectal swabs avoid contamination by lactobacilli Lactobacilli do not prevent GBS culture.
- The organism is killed by vaginal acidity GBS survives in the vagina and colonises it.
- Cervical mucus blocks culture of the organism Cervical mucus is not the reason.
- The rectum is where neonates acquire it Babies are exposed in the birth canal.
Where this sits in the CPSP syllabus
- Obstetrics & Gynaecology, Paper 2: Infection in obstetrics and gynaecology, Puerperal and postoperative infection: common organisms, group B streptococcus
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