Gram-negativeBacilliEnterobacterales

Shigella

Gram-negative, non-motile, facultatively anaerobic bacillus of the family Enterobacteriaceae that causes bacillary dysentery (shigellosis) characterized by invasive bloody, mucoid diarrhea.

Organism Card

DomainMust know
Identity
  • G−ve rod, non-motile (vs Salmonella which is motile), non-capsulated [1]
  • Family Enterobacteriaceae; genus Shigella
  • 4 serogroups: S. dysenteriae (group A), S. flexneri (B), S. boydii (C), S. sonnei (D) [1]
  • S. sonnei commonest in developed countries; S. flexneri commonest in developing countries
  • S. dysenteriae type 1 produces Shiga toxin → most severe disease [1]
Lab discriminator
  • Lactose non-fermenting on MacConkey agar (colourless colonies) [1]
  • Non-motile, no H₂S production, no gas from glucose (vs Salmonella: motile, H₂S +, gas +) [1][2]
  • Oxidase −ve; facultative anaerobe
  • On XLD agar: red/pink colonies (no black centre, vs Salmonella black centre)
  • No Vi antigen (vs Salmonella Typhi) [1]
Reservoir / transmission
  • Humans are the ONLY reservoir (no animal reservoir) [1]
  • Faecal–oral: person-to-person, contaminated food/water [1]
  • Very low infective dose (~10–100 organisms) → highly contagious, facilitates person-to-person spread [1][2]
  • Outbreaks in institutions (day-care centres, residential care homes), travellers to endemic areas
  • HK: notifiable disease; associated with travellers returning from South/Southeast Asia [1][3]
Key virulence
  • Intracellular pathogen: invades colonic/rectal epithelial cells via M cells [1]
  • Type III secretion system (T3SS) → injects Ipa proteins → triggers bacterial-directed endocytosis [1]
  • Shiga toxin (S. dysenteriae type 1 only): AB toxin → cleaves 28S rRNA → inhibits protein synthesis → cytotoxic to colonic epithelium AND endothelial cells [1]
  • Shiga toxin → endothelial damage in renal glomeruli → HUS (haemolytic uraemic syndrome) [1][2]
  • Cell-to-cell spread via actin polymerisation (actin rockets) → avoids extracellular immune defences [1]
Clinical syndromes
  • Bacillary dysentery: bloody mucoid diarrhoea (blood + mucus + pus), tenesmus, fever, abdominal cramps [1][2]
  • Colonic/rectal inflammation predominant (vs Salmonella small bowel)
  • S. dysenteriae type 1: most severe → toxic megacolon, HUS, high mortality [1]
  • S. sonnei: usually mild, self-limiting watery diarrhoea
  • Complications: HUS (microangiopathic haemolytic anaemia + thrombocytopenia + AKI), seizures in children, reactive arthritis (HLA-B27), Reiter syndrome
  • Dehydration less prominent than cholera (smaller volume stool) [1]
Diagnosis
  • Stool culture is gold standard: fresh stool or rectal swab on selective media (MacConkey, XLD, SS agar) [1]
  • Stool microscopy: WBCs and RBCs in stool (inflammatory diarrhoea)
  • Blood cultures usually negative (Shigella rarely causes bacteraemia, unlike Salmonella Typhi) [1]
  • Serotyping for epidemiological investigation
  • Pitfall: dies quickly in transit → specimen must be processed rapidly or use transport medium (Cary-Blair)
Treatment
  • Fluid and electrolyte replacement is mainstay [1]
  • Antibiotics shorten duration and reduce transmission: ciprofloxacin (fluoroquinolone) is first-line in adults [1][2]
  • Alternatives: azithromycin, third-generation cephalosporins (ceftriaxone)
  • Children: azithromycin preferred (avoid FQ in children)
  • Increasing multidrug resistance is a major concern (resistance to ampicillin, TMP-SMX common) → always check local susceptibility [1][3]
  • Anti-motility agents (e.g. loperamide) are CONTRAINDICATED → prolong illness, risk of toxic megacolon [1][2]
Prevention
  • Statutory notifiable disease in Hong Kong [1][3]
  • Strict hand hygiene, food and water hygiene, proper sanitation [1]
  • Contact precautions + enteric precautions for hospitalised patients
  • No commercially available vaccine currently
  • Clearance stool cultures required before food handlers return to work [3]
Classic traps
  • Shigella vs EHEC (E. coli O157:H7): both cause bloody diarrhoea + HUS, but Shigella = invasive (WBCs in stool, fever prominent) vs EHEC = non-invasive (no WBCs, no fever, sorbitol non-fermenting) [1][2]
  • Shigella vs Salmonella: Shigella = non-motile, no H₂S, human-only reservoir, very low infective dose, dysentery (colon); Salmonella = motile, H₂S +, animal reservoir, higher infective dose, enteritis (small bowel) or typhoid [1]
  • Shigella vs Entamoeba histolytica (amoebic dysentery): Shigella = acute, fever, WBCs in stool; Amoeba = subacute, flask-shaped ulcers, trophozoites with ingested RBCs, liver abscess [1][2]
  • Shiga toxin in Shigella vs Shiga-like toxin (Stx) in EHEC: same mechanism but different organisms

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