MicrobiologyTier 1Medical Sciences concept

Mechanisms of infectious diarrhoea (secretory vs osmotic vs inflammatory)

Core concept

Three mechanistic categories, distinguished by where/how the pathogen disrupts normal gut function -- determines expected stool character and whether the diarrhoea persists with fasting
Secretory: enterotoxin drives active chloride/fluid secretion by intact enterocytes -- large-volume, watery diarrhoea that persists despite fasting (fluid loss is toxin-driven, not intake-driven)
Osmotic: unabsorbed solute in the gut lumen draws water in osmotically -- improves/stops with fasting (removing the malabsorbed substrate removes the osmotic drive)

Cholera (Vibrio cholerae) is the classic secretory example: cholera toxin activates adenylate cyclase -> inc intracellular cAMP -> opens CFTR chloride channels -> massive Cl-/fluid secretion into the gut lumen, overwhelming absorptive capacity -- "rice-water stool", no blood, no faecal leukocytes
Inflammatory: pathogen invades or damages the mucosa directly -- Shigella, Salmonella (invasive), Campylobacter, enteroinvasive/enterohaemorrhagic E. coli -- blood and faecal leukocytes/lactoferrin present, smaller volume, associated with fever/tenesmus
Osmotic examples: lactose intolerance, laxative abuse (osmotic agents), some malabsorption syndromes -- stool osmotic gap is elevated

Stool testing for faecal leukocytes/lactoferrin and occult blood distinguishes inflammatory from secretory/osmotic causes at the bedside -- guides likely organism and need for antimicrobial vs supportive-only management
Trap: treating all severe watery diarrhoea the same -- secretory diarrhoea (cholera) needs aggressive oral/IV rehydration as the primary intervention (antibiotics are adjunctive), while inflammatory diarrhoea may need targeted antimicrobial therapy and antimotility agents are relatively contraindicated (risk of toxic megacolon/HUS with Shiga-toxin organisms)
Persistence of diarrhoea despite fasting is the key bedside discriminator pointing toward secretory (or inflammatory) mechanism over osmotic

Cholera toxin's cAMP/CFTR mechanism is directly analogous to E. coli heat-labile enterotoxin (LT) -- same G-protein/adenylate cyclase pathway, different organism
Contrast with Shiga toxin (EHEC, Shigella dysenteriae), which causes inflammatory/bloody diarrhoea via direct cytotoxic ribosomal inactivation, and carries haemolytic uraemic syndrome risk -- a separate note covers this mechanism in detail
C. difficile toxin-mediated colitis is a distinct inflammatory mechanism (cytoskeletal disruption via toxin A/B) rather than classic invasive inflammatory diarrhoea

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