Diarrheagenic E. coli, Shigellosis, Nontyphoidal Salmonellosis and Yersiniosis

Scope

E. coli pathotypes + NTS + Yersinia. Shigella = see Bacillary/Amoebic Dysentery topic. Typhoidal Salmonella = see Enteric Fever topic.

Diarrheagenic E. coli Pathotypes

ETEC: LEADING traveler’s diarrhea cause. LT (=cholera toxin mechanism, GM1/adenylate cyclase/cAMP) ± ST (guanylate cyclase/cGMP). Watery non-bloody, secretory mechanism.

EPEC: infantile diarrhea (developing countries). ATTACHING-EFFACING (A/E) lesion — intimate adherence + destroys microvillus brush border. NO classical toxin, structural damage mechanism.

EHEC (O157:H7 notorious): SHIGA-LIKE TOXIN (related to S. dysenteriae’s, likely horizontal gene transfer). Bloody diarrhea (hemorrhagic colitis) + HUS risk. MORE CLASSICALLY TAUGHT HUS cause than Shigella. Source: undercooked ground beef, unpasteurized milk/juice.

EIEC: genetically/pathogenically close to Shigella, invades colon same mechanism, dysentery-like illness.

EAEC: “STACKED-BRICK” adherence pattern. PERSISTENT (not acute) watery diarrhea, esp. children + HIV patients.

Non-Typhoidal Salmonellosis (NTS)

S. Enteritidis, S. Typhimurium (vs human-restricted S. Typhi/Paratyphi — Enteric Fever topic). Sources: poultry/eggs, undercooked meat, reptile/amphibian contact. Self-limited gastroenteritis: fever, cramps, non-bloody (±streaked) diarrhea, resolves ~1wk. Up to 8% → bacteremia (infants, elderly, immunocompromised/HIV risk). Bacteremic NTS: seeds atherosclerotic plaque/damaged valves → endovascular infection (see Enteric Fever topic).

Yersiniosis

Y. enterocolitica + Y. pseudotuberculosis. Source: PORK products (contrast most enteric pathogens’ more limited pork role), less commonly unpasteurized milk/water.

Tropism: TERMINAL ILEUM + MESENTERIC LYMPH NODES. Fever+RLQ pain+mesenteric lymphadenitis = MIMICS ACUTE APPENDICITIS clinically (sometimes → unnecessary appendectomy). Important differential point.

Y. enterocolitica: COLD ENRICHMENT — grows at 4°C better than competing flora (lab culture technique).

Sequelae: reactive arthritis + erythema nodosum, esp. HLA-B27+ (same post-infectious pattern as Campylobacter).

Laboratory Diagnosis (General)

Stool culture: MacConkey (general). SORBITOL-MacConkey for O157:H7 SPECIFICALLY — O157:H7 can’t ferment sorbitol (unlike most E. coli) → pale/colorless colonies vs pink background.

Pathotype ID (diarrheagenic E. coli): can’t distinguish from commensal biochemically (virulence GENE difference only) → PCR (toxin/virulence genes) OR O-antigen serotyping + Shiga toxin immunoassay/PCR (EHEC O157:H7 practical proxy).

Yersinia: cold enrichment + standard culture.

Multiplex GI PCR panels: screen single specimen for many pathogens simultaneously, faster than sequential testing.

Treatment

MOST = SELF-LIMITED, supportive ORT alone — antibiotics add little for mild disease.

EHEC O157:H7 — ANTIBIOTICS ACTIVELY AVOIDED: killing → ↑Shiga toxin release from dying organisms → ↑HUS risk. Important counterintuitive exception to “always treat bacterial infection.”

Antibiotics (fluoroquinolone/azithromycin) reserved: severe disease, immunocompromised, invasive/bacteremic NTS.

Scope of This Topic

This topic covers the Enterobacteriaceae-family causes of gastrointestinal infection not already covered elsewhere: the diarrhoeagenic E. coli pathotypes, non-typhoidal salmonellosis, and yersiniosis. Shigella (bacillary dysentery) is covered in full under Bacillary and Amoebic Dysentery and only cross-referenced here; typhoidal Salmonella is covered under Enteric (Typhoid) Fever.

Diarrhoeagenic E. coli

E. coli is normally a harmless gut commensal, but several distinct pathotypes — defined by their specific virulence gene complement, not by any visible morphological difference — cause genuinely different diarrhoeal syndromes through genuinely different mechanisms:

Enterotoxigenic E. coli (ETEC) — the leading cause of traveller’s diarrhoea worldwide, produces heat-labile (LT, mechanistically identical to cholera toxin — same GM1-binding, adenylate-cyclase-activating, cAMP-driven secretory mechanism) and/or heat-stable (ST, activates guanylate cyclase instead, raising cGMP) enterotoxins, causing watery, non-bloody diarrhoea via the same purely secretory logic as cholera, just a milder version.
Enteropathogenic E. coli (EPEC) — a significant cause of infantile diarrhoea in developing countries, causing a characteristic attaching-and-effacing (A/E) lesion: the organism adheres intimately to enterocytes and destroys the microvillus brush border, without producing a classical toxin, impairing absorption directly through this structural damage.
Enterohaemorrhagic E. coli (EHEC), most notoriously serotype O157:H7, produces Shiga-like toxin (mechanistically and genetically related to S. dysenteriae’s Shiga toxin, likely acquired by horizontal gene transfer between the two organisms) causing bloody diarrhoea (haemorrhagic colitis) and carrying the same haemolytic uraemic syndrome (HUS) risk described under Shigellosis — EHEC is, in fact, the more classically taught cause of HUS in most curricula, transmitted characteristically via undercooked ground beef and unpasteurised milk/juice.
Enteroinvasive E. coli (EIEC) — genetically and pathogenically very close to Shigella (again, close enough that the distinction is more historical/clinical convention than a clean genomic line), invading colonic epithelium by the same mechanism and producing a dysentery-like illness.
Enteroaggregative E. coli (EAEC) — adheres to enterocytes in a characteristic “stacked-brick” pattern, causing persistent (rather than acute, self-limited) watery diarrhoea, notably in children and in HIV-infected patients.

Non-Typhoidal Salmonellosis (NTS)

Non-typhoidal Salmonella serotypes (chiefly S. Enteritidis and S. Typhimurium — as opposed to the human-restricted, systemic-disease-causing S. Typhi/Paratyphi covered under Enteric Fever) are acquired from a broad range of animal sources — poultry and eggs, undercooked meat, reptile/amphibian contact — and cause a self-limited gastroenteritis: fever, abdominal cramps, and non-bloody (occasionally blood-streaked) diarrhoea, typically resolving within about a week without treatment. As covered under Enteric Fever, a small but clinically important minority of NTS gastroenteritis (up to 8%) progresses to bacteraemia, with elevated risk in infants, the elderly, and immunocompromised patients (notably HIV), and, once bacteraemic, a specific tendency to seed pre-existing atherosclerotic plaque or damaged heart valves, causing endovascular infection.

Yersiniosis

Yersinia enterocolitica and Y. pseudotuberculosis cause a genuinely distinctive GI syndrome, acquired chiefly from contaminated pork products (and, less commonly, unpasteurised milk or contaminated water) — a real point of epidemiological contrast with most other enteric pathogens, given pork’s more limited role as a diarrhoeal-disease vehicle generally. Both organisms show a striking, clinically important tropism for the terminal ileum and mesenteric lymph nodes, producing a syndrome — fever, right lower quadrant abdominal pain, and mesenteric lymphadenitis — that can closely mimic acute appendicitis clinically (sometimes leading to unnecessary appendectomy before the true diagnosis is recognized), a genuinely important differential-diagnosis point worth remembering specifically. Y. enterocolitica also has a distinctive cold enrichment growth property — it grows at refrigeration temperatures (4°C) better than most competing bacterial flora, a property exploited in some laboratory culture protocols to selectively enrich for it from a mixed specimen. Post-infectious reactive arthritis and erythema nodosum are recognized sequelae, particularly in HLA-B27-positive individuals — mirroring the same post-infectious immune-mediated pattern seen with Campylobacter and other enteric pathogens.

Laboratory Diagnosis (General, Across This Topic)

Stool culture on standard enteric media (MacConkey, and for E. coli O157:H7 specifically, sorbitol-MacConkey agar, which exploits O157:H7’s distinctive inability to ferment sorbitol — unlike most other E. coli — to distinguish it as pale/colourless colonies against the pink sorbitol-fermenting background of normal flora) identifies the organism at genus/species level; pathotype-specific identification of diarrhoeagenic E. coli (which cannot be distinguished from normal commensal E. coli by ordinary biochemical testing, since the difference is purely in virulence gene content) requires PCR targeting the specific toxin/virulence genes, or, for EHEC O157:H7 specifically, O-antigen serotyping plus Shiga-toxin detection (by immunoassay or PCR) as a practical proxy. Yersinia benefits from the cold-enrichment technique described above alongside standard culture. Multiplex GI PCR panels, now increasingly available, can screen a single stool specimen for many of these pathogens simultaneously, substantially speeding diagnosis compared with sequential single-organism testing.

Treatment

Most of these infections are self-limited and managed with supportive oral rehydration alone — a genuinely important general principle for uncomplicated bacterial gastroenteritis, since antibiotics often add little benefit for mild disease and, in the specific case of EHEC O157:H7, are actively avoided: antibiotic-induced bacterial killing can trigger increased Shiga-toxin release from dying organisms, raising rather than lowering HUS risk — a genuinely important, counterintuitive exception to “always treat a bacterial infection with antibiotics” worth remembering precisely. Antibiotics (fluoroquinolones or azithromycin) are reserved for severe disease, immunocompromised patients, or invasive/bacteraemic NTS.