Diarrhoeagenic Bacteria: E. coli, Shigella and Vibrio — Exam Revision

Organise E. coli, Shigella and Vibrio cholerae by what they do to the intestine. Secretory toxins cause watery diarrhoea by disturbing electrolyte transport. Invasion produces inflammatory colitis and dysentery. Shiga toxin injures cells through inhibition of protein synthesis and can also cause systemic endothelial injury. The syndrome and the mechanism are more useful than treating all Gram-negative enteric organisms as interchangeable.

The abbreviation matters: ETEC is enterotoxigenic E. coli, EHEC/STEC is enterohaemorrhagic or Shiga toxin-producing E. coli, EIEC is enteroinvasive, EPEC is enteropathogenic, and EAEC is enteroaggregative. They are pathotypes within the same species, defined by virulence and disease behaviour. Ordinary culture identification of E. coli does not automatically establish which diarrhoeal pathotype is present.

Start a vignette with stool character, fever, abdominal pain, exposure and complications. Travel-associated watery diarrhoea suggests ETEC; bloody diarrhoea followed by anaemia, low platelets and renal injury suggests STEC-associated HUS. Fever, tenesmus and inflammatory dysentery support Shigella or another invasive pathogen. Profuse watery diarrhoea with rapid volume depletion in an outbreak setting supports cholera. These are clues, not substitutes for diagnostic testing.

ETEC is the classic traveller’s-diarrhoea association, but it is not the only cause of diarrhoea in travellers. EAEC can also occur in that setting. EPEC is particularly associated with young children and epithelial attachment. EIEC is closely related to Shigella in its invasion biology. EHEC/STEC draws attention because complications extend beyond the gut to a thrombotic microangiopathy.

The O antigen is associated with the lipopolysaccharide somatic antigen, while the H antigen identifies the flagellar antigen. O157:H7 is an important STEC serotype, but Shiga toxin-producing disease is not restricted to that serotype. A non-O157 result does not rule out STEC. Modern evaluation includes toxin detection or toxin-gene testing alongside the appropriate culture approach.

Colonising fimbriae help ETEC attach to the intestinal wall. The organism then expresses a heat-labile toxin, a heat-stable toxin or both. Their genes are plasmid-associated. LT stimulates adenylate cyclase; ST stimulates guanylate cyclase. Each pathway increases intestinal electrolyte secretion and disturbs absorption, so water follows into the lumen. The result is typically watery rather than invasive dysenteric diarrhoea.

Connect the second messenger to the clinical effect. The answer is not simply “cyclic nucleotide”; the question may demand which nucleotide is increased by a particular toxin. When LT is named, choose cAMP. When ST is named, choose cGMP. Cholera toxin also drives an adenylate-cyclase/cAMP pathway, whereas Shiga toxin acts through ribosomal injury. Keeping these pathways separate prevents a very common toxin-matching error.

“Heat-stable” and “heat-labile” describe toxin behaviour, not the patient’s fever pattern. Nor does “toxin-producing” imply that all antibiotics are either required or forbidden. Hydration is central, while antimicrobial decisions depend on the pathogen, illness severity and current resistance context. The special STEC warning should not be incorrectly generalised to every E. coli pathotype.

EHEC/STEC expresses Shiga toxins, which inhibit protein synthesis and damage susceptible cells. Intestinal injury can cause haemorrhagic colitis. Toxin-mediated endothelial injury can also cause a systemic thrombotic microangiopathy. The association connects a diarrhoeal history with later renal and haematological findings rather than restricting the infection to a bowel syndrome.

Recognised exposures include contaminated food or water, undercooked beef, unpasteurised dairy products and contaminated produce. These associations are helpful, but absence of a meat history does not exclude STEC. Outbreaks involving leafy vegetables illustrate why an exposure mnemonic must not become a diagnostic requirement. The laboratory should be asked to evaluate Shiga toxin or its genes rather than relying only on a generic stool-culture label.

CDC warns that antibiotics in a syndrome suggesting STEC can increase the risk of HUS. Antimotility agents should also be avoided in STEC infection and bloody diarrhoea. Supportive care includes careful fluid and electrolyte management and monitoring for renal and haematological complications. A child with bloody diarrhoea followed by oliguria, pallor and thrombocytopenia requires urgent evaluation rather than symptomatic suppression of diarrhoea.

EPEC attaches to enterocytes and produces an attaching-and-effacing lesion with microvillus loss. Typical EPEC uses bundle-forming pili for localised attachment, followed by intimate adherence involving intimin. Loss of the absorptive brush border and disturbed epithelial transport contribute to watery diarrhoea. The main association is infantile diarrhoea, not the LT/ST secretory-toxin pair used for ETEC.

EAEC is named for its aggregative pattern of adherence, classically described as stacked bricks. Adherence factors, regulatory pathways and toxin effects contribute to intestinal colonisation and diarrhoea. It can cause acute as well as persistent watery illness and may affect travellers. Do not convert “aggregative” into “invasive”: the exam clue is the attachment pattern rather than deep colonic penetration.

EIEC invades colonic epithelium, replicates and spreads between cells, producing inflammatory colitis. Its clinical and pathogenic overlap with Shigella explains why a dysentery stem may list both as plausible causes. The word invasive is the useful anchor. It distinguishes EIEC from a typical secretory watery diarrhoea caused by ETEC and from the toxin-mediated complications of STEC.

Shigella is a Gram-negative, nonmotile bacillus transmitted by the faecal–oral route. It survives gastric acid relatively well, so a small inoculum can cause infection. The organism reaches the colon, invades the epithelium and produces marked inflammation. Fever, abdominal cramps, tenesmus and small-volume bloody or mucoid stools are characteristic associations, although the illness can begin with watery diarrhoea.

Shigella dysenteriae is the classic organism associated with Shiga toxin, but toxin biology should not be used to imply that every Shigella isolate has an identical virulence profile. Shigellosis can cause intestinal and extraintestinal complications. Severe disease, dehydration and host vulnerability influence treatment. Antimotility agents are inappropriate because slowing intestinal transit can worsen complications of invasive inflammatory illness.

Hydration remains the foundation of care. Antibiotics can be useful for selected patients, but susceptibility testing is increasingly important because resistance is widespread and extensively drug-resistant strains exist. Avoid memorising a single antibiotic as permanently correct everywhere. Stool culture contributes both identification and resistance information, so a rapid molecular result may need culture follow-up when treatment or outbreak investigation requires it.

Vibrio cholerae is a curved or comma-shaped Gram-negative bacillus. It colonises the small intestine and secretes cholera toxin. The toxin activates adenylate cyclase, increasing cAMP and driving electrolyte secretion with water loss. The mechanism is predominantly secretory. Severe disease can rapidly produce hypovolaemia and shock without the destructive inflammatory dysentery pattern typical of an invasive colonic infection.

Classical severe cholera has profuse, watery diarrhoea described as rice-water stool, often with vomiting and rapid dehydration. Not every infection is severe: WHO notes that many people have mild symptoms or no symptoms. The appearance is a useful clinical clue rather than a laboratory identification method. Assess circulation and dehydration while arranging appropriate microbiological confirmation and public-health evaluation.

WHO identifies O1 and O139 as the serogroups associated with cholera outbreaks. A stool specimen can establish the organism; rapid diagnostic tests may support surveillance, but culture or molecular confirmation has a different role from immediate bedside fluid management. Do not wait for a laboratory name before treating profound dehydration. The urgent physiological problem is loss of water and electrolytes.

E. coli generally ferments lactose and can be recovered on MacConkey agar, but identification to species does not establish diarrhoeal virulence. CDC recommends culture for O157 alongside testing for non-O157 STEC using Shiga toxin or toxin-gene detection. Sorbitol-containing media are relevant to STEC work-up, but a single culture phenotype should not be treated as a universal rule that detects every STEC strain.

For diarrhoeal illness, assess hydration first. Oral rehydration is central when the patient can drink, while severe dehydration requires intravenous fluids. Cholera treatment works because glucose–sodium-linked intestinal transport can support water and electrolyte absorption despite toxin-driven secretion. WHO recommends antibiotics for severe cholera alongside fluids, and discourages mass antibiotic chemoprophylaxis for outbreak prevention.

• Watery travel illness with LT/ST: think ETEC and distinguish cAMP from cGMP.
• Bloody diarrhoea with renal injury, low platelets and haemolysis: evaluate STEC-associated HUS.
• Stacked-brick adherence: EAEC; attaching-and-effacing lesion: EPEC; colonic invasion: EIEC.
• Fever, tenesmus and inflammatory dysentery: consider Shigella and confirm with testing.
• Profuse rice-water diarrhoea with rapid volume depletion: treat suspected cholera dehydration urgently.
• Suspected STEC: avoid routine antibiotics and antimotility treatment; monitor for complications.