Aetiology

The vast majority of intestinal Escherichia coli infections are foodborne, accounting for:[18]

  • 80% of cases of enterohaemorrhagic E coli (EHEC) infection

  • 70% of cases of enterotoxigenic E coli (ETEC) infection

  • 30% of cases of other types of E coli infection.

Over a 20-year period, there were 350 outbreaks of E coli O157:H7 in the US, reported from 49 US states.[14] Of these outbreaks, 52% were associated with contaminated food, including ground beef (41%), produce (21%), other beef (6%), dairy products (4%), and unknown/other foods (28%).[14]E coli O157:H7 outbreaks have also been associated with spinach, romaine lettuce, unpasteurised milk, and infected food handlers.[14][15]​ Spread occurs via faecal-oral transmission.[19]

There have been sporadic reports of pathogen transmission purely from contact with animals carrying the E coli, including petting zoo animals, farm animals, and household pets.[20][21][22][23]​ However, incidence is low and transmission via this route is considered a weak risk factor for E coli infection.

There is an increasing prevalence of antibiotic-resistant strains worldwide.[24] This may be related to greater use of antibiotics in animals, which has been shown to contribute to the development of pathogenic E coli serotypes (including E coli O157:H7).[25]

E coli isolates carrying blaNDM-5 that are resistant to carbapenems and other antibiotics have been identified and pose additional economical and health-related burdens.[26]

Epidemiological surveillance data indicate that transmission of antibiotic-resistant extended-spectrum beta-lactamase-producing (ESBL) E coli occurs most frequently from interspecies spreading via faecal-oral route and through ineffective treatment of urinary tract infections, rather than via the food chain.[27]

Pathophysiology

E coli is a gram-negative, rod-shaped bacterium that propels itself via flagella. It is a commensal organism that colonises the gastrointestinal tract within a few hours of birth. E coli becomes pathogenic by acquiring virulence factors or genetic mutations. Infection by pathogenic strains occurs through ingestion, usually via contaminated food or water. Diarrhoea is caused by a combination of intestinal inflammation, loss of absorptive surface, increased mucosal permeability, and ion secretion.

Each of the pathological subtypes of E coli exerts a pathological response via different mechanism.[1][2]

  • Enterohaemorrhagic E coli (EHEC) attaches to colonic enterocytes and releases virulence factors, most commonly Shiga-like toxin, which disrupts protein synthesis, leading to cell death and bloody diarrhoea; low dose (<100 cells) inoculation produces an infectious response and systemically absorbed toxins can lead to complications like renal damage and haemolytic uraemic syndrome.

  • Enteropathogenic E coli (EPEC) binds to small bowel epithelial cells, subsequently destroying the normal microvillar architecture.

  • Enteroinvasive E coli (EIEC) closely resembles Shigella infection, causing a secretory diarrhoea/dysentery; EIEC is an intracellular pathogen that invades and replicates within, human macrophages and epithelial cells.

  • Enterotoxigenic E coli (ETEC) is a non-invasive strain that binds to small bowel enterocytes and produces heat-labile or heat-stable enterotoxins.

  • Enteroaggregative E coli (EAEC) is a non-invasive strain that binds to intestinal mucosa, adhering and creating a thick biofilm with subsequent release of secretory enterotoxins and cytotoxins.

  • Diffusely adherent E coli (DAEC) colonises the small bowel, leading to the development of finger-like projections that wrap around the bacteria.

Classification

Classification of intestinal pathogenic forms of E coli[1][2][3]

Pathogenic E coli are divided into six different groups based on epidemiology, phenotypic attributes, clinical features of disease, and specific virulence factors.

  • Enteropathogenic E coli (EPEC):

    • Utilises an adhesion protein, intimin, to bind to small bowel epithelial cells, subsequently destroying the normal microvillar architecture

    • Is a leading cause of diarrhoea in infants.

  • Enterotoxigenic E coli (ETEC):

    • A non-invasive strain that binds to small bowel enterocytes and produces heat-labile or heat-stable enterotoxins

    • The most common cause of traveller's diarrhoea.

  • Enteroaggregative E coli (EAEC):

    • A strain of non-invasive bacteria that bind to the intestinal mucosa and creates a thick biofilm through self-adhesion that releases secretory enterotoxins and cytotoxins

    • Usually associated with chronic diarrhoea in children in developing countries.

  • Enteroinvasive E coli (EIEC):

    • Similar to Shigella infection, leads to a secretory diarrhoea/dysentery 

    • An intracellular pathogen, which can invade and replicate within macrophages and epithelial cells.

  • Enterohaemorrhagic E coli (EHEC):

    • Attaches to colonic enterocytes and releases virulence factors, most commonly Shiga-like toxins that disrupt protein synthesis, leading to cell death and subsequent bloody diarrhoea

    • Release of toxins can lead to systemic complications

    • E coli O157:H7 is the most common EHEC serotype.

  • Diffusely adherent E coli (DAEC):

    • Colonises the small bowel, leading to the development of finger-like projections that wrap around the bacteria

    • Causes childhood diarrhoea and diarrhoeal illness in people travelling in North Africa and Mexico.

Serotyping classification[1]

Based on serotyping of O (lipopolysaccharide), H (flagellar), and K (polysaccharide capsule) antigens. Serotyping is a complex classification system, owing to the high number of antigens (173 O antigens, 80 K antigens, and 56 H antigens), resulting in more than 50,000 serotypes. Serotyping can be used to identify particularly virulent strains (e.g., EHEC O157:H7).[4]

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