TABLE 4.

Mechanisms of virulence in pathogenic Escherichia coli.

Pathogenic strain	Primary virulence mechanisms	Reference
Enterotoxigenic E. coli	Adhesion: caused by fibrillar colonisation factors (colonisation factor antigen [CFA]/I, CFA/II, or CFA/IV). Toxin production: Heat-labile enterotoxins (LTs) and/or heat-stable enterotoxins (STs) are produced. LTs activate the main chloride channels of epithelial cells, and STs activate guanylate cyclase activity. The activity of either toxin results in influx of water into the intestines.	6, 52
Enteropathogenic E. coli	Adhesion and mucosal damage: an attaching and effacing (A/E) histopathological lesion is induced by a protein, intimin, and various other chaperones and effector proteins (such as a translocated intimin receptor) which are coded for by genes on a pathogenicity island called the locus of enterocyte effacement. Immune suppression: lymphostatin inhibits lymphocyte activation. Toxin production: some enteropathogenic E. coli strains produce an enterotoxin called EspC causing direct cytotoxic effects in epithelial cells.	6, 52
Enteroinvasive E. coli	Intestinal invasion and damage: invasion and dissemination into epithelial cells are as a result of gene products present on a large virulence plasmid. After epithelial cell penetration, there is endocytic vacuole lysis, intracellular multiplication and finally spread to neighbouring cells, resulting in tissue destruction and inflammation.	6, 52
Enterohaemorrhagic E. coli	Adhesion and mucosal damage: enterohaemorrhagic E. coli also produce an attaching and effacing (A/E) histopathological lesion due to the secretion system of the locus of enterocyte effacement pathogenicity island. Toxin production: potent shiga toxins (Stx1 and Stx2) are produced. Shiga toxin is composed of two major subunits, A and B. The B subunit binds to globotriaosylceramide-3, found on many different cell types, and causes damage via a combination of direct toxicity and cytokine induction. The A subunit cleaves ribosomal RNA which results in protein synthesis inhibition and induction of apoptosis. Shiga toxins also mediate local damage in the colon, which results in intestinal perforation, haemorrhagic colitis, bloody diarrhoea and necrosis.	6, 52, 53
Enteroaggregative E. coli	Adhesion: adherence in an aggregative, stacked-brick-type pattern to the intestinal mucosa is thought to occur via one of several different aggregative adherence fimbriae. Toxin production: Several toxins have been described. Shigella enterotoxin 1 is one of the toxins produced, but the mode of action is not yet understood.	6, 52, 54