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What causes escherichiosis?
Last reviewed: 06.07.2025
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Escherichiosis is caused by Escherichia coli - motile gram-negative rods, aerobes, belonging to the species Escherichia coli, genus Escherichia, family Enterobacteriaceae. They grow on ordinary nutrient media, secrete bactericidal substances - colicins. Morphologically, serotypes do not differ from each other. Escherichia contain somatic (O-Ag - 173 serotypes), capsular (K-Ag - 80 serotypes) and flagellate (H-Ag - 56 serotypes) antigens. Diarrheagenic intestinal bacteria are divided into five types:
- enterotoxigenic (ETKP, ETEC);
- enteropathogenic (EPEC, EPEC);
- enteroinvasive (EIKP, EIEC):
- enterohemorrhagic (EHEC, EHEC);
- enteroadhesive (EACP, EAEC).
The pathogenicity factors of ETEC (pili, or fimbrial factors) determine the tendency to adhesion and colonization of the lower parts of the small intestine, as well as to toxin formation. Heat-labile and heat-stable enterotoxins are responsible for increased excretion of fluid into the intestinal lumen. The pathogenicity of ETEC is due to the ability to adhere. ETEC are capable, having plasmids, of penetrating into intestinal epithelial cells and multiplying in them. ETEC secrete cytotoxin, Shiga-like toxins of types 1 and 2, and contain plasmids that facilitate adhesion to enterocytes. The pathogenicity factors of enteroadhesive E. coli have not been sufficiently studied.
Escherichia coli are resistant in the environment and can survive for months in water, soil, and excrement. They remain viable in milk for up to 34 days, in infant formulas for up to 92 days, and on toys for up to 3-5 months. They tolerate drying well. They have the ability to reproduce in food products, especially in milk. They quickly die when exposed to disinfectants and when boiled. Many strains of E. coli have been noted to have polyresistance to antibiotics.
Pathogenesis of Escherichia coli infections
Escherichia coli enter through the mouth, bypassing the gastric barrier, and, depending on the type, have a pathogenic effect.
Enterotoxigenic strains are capable of producing enterotoxins and a colonization factor, through which attachment to enterocytes and colonization of the small intestine are achieved.
Enterotoxins are heat-labile or heat-stable proteins that affect the biochemical functions of the crypt epithelium without causing visible morphological changes. Enterotoxins enhance the activity of adenylate cyclase and guanylate cyclase. With their participation and as a result of the stimulating effect of prostaglandins, the formation of cAMP increases, as a result of which a large amount of water and electrolytes are secreted into the intestinal lumen, which do not have time to be reabsorbed in the large intestine - watery diarrhea develops with subsequent disturbances of the water-electrolyte balance. The infectious dose of ETEC is 10x10 10 microbial cells.
EICP have the property of penetrating into the cells of the colon epithelium. Penetrating into the mucous membrane, they cause the development of an inflammatory reaction and the formation of erosions of the intestinal wall. Due to damage to the epithelium, the absorption of endotoxins into the blood increases. Mucus, blood and polymorphonuclear leukocytes appear in the feces of patients. The infectious dose of EICP is 5x10 5 microbial cells.
The pathogenicity mechanism of EPKP has not been studied sufficiently. In strains (055, 086,0111, etc.), the adhesion factor to Hep-2 cells was identified, due to which colonization of the small intestine occurs. In other strains (018, 044, 0112, etc.), this factor was not found. The infectious dose of EPKP is 10x10 10 microbial cells.
EHEC secrete a cytotoxin (SLT - shiga-like toxin), which destroys the endothelial cells lining the small blood vessels of the intestinal wall of the proximal colon. Blood clots and fibrin impede the blood supply to the intestine - blood appears in the feces. Intestinal wall ischemia develops, up to necrosis. Some patients experience complications with the development of disseminated intravascular coagulation syndrome (DIC), ISS and acute renal failure.
EACP are capable of colonizing the epithelium of the small intestine. The diseases they cause in adults and children are long-lasting but mild. This is due to the fact that the bacteria firmly attach to the surface of epithelial cells.