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What causes food toxic infections?
Last reviewed: 06.07.2025

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Food toxic infections include a large number of etiologically different, but pathogenetically and clinically similar diseases.
The unification of food toxic infections into a separate nosological form is caused by the need to unify measures to combat their spread and the effectiveness of the syndromic approach to treatment.
The most frequently recorded foodborne toxic infections are caused by the following opportunistic microorganisms:
- family Enterobacteriaceae genus Citrobacter, Klebsiella, Enterobacter, Hafnia, Serratia, Proteus, Edwardsiella, Erwinia;
- family Micrococcaceae genus Staphilococcus;
- family Bacillaceae genus Clostridium, genus Bacillus (including the species B. cereus );
- family Pseudomonaceae genus Pseudomonas (including species Aeruginosa);
- Family Vibrionaceae, genus Vibrio, species NAG-vibrios (non-agglutinating vibrios), V. parahaemoliticus.
Most of the above bacteria live in the intestines of practically healthy people and many representatives of the animal world. The pathogens are resistant to the action of physical and chemical environmental factors; they are capable of reproduction both in living organisms and outside them, for example, in food products (in a wide range of temperatures).
Pathogenesis of food toxic infections
Food toxic infections occur under 2 conditions:
- infectious dose - not less than 10 5 -10 6 microbial bodies in 1 g of substrate;
- virulence and toxigenicity of microorganism strains.
Of primary importance is intoxication with bacterial exo- and endotoxins of pathogens contained in the product.
When bacteria in food products and the gastrointestinal tract are destroyed, endotoxin is released, which, by stimulating the production of cytokines, activates the hypothalamic center, contributing to the development of fever, disruption of vascular tone, and changes in the microcirculation system.
The complex effect of microorganisms and their toxins leads to the development of local (gastritis, gastroenteritis) and general (fever, vomiting, etc.) signs of the disease. The excitation of the chemoreceptor zone and the vomiting center, located in the lower part of the bottom of the fourth ventricle, by impulses from the vagus and sympathetic nerves is important. Vomiting is a protective reaction aimed at removing toxic substances from the stomach. With prolonged vomiting, the development of hypochloremic alkalosis is possible.
Enteritis is caused by enterotoxins secreted by the following bacteria: Proteus, B. cereus, Klebsiella, Enterobacter, Aeromonas, Edwardsiella, Vibrio. Due to the disruption of the synthesis and balance of biologically active substances in enterocytes, increased activity of adenylate cyclase, there is an increase in the synthesis of cAMP. The energy released in this case stimulates the secretory function of enterocytes, resulting in an increased release of isotonic, protein-poor fluid into the lumen of the small intestine. Profuse diarrhea occurs, leading to disturbances in water-electrolyte balance, isotonic dehydration. In severe cases, dehydration (hypovolemic) shock may develop.
Colitis syndrome usually appears in mixed infections involving pathogenic flora.
In the pathogenesis of staphylococcal food poisoning, the action of enterotoxins A, B, C1, C2, D and E is important.
The similarity of pathogenetic mechanisms in food toxic infections of various etiologies determines the commonality of clinical symptoms and determines the scheme of therapeutic measures.