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What causes salmonellosis?
Medical expert of the article
Last reviewed: 04.07.2025
Causes of salmonellosis
According to the structure of the O-antigen, salmonella are divided into groups A, B, C, D, E, etc., and according to the flagellar H-antigen - into serovars. There are about 2000 serovars. More than 700 serovars have been isolated from humans. More than 500 have been registered in our country. Among them, salmonella of groups B, C, D dominate. E - Salmonella enteritidis, S. typhimurium, S. derby, S. panama, S. anatum, S. choleraesuis.
Pathogenesis of salmonellosis
The development of the infectious process largely depends on the mechanism of infection (food, contact, etc.), the size of the infectious dose and the degree of pathogenicity of the pathogen, the immune defense of the macroorganism, age, etc. In some cases, intestinal infection proceeds rapidly, with the development of endotoxin shock, severe toxicosis with exsicosis or a generalized infectious process (septic forms) and with significant bacteremia (typhoid-like forms), while in others, latent, subclinical forms or bacterial carriage occur. Regardless of the form of the disease, the main pathological process develops in the gastrointestinal tract and mainly in the small intestine.
- Live bacteria are destroyed in the upper sections of the gastrointestinal tract (in the stomach, small intestine), resulting in the release of a large amount of endotoxins, which, being absorbed into the blood, cause toxic syndrome ("toxemia phase"), which determines the clinical picture of the initial period of the disease.
- If bacteriolysis is insufficient and the factors of non-specific protection of the gastrointestinal tract are imperfect (young children, newborns, weakened individuals, etc.), salmonella freely enter the small intestine and then the large intestine, where the primary localization of the pathological process occurs (“enteral phase”).
Possessing pronounced invasiveness and cytotoxicity for the intestinal epithelium and, to a greater extent, for the underlying tissue, salmonella are not only capable of initial colonization of the epithelial surface, but can also penetrate (as part of phagosome-like vacuoles) into epithelial cells, into the proper plate of the mucous membrane, into macrophages and multiply in them. Colonization of the epithelium of both the small and large intestines, reproduction of salmonella in epithelial cells (and in macrophages) lead to thinning, fragmentation and rejection of microvilli, destruction of enterocytes and the development of pronounced catarrhal and granulomatous inflammation, which serves as the main pathogenetic mechanism for the development of diarrheal syndrome (enteritis or enterocolitis).
- Depending on the state of the body's immune system and, first of all, the cellular link of immunity, other factors of non-specific protection, either only a local inflammatory process occurs, or a breakthrough of the intestinal and lymphatic barriers occurs and the next stage of the infectious process begins ("bacteremia phase"). With the blood flow, salmonella enters various organs and tissues, where they can also multiply ("secondary localization") with the development of lymphohistiocytic and epithelioid granulomas in cells and the formation of septic foci (meningitis, endocarditis, osteomyelitis, peritonitis, etc.) (septic form).
As a result of pronounced diarrhea syndrome, repeated vomiting and other factors, toxicosis syndrome with exicosis develops. as well as hemodynamic disorders. functions of the cardiovascular, central and autonomic nervous system, metabolism, with suppression of the function of the kidneys, liver and often the adrenal cortex. The development of toxicosis with exicosis aggravates the underlying infectious process and can often be the cause of an unfavorable outcome.
Intracellular parasitism of salmonella in intestinal epithelial cells (including macrophages) determines the possibility of their long-term persistence in the body, the occurrence of exacerbations and relapses, as well as the formation of long-term bacterial excretion and low effectiveness of antibiotic therapy.