What causes iersiniosis?
Last reviewed: 23.04.2024
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Causes of yersiniosis
The cause of iersiniosis is the gram-negative bacillus Yersinia enterocolitica of the Enterobacteriaceae family . It is a heterotrophic facultative-anaerobic microorganism with psychrophilic and oligotrophic properties. Rastetna "hungry" environments and on media with a depleted composition. It retains viability in a wide temperature range: from 40 to -30 ° C. Optimal temperature for growth: 22-28 ° C. Actively multiplies in conditions of household refrigerator and vegetable stores (from 4 to -4 ° C). Metabolism is oxidizing and fermenting. Has a weak urease activity. 76 serotypes of Y. enterocolitica are known . of which only 11 cause disease in humans. Pathogenic Y. Enterocolitica are united in the biological group 1b. They have H- and O-antigens. Some strains contain V- and W-virulence antigens located in the outer membrane. They have specific and cross-reacting antigens that determine intraspecific and antigenic links common for enterobacteria with Y. pseudotuberculosis, Brucellae, Escherichia, Salmonellae, Shigellae, Klebsiellae, etc. This should be taken into account when interpreting the results of serological studies.
In the development of the disease, the leading role is played by the pathogenicity factors of Y. enterocolitica: adhesion, colonization on the surface of the intestinal epithelium, enterotoxigenicity, invasiveness and cytotoxicity. Most strains are not invasive. Not all invasive strains are capable of intracellular reproduction. This explains the variety of forms and variants of the disease.
Controlling the virulence of Yersinia is carried out by chromosomal and plasmid genes. One- and two-plasmid strains are circulating. The proteins of the outer membrane ensure the penetration of the pathogen through the intestinal mucosa by a non-invasive route. Bacterial adhesion that binds to collagen can promote the development of arthritis in patients. IgA-genes - "islands of high pathogenicity" Yersinia - control the synthesis of serine protease, which destroys the secretory IgA of the mucous membranes.
Yersinia enterocolitica perishes by drying, boiling, exposure to sunlight and various chemicals (chloramine, mercuric chloride, hydrogen peroxide, alcohol). Pasteurization and short-term exposure to temperatures of up to 80 ° C do not always lead to the death of Y. Enterocolitica.
[Pathogenesis of iersiniosis
The nature of the interaction of Yersinia with the macroorganism depends on the immunological reactivity of the second, a set of pathogenicity factors of the strain, the dose of the infection and the route of administration. The majority of bacteria overcomes the protective barrier of the stomach. Catarrhal-erosive, less often catarrhal ulcer gastroduodenitis develops. Then the development of the pathological process can go in two directions: either there will be inflammatory changes only in the intestine, or a generalized process with lympho- and hematogenous dissemination of the pathogen will develop.
For yersiniosis caused by weakly invasive strains of Y. Enterocolitica with pronounced enterotoxigenicity, a localized process, which is clinically manifested by intoxication and lesion of the gastrointestinal tract (catarrhal-desquamative, catarrhal-ulcerative enteritis and enterocolitis), is typical.
The penetration of the Yersinia into the mesenteric nodes causes the development of the abdominal form with mesenteric lymphadenitis, terminal ileitis, or acute appendicitis. Gastrointestinal and abdominal forms of the disease can be either independent, or one of the phases of the generalized process.
Iersiniosis spreads invasively and non-invasively. In the first method, Yersinia penetrates the intestinal epithelium, and then a cyclic disease develops with the gastrointestinal, abdominal and generalized phases of the disease. The second way, carried out through the intestinal mucosa inside the phagocyte, is possible if the infection is caused by a cytotoxic and invasive strain. Often it leads to rapid dissemination of the pathogen.
During the period of convalescence, the organism is freed from iersinia and the disturbed functions of organs and systems are restored. With an adequate immune response, the disease ends with recovery. Mechanisms for the formation of protracted flow and secondary focal forms of yersiniosis have not been adequately studied. The leading role is given to the already formed in the acute period of the disease immunopathological reactions, the long persistence of Y. Enterocolitica and hereditary factors. Within 5 years after acute yersiniosis, a number of patients develop systemic diseases (autoimmune thyroiditis, Crohn's disease, Reiter's syndrome, rheumatoid arthritis, etc.).