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What causes yersiniosis?
Last reviewed: 04.07.2025
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Causes of Yersiniosis
Yersiniosis is caused by the gram-negative bacillus Yersinia enterocolitica of the Enterobacteriaceae family . It is a heterotrophic facultative anaerobic microorganism with psychrophilic and oligotrophic properties. It grows in "starved" environments and on environments with a depleted composition. It remains viable in a wide temperature range: from 40 to -30 ° C. The optimum temperature for growth is 22-28 ° C. It actively reproduces in household refrigerators and vegetable stores (from 4 to -4 ° C). Its metabolism is oxidative and fermentative. It has weak urease activity. There are 76 known serotypes of Y. enterocolitica, of which only 11 cause disease in humans. Pathogenic Y. enterocolitica are combined into biogroup 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 common enterobacterial antigenic links with Y. pseudotuberculosis, Brucellae, Escherichia, Salmonellae, Shigellae, Klebsiellae, etc. This must be taken into account when interpreting the results of serological studies.
In the development of the disease, the leading role is given to 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 diversity of forms and variants of the disease.
Control of yersinia virulence is carried out by chromosomal and plasmid genes. Single- and double-plasmid strains circulate. Proteins of the outer membrane ensure penetration of the pathogen through the intestinal mucosa in a non-invasive way. Bacterial adhesion, binding to collagen, can contribute to the development of arthritis in patients. IgA genes - "islands of high pathogenicity" of yersinia - control the synthesis of serine protease, which destroys secretory IgA of the mucous membranes.
Yersinia enterocolitica dies when dried, boiled, exposed to sunlight and various chemicals (chloramine, corrosive sublimate, hydrogen peroxide, alcohol). Pasteurization and short-term exposure to temperatures up to 80 °C do not always lead to the death of Y. enterocolitica.
[ Pathogenesis of yersiniosis
The nature of the interaction of Yersinia with the macroorganism depends on the immunological reactivity of the latter, the set of pathogenicity factors of the strain, the dose of the infection and the route of administration. The bulk of the bacteria overcomes the protective barrier of the stomach. Catarrhal-erosive, less often catarrhal-ulcerative gastroduodenitis develops. Then the development of the pathological process can go in two directions: either inflammatory changes will occur only in the intestine, or a generalized process with lympho- and hematogenous dissemination of the pathogen will develop.
Yersiniosis caused by weakly invasive strains of Y. enterocolitica with pronounced enterotoxigenicity is usually characterized by a localized process, clinically manifested by intoxication and damage to the gastrointestinal tract (catarrhal-desquamative, catarrhal-ulcerative enteritis and enterocolitis).
Penetration of Yersinia into the mesenteric nodes causes the development of the abdominal form with mesenteric lymphadenitis, terminal ileitis or acute appendicitis. The gastrointestinal and abdominal forms of the disease can be either independent or one of the phases of a generalized process.
Yersiniosis is spread by invasive and non-invasive routes. In the first route, Yersinia penetrates through the intestinal epithelium, and then a cyclic disease develops with gastrointestinal, abdominal and generalized phases of the disease. The second route, carried out through the intestinal mucosa inside the phagocyte, is possible if the infection is caused by a cytotoxic and invasive strain. It often leads to rapid dissemination of the pathogen.
During the recovery period, the body is freed from yersinia and the impaired functions of organs and systems are restored. With an adequate immune response, the disease ends in recovery. The mechanisms of the formation of a protracted course and secondary focal forms of yersiniosis have not been sufficiently studied. The leading role is given to immunopathological reactions that are formed already in the acute period of the disease, long-term persistence of Y. enterocolitica and hereditary factors. Within 5 years after acute yersiniosis, some patients develop systemic diseases (autoimmune thyroiditis, Crohn's disease, Reiter's syndrome, rheumatoid arthritis, etc.).