What causes pseudotuberculosis: main causes and pathogenesis
Last reviewed: 23.04.2024
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Causes of pseudotuberculosis
The cause of pseudotuberculosis is Yersinia pseudotuberculosis, a gram-negative rod-like bacterium with peri-trichial flagella, and belongs to the family Enterobacteriaceae. The capsule does not contain. The dispute does not form. It has morphological, cultural and biochemical properties similar to Y. Enterocolitica.
Y. Pseudotuberculosis has flagellate (H) antigen, two somatic (O) antigens (S and R) and virulence antigens - V and W. Sixteen serotypes of Y. Pseudotuberculosis or O-groups are described. Most strains occurring on the territory of Ukraine belong to I (60-90%) and III (83.2%) serotypes. O-antigens bacteria have an antigenic similarity between serotypes within the species and other representatives of the enterobacteria family ( Y. Pestis, Salmonella of group B and D, Y. Enterocolitica 0: 8, 0:18 and 0:21), which must be taken into account in interpreting the results of serological research.
The leading role in the development of pseudotuberculosis is attributed to the pathogenicity factors of Y. Pseudotuberculosis: adhesion, colonization on the surface of the intestinal epithelium, invasiveness, the ability for intracellular multiplication in epithelial cells and macrophages and cytotoxicity. Enterotoxigenicity of strains is weak. Control of virulence is carried out by chromosomal and plasmid genes.
Y. Pseudotuberculosis bacteria are a fairly homogeneous group both within the species and within individual serotypes. All known strains are unconditionally pathogenic. Differences in the manifestation of the pathogenic properties of Y. Enterocolitica and Y. Pseudotuberculosis determine the features of the course of yersiniosis and pseudotuberculosis.
The resistance of Y. Pseudotuberculosis and Y. Enterocolitica to physicochemical effects does not differ.
[Pathogenesis of pseudotuberculosis
The introduction of Y. Pseudotuberculosis begins immediately in the oral cavity, which is clinically manifested by tonsillitis syndrome. A significant part of the pathogen, breaking the gastric barrier, colonizes the epithelium of mainly lymphoid formations of the iliac and cecum (first phase). Then there is an invasion of the epithelium of the intestinal mucosa; the causative agent penetrates into the mucous layer and overcomes the epithelium of the blood vessels - primary bacteremia and hematogenous dissemination develop (second phase). Further, generalization of the infection characterized by dissemination of the pathogen in organs and tissues, reproduction in them and the development of systemic disorders (the third phase) are observed. The main role in this process is played by the invasiveness and cytotoxicity of Y. Pseudotuberculosis. Penetration through the intestinal epithelium is carried out through epithelial cells and intercellular spaces with the help of M-cells and migrating phagocytes. Reproduction of Y. Pseudotuberculosis in epithelial cells and macrophages leads to the destruction of these cells, the development of ulcers and extracellular reproduction of Yersinia in the center of the emerging miliary abscesses in the internal organs.
Microcolonies of bacteria, located extracellularly, cause the karyorexis of polynuclears. Which surround them. In place of these foci, granulomas form in many internal organs.
Thus, pseudotuberculosis is characterized by hematogenous and lymphogenous dissemination of Y. Pseudotuberculosis and a pronounced toxic-allergic syndrome. Maximum clinical and morphological changes develop not in the entrance gates of the infection (oropharynx, upper parts of the small intestine), but in secondary foci: in the liver, lungs, spleen, ileocecal angle of the intestine and regional lymph nodes. In this regard, any clinical form of the disease begins as a generalized infection.
During the period of convalescence (the fourth phase), release from the pathogen occurs and the disturbed functions of organs and systems are restored. Y. Pseudotuberculosis is eliminated step by step: first from the bloodstream, then from the lungs and liver. Long iersiniy persist in the lymph nodes and spleen. The cytopathic effect of bacteria and their prolonged persistence in the lymph nodes and spleen can lead to repeated bacteremia, clinically manifested by exacerbations and relapses.
With an adequate immune response, the disease ends with recovery. A single concept of the mechanism of formation of secondary focal forms, a protracted and chronic course of infection is not present. In 9-25% of patients who underwent pseudotuberculosis, Reiter syndrome, Crohn's disease, Guzero-Sjogren's disease, chronic connective tissue diseases, autoimmune hepatitis, endo-, myo-, peri- and pancarditis, thrombocytopenia, etc., are formed.