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What causes pseudotuberculosis: main causes and pathogenesis
Last reviewed: 06.07.2025
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Causes of pseudo tuberculosis
The cause of pseudo-tuberculosis is Yersinia pseudotuberculosis, a gram-negative rod-shaped bacterium with peritrichous flagella, belonging to the Enterobacteriaceae family. It does not contain capsules. It does not form spores. It has morphological, cultural and biochemical properties similar to Y. enterocolitica.
Y. pseudotuberculosis has a flagellar (H) antigen, two somatic (O) antigens (S and R) and virulence antigens - V and W. 16 serotypes of Y. pseudotuberculosis or O-groups have been described. Most strains found in Ukraine belong to serotypes I (60-90%) and III (83.2%). O-antigens of the bacterium have antigenic similarity between serotypes within the species and other representatives of the enterobacteria family ( Y. pestis, salmonella groups B and D, Y. enterocolitica 0:8, 0:18 and 0:21), which must be taken into account when interpreting the results of serological studies.
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 to intracellular reproduction in epithelial cells and macrophages, and cytotoxicity. Enterotoxigenicity of strains is weak. Virulence is controlled 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 considered unconditionally pathogenic. Differences in the manifestation of 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 influences 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, having overcome the gastric barrier, colonizes the epithelium of mainly lymphoid formations of the ileum and cecum (first phase). Then there is an invasion of the epithelium of the intestinal mucosa; the pathogen penetrates the mucous layer and overcomes the epithelium of the blood vessels - primary bacteremia and hematogenous dissemination develop (second phase). Then generalization of the infection is observed, characterized by dissemination of the pathogen in organs and tissues, reproduction in them and the development of systemic disorders (third phase). 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. The proliferation of Y. pseudotuberculosis in epithelial cells and macrophages leads to the destruction of these cells, the development of ulcers and extracellular proliferation of Yersinia in the center of forming miliary abscesses in internal organs.
Microcolonies of bacteria located extracellularly cause karyorrhexis of polynuclear cells that surround them. Granulomas form in many internal organs at the site of these foci.
Thus, pseudotuberculosis is characterized by hematogenous and lymphogenous dissemination of Y. pseudotuberculosis and a pronounced toxic-allergic syndrome. The maximum clinical and morphological changes develop not at the entry point of 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 convalescence period (the fourth phase), the pathogen is eliminated and the impaired functions of organs and systems are restored. Y. pseudotuberculosis is eliminated in stages: first from the bloodstream, then from the lungs and liver. Yersinia persists for a long time in the lymph nodes and spleen. The cytopathic action of bacteria and their long-term 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 in recovery. There is no single concept of the mechanism of formation of secondary focal forms, protracted and chronic course of infection. In 9-25% of patients who have had pseudo-tuberculosis, Reiter's syndrome, Crohn's disease, Gougerot-Sjögren's, chronic connective tissue diseases, autoimmune hepatitis, endo-, myo-, peri- and pancarditis, thrombocytopenia, etc. are formed.