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Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth
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Quantifying Yersinia pseudotuberculosis Type III Secretion System Activity Following Iron Starvation and Anaerobic Growth

Published on: May 31, 2024

859

[PLASMID-ASSOCIATED VIRULENCE OF YERSINIA PSEUDOTUBERCULOSIS AND INFECTIOUS PROCESS]

L M Somova, F N Shubin, E I Drobot

    Zhurnal Mikrobiologii, Epidemiologii I Immunobiologii
    |January 30, 2019
    PubMed

    Insights

    Genetically determined factors, including plasmids like pYV and pVM82, influence the pathogenicity of Yersinia pseudotuberculosis. Understanding these factors improves diagnostics and prognosis for pseudotuberculosis and yersiniosis.

    Area of Science:

    • Microbiology
    • Immunology
    • Pathogenesis

    Background:

    • Yersinia pseudotuberculosis causes various infections, with pathogenicity linked to genetic factors.
    • Virulence plasmids, particularly pYV, play a key role in Y. pseudotuberculosis pathogenesis.
    • The pVM82 plasmid is associated with Far East scarlet-like fever (FESLF), a specific manifestation.

    Purpose of the Study:

    • To generalize literature data on genetically determined pathogenicity factors of Yersinia pseudotuberculosis.
    • To investigate the role of virulence plasmids (pYV and pVM82) in Y. pseudotuberculosis infections.
    • To explore the molecular basis of FESLF pathogenesis.

    Main Methods:

    • Literature review and generalization of existing data.
    • Analysis of cell-tissue alterations mediated by virulence plasmids.
    • Investigation of YPMa superantigen production by Far Eastern strains.

    Main Results:

    • Virulence plasmid pYV mediates cell-tissue alterations in Y. pseudotuberculosis infections.
    • The pVM82 plasmid is crucial for strains causing FESLF.
    • Far-Eastern strains produce YPMa superantigen, likely key in FESLF pathogenesis.
    • Plasmid variability influences damage to innate immunity cells and target organs, leading to diverse clinical manifestations.

    Conclusions:

    • Plasmid type variability in Y. pseudotuberculosis dictates the spectrum of clinical and morphological manifestations.
    • Understanding the interplay between bacterial molecular characteristics and immune pathogenesis offers improved diagnostics and prognosis for pseudotuberculosis and yersiniosis.

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