Mechanisms involved in the pathogenesis of Yersinia infections

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Abstract
Yersinia enterocolitica and Yersinia pseudotuberculosis are food-borne enterobacterial pathogens which may initiate rheumatoid diseases. By molecular genetic analysis of the pathogenicity of these species virulence gene loci could be identified on the chromosome and on a plasmid. Plasmidencoded proteins mediate cell adherence, phagocytosis resistance, survival in serum, cytotoxicity, and collagen binding. Y. enterocolitica of serotype 0 : 8 is mouse-lethal and arthritogenic for Lewis rats. Mouse lethality is closely associated with the expression of a chromosome-encoded high-affinity iron transport system which enables the pathogen to acquire iron for growth in iron-deficient environments. The antibody response to virulence-associated antigens of arthritis-susceptible Lewis rats differed from that of arthritis-resistant Fisher rats: Lewis rats respond strongly to the collagen-binding protein Yop1 and weakly to the iron-transport receptor protein FyuA, whereas the reverse is found with Fisher rats. This specific antibody response of Lewis rats is suggested to be important for induction of arthritis.