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In this study, an oral minipig infection model was established to investigate the pathogenicity ofYersinia enterocolitica bioserotype 4/O:3. O:3 strains are highly prevalent in pigs, which are usually symptomless carriers, and they represent the most common cause of human yersiniosis. To assess the pathogenic potential of the O:3 serotype, we compared the colonization properties ofY. enterocolitica O:3 with O:8, a highly mouse-virulentY. enterocolitica serotype, in minipigs and mice. We found that O:3 is a significantly better colonizer of swine than is O:8. Coinfection studies with O:3 mutant strains demonstrated that small variations within the O:3 genome leading to higher amounts of the primary adhesion factor invasin (InvA) improved colonization and/or survival of this serotype in swine but had only a minor effect on the colonization of mice. We further demonstrated that a deletion of theinvA gene abolished long-term colonization in the pigs. Our results indicate a primary role for invasin in naturally occurringY. enterocolitica O:3 infections in pigs and reveal a higher adaptation of O:3 than O:8 strains to their natural pig reservoir host.

Essential Role of Invasin for Colonization and Persistence of Yersinia enterocolitica in Its Natural Reservoir Host, the Pig