Essential role of invasin for colonization and persistence of Yersinia enterocolitica in its natural reservoir host, the pig.

ABSTRACT

In this study, an oral minipig infection model was established to investigate the pathogenicity of Yersinia enterocolitica bioserotype 4/O3. O3 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 O3 serotype, we compared the colonization properties of Y. enterocolitica O3 with O8, a highly mouse-virulent Y. enterocolitica serotype, in minipigs and mice. We found that O3 is a significantly better colonizer of swine than is O8. Coinfection studies with O3 mutant strains demonstrated that small variations within the O3 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 the invA gene abolished long-term colonization in the pigs. Our results indicate a primary role for invasin in naturally occurring Y. enterocolitica O3 infections in pigs and reveal a higher adaptation of O3 than O8 strains to their natural pig reservoir host.