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Infect Immun. 1989 January; 57(1): 121-131

The ail locus is found uniquely in Yersinia enterocolitica serotypes commonly associated with disease.

V L Miller, J J Farmer 3rd, W E Hill and S Falkow

Department of Medical Microbiology, Stanford University, California 94305.

ABSTRACT

Yersinia enterocolitica is a heterogeneous group of organisms with more than 50 serotypes and several biotypes. Only a few of these serotypes cause gastrointestinal disease in otherwise healthy hosts; these serotypes are the pathogenic serotypes. Although Y. enterocolitica requires a high-molecular-weight plasmid to cause disease, chromosome-encoded determinants are required for the full expression of virulence. The ability of Yersinia spp. to invade eucaryotic cells is thought to be a virulence factor, because nonpathogenic serotypes are noninvasive in animals and in tissue culture cell models. Current evidence indicates that invasion ability is chromosome encoded. We recently reported cloning two loci, inv and ail, from Y. enterocolitica O8 strain 8081c that allow Escherichia coli to invade tissue culture cells. We investigated the link between invasion in an in vitro tissue culture invasion (TCI) model and hybridization to probes derived from the two invasion loci, inv and ail. We examined 177 Yersinia strains. Strains of serotypes and species associated with disease were TCI+, whereas strains of serotypes and species not associated with disease were TCI-. Only TCI+ strains had DNA homologous to probes derived from ail. All strains (TCI+ and TCI-) had DNA homologous to probes derived from inv, but there were certain restriction fragment-linked polymorphisms that were associated primarily with TCI+ strains. These observations held true for strains epidemiologically associated with disease. Both the inv and ail loci were found to be clearly located on the chromosome. No other genera, including other invasive organisms, had DNA homologous to inv or ail. These data support the hypothesis that the ail locus encodes a Y. enterocolitica invasion factor that may be involved in pathogenesis.

Infect Immun. 1989 January; 57(1): 121-131




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