RESUMO
The Listeria monocytogenes gene inlA, encoding a surface virulence protein, was examined for the presence of premature stop codon (PMSC) mutations in 82 isolates obtained by the Canadian Food Inspection Agency (CFIA) from foods and food contact surfaces. These mutations were coanalyzed for the presence of stress survival islet 1 (SSI-1) and for the abilities of the isolates to invade Caco-2 intestinal epithelial cells and form biofilms on polystyrene. PMSC mutations were present in one-third of the isolates (predominantly those of serogroup 1/2a), and their presence was correlated with a noninvasive phenotype. The presence of SSI-1 and the ability to form biofilms were also linked to the 1/2a serogroup. Serogroup 4b isolates lacked inlA PMSC mutations and were invasive, but neither formed biofilms nor carried SSI-1. To expand upon these experimental findings, an in silico analysis was performed on L. monocytogenes genomes from Canadian databases of 278 food isolates and 607 clinical isolates. The prevalence of inlA PMSC mutations in genomes of food isolates was significantly higher (P < 0.0001) than that in clinical isolates. Also, a three-codon deletion in inlA associated with a hyperinvasive phenotype was more prevalent in genomes from clinical isolates (primarily of clonal complex 6, serogroup 4b) than in those from food isolates (P < 0.001). In contrast, SSI-1 was significantly overrepresented (P < 0.001) in genomes from food isolates. We propose the hypothesis that SSI-1 and inlA play a role in the evolution of Canadian L. monocytogenes strains into either a virulent (represented by serogroup 4b clinical isolates) or an environmentally persistent (represented by serogroup 1/2a food isolates) phenotype. The combined presence of SSI-1 and inlA PMSC mutations have potential for use as genetic markers for risk assessment when L. monocytogenes is recovered from foods, indicating low potential for pathogenesis.