Potential Ad Hoc Markers of Persistence and Virulence in Canadian Listeria monocytogenes Food and Clinical Isolates

Abstract

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.

Atypical Serogroup IVb-v1 of Listeria monocytogenes Assigned to New ST2801, Widely Spread and Persistent in the Environment of a Pork-Meat Producing Plant of Central Italy

“…Although not presenting a Premature Stop Codon Mutation in the inlA gene nor the SSI-1, both associated with an increased production of biofilm, as reported in previous studies (Keeney et al, 2018;Upham et al, 2019;Mahoney et al, 2022), all the strains carried several genetic markers for biofilm production. In particular luxS, for a S-ribosylhomocysteinase, recO encoding the DNA repair protein RecO and lmo2504 for a cell wall-binding protein were found in all the genomes (Pasquali et al, 2018;Gorski et al, 2022).…”

Presence of Listeria monocytogenes in Ready-to-Eat Artisanal Chilean Foods

“…This strain had PMSC in nucleotide 1380, truncated inlA gene, and replacement mutation G → A; it is categorized as PMSC number 8. Upham et al [72] genomically analyzed clinical and food strains and detected that the prevalence of the inlA gene PMSC mutations in genomes of food strains was significantly higher (p < 0.0001) than in clinical strains. However, a three-codon deletion in the inlA gene associated with a highly invasive phenotype was more prevalent in genomes from clinical strains, mainly from serotype 4b, than from food strains (p < 0.001).…”

PervasiveListeria monocytogenesare common in the Norwegian food system and associated with increased prevalence of stress survival and resistance determinants

“…For statistical analyses, the accessory stress survival genes were grouped into categories of cadmium resistance, arsenic resistance, QAC resistance, stress survival islets, biofilm-associated genes, and inlA PMSC mutations (the identified inlA 3-codon deletion (3CD) inlA mutation associated with an increased Caco-2 cell invasion phenotype (68, 69) was not included in this category) (Fig. 2B).…”