Listeria monocytogenes (L. monocytogenes) is a Gram-positive, facultative intracellular foodborne pathogen. The distribution of L. monocytogenes is wide. It has been isolated in humans and animals in all continents except Antarctica[1]. Linked to its ability to tolerate extreme temperatures, acidity and osmolarity, L. monocytogenes can persist and grow in soil, plants, water, food and silage[2].
Listeriosis is a foodborne infection with high morbidity and fatality rate (approximately 20% to 30%, despite effective antibiotic treatment). Human listeriosis is characterized by septicemia and central nervous system (CNS) infections, which mostly occur in immunocompromised and/or elderly individuals, and by maternal-fetal infections, as well as by rare, anatomically localized infections[3].
L. monocytogenes diversity can be classified into lineages (I, II, III, IV), genoserogroups, clonal complexes (CCs), and sequence types (STs). Core-genome MLST further identifies sublineages (SLs) and cgMLST types (CTs)[4]. The biodiversity of L. monocytogenes was identified the four main serotypes (1/2a, 1/2b, 1/2c, and 4b) associated with listeriosis based on Listeria somatic and flagellar antigens, with serotype 4b (lineages I) including the major hypervirulent clones[5]. Most cases of human listeriosis are involving lineages I (serotypes 1/2b and 4b) and II (serotypes 1/2a and 4c). The most prevalent CCs and SLs are geographically and temporally widespread[6]. However, an uneven prevalence is observed among CCs and SLs of food versus clinical cases isolates, as previously noted at the lineage and serotype levels. While lineage II, in particular SL9 (CC9) and SL121 (CC121), is mostly associated with food, lineage I isolates, in particular SL1 (CC1), SL2 (CC2), SL4 (CC4), and SL6 (CC6), is strongly associated with clinical cases in the Western world[7]. In Asia, specifically in China, the most prevalent SL in both food and clinical cases is SL87 (CC87, lineage I, serotype 1/2b)[8].
The virulence of L. monocytogenes depends on its ability to colonize the gut and disseminate in the host. Internalin (InlA) is a leucine-rich repeats (LRR)-containing protein. The receptor of InlA is E-cadherin (Ecad). The InlA–Ecad interaction is critical for L. monocytogenes to cross the intestinal barrier, at the villus level, by transcytosis across goblet cells [50]. While inlA is present in all L. monocytogenes strains, some strains express a truncated and therefore nonfunctional InlA. Hypovirulence can therefore, at least in part, be accounted for by InlA truncation, leading to decreased translocation across the intestinal barrier and placental infection[9]. Similarly to inlAB, Listeria pathogenicity island 1 (LIPI-1) is core virulence genes present in all L. monocytogenes SLs, which are all encoded by prfA, hly, actA, plcA, mpl, plcB, and the nucleomodulin orfX [10]. The LIPI-3 virulence cluster consists of eight genes, and its presence in L. monocytogenes SL1, SL4, and SL6, which are the most associated with clinical cases[4]. LIPI-4, a putative phosphotransferase system is present in SL4, is strongly associated with a clinical origin, particularly in CNS and placental infections[11].
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