Abstract

Listeria genus comprises two pathogenic species, L. monocytogenes (Lm) and L. ivanovii, and non-pathogenic species. All can thrive as saprophytes, whereas only pathogenic species cause systemic infections. Identifying Listeria species’ respective biotopes is critical to understand the ecological contribution of Listeria virulence. In order to investigate the prevalence and abundance of Listeria species in various sources, we retrieved and analyzed 16S rRNA datasets from MG-RAST metagenomic database. 26% of datasets contain Listeria sensu stricto sequences, and Lm is the most prevalent species, most abundant in soil and host-associated environments, including 5% of human stools. Lm is also detected in 10% of human stool samples from an independent cohort of 900 healthy asymptomatic donors. A specific microbiota signature is associated with Lm faecal carriage, both in humans and experimentally inoculated mice, in which it precedes Lm faecal carriage. These results indicate that Lm faecal carriage is common and depends on the gut microbiota, and suggest that Lm faecal carriage is a crucial yet overlooked consequence of its virulence.

Highlights

  • Listeria genus comprises two pathogenic species, L. monocytogenes (Lm) and L. ivanovii, and non-pathogenic species

  • Listeria monocytogenes is more host-associated than nonpathogenic Listeria species

  • A few water samples (42/1980, ≥2.12%) and no air sample (0/53) were positive for any Listeria species (Figs. 1a, 2a for normalised data per category). Note that these Lm prevalence are likely an underestimate, as the sequenced 16S rRNA region varies among the samples studied and does not always allow to discriminate between Listeria species, and that the distribution of undefined Listeria hits followed a similar distribution to those obtained from discriminant regions of the 16S rRNA gene (Fig. 2b)

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Summary

Introduction

Listeria genus comprises two pathogenic species, L. monocytogenes (Lm) and L. ivanovii, and non-pathogenic species. The incidence of microbiologically proven invasive human listeriosis is extremely low, with 0.28 and 0.6 cases per 100,000 people in the United States and Europe, respectively[12,13] This implies that in most cases, human exposure to Lm leads to either absence of clinically detectable infection and/or clinically silent gut colonisation, suggesting that Lm virulence genes are likely not selected for their capacity to induce clinically-overt disease. We show that Lm is more host-associated than non-pathogenic Listeria species, and, in contrast to nonpathogenic Listeria species, is present in the faeces of healthy humans, both in publicly available 16S rRNA datasets and in an independent cohort of asymptomatic individuals. Asymptomatic carriage might represent an important outcome of Lm virulence, in addition to clinicallyovert disease[28]

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