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Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.


Bacterial Infections and Mycoses | Bacteriology | Biology | Biotechnology | Food Biotechnology | Food Microbiology | Genetics and Genomics | Genomics | Immunology and Infectious Disease | Medical Microbiology | Medical Sciences | Medicine and Health Sciences | Microbiology | Organisms | Pathogenic Microbiology

Publication Details

Frontiers In Nutrition / Food Microbiology

Received: 05 July 2016; Accepted: 07 December 2016;
Published: 21 December 2016

Edited by:

Andrea Gomez-Zavaglia, Center for Research and Development in Food Cryotechnology (CIDCA, CONICET), Argentina

Reviewed by:

David Rodriguez-Lazaro, University of Burgos, Spain
Learn-Han Lee, Monash University Malaysia Campus, Malaysia
Gonçalo Nieto Almeida, Catholic University of Portugal, Portugal
Pio Maria Furneri, University of Catania, Italy

Copyright: © 2016 Casey, Jordan, Coffey, Fox and McAuliffe. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Olivia McAuliffe,


The vast majority of clinical human listeriosis cases are caused by serotype 1/2a, 1/2b, 1/2c, and 4b isolates of Listeria monocytogenes. The ability of L. monocytogenes to establish a systemic listeriosis infection within a host organism relies on a combination of genes that are involved in cell recognition, internalization, evasion of host defenses, and in vitro survival and growth. Recently, whole genome sequencing and comparative genomic analysis have proven to be powerful tools for the identification of these virulence-associated genes in L. monocytogenes. In this study, two serotype 1/2b strains of L. monocytogenes with analogous isolation sources, but differing infection abilities, were subjected to comparative genomic analysis. The results from this comparison highlight the importance of accessory genes (genes that are not part of the conserved core genome) in L. monocytogenes pathogenesis. In addition, a number of factors, which may account for the perceived inability of one of the strains to establish a systemic infection within its host, have been identified. These factors include the notable absence of the Listeria pathogenicity island 3 and the stress survival islet, of which the latter has been demonstrated to enhance the survival ability of L. monocytogenes during its passage through the host intestinal tract, leading to a higher infection rate. The findings from this research demonstrate the influence of hypervariable hotspots in defining the physiological characteristics of a L. monocytogenes strain and indicate that the emergence of a non-pathogenic isolate of L. monocytogenes may result from a cumulative loss of functionality rather than by a single isolated genetic event.

Table S1 Locations of hypervariable hotspots within each of the input strains.pdf (108 kB)
Locations of hypervariable hotspots within each of the input strains

Table S2.pdf (193 kB)
Strain-specific genes in L. monocytogenes strain DPC6895 when compared to strain FSL J2-064

Table S3.pdf (190 kB)
Strain-specific genes in L. monocytogenes strain FSL J2-064 when compared to strain DPC6895

Table S4.pdf (209 kB)
Antibiotic / Heavy Metal resistance genes in each input L. monocytogenes strain

Table S5.pdf (111 kB)
L. monocytogenes strain DPC6895 Cadmium Resistance Islet

Table S6.pdf (20 kB)
A list of internalin genes present in each of the L. monocytogenes input strains