L. monocytogenes is a widely distributed, if not ubiquitous, bacterial pathogen. While the importance of feed- and food-borne transmission to ruminant and human hosts has been well defined, its routes of transmission among different ecosystems and compartments within food production systems appear complex and remain to be clearly elucidated. Despite the fact that human infections with L. monocytogenes appear rare, particularly given the frequent prevalence and occasional high load of L. monocytogenes in many different environments, including in human foods and animal feeds, it is tempting to propose an anthropocentric transmission pathway for L. monocytogenes from the general environment through animal populations to food processing environments and foods to humans. While subtyping studies have clearly shown that human disease-associated L. monocytogenes strains, including epidemic clones, can be found in many environments, including natural, urban, and farm environments, directionality of transfer and transmission is difficult to establish. Consequently, future work remains to identify and characterize L. monocytogenes hosts, reservoirs, and transmission pathways, with consideration given to the possibility that the true natural host(s) of L. monocytogenes could be currently unidentified mammalian or even nonmammalian species. The ecological success of L. monocytogenes as a globally distributed microorganism may lie in its ability to survive in a large number of hosts as well as in non-host-associated environments, with the ability to establish high population densities in some host-associated ecosystems.
A number of distinct L. monocytogenes phylogenetic lineages and clonal groups have been identified and classified based on differences in abilities to cause human disease. Key groups important to the overall picture of L. monocy-togenes ecology and transmission include (1) virulence-attenuated strains (such as those characterized by premature stop codons in inlA (Nightingale et al. 2005) or by mutations in other virulence genes (Roberts et al. 2005)), (2) epidemic clones, which appear to show increased human virulence as compared to other strains, and (3) lineage III strains that appear to be associated with animal hosts (Jeffers et al. 2001) and that have limited ability to survive or multiply in non-host-associated environments (Gray et al. 2004; Roberts et al. 2006). Evolution of L. monocytogenes strains and lineages likely represents adaptation of specific strains to different niches, including many that may remain to be defined (e.g., in alternate host species). An improved understanding of the evolution of different L. monocytogenes ecotypes will thus provide an opportunity to better understand the ecology and transmission of L. monocytogenes, including its reservoirs and hosts.
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