Severe infection caused by Listeria monocytogenes in humans is primarily linked to the pathogen's ability to cross the intestinal barrier and disseminate within the host. Once internalised, L. monocytogenes exhibits intracellular motility that enables colonisation of secondary target organs, including the brain and placenta. This review aims to critically compare the infection pathways of L. monocytogenes in humans and ruminant hosts, highlighting the molecular mechanisms that enable bacterial survival, organ tropism, and adaptation to host-specific stressors. By focusing on these comparative pathways, we aim to clarify how differences in virulence and stress-response factors, influenced by clonal complex, strain type, and lineage, affect host susceptibility and disease outcome. Using a comparative approach, we explore how variation in virulence and stress-response determinants, influenced by lineage, clonal complex, and strain type, may shape host susceptibility and disease outcomes across species. While ruminant listeriosis is well recognized clinically, key aspects of infection dynamics, tissue tropism, and host-pathogen interactions in these hosts remain poorly understood. Addressing these knowledge gaps will strengthen comparative pathogenesis frameworks and enhance the interpretation of strain diversity and host association patterns, contributing to a more integrated understanding of L. monocytogenes biology in human and animal hosts.
Teixeira et al. (Sun,) studied this question.
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