Intracellular Listeria monocytogenes Comprises a Minimal but Vital Fraction of the Intestinal Burden following Foodborne Infection
Listeria monocytogenesis a highly adaptive bacterium that replicates as a free-living saprophyte in the environment as well as a facultative intracellular pathogen that causes invasive foodborne infections. The intracellular life cycle ofL. monocytogenesis considered to be its primary virulence determinant during mammalian infection; however, the proportion ofL. monocytogenesthat is intracellularin vivohas not been studied extensively. In this report, we demonstrate that the majority of wild-type (strain EGDe) and mouse-adapted (InlAm-expressing)L. monocytogenesrecovered from the mesenteric lymph nodes (MLN) was extracellular within the first few days after foodborne infection. In addition, significantly lower burdens ofL. monocytogeneswere recovered from the colon, spleen, and liver of gentamicin-treated mice than of control mice. This led us to investigate whether intracellular replication ofL. monocytogeneswas essential during the intestinal phase of infection. We found that lipoate protein ligase-deficientL. monocytogenes(ΔlplA1) mutants, which display impaired intracellular growth, were able to colonize the colon but did not persist efficiently and had a significant defect in spreading to the MLN, spleen, and liver. Together, these data indicate that the majority of theL. monocytogenesburden in the gastrointestinal tract is extracellular, but the small proportion of intracellularL. monocytogenesis essential for dissemination to the MLN and systemic organs.