ABSTRACTInternalin A (InlA; encoded byinlA) facilitates the crossing of the intestinal barrier byListeria monocytogenes. Mutations leading to a premature stop codon (PMSC) ininlAand thus attenuated mammalian virulence have been reported. We recently characterized 502L. monocytogenesfood isolates from a retail survey and 507 human clinical isolates from multiple U.S. states with respect to the presence/absence ofinlAmutations. The objective of this study was to investigate the hypothesis that dose responses for human listeriosis vary betweenL. monocytogenesstrains with and those without a PMSC ininlA. Subtype-specific prevalence and concentration distributions in food, along with epidemiologic and consumption data, were input into established dose-response models to generate anrvalue (probability of a cell causing illness). Under the conservative assumption thatL. monocytogeneslevels at retail represent levels consumed, mean log10rvalues were −8.1 and −10.7 forL. monocytogenessubtypes with genes encoding a full-length and a truncated InlA, respectively.L. monocytogenescarrying a 5′ frameshift mutation in a homopolymeric tract showed a mean log10rvalue of −12.1. Confidence intervals for thervalues and their differences varied depending on subtypes. When the increase in concentration ofL. monocytogenessubtypes between retail and consumption was considered, mean log10rvalues were reduced to −10.4, −13.8, and −12.8 for the subtypes with genes encoding a full-length InlA, for the subtypes carrying a PMSC ininlA, and for allL. monocytogenesisolates regardless of subtype, respectively. Our study provides further quantitative evidence thatL. monocytogenessubtypes vary in abilities and relative likelihoods of causing human disease, which were mechanistically related to defined genetic markers.
Listeria adhesion protein-expressing bioengineered probiotics prevent fetoplacental transmission of Listeria monocytogenes in a pregnant Guinea pig model
