While serotyping studies indicated that a number of isolates from RTE foods represented serotypes associated with human disease (i.e., serotypes 1/2a, 1/2b, and 4b) (Ryser 1999), a number of food isolates also represented serotypes rarely associated with human infections; in particular, serotype 1/2c (Farber and Peterkin 1991). The observations that serotypes 1/2b and 4b were often overrepresented among human clinical isolates as compared to their prevalence among food-associated isolates, while serotypes 1/2a, and particularly 1/2c, were generally overrepresented among food isolates as compared to their prevalence among human clinical isolates, provided initial evidence that L. monocytogenes strains and serotypes differ in their abilities to cause human disease. Molecular subtyping studies further supported these observations by showing that L. monocytogenes strains grouped into lineage I (which includes serotypes 1/2b and 4b) were more common among human clinical isolates as compared to food isolates, while strains grouped into lineage II (which includes serotypes 1/2a and 1/2c) were more common among food isolates than human clinical isolates (Wiedmann et al. 1997; Jeffers et al. 2001). A study of almost 1,000 L. monocytogenes isolates from human clinical cases and foods showed that a number of specific ribotypes within the different L. monocytogenes lineages differed significantly in their prevalences among food and human isolates (Gray et al. 2004). Three ribotypes that were overrepresented among isolates from human listeriosis patients represented subtypes previously associated with multiple human listeriosis cases (i.e., epidemic clones), and also showed significantly higher ability to spread from cell to cell in a tissue culture plaque assay, providing phenotypic data supporting enhanced mammalian virulence of these subtypes and epidemic clones (Gray et al. 2004). Conversely, a number of the specific subtypes that were more common among food isolates in both the United States and France also showed reduced invasion efficiencies for human intestinal epithelial Caco-2 cells. Interestingly, the reduced invasion phenotype was found to be caused by one of several possible mutations leading to premature stop codons in inlA, which encodes for internalin A, a listerial surface molecule critical for invasion of human intestinal epithelial cells, thus providing a clear biological explanation for attenuated human virulence in these strains. Importantly, strains with premature stop codon mutations in inlA appear to represent about 30% of food isolates as established by independent studies in France (Jacquet et al. 2004) and the USA (Gray et al. 2004; Nightingale et al. 2005) supporting that a number of food isolates show reduced virulence. In addition, a smaller proportion of food isolates appears to show attenuated human virulence due to mutations in other virulence genes, including hly and prfA (Roberts et al. 2005; Roche et al. 2005). The combination of molecular subtyping with phenotypic characterization has thus provided substantial evidence for virulence differences among L. monocy-togenes subtypes. These experimental observations have also been supported by mathematical modeling data that indicate greater than 5 log differences in the likelihood of different L. monocytogenes subtypes to cause human disease (Chen et al. 2006).
Subtyping studies on L. monocytogenes isolated from food processing and retail environments showed that plant- or retail-specific L. monocytogenes subtypes can persist in these environments and also showed that the subtypes found in these environments represent both subtypes rarely associated with human disease, as well as those commonly associated with human disease, including subtypes that have caused multiple human listeriosis outbreaks (i.e., epidemic clones, Sauders et al. 2004). The observation that human disease-associated L. monocytogenes can persist in the environment without apparent loss of human virulence is further supported by the observation that a human listeriosis outbreak in 2000 was linked to contaminated RTE deli turkey produced in a processing plant in which the causative strain appears to have persisted for more than 10 years (Olsen et al. 2005). The strain responsible for the outbreak in 2000 also caused a single human listeriosis case in 1989 that was linked to consumption of contaminated hot dogs produced (and contaminated) in the same plant (Olsen et al. 2005).
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