Abstract:The genus Listeria consists of six species: L. monocytogenes, L. innocua, L. welshimeri, L. ivanovii, L. seeligeri and L. grayi. Two of the species, L. monocytogenes and L. ivanovii are pathogenic. The heterogeneity of remaining species, previously assumed to be nonpathogenic, regarding their capability of acquiring virulence-associated genes may reflect their potential ability to be causative agents of diseases, especially in immunocompromised mannals. Virulence determinants involved in environmental tolerance, adhesion and invasion of eukaryotic cells and intracellular life function interactively. The virulence genes are mostly organized into discrete genetic units known as pathogenicity islands (PAIs), among which Listeria pathogenicity island 1 (LIPI-1) and island 2 (LIPI-2) are the most important. During the evolution of pathogenicity, a common ancestor bearing PAIs gave rise to the currently prevailing typical strains of six species through horizontal transfer of virulence determinants or by events such as recombination and natural selection. Bacteriophages, transposons and plasmids might play critical roles in these processes as the executants. Compred to pathogenic species, the nonpathogenic species lost LIPI-1 (L. innocua, L. welshimeri and L. grayi) or harbored corrupted LIPI-1 (L. innocua, L. welshimeri). Some types of natural atypical Listeria strains such as nonhemolytic L. seeligeri and hemolytic L. innocua, although complicating taxonomic identification, should contribute fruitful insights into the evolution events of pathogenicity underlying the phylogeny of the genus Listeria.
