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Chapter 41 : Evolution of Listeria monocytogenes
Category: Fungi and Fungal Pathogenesis; Bacterial Pathogenesis
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In the mid-1980s, molecular biology coupled with bacterial genetics and cell biology approaches allowed detailed investigations of the genetic basis of Listeria monocytogenes virulence. L. monocytogenes infects humans and animals, although its presence has been reported in an impressive number of animal species, which are probably healthy carriers. Southern blot hybridization highlighted that the virulence gene cluster and the internalin locus were absent in L. innocua. The most abundant class of surface proteins are lipoproteins, a class of bacterial surface proteins that may be implicated in adherence to different substrates, host tissues, or other bacteria, as well as in conjugation, signalling, or metabolic functions. The origin of the known virulence genes is still unclear, but comparative sequence analysis gives insight into the possible evolution of pathogenesis in Listeria. Further analysis of the gene content of these strains with respect to virulence genes revealed that all known virulence factors (inlAB, prfA, plcA, hly, mpl, actA, plcB, uhpT, and bsh) are present in all L. monocytogenes strains tested. Interestingly, the distribution of surface proteins among the L. monocytogenes strains mirrored the three lineages, as each lineage and each subgroup within a lineage is characterized by a specific surface protein combination. The many fascinating strategies used by Listeria to invade cells, escape from the internalization vacuole, spread from cell to cell, and escape the host as early defense mechanisms are providing unexpected clues to how microbes can establish an infection.
Phylogenetic tree of the genus Listeria. This tree is based on the concatenated nucleic acid sequences of 16S and 23S rRNA, iap, prs, vclB, and ldh. The bar indicates 10% estimated sequence divergence. (Reproduced with permission from Schmid et al., 2005.)
Schematic representation of the infection cycle of L. monocytogenes. The successive steps are entry (1), lysis of the vacuole (2), intracellular replication (3), intracellular movement (4), cell to cell spread (5), and formation and lysis (6) of two-membrane vacuole. Virulence factors involved at the different steps are indicated in the text.