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Title Evolution of Shigella: Gene Gain and Gene Loss (and Gene Gain?)

Presented by Anthony T. Maurelli, Ph.D. Professor Department of Microbiology & Immunology Uniformed Services University of the Health Sciences Bethesda, MD

Bacteria of the genus Shigella aregram negative rods that are the causative agents of bacillary dysentery or shigellosis. The four species of Shigella (iS. dysenteriae, S. flexneri, S. goydii, and S. sonnei) are so closely related to E. coli that they should be included in a single species. Acquisition of the large virulence plasmid was the crucial event in the evolution of Shigella and this plasmid is what distinguishes Shigella from the non-pathogenic commensal E. coli. The virulence plasmid and subsequent acquisition of Shigella unique pathogenicity islands represent evolution via gain-of-function events.

Ancestral traits that interfere with virulence are successively lost from the newly evolved pathogen genome due to selection for increased fitness in the host niche. Thus, pathogen evolution is also driven by loss-of-function mutations which silence/inactivate antivirulence phenotypes. Evidence in support of this new model of pathogen evolution is provided by comparison of Shigella with its commensal ancestor E. coli and identification of antivirulence genes (genes expressed by ancestral E. coli strains but lost in Shigella). Thus, the convergent evolution of the seven Shigella lineages presents a unique opportunity for the study of pathogen evolution via gene acquisition as well as pathoadaptive mutation and loss of antivirulence genes. The potential for emergency of new pathotypes of Shigella will be discussed in the context of newly isolated strains of S. flexneri that produce Shiga toxin.

Refreshments will be provided.