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Shigella  spp. are responsible for bacillary dysentery in humans. The acquisition or the modification of the virulence plasmid encoding factors promoting entry of bacteria into and dissemination within epithelial cells was a critical step in the evolution of these bacteria from their  Escherichia coli  ancestor(s). Incorporation of genomic islands (GI) and gene inactivation also shaped interactions between these pathogens and their human host. Sequence analysis of the GI inserted next to the  leuX  tRNA gene in  S .  boydii ,  S .  dysenteriae ,  S .  flexneri ,  S .  sonnei  and enteroinvasive  E .  coli  (EIEC) suggests that this region initially carried the  fec ,  yjhATS  and  fim  gene clusters. The  fim  cluster encoding type I fimbriae is systematically inactivated in both reference strains and clinical isolates and distinct mutations are responsible for this inactivation in at least three phylogenetic groups. To investigate consequences of the presence of fimbriae on the outcome of the interaction of  Shigella  with host cells, we used a  S .  flexneri  strain harboring a plasmid encoding the  E .  coli fim  operon. Production of fimbriae by this recombinant strain increased the ability of bacteria to adhere to and enter into epithelial cells and had no effect on their ability to disseminate from cell to cell. The observations that production of type I fimbriae increases invasion of epithelial cells and that independent mutations abolish fimbriae production in  Shigella  suggest that these mutations correspond to pathoadaptive events.

Distinct Mutations Led to Inactivation of Type 1 Fimbriae Expression in Shigella spp.