Table 6

Shigella model of elements acquired or disposed of during pathoadaptation a

AdaptationCategory and element(s)Role in pathogenesis b
AcquisitionInvasion plasmid elements
    T3SSTranslocation of T3S effectors into host
    T3SS substrates/translocatorsSubversion of host cell processes for bacterial invasion, intracellular survival, and intra- and intercellular motility
    Transcriptional regulatorsCoordination of T3SS-associated gene transcription, stabilization of T3S effectors in bacterial cytosol
    ChaperonesWatery diarrhea, inflammation
    Enterotoxin ShET2
Chromosomal Shigella PAIs
    SHI-1(including enterotoxin ShET1 and SPATEs Pic and SigA)Watery diarrhea, mucus permeabilization, serum resistance and hemagglutination
    SHI-2/3Iron acquisition, regulation of inflammation
    SHI-OHost immune evasion
    SRLIron acquisition, multidrug resistance
    Shiga toxin (primarily in S. dysenteriae 1)Inhibition of host protein synthesis, induction of apoptosis
Loss or inactivationAntivirulence genes
    ompT Inhibition of intra- and intercellular motility
    cadA (for EIEC often cadC)Attenuation of PMN transepithelial migration, enterotoxin activity, and phagosomal escape
    nadA, nadB Inhibition of PMN transepithelial migration, cell-to-cell spread, and T3SS
    speG Decrease of oxidative stress tolerance
    argT Inhibition of cell invasion
Surface structures
    Flagella, fimbriaeActivators of host immune system; flagella negligible due to acquired T3S effector-mediated, actin-based motility
Diverse catabolic pathwaysRedundant due to pathogenic lifestyle
  • a PAI, pathogenicity island; PMN, polymorphonuclear leukocyte; SPATEs, serine protease autotransporters from Enterobacteriaceae.

  • b See references 38 and 424.