The role of toxin-coregulated pili in the pathogenesis of Vibrio cholerae O1 El Tor

Microb Pathog. 1993 Dec;15(6):421-31. doi: 10.1006/mpat.1993.1091.

Abstract

Studies in the infant mouse cholera model have evaluated the significance of toxin-coregulated pili (TCP) in the pathogenesis of Vibrio cholerae strains of El Tor biotype. Four El Tor strains--two which produce TCP during in vitro growth and two which do not--were mutated by the insertion of an antibiotic-resistance cartridge into the tcpA gene (encoding the pilin monomer). The resulting mutants were otherwise indistinguishable from wild-type and in particular were unaltered in their sensitivity to antibody-dependent, complement-mediated bacteriolysis. All were dramatically attenuated and showed a marked impairment in terms of in vivo persistence in mixed-infection competition experiments. Virulence was restored by provision of a functional tcp operon in trans, confirming that the pathogenic potential of El Tor strains is critically dependent upon product(s) of this operon.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacterial Proteins / genetics
  • Bacterial Toxins / metabolism
  • Base Sequence
  • Blotting, Southern
  • Cholera / microbiology
  • Cloning, Molecular
  • DNA, Bacterial
  • Fimbriae Proteins*
  • Fimbriae, Bacterial / physiology*
  • Immunoblotting
  • Mice
  • Molecular Sequence Data
  • Mutation
  • Vibrio cholerae / genetics
  • Vibrio cholerae / pathogenicity*
  • Virulence

Substances

  • Bacterial Proteins
  • Bacterial Toxins
  • DNA, Bacterial
  • TcpA protein, Vibrio cholerae
  • Fimbriae Proteins