The role of toxin-coregulated pili in the pathogenesis of Vibrio cholerae O1 El Tor.
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.
Attridge
S R
SR
Department of Microbiology and Immunology, University of Adelaide, Australia.
Voss
E
E
Manning
P A
PA
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics; D001427:Bacterial Toxins / Q000378:metabolism; D001483:Base Sequence; D015139:Blotting, Southern; D002771:Cholera / Q000382:microbiology; D003001:Cloning, Molecular; D004269:DNA, Bacterial; D036781:Fimbriae Proteins; D010861:Fimbriae, Bacterial / Q000502:physiology*; D015151:Immunoblotting; D051379:Mice; D008969:Molecular Sequence Data; D009154:Mutation; D014734:Vibrio cholerae / Q000235:genetics / Q000472:pathogenicity*; D014774:Virulence
D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004269:DNA, Bacterial; C085807:TcpA protein, Vibrio cholerae; D036781:Fimbriae Proteins