Colonization factors of Escherichia coli O157:H7 in pigs

Escherichia coli O157:H7 causes severe hemorrhagic colitis in people. The main source of infection by E. coli O157:H7 is improperly cooked, or handled, contaminated food. E. coli O157:H7 has two well-described virulence factors: intimin and Shiga toxins. Research presented in this document utilized strains of E. coli O157:H7 that were mutated in genes that encoded a quorum sensing molecule, long polar fimbriae, and intimin. Gnotobiotic and conventionally reared pigs were infected to demonstrate whether the mutated strains were impaired in their ability to colonize or create disease when compared to the parent strain of E. coli O157:H7.;Mutation of the luxS gene, the product of which was a quorum sensing communicative molecule Al-2, was the first mutant of E. coli O157:H7 presented. AI-2 positively influences the bacterium to transcribe and translate genes that are necessary for bacterial attachment to enterocytes. Natural host hormones, epinephrine and norepinephrine, can override the luxS mutation given to the bacteria. The mutation in luxS had minimal effect on the colonization capability for E. coli O157:H7 possibly due to the provision of hormones from the intestinal tract of the pigs.;The second set of E. coli O157:H7 mutants had genes disrupted that were homologous to long polar fimbriae genes in Salmonella. The fimbriae may contribute to the initial adherence of E. coli O157:H7 to the enterocytes. The results of the long polar fimbriae studies indicated the lpf genes are not critical for virulence; however, they may aid E. coli O157: H7 in the colonization of gnotobiotic and conventionally reared pigs.;The third E. coli O157:H7 mutant was an intimin mutant. Several studies have shown that E. coli O157:H7 can be recovered from the tonsils from infected conventional pigs. In some instances, the recovery from tonsils exceeded that from the feces or any intestinal organ. It was concluded that intimin is not required for colonization of conventional pigs by E. coli O157:H7; nor does it preferentially colonize a particular area of the alimentary tract, but can remain at low levels throughout the tract.;These three studies may contribute to the idea that redundancy of adherence mechanisms may allow E. coli O157:H7 a competitive advantage in the colonization process

Colonization factors of Escherichia coli O157:H7 in pigs

Escherichia coli O157:H7 causes severe hemorrhagic colitis in people. The main source of infection by E. coli O157:H7 is improperly cooked, or handled, contaminated food. E. coli O157:H7 has two well-described virulence factors: intimin and Shiga toxins. Research presented in this document utilized strains of E. coli O157:H7 that were mutated in genes that encoded a quorum sensing molecule, long polar fimbriae, and intimin. Gnotobiotic and conventionally reared pigs were infected to demonstrate whether the mutated strains were impaired in their ability to colonize or create disease when compared to the parent strain of E. coli O157:H7.;Mutation of the luxS gene, the product of which was a quorum sensing communicative molecule Al-2, was the first mutant of E. coli O157:H7 presented. AI-2 positively influences the bacterium to transcribe and translate genes that are necessary for bacterial attachment to enterocytes. Natural host hormones, epinephrine and norepinephrine, can override the luxS mutation given to the bacteria. The mutation in luxS had minimal effect on the colonization capability for E. coli O157:H7 possibly due to the provision of hormones from the intestinal tract of the pigs.;The second set of E. coli O157:H7 mutants had genes disrupted that were homologous to long polar fimbriae genes in Salmonella. The fimbriae may contribute to the initial adherence of E. coli O157:H7 to the enterocytes. The results of the long polar fimbriae studies indicated the lpf genes are not critical for virulence; however, they may aid E. coli O157: H7 in the colonization of gnotobiotic and conventionally reared pigs.;The third E. coli O157:H7 mutant was an intimin mutant. Several studies have shown that E. coli O157:H7 can be recovered from the tonsils from infected conventional pigs. In some instances, the recovery from tonsils exceeded that from the feces or any intestinal organ. It was concluded that intimin is not required for colonization of conventional pigs by E. coli O157:H7; nor does it preferentially colonize a particular area of the alimentary tract, but can remain at low levels throughout the tract.;These three studies may contribute to the idea that redundancy of adherence mechanisms may allow E. coli O157:H7 a competitive advantage in the colonization process.</p