Reduced Virulence of an fliC Mutant of Shiga-Toxigenic Escherichia coli O113:H21

• Published in: Infection and Immunity Vol. 74; no. 3; pp. 1962 - 1966
• Main Authors: Rogers, Trisha J, Paton, James C, Wang, Hui, Talbot, Ursula M, Paton, Adrienne W
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society for Microbiology 01.03.2006
• Subjects: Animals; Bacteriology; Biological and medical sciences; Escherichia coli; Escherichia coli - genetics; Escherichia coli - immunology; Escherichia coli - pathogenicity; Escherichia coli Infections - etiology; Flagellin - genetics; Flagellin - metabolism; Fundamental and applied biological sciences. Psychology; Mice; Microbiology; Miscellaneous; Molecular Pathogenesis; Mutation; Shiga Toxins - genetics; Streptomycin - pharmacology; Virulence - genetics; Microbiology; Escherichia coli; Virulence; Bacteria; Mutation; Immunity; Enterobacteriaceae
• ISSN: 0019-9567; 1098-5522
• DOI: 10.1128/IAI.74.3.1962-1966.2006

The contribution of flagellin to the virulence of the O113:H21 Shiga-toxigenic Escherichia coli (STEC) strain 98NK2 was investigated in the streptomycin-treated mouse model. Groups of mice were challenged with either the wild-type STEC or a fliC deletion derivative thereof. There was no difference in the level of gut colonization by the two strains, but the fliC mutant was significantly less virulent than its parent; the overall survival rates were 43.7% and 81.2%, respectively (P < 0.025). This is the first report of a nontoxic accessory virulence factor contributing to a fatal outcome of STEC infection in this model. Although H21 FliC is known to be a potent inducer of CXC chemokines, including interleukin 8, there was no obvious difference in the recruitment of polymorphonuclear leukocytes to the intestinal epithelium of mice challenged with either strain. However, immunofluorescence microscopy suggested that the fliC mutant was less capable of forming a close association with the colonic epithelium. This may have reduced the uptake of Stx2 by mice infected with the mutant.