OxyR contributes to the virulence of a Clonal Group A Escherichia coli strain (O17:K+:H18) in animal models of urinary tract infection, subcutaneous infection, and systemic sepsis

• The Escherichia coli OxyR regulon includes multiple oxidative stress response genes.
• An oxyR mutant of a Clonal Group A (CGA) E. coli strain was attenuated in three rodent infection models.
• A complemented mutant showed virulence levels comparable to the parent strain.
• These data implicate OxyR as a virulence factor in both urinary and extra-urinary E. coli infections.

The oxidative stress response regulator OxyR was assessed as both a urinary and extra-urinary virulence factor in Escherichia coli strain UCB34 (O17:K+:H18), a representative of the emergent Clonal Group A (CGA). Compared to UCB34, the isogenic oxyR mutant exhibited increased H2O2 sensitivity, indistinguishable in vitro growth, and attenuated virulence in rodent models of urinary tract, subcutaneous infection, and systemic sepsis. Complemented mutants showed virulence levels comparable to parent strains in all models. These findings uniquely fulfill molecular Koch's postulates for a putative virulence factor of CGA, provide experimental evidence of an extra-urinary virulence promoting trait in CGA, and document a role for OxyR in local and systemic extra-urinary E. coli infections.