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Avian pathogenicEscherichia coli (APEC) infection causes avian colibacillosis, which refers to any localized or systemic infection, such as acute fatal septicemia or subacute pericarditis and airsacculitis. The RfaH transcriptional regulator inE. coli is known to regulate a number of phenotypic traits. The direct effect of RfaH on the virulence of APEC has not been investigated yet. Our results showed that the inactivation ofrfaH significantly decreased the virulence of APEC E058. The attenuation was assessed byin vivo andin vitro assays, including chicken infection assays, an ingestion and intracellular survival assay, and a bactericidal assay with serum complement. The virulence phenotype was restored to resemble that of the wild type by complementation of therfaH gene intrans . The results of the quantitative real-time reverse transcription-PCR (qRT-PCR) analysis and animal system infection experiments indicated that the deletion ofrfaH correlated with decreased virulence of the APEC E058 strain.

RfaH Promotes the Ability of the Avian Pathogenic Escherichia coli O2 Strain E058 To Cause Avian Colibacillosis