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      RfaH promotes the ability of the avian pathogenic Escherichia coli O2 strain E058 to cause avian colibacillosis.

      Journal of Bacteriology
      Animals, Chickens, Coinfection, DNA Primers, genetics, Disease Resistance, Escherichia coli, growth & development, pathogenicity, Escherichia coli Infections, immunology, microbiology, veterinary, Escherichia coli Proteins, metabolism, Genetic Complementation Test, Macrophages, Peptide Elongation Factors, Phenotype, Poultry Diseases, Sequence Deletion, Specific Pathogen-Free Organisms, Trans-Activators, Virulence, Virulence Factors

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          Abstract

          Avian pathogenic Escherichia 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 in E. 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 of rfaH significantly decreased the virulence of APEC E058. The attenuation was assessed by in vivo and in 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 the rfaH gene in trans. The results of the quantitative real-time reverse transcription-PCR (qRT-PCR) analysis and animal system infection experiments indicated that the deletion of rfaH correlated with decreased virulence of the APEC E058 strain.

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