The avian pathogenic Escherichia coli O2 strain E058 carrying the defined aerobactin-defective iucD or iucDiutA mutation is less virulent in the chicken.

The expression of aerobactin accounts for much of the pathogenesis of avian pathogenic Escherichia coli (APEC). iucA, iucB, iucC and iucD are involved in aerobactin synthesis and iutA is responsible for the expression of a specific outer membrane receptor protein for ferric aerobactin. Knockout mutants of iucD and iucDiutA in the APEC O2 strain E058 were constructed and named E058ΔiucD and E058ΔiucDΔiutA, respectively. To evaluate the pathogenicity of these mutants, we used multiple approaches to assess the effects of mutations on the virulence of APEC E058. Aerobactin-defective mutants E058ΔiucD and E058ΔiucDΔiutA showed significantly decreased pathogenicity compared with the wild-type strain E058, evidenced by the low extent of colonization in selected organs or being outcompeted by E058 in vivo. Chickens challenged with APEC E058 exhibited typical signs and lesions of avian colibacillosis, while those inoculated with the mutants E058ΔiucD or E058ΔiucDΔiutA showed moderate airsacculitis, mild pericarditis and perihepatitis. However, no significant differences in resistance to specific-pathogen-free chicken serum, ingestion by HD-11 cells, and growth rates in LB were observed between the mutants and the wild-type strain. These results indicated that the IucD- and IutA-related virulence factors play a significant role in the pathogenesis of the APEC strain E058.