Prophage phiv205-1 facilitates biofilm formation and pathogenicity of avian pathogenic Escherichia coli strain DE205B

Avian colibacillosis caused by avian pathogenic Escherichia coli (APEC) causes significant economic losses to the poultry industry worldwide and is also a leading potential threat to human health. Bacteriophages integrate into the host bacterial chromosome, and are an important source of genetic variation and have a major impact on bacterial evolution. Previously, we predicted prophage phiv205-1 in APEC strain DE205B. Here, to determine the function of prophage phiv205-1, we constructed the prophage deletion mutant DE205B Delta phiv205-1. Compared with the wild-type (WT) APEC strain DE205B, the adherence and invasive abilities of DE205B Delta phiv205-1 were reduced by 41.88 %(P < 0.05). Further, the mutant strain had 52.38 % reduced biofilm formation compared with the WT strain (P < 0.001). Chick challenge showed that the median lethal dose (LD50) of the mutant strain and WT strain was 3.13 x 10(5) colony-forming units (CFU) and 3.86 x 104 CFU, respectively, indicating that the mutant strain had decreased virulence compared with the WT strain. Furthermore, in vivo studies showed that, compared with the WT strain, DE205B Delta phiv205-1 bacterial loads were reduced by 1.6-fold (P < 0.05) and 4.8-fold (P < 0.001) in the lungs and brains, respectively, of the infected chicks. In conclusion, the prophage phiv205-1 contributes to the virulence of APEC strain DE205B by facilitating the adherence, biofilm formation, and colonization abilities of its host strain.