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 DE205BΔphiv205-1. Compared with the wild-type (WT) APEC strain DE205B, the adherence and invasive abilities of DE205BΔphiv205-1 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 × 105 colony-forming units (CFU) and 3.86 × 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, DE205BΔphiv205-1 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.
Keywords: Avian pathogenic Escherichia coli; Biofilm formation; Colonization; Prophage; Virulence.
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