Effects of myo-inositol, sialic acid and L-fucose metabolic pathways on pathogenicity of Aeromonas hydrophila strain NJ-35

Abstract:

[Objective] This study aims to investigate the effect of inositol, sialic acid, and L-fucose metabolic pathways on pathogenicity in the process of Aeromonas hydrophila infection. [Methods] By homologous recombination technology, the genes associated with myo-inositol, sialic acid and L-fucose metabolism, iolC, fucK and nanA, were inactivated. Then fifty percent lethal doses (LD₅₀) of the deletion mutants were determined in zebrafish and the bacterial loads in different tissues were assayed in crucian carp co-infected with the wild-type and its derivative mutant strains. [Results] The inactivation of all the three metabolic genes successfully blocked the ability of A. hydrophila to degrade the corresponding substrates. Deletion of iolC resulted in a nearly 12-fold increase in LD₅₀ in zebrafish, whereas deletion of nanA and fucK had no significant effect on LD₅₀. The bacterial loads of the wild strain were significantly higher than that of the iolC deletion strain in liver, spleen and kidney after co-infection, indicating an obvious competitive growth advantage of the wild strain. But for nanA and fucK mutant strains, after co-infection with the wild strain, there was no significant difference in bacterial loads of the wild-type and its derivative mutant strains in different tissues. [Conclusion] The inositol metabolic pathway plays an important role during A. hydrophila infection, while sialic acid and L-fucose metabolic pathways have no significant effect on the pathogenicity of this bacterium.