Abstract
Abstract
The objective of this paper was to analyze of antibiotic resistance genes and mechanisms of antibiotic resistance in the causal agent of kiwifruit bacterial canker in western China. Pseudomonas syringae pv. actinidiae (Psa) strain L211, previously isolated from canker-infected kiwifruit (Actinidia chinensis)and identified in the laboratory, was used as the study material for whole-genome sequencing and annotation of gene functions. The antibiotic resistance genes and resistance mechanisms were predicted by comparison with the CARD database, and verified by antibiotic sensitivity tests. Our results showed that in total, 482 resistance genes were predicted in the strain L211 genome involved in resistance to28 antibiotics. Thepredicted genes were classified in six categories of resistance mechanisms, namely antibiotic efflux, antibiotic inactivation, antibiotic target alteration, antibiotic target protection, reduced antibiotic penetration, and mixed resistance mechanisms. Resistance was mainly characterized as active efflux, β-lactamase degradation, mutation of target genes, plasmid mediated, and reduced biofilm permeability. Antibiotic sensitivity tests revealed that strain L211 was resistant to carbenicillin, cefadroxil, clindamycin, isoniazid, sulfadiazine, bacitracin, norfloxacin, dapsone, and chloramphenicol, and sensitive to oxytetracycline, streptomycin, triclosan, and rifampin. Psa may be a broad-spectrum antibiotic-resistant bacterium, with antibiotic efflux as its main resistance mechanism.Multiple resistance mechanisms were predicted to act in concert, resulting in increased antibiotic resistance and resistance to multiple antibiotics. Frequent use of agricultural antibiotics is interpreted to have led to proliferation in resistance genes that target two antibiotics.To avoid further increase in the resistance spectrum of Psa, the use of chemical antibiotics in agriculture should be strictly controlled.
Publisher
Research Square Platform LLC