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Aeromonas salmonicida AS09, isolated from spoiled salmon, was investigated through whole-genome sequencing coupled with phenotypic characterization. The 4.91 Mb chromosome and two plasmids harbor genes involved in proteolysis (hap, inhA, ahe2), hemolysis (aerA, hlyA/B/D), TMAO reduction (torZ/C/D), and genes encoding components of three quorum sensing circuits (AI-1, AI-2, AI-3). Phenotypic assays confirmed extracellular protease and hemolysin activities, TMA production, and biofilm formation on multiple surfaces, and demonstrated production of the AI-1 signal C4-HSL. However, the functionality of the AI-2 and AI-3 systems and QS-mediated regulation of these phenotypes were not experimentally established. Antimicrobial susceptibility testing showed no inhibition zones for ampicillin or tetracycline, measurable inhibition zones for ciprofloxacin (9.50 ± 0.87 mm) and gentamicin (13.00 ± 0.50 mm), and a narrow zone for triclosan (7.50 ± 0.50 mm); because CLSI Enterobacteriaceae breakpoints are not validated for Aeromonas, these values are reported descriptively rather than as clinical categories. Genome-based resistance analysis identified 345 resistance-associated genes, with ResFinder confirming 12 acquired determinants, including chromosome-borne cphA5, blaFOX, blaOXA-10, qnrVC6, and integron-associated sul1. The localization of these genes on mobile elements suggests potential for horizontal dissemination. Collectively, the genomic and phenotypic data indicate that AS09 carries multiple spoilage- and virulence-associated traits together with acquired resistance determinants, marking it as a strain of potential dual concern for seafood spoilage and public health, underscoring the value of integrating genome-based surveillance with conventional testing for Aeromonas from aquatic products.
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Xu et al. (2026) studied this question.
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