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The incidence of furunculosis in juvenile Atlantic salmon, Salmo salar, has increased in recent years in Chile, with isolates of Aeromonas salmonicida being the primary cause. However, in some cases, molecular diagnostics failed to identify the etiological agent. We previously demonstrated that a proportion of undiagnosed cases was produced by a new A. salmonicida strain. In those cases where the pathogen remained unidentified, we isolated colonies with an A. salmonicida-like appearance. Subsequent phylogenetic analysis presented in this work grouped those A. salmonicida-like isolates within the Aeromonas piscicola clade. Whole genome sequencing confirmed the taxonomic affiliation, giving additional insights into virulence and antibiotic resistance markers. Indeed, one of the strains showed reduced susceptibility to oxytetracycline. Virulence potential was assessed by in vivo testing in S. salar, which resulted in disease with pathognomonic signs of furunculosis. Although the pathogen presents common antigens with A. salmonicida, the current vaccine triggered only a modest IgM response against A. piscicola in the field. Our results support the hypothesis that the increasing incidence of furunculosis in Chile cannot solely be ascribed to the emergence of the new less-virulent A. salmonicida strain, but may partially result from furunculosis-like infections caused by A. piscicola strains which exhibit a comparable virulence level.

The incidence of furunculosis in juvenile Atlantic salmon, Salmo salar, has increased in recent years in Chile, with isolates of Aeromonas salmonicida being the primary cause. However, in some cases, molecular diagnostics failed to identify the etiological agent. We previously demonstrated that a proportion of undiagnosed cases was produced by a new A. salmonicida strain. In those cases where the pathogen remained unidentified, we isolated colonies with an A. salmonicida-like appearance. Subsequent phylogenetic analysis presented in this work grouped those A. salmonicida-like isolates within the Aeromonas piscicola clade. Whole genome sequencing confirmed the taxonomic affiliation, giving additional insights into virulence and antibiotic resistance markers. Indeed, one of the strains showed reduced susceptibility to oxytetracycline. Virulence potential was assessed by in vivo testing on S. salar, which resulted in disease with pathognomonic signs of furunculosis. Although the pathogen presents common antigens with A. salmonicida, the current vaccine triggered only a modest IgM response against A. piscicola in the field. Our results support the hypothesis that the incidence of furunculosis in Chile cannot be ascribed to the emergence of the new A. salmonicida strain, but may partially result from infections caused by A. piscicola strains which exhibit a comparable virulence level.

The emergence and spread of pathogens pose significant challenges to the sustainability and productivity of aquaculture globally. For the Chilean salmon farming industry, salmonid rickettsial septicemia (SRS), caused by the facultative intracellular bacterium Piscirickettsia salmonis, constitutes one of the main disease challenges. In this study, the efficacy of various oral doses of florfenicol (FFC) (5, 7.5, and 10 mg/kg BW/day) against SRS was assessed in Atlantic salmon, when treatment was initiated at an early stage of infection. Since salmonids infected with P. salmonis typically lose appetite as the disease progresses, and the therapeutic FFC dose is dependent on a normal specific feeding rate (SFR), the treatments were administered 5 days post-challenge (DPC5). On the day of challenge, experimental fish were intraperitoneally (IP) injected with 0.2 mL of P. salmonis genogroup LF-89 inoculum (9.07 × 10⁷ CFU mL⁻¹). Fish mortality, behavior, clinical signs of disease, feed intake and SFR were monitored throughout the study. Conclusions: An important finding in this study was that all tested antibiotic doses halted disease progression and prevented mortality in fish challenged with P. salmonis when administered DPC5. In the control group, mortality reached 32.2% with fish displaying clinical signs of SRS.