The innate immune response in Salmo salar, mediated by pattern recognition receptors (PRRs), is crucial for defending against pathogens. This study examined DDX41 protein functions as a cytosolic/nuclear sensor for cyclic dinucleotides, RNA, and DNA from invasive intracellular bacteria. The investigation determined the existence, conservation, and functional expression of the ddx41 gene in S. salar. In silico predictions and experimental validations identified a single ddx41 gene on chromosome 5 in S. salar, showing 83.92% homology with its human counterpart. Transcriptomic analysis in salmon head kidney confirmed gene transcriptional integrity. Proteomic identification through mass spectrometry characterized three unique peptides with 99.99% statistical confidence. Phylogenetic analysis demonstrated significant evolutionary conservation across species. Functional gene expression analysis in SHK-1 cells infected by Piscirickettsia salmonis and Renibacterium salmoninarum indicated significant upregulation of DDX41, correlated with increased proinflammatory cytokine levels and activation of irf3 and interferon signaling pathways. In vivo studies corroborated DDX41 activation in immune responses, particularly when S. salar was challenged with P. salmonis, underscoring its potential in enhancing disease resistance. This is the first study to identify the DDX41 pathway as a key component in S. salar innate immune response to invading pathogens, establishing a basis for future research in salmonid disease resistance.

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 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.