Isolation and identification of Edwardsiella tarda from naturally diseased largemouth bass (Micropterus salmoides) and its impact on host immune responses.

Abstract

The largemouth bass (Micropterus salmoides) industry in China has expanded rapidly under high-density intensive farming, yet is increasingly threatened by bacterial diseases whose pathogenesis remains poorly understood. This study constitutes the first report of Edwardsiella tarda infection in largemouth bass in Chongqing, China. A novel strain (LY-01) was isolated from diseased fish and identified as E. tarda through integrated phenotypic, biochemical, and molecular phylogenetic (16S rRNA and gyrB sequencing) analyses. Notably, the isolate harbored a unique virulence gene profile (gadB, mukF, esaV, fimA, citC), distinguishing it from previously reported strains. Artificial infection experiments confirmed high virulence, inducing systemic edema and histopathological damage in the liver, spleen, and intestine. Infected fish displayed extensive inflammatory infiltration, hemorrhage, and necrosis, along with significant alterations in serum immune-related parameters (T-AOC, SOD, MDA, LZM, ACP, AKP, ALT, AST), indicating systemic oxidative stress and immune dysregulation. Comparative transcriptomics of spleen tissue revealed 3610 differentially expressed genes (1924 up- and 1686 down-regulated), with KEGG enrichment highlighting key immune pathways such as IL-17 and PI3K-Akt signaling, and ECM-receptor interaction. Functionally, E. tarda infection activated the IL-17 signaling pathway, promoting the release of inflammatory cytokines (TNF-α, IL-6, IL-1β) and mediating splenic inflammatory responses. These findings systematically elucidate the molecular pathogenesis of E. tarda in largemouth bass and provide a theoretical foundation for developing targeted disease-control strategies in commercial aquaculture.