Experimental study reveals renal granulomatous inflammation and metabolic shifts in Vibrio harveyi-infected greater amberjack, highlighting key immune mechanisms.
In July 2024, an outbreak of disease characterized by skin ulcers, blindness, tail rot, and multiple white granulomatous lesions in internal organs was reported in cultured Seriola dumerili on Naozhou Island, Zhanjiang, China. A bacterial isolate, VH-0801, was isolated from diseased fish and identified as Vibrio harveyi based on morphological characteristics and 16S rRNA and gyrB sequence analyses, while its pathogenic potential was further evaluated through challenge infection experiments. Histopathological examination revealed severe granulomatous inflammation in the kidneys of diseased fish, characterized by central necrosis, extensive inflammatory cell infiltration, abnormal melanin deposition, vacuolar degeneration, and steatosis. Virulence genetic testing showed that strain VH-0801 carried multiple virulence-associated genes, including vhhA , vhhB , vhpB , pap6 , luxR , toxR , and toxS . To investigate host responses associated with V. harveyi infection, RNA-Seq analysis was conducted on kidney tissues from naturally diseased and healthy control S. dumerili . A total of 512 differentially expressed genes (DEGs) were identified, comprising 250 down-regulated and 262 up-regulated genes. Functional enrichment analysis indicated that these DEGs were primarily associated with the extracellular space, extracellular region, extracellular exosomes, and the apical plasma membrane, as well as pathways related to amino acid and carbohydrate metabolism, cytoskeletal regulation in muscle cells, nicotinate and nicotinamide metabolism, and the C-type lectin receptor (CLR) signaling pathway. In conclusion, this study characterized the pathological features of visceral nodular disease and the host immune-metabolic responses associated with V. harveyi infection in cultured greater amberjack ( S. dumerili ), providing new insights into disease progression and host–pathogen interactions.
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