Whole-Genome-Sequencing Analysis of the Pathogen Causing Spotting Disease and Molecular Response in the...

Sea urchin aquaculture has experienced remarkable growth in recent years. However, this growth has been accompanied by increased disease prevalence. Notably, spotting disease has particularly severe impacts. In this study, we isolated the pathogen HZ-3-2 from 10 sea urchins with spotting disease, and it was identified as Vibrio splendidus through morphological observations, 16S rDNA sequencing, and whole-genome sequencing. Subsequently, experimental infection confirmed that V. splendidus (HZ-3-2) is the causative agent of spotting disease in this outbreak. The drug sensitivity confirmed the presence of drug resistance genes, such as CPR, QNRS5, and rsmA, which were identified in the genome. The tests indicated that V. splendidus was sensitive to various antibiotics, including fluoroquinolones and florfenicol. Finally, we used the transcriptome to explore the molecular response of the diseased sea urchin. Compared to the control group, a group of sea urchins immersed in a pathogen suspension with a concentration of 10⁷ CFU/mL (group M) resulted in 439 annotated differentially expressed genes. KEGG pathway analysis indicated significant activation of cholesterol metabolism and starch and sucrose metabolism in the S. intermedius. This study highlights the genes NPC1, AMY2A, and MGAM as critical regulators of energy metabolism, and cholesterol synthesis in infected sea urchins. These findings confirm V. splendidus as the bacterium responsible for spotting disease and provide valuable insights into the intestinal molecular response of S. intermedius to infection.