Shen, Xueyan, Gibson-Kueh, Susan, Nelson, Sarah Priyanka, Poon, Zhi Weng Josiah, Terence, Celestine, Vu, Nguyen Thanh, Carrai, Maura, Awate, Sunita, Vij, Shubha, Tan, Marie R., Jerry, Dean R., and Domingos, Jose A. (2026) Scale Drop Disease Virus (SDDV) infection induces intestinal dysbiosis and secondary Vibrio expansion in Asian seabass (Lates calcarifer). Fish and Shellfish Immunology, 174. 111344.

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Abstract

Scale drop disease virus (SDDV) is a major viral pathogen causing high mortality in farmed Asian seabass (Lates calcarifer), yet its impacts on host-associated microbiota remain poorly understood. In this study, juvenile L. calcarifer were intraperitoneally challenged with 107 viral copies (0.1 ml SDDV), resulting in 94.2% cumulative mortality over a 24-day experimental period. A total of 36 intestinal content samples were collected at defined time points relative to challenge (dpc) from clinically healthy (H) and sick (S) fish, representing five stages: pre-infection baseline (H0 dpc), early infection (H6 dpc), peak mortality (H10 dpc and S10 dpc), declining mortality (S15 dpc) and recovery (H24 dpc). Histopathological examination revealed progressive intestinal pathology, characterised by multifocal vesicle formation and epithelial necrosis, consistent with SDDV-associated enteropathy. 16S rRNA gene sequencing demonstrated pronounced intestinal dysbiosis during infection, with a significant collapse of alpha diversity at peak mortality (10 dpc; Kruskal-Wallis test with Dunn's post-hoc comparisons, p < 0.05) where Chao1 decreased from 942 at baseline to 416 and Shannon from 4.3 to 1.9. At peak disease, the gut microbiome was overwhelmingly dominated by Vibrio (>80% relative abundance), suggesting secondary opportunistic expansion associated with virus-induced intestinal damage. Co-occurrence network analysis further revealed fragmentation of microbial interactions during peak infection, followed by partial restoration of network connectivity and re-emergence of taxa such as Photobacterium and Rhodobacteraceae during recovery from infection. Collectively, these findings demonstrated that SDDV infection induced severe intestinal pathology accompanied by dynamic restructuring of the gut microbiome in L. calcarifer, linking viral epithelial damage to destabilization of the intestinal microbial homeostasis and secondary Vibrio overgrowth. Distinct microbiome features, including reduced community diversity and Vibrio dominance at peak disease, as well as recovery-associated taxa in surviving fish, may represent potential microbial indicators of disease progression and intestinal recovery, providing a reference framework for future microbiome-informed health management strategies aimed at mitigating SDDV impacts in L. calcarifer aquaculture.

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