Objective This review elucidates the pivotal virulence evolution pathway of Vibrio spp. causative of translucent post-larva vibriosis (Vp_TPV) that underlies high mortality in post-larval shrimp, clarifies the mechanisms underlying their high lethality, and provides a basis for the development of inhibitors that attenuate virulence factors as well as pathogen-specific control strategies, thereby safeguarding broodstock security and supporting the sustainable development of aquaculture.

Progress TPV, also referred to as highly lethal Vibrio disease (HLVD), is a severe bacterial affliction that poses a significant threat to the global shrimp aquaculture sector. This disease predominantly affects Penaeus vannamei during the post-larval developmental stages (PL4−PL12), inducing mortality rates as high as 90% within 48 hours of onset, leading to substantial economic losses across major shrimp-producing nations, including China and Vietnam. The disease exhibits multi-source pathogenicity, predominantly caused by V. parahaemolyticus, but V. alginolyticus and V. campbellii can also be implicated. Importantly, TPV pathogens pose risks of cross-host and cross-regional transmission. Plasmid-encoded toxins represent the core virulence determinants mediating host invasion and tissue damage. Through the expression of toxin complexes (Tc) or Vibrio high virulent psrotein 2 (VHVP-2), these pathogens induce intestinal barrier collapse and hepatopancreatic necrosis, ultimately leading to tissue degeneration and structural dissolution. At the evolutionary level, plasmid-borne virulence genes undergo frequent transfer and recombination driven by transposons and type Ⅳ secretion systems (T4SS), generating novel hybrid plasmids and enhancing both adaptability and pathogenicity.To address this bacteriological epizootic that severely compromises penaeid aquaculture, the present work systematically integrates TPV’s etiological foundations, molecular pathogenesis, and sustainable mitigation paradigms. This synthesis delineates the diversity of pathogenic Vibrio and the mechanisms of virulence evolution, elucidates toxin-mediated host cellular injury pathways, and establishes sustainable control strategies based on early diagnostics and ecological interventions.

Significance In response, this review proposes an integrated, ecology-based strategy for disease management: blocking pathogen introduction via broodstock quarantine and specific pathogen free lines, monitoring and regulating water quality and microbial communities, and complementing with phage therapy, probiotics, and immune enhancers to establish a “source blocking-environmental optimization-targeted intervention-rapid response” defense framework. By utilizing this conceptual framework, it is imperative that future research include a thorough examination of toxin-host interaction dynamics, alongside the advancement of disease-resistant germplasm development and environmentally adaptive intervention technologies. These technologies are necessary to mitigate the risks of epizootic emergence and pathogen dissemination.