Metabolomic variation along the gastrointestinal tract of shrimps with white feces syndrome
Wananit Wimuttisuk1, Pisut Yotbuntueng1, Piyachat Sanguanrat1, Pacharawan Deenarn2, Punsa Tobwor1, Surasak Jiemsup3, and Suganya Yongkiettrakul3
1Integrative Aquaculture Biotechnology Research Group, National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency (NSTDA), Khlong Luang, Pathum Thani, Thailand
2Biorefinery and Bioproduct Technology Research Group, National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency (NSTDA), Khlong Luang, Pathum Thani, Thailand
3Medical Molecular Biotechnology Research Group, National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency (NSTDA), Khlong Luang, Pathum Thani, Thailand
White Feces Syndrome (WFS) is a devastating disorder that threatens the global production of the Pacific white shrimp, Litopenaeus vannamei. WFS is caused by a coinfection of Enterocytozoon hepatopenaei (EHP) and opportunistic bacteria, such as Vibrio spp. WFS leads to significant economic losses through reduced feeding, stunted growth, and up to 30% mortality in the infected ponds. However, not all shrimp infected with EHP and Vibrio display the WFS symptoms, suggesting the presence of specific pathways involved in WFS progression. In this study, a comprehensive metabolomic analysis was performed to compare the metabolomic profiles in hepatopancreases and stomachs of healthy shrimp (control), shrimp infected with EHP and Vibrio parahaemolyticus but without symptoms (IF), and shrimp with WFS. Using the ultra-high performance liquid chromatography high-resolution tandem mass spectrometry, the metabolomic analysis of shrimp hepatopancreas and stomachs was performed in both positive and negative modes. The principal component analysis revealed a clear separation between the control group and the IF and WFS groups, indicating significant metabolic changes associated with pathogenic infection in shrimp hepatopancreases. Heatmap analysis further highlighted distinct variations in metabolite levels among the three groups. Specifically, out of 257 metabolites identified in positive mode, 21 were significantly upregulated, and 53 were downregulated in WFS shrimp compared to controls. Negative mode analysis of hepatopancreas samples showed 8 metabolites upregulated and 35 downregulated in WFS shrimp. A smaller set of metabolites differentiated IF from WFS shrimp. The metabolites that were upregulated in WFS included two organic oxygen compounds and one organic acid/derivative, while downregulated compounds included various lipids, heterocyclic, nitrogen, and benzenoid compounds. In contrast, the stomach samples did not show distinct metabolic profiles between groups, suggesting that WFS primarily alter the metabolic pathway in the hepatopancreas. These findings reveal that WFS alters the metabolic profiles in shrimp hepatopancreases and that these metabolic shifts may serve as early predictors of the WFS. Moreover, the supplementation of metabolites that were downregulated in WFS could offer a new strategy to reduce the severity of WFS.
