Analysis of intestinal metabolites in Litopenaeus vannamei infected with white faeces syndrome based on untargeted metabolomics

White faeces syndrome (WFS) has always been one of the main intestinal diseases of Litopenaeus vannamei, which has caused huge economic losses to shrimp farming. WFS infection is known to result from a combination of pathogens, but the changes in intestinal metabolites following WFS infection are unknown. In this study, morphological sections of the hepatopancreas and intestine of WFS infected shrimp were analyzed, and lesions were found in the hepatopancreas and intestine of infected shrimp. The hepatopancreatic bodies of shrimp infected with WFS were arranged and scattered, and the stellate cavity was deformed. The connective tissue within the intestinal fold's atrophies to the point where the muscular layer almost disappeared. The enzyme linked kit results showed that lysozyme activity in hepatopancreas was significantly increased, total antioxidant capacity was significantly decreased, intestinal total antioxidant capacity and superoxide dismutase activities were significantly decreased in WFS infected shrimp, indicating that the antioxidant capacity of hepatopancreas and intestine were impaired. The intestinal metabolites of WFS shrimp and healthy shrimp were analyzed by non-targeted metabolic technology, and 10 differential metabolites and 7 differential metabolic pathways were screened. Among them, arginine, a significant differential metabolite, may positively activate the mTOR pathway, leading to the high expression of mTOR pathway, which is closely related to intestinal health. This indicates that when L. vannamei. is infected with WFS, the arginine content in the intestine is up-regulated, which positively activates the mTOR signaling pathway leading to pathway disorder, thereby destroying the intestinal health of L. vannamei. Through this study, we can not only understand the intestinal metabolic characteristics of WFS, but also provide a theoretical reference for the prevention and treatment of WFS in L. vannamei.