Metabolic responses of penaeid shrimp to acute hepatopancreatic necrosis disease caused by Vibrio parahaemolyticus

Abstract

Vibrio parahaemolyticus is a causative agent of the acute hepatopancreatic necrosis disease (AHPND) that leads to massive mortalities in penaeid shrimp aquaculture worldwide. Mitigation of the significant economic losses caused by AHPND are hampered by knowledge gaps in the pathogenic mechanism of V. parahaemolyticus infection in shrimp. To provide insights into this infection mechanisms, molecular responses of shrimp exposed to V. parahaemolyticus were measured via a metabolomics approach. A gas chromatography–mass spectrometry (GC–MS) platform was employed to generate metabolite profiles of haemolymph from Penaeus vannamei shrimp challenged with V. parahaemolyticus and control shrimp (not exposed to the pathogen). The results revealed increases of several intermediates in the citric acid (TCA) cycle (cis-aconitic acid, citric acid, fumaric acid, isocitric acid and succinic acid) and phosphoenolpyruvic acid (PEP), as well as decreases of six amino acids (threonine, asparagine, 4-aminobutyric acid, histidine, ornithine, glutamine) in challenged shrimp compared to controls. A pathway analysis identified 11 significantly changed pathways due to V. parahaemolyticus infection, which were mostly amino acid metabolisms, TCA cycle and gluconeogenesis. The results suggest an increase in metabolic rate and elevated TCA cycle and gluconeogenesis activities in Vibrio-challenged shrimp due to the high energy demand of the associated immune response. The study provides important new findings about the pathogenic mechanisms of V. parahaemolyticus invasion in shrimp at the metabolic level. Further metabolomics investigations may lead for identification of metabolite biomarkers of V. parahaemolyticus infection for early detection of AHPND.