Abstract:Acute Hepatopancreatic Necrosis Syndrome (AHPNS), also know as Early Mortality Syndrome (EMS), was officially reported in China in 2010 and has caused large-scale die-offs of cultivated shrimp in several Asian countries. A research team of the University of Arizona has identified that the pathogen is Vibrio parahaemolyticus which is a strain of a bacterium commonly found in brackish coastal waters around the globe. Because V. parahaemolyticus is a conditioned pathogen, it is very important to study the effects of ammonia nitrogen on the toxicity of this pathogen to Litopenaeus vannamei. To evaluate the effects of total ammonia nitrogen during the outbreak of AHPNS in L. vannamei, we examined the susceptibility to the pathogen, the non-specific immunity and the expression of LvLT mRNA in the hepatopancreas of the shrimp. Shrimp underwent the ammonia stress for 20 days with different ammonia nitrogen concentrations: 2.5 mg/L, 5.0 mg/L, 7.5 mg/L, 10.0 mg/L and the control concentration. After the exposure to V. parahaemolyticus, the death rate of shrimp perked in 6–24 h. The accumulative mortality rates of the treated groups were 0, 8%, 12%, 20% and 36% respectively at 120 h. The activities of phenoloxidase (PO) reached the lowest at 12 h in the control, 2.5 and 5.0 mg/L groups, and at 24 h in the 7.5 and 10.0 mg/L groups. The activity of superoxide dismutase (SOD) increased at first and then gradually declined, and lysozyme (LSZ) exhibited the same trend. The expression of LvLT mRNA in the hepatopancreas increased at 6 h in all groups and was significantly higher in the control, 2.5, 5.0 and 7.5 mg/L group than that in the 10.0 mg/L group. The LvLT mRNA expression reached the maximum at 12 h and then declined gradually at 24 h. The results indicated that high ammonia nitrogen could cause depression in the immunity of L. vannamei, and subsequently increase their susceptibility to V. parahaemolyticu and the resultant mortality rate. Therefore it is crucial to regulate the concentration of total ammonia nitrogen in aquatic environment to prevent the breakout of Acute Hepatopancreas Necrosis Syndrome.
