Acute hepatopancreatic necrosis disease (AHPND) recently escalate into panzootic, leading to severe losses in shrimp industries. Three types of quorum sensing (QS) signal molecules namely N-acyl-homoserine lactone (AHL) (Figure 1), Autoinducer-2 (AI-2) and Cholerae autoinducer-1-like (CAI-1) molecules were detected in cell-free fluid from AHPND causing strains. The LuxR and LuxS genes screening were positive for all the AHPND positive Vibrio strains.
In vivo expression of AHPND virulence genes (pirA and pirB), quorum sensing regulator luxR and virulence regulator toxR in V. parahaemolyticus strain BpShHep31 and V. harveyi strain BpShHep24, causing AHPND were further investigated. A significant (P < 0.05) increase in the expression levels of the quorum-sensing master regulator luxR were detected when compared with the control shrimp (unchallenged group). There was also a substantial difference in pirA, pirB and toxR expressions in the challenged shrimps compared to unchallenged group. The expression of AHPND virulence genes (pirA and pirB), luxR and toxR peaked at 36 h post challenged at 20-30-, 41-59- and 25-39-fold respectively. Furthermore, expression levels of pirA, pirB, luxR and toxR positively correlate with the mortality rate of shrimp in the challenged group.