Molecular epidemiology of acute hepatopancreatic necrosis disease: A review

Acute hepatopancreatic necrosis disease (AHPND) is one of the major shrimp diseases worldwide which affects global economy up to 44 billion USD from 2010 to 2016. The causative agent of AHPND is the binary toxin PirAB, a toxin that causes sloughing effect on shrimp hepatopancreatic cells. This toxin is encoded by pirAB^vp gene located within a 5.5-kb composite transposon Tn6264, on a ∼70-kb plasmid pVA carried by Vibrio parahaemolyticus. Up to date, the pathogenesis and epidemiological links between AHPND-causing strains are still unclear. Therefore, this review aims to collect achieved results about the distribution, origin, transmission, and antibiotic resistance status of AHPND-causing strains, the molecular mechanism of PirAB toxin, and the mobile genetic elements that promote the spread of AHPND to provide valuable insights for future studies. Phylogenetic studies on AHPND reveal its evolutionary history, transmission routes, and genetic variations, with findings suggesting diverse origins of AHPND strains across different regions, facilitated by horizontal gene transfer and adaptation mechanisms in V. parahaemolyticus populations. Antimicrobial resistance profiles of AHPND-causing strains are also diverse and prevalent, particularly in Vietnam, South Korea, and Thailand, encompassing antibiotics like ampicillin, amoxicillin, sulfadiazine sodium, streptomycin, colistin, cefalexin, erythromycin, ceftazidime, and neomycin, raising concerns regarding multidrug resistance. PirAB toxin might function through the pore-forming activity of PirB^vp and the receptor-binding activity of PirA^vp, as predicted by Cry toxin model, while its expression is regulated by the quorum sensing system in V. parahaemolyticus. The pVA plasmid and the composite transposon Tn6264 both facilitates the dissemination of AHPND-causing strains, while the evolutionary mechanisms of these elements have not been widely understood. Transcriptomic and metabolomic studies also identify numerous differentially expressed genes in shrimp infected by AHPND-causing V. parahaemolyticus, and its immunity is also dependent on developmental stage and gut microbiota.