Do acute hepatopancreatic necrosis disease-causing PirAB(VP) toxins aggravate vibriosis?

Gram-negative marine bacterium Vibrio parahaemolyticus is an important aquatic pathogen and has been demonstrated to be the causative agent of acute hepatopancreatic necrotic disease (AHPND) in shrimp aquaculture. The AHPND-causing V. parahaemolyticus strains contain a pVA1 plasmid encoding the binary PirA(VP) and PirB(VP) toxins, are the primary virulence factor that mediates AHPND and mortality in shrimp. Since PirAB(VP) toxins are secreted extracellularly, one can hypothesize that PirAB(VP) toxins would aggravate vibriosis in the aquatic environment. To address this, in vivo and in vitro experiments were conducted. Germ-free Artemia franciscana were co-challenged with PirAB(VP) toxins and 10 Vibrio spp. The in vivo results showed that PirAB(VP) toxin interact synergistically with MM30 (a quorum sensing AI-2 deficient mutant) and V. alginolyticus AQ13-91, aggravating vibriosis. However, co-challenge by PirAB(VP) toxins and V. campbellii LMG21363, V. parahaemolyticus CAIM170, V. proteolyticus LMG10942, and V. anguillarum NB10 worked antagonistically, increasing the survival of Artemia larvae. The in vitro results showed that the addition of PirAB(VP) toxins significantly modulated the production of the virulence factors of studied Vibrio spp. Yet these in vitro results did not help to explain the in vivo results. Hence it appears that PirAB(VP) toxins can aggravate vibriosis. However, the dynamics of interaction is strain dependent.