Do acute hepatopancreatic necrosis disease-causing PirABVP toxins aggravate vibriosis?

Abstract

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 PirAVP and PirBVP toxins, are the primary virulence factor that mediates AHPND and mortality in shrimp. Since, PirABVP toxins are secreted extracellularly, one can hypothesize that PirABVP toxins would aggravate vibriosis in the aquatic environment. To address this, in vivo and in vitro experiments were conducted. The germ-free Artemia franciscana was co-challenged with PirABVP toxins and 10 Vibrio spp. The in vivo results showed that PirABVP toxin interact synergistically with V. harveyi BB120 (wild type), BB152 (HAI-1 deficient mutant), JMH603 (CAI-1 deficient mutant), MM30 (AI-2 deficient mutant) and V. alginolyticus AQ13-91 strain and significantly decreased the survival of Artemia larvae. However, supplementation of PirABVP toxin have significant antagonistic interaction with V. campbellii LMG21363, V. parahaemolyticus CAIM170, V. proteolyticus LMG10942 and V. anguillarum NB10 strain and increased the survival of Artemia larvae. The in vitro results showed that the addition of PirABVP toxins significantly modulated the production of the virulence factors of studied Vibrio spp. Moreover, the in vitro results with respect to virulence factor production did not support the the in vivo results. Hence it appears that PirABVP toxins will not always aggravate vibriosis.