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 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 will not always aggravate vibriosis and the dynamics of interaction is strain dependent.

摘要

革兰氏阴性海洋细菌副溶血弧菌是一种重要的水生病原体，已被证明是虾类水产养殖中急性肝胰腺坏死病（AHPND）的病原体。引起AHPND的副溶血性弧菌菌株含有编码二元PirA ^VP和PirB ^VP毒素的pVA1质粒，是介导虾中AHPND和死亡率的主要毒力因子。由于PirAB ^VP毒素在细胞外分泌，因此可以推测PirAB ^VP毒素会加剧水生环境中的弧菌病。为了解决这个问题，进行了体内和体外实验。无病菌Franciscana卤虫与PirAB ^VP毒素和10 Vibrio spp共同感染。该体内结果显示，PirAB ^VP毒素与MM30协同相互作用（一群体感应AI-2缺陷型突变）和溶藻弧菌AQ13-91，加重弧菌病。然而，PirAB共同挑战^VP毒素和五，坎LMG21363，副溶血弧菌CAIM170，溶蛋白弧菌LMG10942和鳗弧菌NB10工作对抗性，提高生存的卤虫幼虫。该体外结果表明，添加PirAB的^VP毒素显着调节了所研究弧菌的毒力因子的产生。然而，这些体外结果并不能解释体内结果。因此，似乎PirAB ^VP毒素并不总是会加剧弧菌病，并且相互作用的动力学取决于菌株。