Bacteria, especially Vibrio spp., are largely responsible for larval diseases in shellfish aquaculture. Despite the severe impact of bacterial diseases on larval health, only a few direct studies have characterized the pathogenesis of vibriosis in bivalve larvae. To clarify the onset and advancement of vibriosis in blue mussel Mytilus edulis larvae, two known larval pathogens Vibrio splendidus ME9 and Vibrio anguillarum NB10 were tagged with green fluorescence protein (GFP), and combined with synchronous histopathological analyses, we identified a new type of pathogenesis of experimental vibriosis in bivalve larvae. The GFP-tagged Vibrio strains were first filtered by larvae through the velum and entered into the larval stomach through the esophagus. Later, they proliferated rapidly in the style sac and digestive glands, inducing necrosis of the digestive organs in the dorsal region during the first 24 h post challenge. Necrosis continued with esophagus disruption and velar deformation. Ultimately, the loss of distinguishable internal structures further disrupted the associated regulatory functions and rapidly induced larval death. It was confirmed later by ultrastructural observations that the Vibrio strains grew along the digestive tract and disrupted the digestive epithelium as a portal of entry. Moreover, we obtained the first evidence that the microvilli and cilia of the gastrointestinal epithelial cells were most sensitive to the vibriosis since the earliest disruptions of the larvae occurred in these positions, as shown by ultrastructural observations. The progression of the infection pathway as described in this study will facilitate further research that aims at the analysis of the gastrointestinal morphology after the introduction of anti-Vibrio therapy in the culture system.

细菌，尤其是弧菌属细菌，是造成贝类水产养殖中幼虫疾病的主要原因。尽管细菌性疾病对幼虫的健康有严重的影响，但只有很少的直接研究表明了双壳幼虫中弧菌病的发病机理。为了澄清弧菌病的发生和发展中的紫贻贝贻贝幼虫，两个已知的幼虫病原灿烂弧菌ME9和鳗弧菌NB10均标有绿色荧光蛋白（GFP），并与同步组织病理学分析相结合，我们发现了一种新类型的发病机制双壳幼虫的实验性弧菌病 带GFP标签的弧菌菌株首先被幼虫通过膜过滤，并通过食道进入幼虫的胃中。后来，它们在囊和消化腺中迅速增殖，在攻击后的最初24小时内引起背侧消化器官坏死。坏死继续伴随食管破裂和纤维变形。最终，可分辨的内部结构的丧失进一步破坏了相关的调节功能，并迅速引起幼虫死亡。后来通过超微结构观察证实了弧菌菌株沿着消化道生长，并破坏了消化上皮作为入口。此外，我们获得了第一个证据，表明胃肠道上皮细胞的微绒毛和纤毛对弧菌病最敏感，因为幼虫的最早破坏发生在这些位置，如超微结构观察所示。如本研究中所述的感染途径的进展将促进进一步的研究，其旨在在培养系统中引入抗弧菌疗法后分析胃肠道形态。