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Translucent post-larvae disease (TPD) has emerged as a severe threat to shrimp aquaculture, causing substantial economic losses. The causative agent, Vibrio parahaemolyticus, has been primarily identified in China, but this study provides the first confirmed report of its presence in shrimp populations outside China. This research characterizes V. parahaemolyticus strain AG1 (VpTPD AG1), isolated from diseased Penaeus vannamei, through biochemical, molecular, and pathogenic analyses. PCR screening of VpTPD AG1 detected vhvp-1 and vhvp-2, genes previously linked to TPD virulence, while pirA/pirB genes associated with acute hepatopancreatic necrosis disease (AHPND) were absent. Experimental immersion challenges demonstrated high virulence and dose-dependent pathogenicity, with an LC50 of 8.51 × 102 CFU/mL at 96 hours in 15-day-old post-larvae (PL15) of Penaeus vannamei shrimp. Larger post-larvae (PL30) exhibited reduced susceptibility, suggesting a size-dependent resistance mechanism. Histopathological analysis confirmed the degeneration of the hepatopancreas, including tubular necrosis, epithelial cell sloughing, and bacterial invasion, consistent with previously reported TPD pathology. Additionally, hemocytic enteritis, a characteristic histopathological feature associated with infection with VpTPD AG1 strain, was marked by mucosal epithelium loss, intense inflammation, and a thick hemocyte layer in the intestine. Antibiotic susceptibility testing of VpTPD AG1 strain revealed resistance to β-lactams but sensitivity to multiple other antimicrobial classes. These findings highlight the expanding geographical distribution of VpTPD, its distinct pathological features compared to AHPND, and further highlight the urgent need to enhance surveillance and implement effective biosecurity measures to prevent its global dissemination.

透明幼虾病（Translucent Post-larvae Disease, TPD）已成为虾类养殖业的严重威胁，造成巨额经济损失。其病原菌为副溶血性弧菌（Vibrio parahaemolyticus），此前主要在我国被检出，而本研究首次确认该菌在我国以外的虾类种群中存在。本研究对从患病凡纳滨对虾（Penaeus vannamei）中分离得到的副溶血性弧菌菌株AG1（VpTPD AG1）开展了生化、分子及致病性分析。通过对VpTPD AG1进行PCR筛查，检出了此前被证实与TPD毒力相关的vhvp-1与vhvp-2基因，但未检测到与急性肝胰腺坏死病（Acute Hepatopancreatic Necrosis Disease, AHPND）相关的pirA/pirB基因。浸泡感染实验结果表明，该菌株具有高毒力且呈剂量依赖性致病特性；感染96小时后，其对15日龄凡纳滨对虾幼虾（Post-larvae 15, PL15）的半数致死浓度（Lethal Concentration 50, LC50）为8.51×10²菌落形成单位/毫升（Colony Forming Unit/mL, CFU/mL）。30日龄幼虾（Post-larvae 30, PL30）的易感性显著降低，提示存在体型依赖的抗性机制。组织病理学分析证实，感染该菌株的虾类肝胰腺出现变性病变，包括肾小管坏死、上皮细胞脱落及细菌侵袭，与此前报道的TPD病理特征一致。此外，VpTPD AG1菌株感染还可引发血细胞性肠炎——该病害的特征性组织病理学表现为肠黏膜上皮脱落、严重炎症反应及肠腔内出现厚血细胞层。对VpTPD AG1菌株的药敏试验显示，其对β-内酰胺类抗生素耐药，但对多种其他类别的抗菌药物敏感。本研究结果揭示了VpTPD的地理分布范围正在不断扩大，其与AHPND存在截然不同的病理特征，并进一步凸显了加强监测、实施有效生物安全措施以防止其全球扩散的紧迫性。