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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.半透明幼体病害（Translucent post-larvae disease, TPD）已成为对虾养殖业的严重威胁，造成了巨额经济损失。其致病菌副溶血性弧菌（Vibrio parahaemolyticus）此前主要在中国被检出，而本研究首次证实该致病菌在境外对虾种群中存在。本研究针对从患病凡纳滨对虾（Penaeus vannamei）体内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。对VpTPD AG1的PCR筛查结果显示，其携带此前与TPD毒力相关的vhvp-1和vhvp-2基因，但未检出与急性肝胰腺坏死病（acute hepatopancreatic necrosis disease, AHPND）相关的pirA/pirB基因。浸泡感染试验证实该菌株具有高致病性且呈剂量依赖性，在15日龄凡纳滨对虾幼体（PL15）中，96小时的半致死浓度（LC50）为8.51 × 10² CFU/mL。30日龄幼体（PL30）则表现出更低的易感性，提示存在体长依赖的抗性机制。组织病理学分析确认其引发肝胰腺病变，包括小管坏死、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，该菌株感染特有的组织病理学特征——血细胞性肠炎，表现为肠道黏膜上皮脱落、重度炎症及增厚的血细胞层。对VpTPD AG1的药敏试验显示，其对β-内酰胺类抗菌药物具有耐药性，但对多种其他类别抗菌药物敏感。本研究结果表明VpTPD的地理分布正在扩大，且其病理特征与AHPND存在显著差异，同时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。