Department of Aquaculture, College of Animal Science & Technology, Sichuan Agricultural University, Wenjiang 611130, Sichuan, China.
Department of Aquaculture, College of Animal Science & Technology, Sichuan Agricultural University, Wenjiang 611130, Sichuan, China.
Ecotoxicol Environ Saf. 2021 Jun 1;215:112157. doi: 10.1016/j.ecoenv.2021.112157. Epub 2021 Mar 25.
Hepatopancreatic Necrosis Syndrome (HPNS) severely impacts the Chinese mitten crab (Eriocheir sinensis) industry. However, little knowledge of the aetiology and pathogenesis of the disease causes significant difficulties in its prevention and control. In this study, we conducted a pathological analysis of HPNS through time-integrated large-volume sampling, to clarify the disease characteristics and mechanism of HPNS-afflicted crabs; besides, animal models were constructed to verify the pathological diagnosis. The results showed that the hepatopancreas was the principal target organ of HPNS; multiple correspondence analysis revealed that the main histopathological characteristics included non-interstitial atrophic hepatopathy diseases such as hepatic tubule atrophy, dilated hepatic tubules, and hepatic tubule necrosis. Additionally, the muscles also showed signs of disease, including myofibre atrophy, necrosis, and inflammation. Ultrastructural studies showed prominent apoptosis and autophagy-like alterations in the hepatopancreas of HPNS-afflicted crabs. Further, the establishment of animal models revealed that the double variate stimulation of environmental variables such as abamectin/sewage with nutrition deficiency could result in HPNS-similar lesions. Based on these studies, we concluded that HPNS is a chronic hepatopancreas-initiated energy-consumed disease with a low likelihood of pathogen but a high probability of environment and nutrition.
肝胰腺坏死综合征(HPNS)严重影响中华绒螯蟹(Eriocheir sinensis)产业。然而,由于对该疾病的病因和发病机制知之甚少,给其预防和控制带来了重大困难。在这项研究中,我们通过时间整合的大容量采样对 HPNS 进行了病理分析,以阐明 HPNS 患病蟹的疾病特征和发病机制;此外,还构建了动物模型来验证病理诊断。结果表明,肝胰腺是 HPNS 的主要靶器官;多元对应分析显示,主要的组织病理学特征包括非间质萎缩性肝病变,如肝小管萎缩、扩张的肝小管和肝小管坏死。此外,肌肉也出现了疾病迹象,包括肌纤维萎缩、坏死和炎症。超微结构研究表明,HPNS 患病蟹的肝胰腺中存在明显的细胞凋亡和自噬样改变。此外,动物模型的建立表明,阿维菌素/污水等环境变量与营养缺乏的双重变量刺激可能导致 HPNS 类似病变。基于这些研究,我们得出结论,HPNS 是一种慢性由肝胰腺起始的能量消耗性疾病,病原体的可能性较低,但环境和营养的可能性较高。