文章摘要
张丹枫,安树伟,周素明,王国良.大黄鱼(Pseudosciaena crocea)内脏白点病的组织病理和超微病理分析.渔业科学进展,2017,38(4):11-16
大黄鱼(Pseudosciaena crocea)内脏白点病的组织病理和超微病理分析
Histopathology and Ultrastructure of Visceral White-Spots in Pseudosciaena crocea
投稿时间:2016-06-16  修订日期:2016-08-18
DOI:10.11758/yykxjz.20160616001
中文关键词: 大黄鱼  内脏白点病  组织病理  超微病理
英文关键词: Pseudosciaena crocea  Visceral white-spots  Histopathology  Ultrastructure
基金项目:
作者单位
张丹枫 宁波大学 应用海洋生物技术教育部重点实验室 , 浙江宁波 315211 
安树伟 宁波大学 应用海洋生物技术教育部重点实验室 , 浙江宁波 315211 
周素明 宁波大学 应用海洋生物技术教育部重点实验室 , 浙江宁波 315211 
王国良 宁波大学 应用海洋生物技术教育部重点实验室 , 浙江宁波 315211 
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中文摘要:
      利用组织切片及超薄切片电镜技术对患内脏白点病大黄鱼(Pseudosciaena crocea)的肝脏、脾脏和肾脏3种组织进行病理学分析,探讨该病的致病机理。结果显示,大黄鱼的临床症状为为:体表无明显病症,脾、肾、肝等内脏有大量白色结节。;组织病理显示:,肝、肾和脾是感染损伤的主要靶器官,出现组织变性坏死,空泡化严重,炎性细胞浸润;病变组织均出现病理性结节。超微病理显示,病鱼肝、肾、脾细胞超微结构受损严重,尤以线粒体和细胞核损伤明显。线粒体肿胀,嵴断裂消失,空泡化;细胞核核膜破裂,染色质浓缩边集;肾脏和脾脏均发现大量菌聚集成团的病原。研究实验结果表明:,大黄鱼内脏白点病的组织细胞病理变化特征显示了病原菌的入侵和危害,造成鱼体生理代谢紊乱,免疫力和抵抗力下降,鱼体终因无法维持正常的生命活动而导致死亡。
英文摘要:
      The visceral white-spots disease is a serious bacterial disease in cage cultured large yellow croaker (Pseudosciaena crocea) in recent years in Zhejiang Province. The principal clinical signs of visceral white-spots disease among infected fish include multi-focal granulomas in the internal organs, especially in spleen and posterior kidney. In present study, the tissues including liver, spleen, kidney, heart, intestine and muscular tissues collected from infected large yellow croaker, P. crocea were examined histologically and ultrastructurally to elucidate the histological features after being infected by the bacterial disease. The collected diseased fish showed clinical signs of numerous gray, tan or white foci present in the spleen, liver or kidney internally without any external lesions. Histopathological analysis revealed severe degeneration and necrotic changes in multiple internal organs, including liver, spleen and kidney. Moreover, fibrosis in the liver tissue, proliferation of lymphocytes, infiltration of neutrophils and sedimentation of hemoferrin in spleen, and atrophy of glomeruli, deformation of renal tubules and amyloidosis in kidney were observed in this study. Furthermore, serious vacuolization, inflammatory cell infiltration and pathological nodules were observed. The results of ultrastructural analysis showed swelling and distortion of visceral cells in liver, spleen, and kidney. Rarefaction and vacuoles of the mitochondrial structure, disruption and disappearance of the mitochondrial cristae and condensation and margination of the chromatin were also observed in the liver, spleen and liver cells of diseased fish. In addition, large numbers of rod-shaped bacterial cells were packed in kidney and spleen. Our results clearly demonstrated the pathological changes in the cell or tissues among the diseased fish. The changes were characterized by serious visceral granulomas, and the release of toxic metabolites and loss of appetite leading to metabolic disorder and serious mortality of the fish. The study provided valuable data for understanding the pathogenesis of this bacterial pathogen in large yellow croaker.
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