|本期目录/Table of Contents|

[1]许晓芸,陈锦民,冯建军,等.迟缓爱德华氏菌感染美洲鳗鲡后的组织与超微病理观察[J].集美大学学报(自然科学版),2017,22(6):17-23.
 XU Xiaoyun,CHEN Jinmin,FENG Jianjun,et al.Pathological and Ultrastructural Changes of American Eel(Anguilla rostrata)Infected by Edwardsiella tarda[J].Journal of Jimei University,2017,22(6):17-23.
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迟缓爱德华氏菌感染美洲鳗鲡后的组织与超微病理观察(PDF)
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《集美大学学报(自然科学版)》[ISSN:1007-7405/CN:35-1186/N]

卷:
第22卷
期数:
2017年第6期
页码:
17-23
栏目:
水产、食品与生物工程
出版日期:
2017-11-28

文章信息/Info

Title:
Pathological and Ultrastructural Changes of American Eel(Anguilla rostrata)Infected by Edwardsiella tarda
作者:
许晓芸12陈锦民12冯建军12郭松林12
(1.集美大学水产学院,福建 厦门 361021;2.鳗鲡现代产业技术教育部工程研究中心,福建 厦门 361021)
Author(s):
XU Xiaoyun12CHEN Jinmin12FENG Jianjun12GUO Songlin12
(1.Fishery College of Jimei University,Xiamen 361021,China;2.Anguilla Modern Engineering Research Center of Industrial Technology of the Ministry of Education,Jimei University,Xiamen 361021,China)
关键词:
迟缓爱德华氏菌人工感染美洲鳗鲡组织病理超微病理
Keywords:
Edwardsiella tardaartificial infectionAnguilla rostratapathological changesultrastructural pathology
分类号:
-
DOI:
-
文献标志码:
A
摘要:
用迟缓爱德华氏菌(Edwardsiella tarda)人工感染美洲鳗鲡(Anguilla rostrata),采集死亡或濒死鳗鲡的脏器,从组织病理学角度研究其致病性。结果表明:感染迟缓爱德华氏菌的美洲鳗鲡可发生急慢性炎症。急性炎症时可见肝组织多发性坏死灶,周围可见巨噬细胞聚集,肝细胞变性、坏死;慢性感染时易见病鱼肝组织大面积高度纤维化,肝细胞坏死,细胞间质增宽,间质内充满胆汁和单核巨噬细胞,肝脏中央静脉血管壁扩张。急性感染时肾间质与肾小管局灶性坏死,肾小管上皮细胞空泡化,部分上皮细胞脱落入管腔,呈蛋白管形;慢性炎症反应时肾间质血窦内单核巨噬细胞大量增生并形成早期肉芽肿,肾小管管腔内出现大块异物,肾小球毛细血管肿胀,肾小囊内出现红染的纤维素性渗出液。染病鳗鲡脾脏红白髓正常结构消失,红髓内出现大量淋巴细胞,白髓区有崩解的红细胞;白脾区淋巴细胞坏死后纤维化形成增生性结节;心肌纤维出现局灶性坏死,肌纤维溶解、断裂呈索状或团块状。染病鳗鲡的超微病理变化表现为肾小球毛细血管扩张,血管内深染的内皮细胞增多;肾小管上皮细胞肿大,有些肾小管上皮细胞坏死溶解,细胞核消失,肾小管管腔内充满蛋白样物质和坏死细胞碎片;肾间质结缔组织溶解消失,有大量的吞噬细胞和感染菌菌体;部分肾小管上皮细胞胞质内线粒体数量减少,线粒体肿胀,嵴断裂,内质网断裂,核糖体从内质网上分离、散开;坏死的造血细胞核高度浓缩,电子密度极高。
Abstract:
To study the pathogenicity of Edwardsiella tarda to farmed American eels(Anguilla rostrata)and pathological changes,Edwardsiella tarda was used to infect American eel.The general pathological changes were presented as follows:Acute and chronic inflammations were observed in American eels infected by E.tarda.In the acute inflammation,multiple necroses were noticed in the liver,with the accumulation of macrophage and liver cell degeneration and necrosis.In the chronic infections,liver cell showed necrosis and large area of fibrosis;stromal of the cells were widened and full of bile and mononuclear macrophages,and central venous wall in the liver was dilated.Acute infection resulted in renal tubular and renal interstitial focal necrosis,and renal tubular epithelial cell vacuoles and some epithelial cells shedding into the lumen.Chronic inflammation resulted in mononuclear macrophages proliferation in the renal interstitial and early granuloma formation;large pieces of foreign bodies occurred within the lumen of the glomerular and capillary in the glomerular was swelling,and renal capsule appeared red dye cellulose exudate.The normal structure of spleen red and white pith disappeared,while a large number of lymphocytes appeared in the red pulp,and disintegrated red blood cells were presented in white pulp area.Fibrosis hyperplastic nodules were presented in the area of lymphocytes necrosis in spleen.Myocardial fibers showed focal necrosis,muscle fibers dissolution and fractured as cordlike or lumpy.The ultrastructural pathological changes were studied in American eels infected by E.tarda.The glomerular capillary was dilation,and intravascular stained endothelial cells increased;tubular epithelial cells were swelling,and some tubular epithelial cells were necrosis and melting,leaving nuclei disappeared;tubule lumen was filled with proteinlike substances and necrotic cell debris;renal interstitial connective tissue dissolved and disappeared,with a large number of phagocytic cells and infectious bacteria.The number of cytoplasm mitochondria in some epithelial cells of renal tubules reduced;mitochondria were swelling and cristae were broken,and endoplasmic reticulum was broken;ribosomes were left and spread from the endoplasmic reticulum.The nucleuses of necrosis hematopoietic cells were highly concentrated,with high electron density.

参考文献/References:

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备注/Memo

备注/Memo:
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更新日期/Last Update: 2017-12-28