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异育银鲫咽碘泡虫病组织病理与病理生理
引用本文:李振伟,陆宏达,操艮萍,刘俊杰,毛毛.异育银鲫咽碘泡虫病组织病理与病理生理[J].中国水产科学,2016,23(6):1339-1350.
作者姓名:李振伟  陆宏达  操艮萍  刘俊杰  毛毛
作者单位:上海海洋大学水产与生命学院,上海,201306
基金项目:水产动物遗传育种上海市协同创新中心(ZF1206),上海市重点学科建设项目(Y1101)
摘    要:咽碘泡虫(Myxobolus pharynae)病是近几年发生在江苏省盐城地区的大丰、射阳和滨海以及周边地区,引起养殖异育银鲫(Carassius auratus gibelio)大批死亡的一种黏孢子虫病,咽碘泡虫只特异地寄生在异育银鲫的咽部组织内,为了阐明该病对鱼体的损伤作用,我们对不同患病时期的异育银鲫的组织病理和疾病中期的病理生理进行研究。组织病理结果表明:疾病初期病鱼咽部略有轻度充血,咽碘泡虫以营养体阶段寄生在咽部黏膜下层的组织中,并开始形成由成纤维细胞包裹的小孢囊,其他组织器官无病理损伤现象;疾病中期由于小孢囊数量增加和囊内营养体分裂增殖并逐步发育为成熟孢子后体积增大,构成的大孢囊使咽部显著膨大,包裹小孢囊的结缔组织囊壁充血,逐步萎缩而变薄,成纤维细胞核固缩坏死,咽部黏膜层中的上皮细胞淡染、核固缩坏死,味蕾失去应有的结构,鳃组织细胞在鳃小片间严重增生,肾部分区域出现细胞坏死,肾小球肿胀,肾小管上皮细胞出现滴状玻璃样变性,肝、脾、肠和前肾无病理变化现象;疾病后期小孢囊囊壁、黏膜下层和黏膜层组织细胞进一步坏死崩解,出现孔洞,成熟孢子、坏死组织和血液一并流出孔洞,病鱼肠腔中有许多来自坏死的咽部组织细胞和成熟孢子,其他组织器官病理变化与疾病中期相似。疾病中期病鱼的病理生理分析结果表明:病鱼红细胞数量和大小、血红蛋白浓度、血栓细胞数量、血清总蛋白、白蛋白、球蛋白、血糖、谷丙转氨酶、谷草转氨酶和碱性磷酸酶都分别极显著低于健康鱼(P0.01),出现贫血;病鱼红细胞脆性、白细胞数、嗜中性粒细胞数、单核细胞数、总胆红素、肌酐、尿素和乳酸脱氢酶分别都极显著高于健康鱼(P0.01);淋巴细胞数和嗜酸性粒细胞数与健康鱼相比,无显著差异(P0.05)。由于咽碘泡虫的寄生部位鱼咽部严重膨大堵塞口咽腔并引发鳃组织增生、肾的损伤和贫血等变化,进一步发展为咽部组织坏死破裂出现孔洞流血,导致病鱼无法摄食和呼吸困难等功能障碍而死亡。

关 键 词:异育银鲫  咽碘泡虫  疾病  组织病理  病理生理
修稿时间:2016/11/9 0:00:00

Histopathology and pathophysiology of Carassius auratus gibelio infected by Myxobolus pharynae
LI Zhenwei,LU Hongd,CAO Genping,LIU Junjie,MAO Mao.Histopathology and pathophysiology of Carassius auratus gibelio infected by Myxobolus pharynae[J].Journal of Fishery Sciences of China,2016,23(6):1339-1350.
Authors:LI Zhenwei  LU Hongd  CAO Genping  LIU Junjie  MAO Mao
Institution:College of Fisheries and Life Science, Shanghai Ocean University, Shanghai 201306, China
Abstract:Myxosporean disease caused byMyxobolus pharynaehas led to high annual mortality in cultured Carassius auratus gibelio in Yancheng City, Jiangsu Province, China, in recent years. The pathogen specifically parasitizes the pharyngeal tissue ofC. auratus gibelio. To examine the lesions of diseasedC. auratus gibelio, histopathological observations at different stages of the disease, and pathophysiological analyses in the middle stage of the disease, were carried out. Histopathological results showed that, at the trophozoite stage,M. pharynae parasitized the pharyngeal submucosa of fish, resulting in slight hyperemia of the pharynx, and sporocysts were formed by fibroblast packages, but no pathological changes were found in other tissues and organs at this early stage of the disease. The pharynx was greatly enlarged in the middle stage of the disease due to the increasing number of small sporocysts and proliferation of trophozoites, which developed into mature spores that formed a large sporocyst. Serious congestion appeared within the walls of sporocysts, which were mainly composed of the connective tissue of fibrocytes, collagenous fibers and elastic fibers. The nuclei of fibrocytes underwent karyopyknosis and necrosis, and there was atrophy in the connective tissue in the walls, which gradually thinned. Pale staining was seen in epithelial cells and taste buds in the pharyngeal mucosa, which eventually became ne-crotic. Cell hyperplasia mainly appeared in secondary gill lamellae. Renal glomeruli expanded, hyaline degenera-tion appeared in renal tubular epithelial cells and necrocytosis occurred in some parts of the kidney. No patho-logical changes appeared in the liver, spleen, intestine or in the head of the kidney. Further necrotic tissues and cells in the walls of sporocysts, and in the pharyngeal mucosa and submucosa, resulted in holes through which mature spores and necrotic tissues passed into the blood stream during the late stage of the disease. Many necrotic cells and mature spores came from necrotic pharynx regions in the intestine. Histopathological changes in other organs and tissues were similar to those in the middle stage of the disease. Pathophysiological analysis in the mid-dle stage of the disease showed that the number and size of red blood cells, hemoglobin, thrombocytes, total pro-tein, albumin, globin, glucose, alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase in the diseased fish were significantly lower than those in the healthy fish (P<0.01). Erythrocyte osmotic brittleness, numbers of white blood cells, neutrophils and monocytes, and total bilirubin, creatinine, urea and lactate dehy-drogenase were significantly higher in the diseased fish than those in the healthy fish(P<0.01). There were no sig-nificant differences in lymphocytes and eosinophils between diseased fish and healthy fish (P>0.05). Diseased fish eventually died because of feeding difficulty and respiratory dysfunction caused by the enlarged pharynx, which blocked the oropharyngeal cavity, leading to hyperplasia in secondary gill lamellae, kidney lesion, anemia and other changes and further necrotic pharyngeal tissues forming a bleeding hole.
Keywords:Carassius auratus gibelio  Myxobolus pharynae  disease  histopathology  pathophysiology
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