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秦蕾, 王印庚, 张立敬, 戴继勋. 蟹栖异阿脑虫寄生大菱鲆及其组织病理学研究[J]. 水生生物学报, 2007, 31(5): 618-628.
引用本文: 秦蕾, 王印庚, 张立敬, 戴继勋. 蟹栖异阿脑虫寄生大菱鲆及其组织病理学研究[J]. 水生生物学报, 2007, 31(5): 618-628.
QIN Lei, WANG Yin-Geng, ZHANG Li-Jing, DAI Ji-Xun. HISTOPATHOLOGY OF TURBOT ASSOCIATED WITH MESANOPHRY S CARCINI PARASITE[J]. ACTA HYDROBIOLOGICA SINICA, 2007, 31(5): 618-628.
Citation: QIN Lei, WANG Yin-Geng, ZHANG Li-Jing, DAI Ji-Xun. HISTOPATHOLOGY OF TURBOT ASSOCIATED WITH MESANOPHRY S CARCINI PARASITE[J]. ACTA HYDROBIOLOGICA SINICA, 2007, 31(5): 618-628.

蟹栖异阿脑虫寄生大菱鲆及其组织病理学研究

HISTOPATHOLOGY OF TURBOT ASSOCIATED WITH MESANOPHRY S CARCINI PARASITE

  • 摘要: 论文首次报道了蟹栖异阿脑虫(Mesanophryscarcini)在养殖大菱鲆体内的寄生情况以及所引起宿主的组织病理学变化。观察结果表明,感染的苗期大菱鲆的大部分器官组织包括皮肤、鳍、鳃、眼、脑、心脏、肝脏、肾脏、脾脏、胰腺和消化道等以及器官组织间隙中都发现了寄生的蟹栖异阿脑虫,属于全身性感染;而对于成鱼,蟹栖异阿脑虫主要寄生于皮肤、鳍和鳃等器官组织;严重感染者,蟹栖异阿脑虫可侵入其脑、肝脏、肾脏和心脏等器官组织,但数量不多。蟹栖异阿脑虫在大菱鲆体内的寄生能够引起病鱼各器官组织发生不同程度的组织病理学改变。该病在幼鱼和成鱼身上所表现出较一致的病理学特征为:鳃小叶呼吸上皮细胞增生;脑膜炎和脑组织液化性坏死;肾脏和脾脏造血组织坏死;肝脏中央静脉和窦状隙扩张;肌纤维发生凝固性坏死和眼的脉络膜充血、水肿;单核巨噬细胞浸润。研究认为,蟹栖异阿脑虫寄生引起的鳃损害使病鱼呼吸困难,窒息是病鱼发生死亡的主要原因,而虫体寄生导致的各器官组织变性,坏死,使得病鱼器官功能衰竭可加速鱼的死亡。另外,文中还探讨了蟹栖异阿脑虫入侵大菱鲆的可能途径,认为破损的皮肤和鳃是入侵的主要途径。研究结果告诉我们,在大菱鲆养殖过程中防止鱼体擦伤,保持池底清洁对于预防疾病的发生非常重要;对该病的治疗应采取外部杀虫和内部口服药物相结合的方式。

     

    Abstract: Turbot,Scophthalmus maximus(L.) is a very important commercial species in Europe, from where it was introduced into China in 1992. With the success in artificial breeding from 1998, the commercial culture has spread rapidly along the coast of North China. Recently, yields have reached 20,000MT, valued at 200 million RMB. From 2003, a novel disease in turbot associated with Mesanophrys carcini infection was identified in China, causing high mortality and economic losses. This paper first reports the histopathology of this disease, aiming at supplying theoretical foundation for the prevention and therapy. In the case of infected larvae, ciliates could be found infin, skin, gills, eye and internal organs such as brain, heart, kidney, spleen, pancreas, liver and the alimentary tract, which indicated the systemic infection to the larvae. In infected large turbot, the ciliates were predominantlyfound in the skin, fin and gills. And in the severe cases, they could invade the brain, liver, kidney and heart with little numbers. Histopathological studies revealed that various pathological changes to the tissues associated with Mesanophrys carcini. The affected larvae and large turbot showed the consistent histopathological changes, including hyperplasia of the branchial epithelium, meningitis, liquefaction of the brain, necrosis of haemopoietic tissue in the kidney and spleen, dilation of central vein and sinusoids in the liver, coagulative necrosis of muscle fibers, congestion and oedema of choroid in the eye and proliferation of mononuclear macrophages. Mesanophrys carcini caused damage to the gills, resulting in the asphyxia of the diseased turbot. This is probably the major causes of death in affectedfish. And organsfailure as a result of necrosis associated with presence of Mesanophrys carcini is also responsible for the death of affected fish. In addition, we discuss possible route of entry into the host, considering that injured skin and gills are the main route for the Mesanophrys carcini infection. The study tells us that keeping pond cleaning, avoiding scratching the fish surface are very necessaryfor the prevention of the Mesanophrys carcini infection; the therapy should include not only external treatment but also the internal.

     

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