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Clinico-pathological study on the mechanism of anemia in piroplasmosis of domestic animals

家畜梨形虫病贫血机制的临床病理学研究

基本信息

批准号：
03454110
负责人：
MAEDE Yoshimitsu
金额：
$ 3.78万
依托单位：
Hokkaido University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1992
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-03454110/
关键词：
Babesia Piroplasma Anemia Dogs Erythrocytes Macrophage Erythrophagocytosis Babesia gibsoni 酸化障害

项目摘要

In order to establishethe effective therapy and prevention for piroplasmosis in domestic animals, we investigated the mechanism of anemia induced by Babesia gibsoni in dogs. The results were as follows. 1.Babesia gibsoni was successfully cultured in a settled layer of canine erythrocytes. 2. During the cultivation, the concentrations of methemoglobin and malondialdehyde, an end product of lipid peroxidation, in erythrocytes were significantly increased. 3. Glucose consumption and lactate production by infected erythrocytes, and 2,3-DPG concentration were also increased. 4. Erythrocyte deformability was decreased. 5. The erythrophagocytic activity of macrophages obtained from the peripheral blood of the infected dogs showed a marked increase in association with progressive parasitemia. 6. Administration of prednisolone to the infected dogs resuted in a transient recovery from anemia in these dogs. 7. The erythrophagocytic activity of macrophages was not suppressed by the administration of prednisolone in the infected dogs. These results indicate that erythrocytes infected with B.gibsoni were suffered from an oxidative damage by the multiplication of the parasites, and that the erythrophagocytic activity of macrophages against the damaged erythrocytes might be accelerated in infected dogs, resulting in anemia in these dogs.

为了建立有效的治疗和预防家畜梨形虫病的方法，本实验研究了吉氏巴氏杆菌引起犬贫血的机制。结果如下。1.吉氏巴氏杆菌在犬红细胞的沉降层中成功培养。2.在培养过程中，高铁血红蛋白和丙二醛，脂质过氧化的终产物，在红细胞中的浓度显着增加。3.感染红细胞的葡萄糖消耗和乳酸产生以及2，3-DPG浓度也增加。4.红细胞变形能力降低。5.从感染犬外周血中获得的巨噬细胞的吞噬红细胞活性显示出与进行性寄生虫血症相关的显著增加。6.对感染犬给予泼尼松龙，导致这些犬的贫血短暂恢复。7.巨噬细胞的吞噬红细胞的活性并没有受到抑制的泼尼松龙在感染的狗的管理。这些结果表明，受吉氏B.gibsoni感染的红细胞由于寄生虫的繁殖而遭受氧化损伤，并且在感染的狗中，巨噬细胞对受损红细胞的红细胞吞噬活性可能加速，导致这些狗的贫血。