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

为了建立家畜螺形体病的有效治疗和预防方法，我们研究了由巴贝斯虫引起的狗贫血的机制。结果如下：1.成功地在犬红细胞沉淀层中培养了巴贝斯虫。2. 在培养过程中，红细胞中高铁血红蛋白和丙二醛（脂质过氧化的最终产物）的浓度显著增加。3. 感染红细胞的葡萄糖消耗和乳酸生成以及2,3- dpg浓度也增加。4. 红细胞变形能力降低。5. 从感染犬的外周血中获得的巨噬细胞的红细胞活性显示出与进行性寄生虫病相关的显著增加。6. 强的松龙对感染狗的管理导致这些狗从贫血中短暂恢复。7. 强的松龙对感染犬巨噬细胞的红细胞吞噬活性没有抑制作用。这些结果表明，感染了gibsoni的红细胞由于寄生虫的增殖而受到氧化损伤，感染犬的巨噬细胞对受损红细胞的吞噬活性可能加快，从而导致贫血。

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.