Isler C M, Bellamy J E, Wobeser G A
Can J Vet Res. 1987 Apr;51(2):261-70.
Various hypotheses have been proposed for the pathogenesis of the neurological signs associated with bovine enteric coccidiosis. We undertook a prospective study of cases of bovine enteric coccidiosis with and without nervous signs to test the validity of these hypotheses and explore other possible pathophysiological mechanisms. Clinical, pathological and toxicological data from 12 calves with, and 15 calves without, neurological signs were compared. Calves with neurological signs had a lower liver Cu concentration (p less than 0.01) and a higher plasma glucose concentration (p less than 0.05) than did calves without neurological signs. Hyperglycemia and Cu deficiency may increase the susceptibility to central nervous system damage, but are not likely to account for the onset of neurological signs in calves with enteric coccidiosis. The results of the study suggest that the following are not involved in the pathogenesis of "nervous coccidiosis": disturbance of serum Na, K, Ca, P, or Mg concentration, vitamin A deficiency, thiamine deficiency, anemia, lead intoxication, uremia, Haemophilus somnus meningoencephalitis, severity of coccidial infection, gross alterations in intestinal bacterial flora and hepatopathy.
关于与牛肠道球虫病相关的神经症状的发病机制，已经提出了各种假说。我们对有和没有神经症状的牛肠道球虫病病例进行了一项前瞻性研究，以检验这些假说的有效性，并探索其他可能的病理生理机制。比较了12头有神经症状和15头没有神经症状的犊牛的临床、病理和毒理学数据。有神经症状的犊牛肝脏铜浓度较低（p小于0.01），血浆葡萄糖浓度较高（p小于0.05），而没有神经症状的犊牛则不然。高血糖和铜缺乏可能会增加中枢神经系统损伤的易感性，但不太可能解释患有肠道球虫病的犊牛神经症状的发作。研究结果表明，以下因素不参与“神经性球虫病”的发病机制：血清钠、钾、钙、磷或镁浓度紊乱、维生素A缺乏、硫胺素缺乏、贫血、铅中毒、尿毒症、睡眠嗜血杆菌脑膜脑炎、球虫感染的严重程度、肠道细菌菌群的总体变化和肝病。
