Davis T Zane, Stegelmeier Bryan L, Panter Kip E, Cook Daniel, Gardner Dale R, Hall Jeffery O
ARS/USDA Poisonous Plant Research Laboratory, Logan, UT 84321, USA.
J Vet Diagn Invest. 2012 Mar;24(2):319-27. doi: 10.1177/1040638711435407.
Sixteen of approximately 500 yearling steers died of acute selenium (Se) toxicosis after grazing on a Se-contaminated range for only a few days. Field studies and chemical analyses identified the predominant toxic plant as western aster (Symphyotrichum ascendens, previously Aster ascendens), which contained over 4,000 ppm Se (dry weight). Several dead animals that were necropsied had acute severe myocardial necrosis characterized by edema and myocyte swelling, with hypereosinophilia, clumping, and coagulation of myocardial proteins. Whole blood from 36 surviving steers was collected and analyzed, and 10 steers with elevated Se concentrations were selected for close monitoring and clinical evaluations. Each steer was weighed, and serum, blood, liver, skeletal muscle, and hair were regularly collected after removal from the Se-contaminated range. One animal that died 18 days after exposure was necropsied and exhibited severe multifocal myocardial fibrosis with extensive hepatic congestion, degeneration, and hemosiderosis. At 180 days postexposure, 2 of the 10 steers were euthanized, and tissue samples were collected. Both steers had rare, small fibrotic foci in their hearts. The Se elimination half-lives from serum, whole blood, liver, and muscle of the recovering steers were 40.5 ± 8.2, 115.6 ± 25.1, 38.2 ± 5.0, and 98.5 ± 19.1 days, respectively. The Se concentration in hair reached a peak of 11.5 ± 5.3 ppm at 22 days postexposure. The findings indicate that cattle are sensitive to acute Se toxicosis caused by ingestion of Se-accumulator plants, with myocardial necrosis as the primary lesion. Some poisoned animals may develop congestive heart failure weeks after the toxic exposure, and in the current study, Se was slowly excreted requiring a relatively long withdrawal time.
在一片受硒污染的牧场放牧仅几天后，约500头一岁小公牛中有16头死于急性硒中毒。野外研究和化学分析确定主要的有毒植物为西部紫菀（Symphyotrichum ascendens，以前称为Aster ascendens），其含硒量超过4000 ppm（干重）。几只进行了尸检的死亡动物有急性严重心肌坏死，表现为水肿和心肌细胞肿胀，伴有心肌蛋白嗜酸性粒细胞增多、聚集和凝固。采集并分析了36头存活小公牛的全血，选择10头硒浓度升高的小公牛进行密切监测和临床评估。每头小公牛称重后，从受硒污染的牧场转移出来后定期采集血清、血液、肝脏、骨骼肌和毛发。一头在接触后18天死亡的动物进行了尸检，显示有严重的多灶性心肌纤维化，伴有广泛的肝脏充血、变性和含铁血黄素沉着。接触后180天，对10头小公牛中的2头实施安乐死并采集组织样本。两头小公牛心脏中均有罕见的小纤维化病灶。康复小公牛血清、全血、肝脏和肌肉中硒的消除半衰期分别为40.5±8.2天、115.6±25.1天、38.2±5.0天和98.5±19.1天。毛发中的硒浓度在接触后22天达到峰值，为11.5±5.3 ppm。研究结果表明，牛对摄入富硒植物引起的急性硒中毒敏感，主要病变为心肌坏死。一些中毒动物在接触毒物数周后可能会发展为充血性心力衰竭，在本研究中，硒排泄缓慢，需要较长的休药期。
