Malinak Chad M, Hofacre Charles C, Collett Stephen R, Shivaprasad H L, Williams Susan M, Sellers Holly S, Myers Elise, Wang Yun-Ting, França Monique
Avian Dis. 2014 Dec;58(4):642-9. doi: 10.1637/10864-051514-Case.1.
Two broiler chicken houses containing 17,500 chicks each experienced an extreme elevation in chick mortality beginning on day 3 after placement. Clinical signs observed upon farm visit included numerous small chicks for their age; depressed, lethargic, and comatose chicks; and chicks huddling near feed pans and under heaters. Necropsied chicks were markedly pale and had atrophy of the thymus and bursa, swollen and edematous proventriculus, erosions in the koilin and in the proventricular-ventricular junction, pale kidneys, and yellowish to brownish-orange liver often with linear pale areas. The chicks had watery blood and hematocrits measured from 9.5% to 18%. Chicken infectious anemia was initially suspected based on the clinical signs and gross lesions. Histopathology revealed multifocal acute hepatic degeneration and necrosis with golden-brown pigment in the cytoplasm of hepatocytes and Kupffer cells, moderate to severe koilin degeneration and fragmentation, multifocal mild to moderate proventricular necrosis, mild to moderate necrosis and loss of enterocytes, blunting of small intestinal villi, lymphoid depletion in the thymus and bursa, erythrophagocytosis in the liver and spleen, and acute renal tubular degeneration and necrosis. Special stains revealed mild to abundant accumulation of copper pigment in the cytoplasm of hepatocytes and iron pigment in the cytoplasm of Kupffer cells. Feed analysis revealed 2140 to 2393 parts per million of copper in the starter ration, and heavy metal analysis detected markedly elevated copper levels in formalin-fixed samples of the liver. Excessive amounts of tribasic copper chloride in the starter ration caused copper toxicosis in these chicks. Similar clinical signs and lesions were reproduced when the suspect feed was used in an experimental pen trial.
两个肉鸡舍，每个舍有17500只雏鸡，在雏鸡入舍后第3天开始雏鸡死亡率急剧升高。农场巡查时观察到的临床症状包括许多雏鸡比正常同龄雏鸡小；雏鸡精神沉郁、嗜睡、昏迷；雏鸡挤在料盘附近和加热器下方。剖检的雏鸡明显苍白，胸腺和法氏囊萎缩，腺胃肿胀且水肿，角质膜和腺胃 - 肌胃交界处有糜烂，肾脏苍白，肝脏呈淡黄色至棕橙色，常有线状浅色区域。雏鸡血液稀薄，血细胞比容为9.5%至18%。根据临床症状和大体病变，最初怀疑是鸡传染性贫血。组织病理学显示多灶性急性肝变性和坏死，肝细胞和库普弗细胞胞质中有金棕色色素，角质膜中度至重度变性和断裂，多灶性轻度至中度腺胃坏死，肠上皮细胞轻度至中度坏死和脱落，小肠绒毛变钝，胸腺和法氏囊淋巴细胞耗竭，肝脏和脾脏有红细胞吞噬现象，以及急性肾小管变性和坏死。特殊染色显示肝细胞胞质中有轻度至大量的铜色素积聚，库普弗细胞胞质中有铁色素积聚。饲料分析显示开食料中铜含量为百万分之2140至2393，重金属分析检测到福尔马林固定的肝脏样本中铜水平显著升高。开食料中过量的碱式氯化铜导致这些雏鸡铜中毒。在试验围栏试验中使用可疑饲料时，出现了类似的临床症状和病变。
