产蛋鸡脂肪肝综合征的诊治

鸡的脂肪肝综合征 (FLS)发生于产蛋鸡 ,是以过度肥胖和产蛋下降为特征的一种代谢病。脂肪肝同时有肝出血的病例又被称为脂肪肝出血综合征 (FLHS)。本病主要发生于产蛋期的高产鸡群 ,死亡率高 ,给养禽业造成了很大经济损失。笔者对河南省周口市某鸡场鸡脂肪肝综合征进行了诊治 ,现将有关情况报告如下。1　发病情况2 0 0 2年 3月 ,我市北郊某养鸡厂饲养的 5 0 0 0只艾维茵蛋鸡于 15 6日龄时开始发病 ,且发病鸡连续不断。产蛋量突然减少 ,产蛋率下降了 5 6%左右 ,发病率达到 42 %。经采取一定的防治措施后 ,92 %已基本痊愈 ,恢复了正常的产…     

一例产蛋鸡脂肪肝综合征的诊治

脂肪肝综合征是指脂肪代谢发生障碍的一种营养代谢性疾病,以肝脏积累大量的脂肪、出现肝脏脂肪变性、使肝细胞与血管壁变脆而发生肝出血为主要特征。脂肪肝综合征多发生于产蛋母鸡中,尤其发生在笼养的产蛋高峰期的母鸡中。现将本省海安养鸡专业户的鸡发生本病的诊治情况报道如下。一.发病情况及临诊症状2003年7月中旬,海安大公镇一养鸡专业户所饲养的一批2500只的罗曼蛋鸡,饲养到达220日龄时,产蛋率达到92%,不久有下降的趋势,之后每天都有2～3只死亡,多发生在夜间。到240日龄时,产蛋率下降到70%以下,20天累计死亡40多只。该养鸡户以为是天气…     

浅谈"初产蛋鸡综合症"

近几年来 ,通河县养鸡业有了很大发展 ,特别是商品蛋鸡养殖发展较快 ,已成为养殖业中的支柱产业。蛋鸡在初产期常发生一种以呼吸困难 ,体温升高 ,产蛋无力 ,轻度瘫痪等为特征的疾病。本文将其暂定为“初产蛋鸡综合症”。经 2个月的详细观察 ,现将 6 0 0 0只海塞克斯初产蛋鸡发病情况介绍如下。1　发病经过与发病持续期　 当鸡进入初产期 ,在 1 4 4日龄以后陆续发生本病。在 1 4 4日龄第 1只病鸡出现 ,至 1 92日龄最后 1只病鸡出现 ,鸡群发病持续时间为 48d。在发病持续期内日平均发病鸡数为 36只 ,日平均发病率为 0 .60 % ,累计死亡 2 6只鸡…     

产蛋鸡大肠杆菌病的诊疗报告

鸡大肠杆菌病是由致病性埃希氏大肠杆菌引起。该病原体不但严重危害雏鸡，而且也危害成年鸡，尤其是产蛋鸡。随着集约化养鸡场的迅速发展，鸡大肠杆菌病日趋严重。2002年12月，张家港市某鸡场发生了一起产蛋鸡大肠杆菌病例，现将诊疗情况报告如下。     

笼养蛋鸡脂肪肝综合征的防治

脂肪肝出血综合征是由于笼养蛋鸡摄入能量过高的日粮，而运动又受到限制，导致能量代射失调，造成脂肪过度沉积的一种代谢疾病，本病主要发生在笼养鸡。     

产蛋鸡脂肪肝综合症的防治

发生于产蛋鸡的脂肪肝综合症是一种代谢疾病,以过度肥胖和产蛋下降为特征。该病给养禽业造成很大的损失。 发病因素 该病发生的因素包括:遗传、营养过剩、管理不善、环境温度的改变、应激、过量的雌性激素、黄曲霉素等,都是此综合症的诱因。 主要症状 鸡群中患脂肪肝综合症的鸡和其他鸡明显不同,体况良好,但体重却比相应年龄或生产阶段的鸡重。鸡冠和肉髯     

产蛋鸡大肠杆菌病的诊断与防治

1　发病情况我县某个体鸡场饲养的 80 0只罗曼褐商品蛋鸡 ,至2 0 0 3年 1月 18日共计 30周龄 ,按正常早已进入产蛋高峰期 ,但实际只达到 78%的产蛋率 ,还伴有零星死亡情况。2　临床症状整个鸡群采食量低 ,个别鸡缩颈呆立 ,羽毛逆立 ,两翅下垂 ,眼睛微闭 ,有的呼吸困难 ,部分鸡腹泻 ,排出灰白色或黄绿色稀粪。3　剖检变化心包增厚 ,表面覆着黄白色纤维素性附着物。肝肿大 ,表面覆盖着一层纤维素性附着物。脾脏肿大 ,腹部气囊和胸部气囊有黄褐色纤维素性渗出物 ,肠粘连 ,有破裂的卵黄 ,恶臭。直肠粘膜充血、出血 ,充满黄绿色粪便。4　实验室检…     

产蛋鸡传染性鼻炎的防治

山东省临沂市河东区某养殖户饲养 65 0 0只海兰褐商品蛋鸡 ,全部采用笼养。在开产前按常规进行了鸡新城疫等疫苗的免疫 ,但未接种过鸡传染性鼻炎菌苗。 2 0 0 2年 1月 2 9日 ,鸡2 5 3日龄时 ,暴发一种以打喷嚏、咳嗽、头部肿胀为主要特征的疫病。开始时个别鸡零星发病 ,5ｄ内蔓延至全群 ,有 80 %的鸡出现症状 ,并零星死亡。其死亡率虽不高 ,但因持续时间长 ,难以根治 ,严重影响了蛋鸡的产蛋率。产蛋率下降至70 % ,造成极大的经济损失。养殖户对发病鸡群曾用红霉素、环丙沙星等药物内服 ,但效果不明显。用药时症状减轻 ,一旦停药病情又加重。…     

蛋鸡脂肪肝综合征的病因及其发病机理

脂肪肝综合征(Fatty 1iver Syndrome，FLS)或叫脂肪肝出血综合征(FLHS)是一种脂类代谢紊乱疾病。该病普遍发生于笼养蛋鸡，已成为很多国家的常见病。我国各地均有发生，发病率常在5％左右，占全部死亡鸡的8％～10％。此病多发生于产蛋量高峰期膘情良好的蛋鸡，引起产蛋量逐渐下降(2％～50％)。它给现代密集型养禽业带来了严重的经济损失，因此引起世界各国的重视。     

产蛋期肉种鸡脂肪肝综合征的诊治

某场饲养的9500套肉种鸡在产蛋上高峰期间,其中一栋鸡舍鸡只发病并死亡,经检测诊断为鸡脂肪肝综合征。现将诊治情况介绍如下：     

蛋鸡脂肪肝综合征诱因及其营养调控措施

蛋鸡脂肪肝综合征是一种营养代谢疾病,多发于产蛋高峰期蛋鸡.本文综述了诱发蛋鸡脂肪肝综合征的主要因素及降低蛋鸡脂肪肝的营养调控措施.     

Mycoplasma gallinarum infection in commercial layers and onset of fatty liver hemorrhagic syndrome

Fatty liver hemorrhagic syndrome (FLHS) was observed in each of three trials in which commercial layers were utilized to determine the effect of Mycoplasma gallinarum (MGn) on egg and eggshell quality parameters and egg production. In each of three trials, FLHS occurred 31-54 days later in MGn-inoculated hens as compared with the Mycoplasma-clean (control) hens. In trials 1 and 2, no therapeutic intervention was initiated to ameliorate FLHS. In trial 3, therapeutic intervention was instituted and consisted of the addition of 1 pound of choline chloride/ton of feed. Total mortality recorded throughout the duration of each trial and attributable to FLHS was not significantly different between the control and the MGn-inoculated treatment. However, FLHS-associated mortality in each of the three trials was numerically greater for the control treatment.     

Fatty haemorrhagic liver syndrome in laying hens on diets supplemented with rapeseed products.

Livers of laying hens of Hy-Line No 934E on low erucic acid rapeseed meals and rapeseed oil were studied. Gross lesions in the livers of hens on experimental diets were moderate to severe fatty degeneration, focal necrosis and moderate to severe haemorrhage. Histological examination revealed oedematous foci and lysis of hepatocytes along with large amounts of lipid droplets in the necrotic lesions. Necrotic lesions were not always associated with large haemorrhages. Connective tissue infiltration of older degenerative and haemorrhagic lesions was not extensive. Abdominal haemorrhage from livers occurred when extensive necrosis in the form of hepatocyte lysis and some vascular changes were present, suggesting hepatocytic degeneration caused by toxic products or their metabolites present in rapeseed by-products.     

Fatty liver in dairy cows

An increase in liver fat concentration during the peripartum period is extremely common in dairy cows and, to some degree, is probably normal. When severe, it is associated with clinical problems including increased morbidity and mortality and reduced breeding efficiency. Fatty liver develops when serum NEFA concentrations rise and hepatic uptake of NEFA exceeds the liver's ability to synthesize and secrete lipoproteins. In most cases, hepatic lipid accumulation appears to commence prepartum, in association with rising serum NEFA concentrations and declining serum lipoprotein concentrations. Commonly used clinicopathologic tests of liver function do not yield clearly abnormal results except in animals with extremely high concentrations of liver fat. Clinically useful estimates of hepatic lipid concentration can be obtained in the field by determining the buoyancy of needle biopsy samples in liquids of various specific gravities. Clinically ill animals with liver fat concentrations of greater than 35 per cent by weight have a poor prognosis, and those that do survive will have a protracted convalescence. Treatment of dairy cows with clinical fatty liver should be aimed at reducing further adipose lipid mobilization and promoting hepatic lipoprotein synthesis; however, protocols for therapy have not as yet been evaluated critically. Prevention of fatty liver is more rewarding than treatment. Dry cows should be maintained in a moderately fat condition and fed high-quality, palatable feeds in amounts necessary to met or slightly exceed their energy requirements. Free-choice feeding of high-energy feeds should be avoided in late lactation and during the nonlactating period.