基于肠道微生物探讨蛋鸡脂肪肝出血综合征的研究进展

蛋鸡脂肪肝出血综合征(FLHS)是常发生于高产蛋鸡的营养代谢病,其临床表现主要为蛋鸡脂质代谢紊乱引起的肝脏脂质沉积、产蛋量骤降及急性死亡,造成严重经济损失,是当前集约化养殖需要重点关注的疾病。肠道微生物作为参与机体生长发育、免疫代谢的重要角色,参与宿主的脂质合成与转运,保持肠道屏障的完整性以避免有害物质通过血液循环损伤肝脏并影响其功能,同时肠道微生物代谢产物的丰减与转化方向也会对肝脏健康产生或好或坏的影响。目前认为FLHS的发病机制主要包括营养、遗传、激素、肠道微生物等多种因素,“肠-肝轴”也受到当前治疗肝脏疾病的广泛关注。作者以肠道微生物为切入点,通过对蛋鸡常见肠道微生物及其与脂质代谢相关的功能进行总结,回顾了肠道微生物在脂质代谢与FLHS方面的相关研究,着重介绍了肠道微生物及其代谢产物在FLHS发生发展过程中可能产生的作用机理,以期从肠道微生物的角度解释FLHS的可能发病机制,并在生产实践中找到通过调节肠道微生物预防或治疗FLHS的方法,推动养禽业的发展。     

蛋鸡脂肪肝出血综合征的发病原因及其防治

蛋鸡脂肪肝出血综合征是蛋鸡养殖生产中的常见和多发的营养代谢性疾病综合症,临床表现以突然发病、产蛋量下降和高产蛋鸡突然死亡为主要特征。特别是进入产蛋高峰期的鸡发病,常会给养殖户带来很大的经济损失。 近年来,笔者在动物门诊工作中,发现蛋鸡脂肪肝出血综合征（FLHS）有逐年上升的趋势,现笔者对该病的发病及诊疗小结如下,供业界同仁参考     

鹅源新城疫病毒感染鸡的临诊症状及病理变化

用鹅源新城疫病毒BY株人工感染25日龄雏鸡，同时用鸡新城疫病毒标准强毒F48E8株作为攻毒对照，观察2株病毒感染鸡的临诊症状、病理变化，并加以比较。结果，2株病毒都可致试验鸡100％发病和死亡。BY组鸡于感染后51h出现症状，发病后48h全部死亡，主要大体病变为喉头严重出血、腺胃乳头或腺胃与肌胃交界处轻微出血、肠道黏膜局灶性出血坏死，病理组织学变化主要为消化器官和免疫器官内的细胞显著变性、坏死及出血等；F48E8组鸡于感染后72h出现症状，发病后36h感染鸡全部死亡，所表现的病理变化与BY组鸡相似，但腺胃和肠道的出血病变比BY组鸡显著。     

鸡脂肪肝出血综合征(FLHS)的中药防治

脂肪肝出血综合征(Fatty liver hemorrhagic syndrome,FLHS)是由于饲料中营养物质过剩而某些微量营养成分不足或不平衡,造成鸡体内代谢机能紊乱而引起的,以肝脏发生脂肪变性出血而急性死亡为特征的疾病.     

蛋鸡脂肪肝出血综合征的病因研究进展

蛋鸡脂肪肝出血综合征(FLHS)是一种代谢性疾病,营养、内分泌、遗传和环境等因素都可影响其发生。日粮中能量过高或蛋白不足是诱发FLHS的主要因素,能量、蛋白来源也影响FLHS的发生。日粮中脂肪酸来源影响FLHS的发生,动物性脂肪较易引起FLHS,适量添加植物油可降低肝脏脂肪含量。雌激素水平升高可引起肝脏脂肪含量增加,与FLHS存在一定的量效关系。甲状腺素和孕酮可降低肝脏脂肪含量,防止出血发生。FLHS易感品系UCD-3蛋鸡肯定了遗传因素对该病的影响。空间不充足或必要活动受限制,导致能量过剩是FLHS发生的重要诱因。肝脏脂肪沉积并不总是引起肝脏出血,脂质过氧化物分解生成大量脂质自由基引起细胞损伤,可能是肝脏脂肪含量升高导致出血的分子机制。     

笼养产蛋鸡出血性脂肪肝综合症及其防治(二)

五、预防引起FLHS的原因可能与遗传、营养、环境和激素等因素有关,可使肝脂代谢平衡失调。鸡群中如有个别鸡因脂肪肝而死亡,或有脂肪肝症状时,该群鸡就有可能存在着脂肪肝的潜在威胁,影响鸡群产蛋率,就要找出影响肝脂代谢平衡失调的具体原因,来纠正饲养管理,加以防治。     

鹅鸡共发副粘病毒病的诊疗

扬州市某养鹅专业户放养45日龄鹅200只，30日龄和15日龄草鸡各20余只，未防疫。鹅于40日龄左右有少部分发病，精神萎顿、不食、拉黄白色稀粪；在鹅发病后，鸡也有类似症状而先后发病死亡。发病后1周内，第1批鸡已全部死亡，发病后10d，第2批鸡也开始出现同样症状，并死亡2只。鹅、鸡曾服用土霉素等抗菌素治疗无效。1病理变化　　鹅的主要病理变化为全身皮下出血，胸骨出血；肝脏肿大，有白色坏死点；脾脏肿大，表面呈白色花斑状坏死，大小不等；心冠脂肪出血；嗉囊与腺胃连接处有严重出血斑块，腺胃呈条纹状出血；胰腺出血或有坏死灶；整个…     

蛋鸡脂肪肝出血性综合征的病例报告

<正>蛋鸡脂肪肝出血综合征(FLHS)是一种营养代谢性疾病,主要受营养、内分泌、遗传和环境等因素的影响。经剖检后,发现其腹内壁附着一层厚厚脂肪层,肝大明显,呈黄褐色、质脆并有油腻感,包膜下有部分点状出血。个别鸡该病或肝破裂而死亡。本病会造成产蛋率大幅度下降和蛋鸡死亡,从而造成经济损失。近年来该病发生增加,现简要介绍昌邑市下营镇某村庄蛋鸡普遍发生一种产蛋异常情况,供读者参考。1发病情况一养殖户饲养蛋鸡3500羽,近段时间产蛋率由90~95%下降     

疑似鸡出血性脂肪肝综合症的观察

我县永安乡养鸡专业户刘××的蛋鸡场于1985年8月份以来产蛋量下降,产蛋母鸡零星发病、死亡。经剖检及化验室诊断为疑似鸡出血性脂肪肝综合症(FLHS)。现报告下。     

中药防治鸡脂肪肝出血综合征的研究进展

鸡脂肪肝出血综合征（FLHS）几乎是与笼养鸡技术的开发、发展一致的,其普遍发生于笼养蛋鸡,其次为过肥的肉用仔鸡。FLHS的发病率根据鸡的品种、日粮组成、环境等因素而有差异,通常为鸡群的1％-2%,有的高达5％-7％,甚至15％以上。死亡率一般低于5％,有时高达20%.FLHS还能导致鸡群的产蛋量下降,影响产蛋高峰期的出现,目前己成为许多国家养殖业的常见病。随着我国养殖业迅猛发展,集约化养殖规模的不断扩大,浙江、安徽、河南、河北、四川等地都有发生FLHS的报道,且有逐年增多的趋势,对养殖业造成了很大的危害。     

Effects of a high energy and low protein diet on hepatic and plasma characteristics and Cidea and Cidec mRNA expression in liver and adipose tissue of laying hens with fatty liver hemorrhagic syndrome

Cidea and Cidec are two members of Cell death‐inducing DNA fragmentation factor‐alpha‐like effector family proteins, which could be involved in lipid or fat metabolism. To better understand the roles of Cidea and Cidec in fatty liver hemorrhagic syndrome (FLHS), 150 healthy 155‐day‐old Hyline Brown laying hens were randomly divided into control group (fed with basic diet) and experimental group (fed with high‐energy low‐protein [HELP] diet). Analysis of the liver by tissue sectioning and hematoxylin and eosin staining showed that the HELP diet induced micro‐vesicular steatosis in laying hens. Subsequently, based on the liver color scores and the range of lipid accumulation observed in histological examination, we classified livers with <50% vacuolization as mild FLHS and >50% as severe FLHS. The results showed that the levels of Cidea and Cidec mRNA expression were markedly elevated in the liver and adipose tissues with FLHS and the levels of Cidea and Cidec mRNA expression in the liver with severe FLHS were significantly higher than that in the liver with mild FLHS. Thus, the present study revealed that the Cidea and Cidec genes may be involved in pathways of FLHS formation.     

鸡脂肪肝出血综合征发生过程中脂质代谢与血清甲状腺激素水平变化

探讨血清甲状腺激素水平与鸡脂肪肝出血综合征（FLHs）发生之间的关系。选用14日龄青脚麻鸡160只,按体质量随机分为对照组和FLHS组。对照组饲喂基础日粮,FLHs组饲喂高脂日粮（基础日粮＋10％牛油）的同时肌肉注射苯甲酸雌二醇（剂量为2．4mg／kg,每周3次,共3周）,试验期为28d。结果显示,试验期间,FLHS组鸡的体温明显降低;28和42日龄时,FLHS组鸡的平均体质量与平均采食量均显著高于对照组（P〈0．05或P〈10．01）;皮下脂肪厚度、肌间脂肪宽度、肝指数、肝脂率、皮脂率、腹脂率升高;血清TG、TC和LDL—C浓度均显著高于对照组（P〈0．05或P％0．01）,而血清HDL—C浓度均显著低于对照组（P〈0．01）;血清T3、T4和FT3水平降低,特别在试验后期降低更明显,而血清FT4水平变化不显著;同时FLHS组血清TP、ALB和PA浓度均比对照组有所提高。结果提示,FLHS可引起血清甲状腺激素水平的下降,而甲状腺激素水平的下降进一步造成脂质代谢紊乱,参与了鸡FLHS的发生。     

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.     

甜菜碱预防蛋鸡脂肪肝出血综合征的研究

本试验旨在研究甜菜碱对蛋鸡脂肪肝出血综合征的预防效果。选用300日龄海蓝褐蛋鸡120只,随机分为3组,每组4个重复,每个重复10只,在自由采食、饮水和光照16 h的条件下,分别饲喂正常日粮（代谢能11.30 MJ/kg,粗蛋白质17.20%）、高能量低蛋白质日粮（代谢能12.81 MJ/kg,粗蛋白质13.04%）和添加1000 mg/kg甜菜碱的高能量低蛋白质日粮60 d。于试验期第1、30、60天,每组取8只鸡采血制备血清和采集肝脏样品及腹脂,测定血脂含量、肝脂率和腹脂率,结合产蛋性能及病理学变化,综合判定脂肪肝出血综合征(fatty liver hemorrhagic syndrome,FLHS)的发生及甜菜碱的预防效果。结果表明,与对照组相比,饲喂高能量低蛋白质日粮30 d即可引发FLHS,饲喂60 d则病情进一步加重;而在高能量低蛋白质日粮中添加1000 mg/kg甜菜碱后,饲喂30 d时甜菜碱可显著抑制FLHS的发生,具有很好的预防作用,但饲喂60 d时甜菜碱的预防作用减弱。     

Failure of oestradiol administration to induce fatty liver haemorrhagic syndrome in the laying hen

Studies were carried out to investigate whether the administration of oestradiol to laying hens induced fatty liver-haemorrhagic syndrome (FLHS). Short term oestradiol administration (up to 6 d) significantly increased liver size and plasma lipid concentration but had no effect on liver lipid concentration or hepatic lipogenic enzyme activities. Longer-term hormone treatment (up to 28 d) again significantly increased liver size and plasma lipid concentration. Liver lipid concentration was substantially reduced and lipogenic enzyme activity significantly reduced in oestradiol-treated birds. These effects had some similarities to those seen in oestrogenised immature birds and were additive to the effects of endogenous oestrogen in the laying bird. There were no deaths from FLHS and oestradiol treatment did not cause liver haemorrhages or affect egg production.     

Different susceptibility to fatty liver-haemorrhagic syndrome in young and older layers and the interaction on blood LDL-C levels between oestradiols and high energy-low protein diets

1. The objective of the study was to investigate the susceptibility of young and older laying hens to fatty liver-haemorrhagic syndrome (FLHS) and to evaluate the reliability of different blood lipid fractions for predicting or diagnosing FLHS.

2. Forty young hens and 40 older hens were caged individually. Each group of hens was randomly allotted to four treatments for 21 days: either a control, an oestradiol group, a high energy-low protein diet (HELPD) group or a HELPD + oestradiol group. Blood levels of oestradiol, triglyceride (TG), cholesterol (CHOL), high density lipoprotein-cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C), liver total lipids, hepatic haemorrhagic scores and productive performance were assessed.

3. In older hens, β-oestradiol increased (P < 0.05) liver total lipids, hepatic haemorrhagic scores and the incidence of FLHS but reduced (P < 0.05) productive performance; however, such changes were not observed in young hens.

4. In two groups of hens, serum TG, CHOL and HDL-C levels were increased (P < 0.001) by β-oestradiol. Hens with FLHS had higher serum TG, CHOL and HDL-C (P < 0.001) than non-FLHS birds in the older layer group of hens.

5. An interaction (β-oestradiol × HELPD) (P < 0.05) for LDL-C levels was observed in both groups of hens. In young hens, β-oestradiol induced a decrease (P = 0.004) in serum LDL-C levels but the effect was attenuated by HELPD. In older hens, HELPD caused an increase (P = 0.02) in serum LDL-C although the effect depended on the presence of β-oestradiol.

6. In conclusion, older layers were more susceptible to FLHS than young layers after oestradiol treatment. Blood TG, CHOL and HDL-C rather than LDL-C levels can be used as a prediction tool for the overall susceptibility to FLHS in older rather than young layers. There were interactions between oestradiol and HELPD on blood LDL-C levels in laying hens.     

Effect of selected dietary antioxidants on fatty liver‐haemorrhagic syndrome in laying hens

1. Single comb White Leghorn hens of an inbred line highly susceptible to fatty liver haemorrhagic syndrome (FLHS) were fed supplemented dietary ascorbic acid (200 mg/kg), α‐tocopherol (75 mg/kg), or L‐cysteine (3 g/kg, and 6 g/kg) for 28 d in order to evaluate the potential therapeutic effect of these compounds against the disease.

2. Supplementation of ascorbic acid, α‐tocopherol, or a low level of L‐cysteine (3 g/kg) did not significantly affect any of the hepatic variables evaluated. Hepatic glutathione was not increased by the supplementation of dietary L‐cysteine.

3. L‐cysteine supplemented at a level of 6 g/kg decreased hepatic dry matter and fat contents without affecting the hepatic malondialdehyde or the liver haemorrhagic score.

4. Because one of the predisposing factors of FLHS is a high hepatic fat content it was concluded that dietary supplementation of L‐cysteine (6 g/kg) may be useful in the prevention of the disease.     

Effect of dietary flaxseed, flax oil and n-3 fatty acid supplement on hepatic and plasma characteristics relevant to fatty liver haemorrhagic syndrome in laying hens

1. Two experiments were carried out to investigate the effect of dietary flaxseed, flax oil and n-3 fatty acid supplementation (Dry n-3) on hepatic fat content, plasma triglycerides, hepatic haemorrhage score, egg production, food intake and body weight in an inbred line of Single Comb White Leghorns (UCD-003) predisposed to fatty liver haemorrhagic syndrome (FLHS) and normal SCWL hens. 2. Feeding diets containing 100 g/kg ground flaxseed, 40 g/kg flax oil, or 100 g/kg Dry n-3 reduced body weight and significantly reduced hepatic fat content compared to feeding the control diet with animal and vegetable oil as a fat source. 3. Hepatic malondialdehyde, an indicator of lipid peroxidation within the liver, was not significantly affected by dietary treatment. 4. Normal SCWL hens tended to have higher egg production, greater body weight, greater food intake and higher blood triglyceride concentrations than UCD-003 hens, although the strain effects were not significant. Liver weight as a percent of body weight was significantly lower in normal SCWL hens. Treatments by strain interactions were not found. 5. The result suggested that dietary flaxseed, flax oil and Dry n-3 decrease hepatic fat content and reduce body weight, 2 of the predisposing factors believed to contribute to FLHS onset. However, haemorrhages were still apparent in both strains regardless of treatment, indicating that other unknown underlying mechanisms may also be responsible for FLHS.     

苜草素对产蛋后期蛋鸡脂肪肝出血综合征的预防作用

本试验旨在研究苜草素对产蛋后期蛋鸡脂肪肝出血综合征(FLHS)的预防作用。选用500日龄京红1号产蛋鸡1 008只,随机等分为7组,每组6个重复,每个重复24只鸡。Ⅰ组为对照组,饲喂常规饲粮(代谢能11.10 MJ/kg,粗蛋白质17.68%);Ⅱ~Ⅶ组为试验组,饲喂高能低蛋白质饲粮(代谢能12.87 MJ/kg,粗蛋白质13.84%),并分别在饲粮中添加0、200、400、600、800、1 000 mg/kg苜草素。试验期60 d。结果表明:1)与对照组相比,高能低蛋白质饲粮组(Ⅱ组)蛋鸡第30天时即可表现出明显的FLHS病理特征,第1~30天平均日采食量、产蛋率、蛋重、产蛋量显著降低(P0.05),料蛋比显著升高(P0.05),第1~60天趋势更加显著(P0.05);第42天蛋白高度和哈氏单位显著降低(P0.05)。2)在高能低蛋白质饲粮中添加不同梯度的苜草素均能降低FLHS发生率,提高第1~60天的平均日采食量、产蛋率、产蛋量,降低料蛋比;提高第42天的蛋白高度、哈氏单位。由此可见,高能低蛋白质饲粮能够诱导蛋鸡FLHS,补充苜草素具有预防作用。