肉鸡腹水综合征及肉鸡猝死综合征

肉鸡腹水综合征与猝死综合征是严重影响肉鸡生产的 2种非传染性疾病。据全球 18个国家统计 ,二者的发病率分别为 4 7%与 4 0 % ,年经济损失超过 10亿美元。目前认为 ,这 2种疾病具有同一性质的代谢与病理变化 ,但临床上的表现不同 ,即发病快者为猝死综合征 ,发病慢者为腹水症。主要原因是生长过快 ,使得心肺功能不能适应整体代谢的需求 ,引起肺动脉高压所致。     

A study on pathogenesis of sudden death syndrome in broiler chickens

Sudden death syndrome (SDS) in fast growing broiler chickens has been recognized as a patho-physiological entity for four decades, but its pathogenesis still remains unknown. More recent investigations provided evidence that link SDS to cardiac arrhythmia, but the mechanism triggering arrhythmogenesis and factors responsible for fatal outcome are poorly understood. In order to understand the chain of events leading to SDS in broilers, the present study focused on putative mechanisms that trigger arrhythmia and mechanisms that predispose the myocardium to fatal arrhythmia. Susceptibility of broilers to cardiac arrhythmia under stress conditions was evaluated using a simulated stress test with epinephrine. Detailed histopathological evaluation of the broiler heart was undertaken to identify structural features that may predispose the myocardium to fatal arrhythmia. The simulated stress challenge revealed that many broilers are highly susceptible to stress induced cardiac arrhythmia. In some broilers the stress challenge induced severe ventricular arrhythmia, and the life threatening nature of this arrhythmia was evidenced by the fact that several birds showing the most severe arrhythmic responses, died suddenly within several days after the stress challenge. Examination of hearts of broilers that died of SDS revealed microscopic lesions in the cardiomyocytes, and widespread changes in the sub-endocardial and mural His-Purkinje system (HPS). Immune staining for Caspase-3 confirmed that numerous Purkinje cells in the left ventricular myocardium from broiler chickens that died of SDS were undergoing apoptosis. The observed lesions suggest that the electrical stability of the myocardium was compromised. Taken together, our findings indicate that stress is a most likely trigger of cardiac arrhythmia in broilers, whereas the pathological changes seen in the myocardium and in the HPS in fast growing broilers provide a very conducive milieu for sustained ventricular arrhythmia. In cases where the electrical stability of the myocardium is compromised, even an episodic arrhythmic event may readily degenerate to catastrophic ventricular fibrillation and sudden death. We conclude that the combination of stress and changes in the cardiomyocytes and HPS are the key requisite features in the pathogenesis of SDS.     

Organ weights of normal broiler chickens and those dying of sudden death syndrome

Sudden death syndrome is an economically important condition of fast-growing broiler chickens in which death occurs suddenly with a short, wing-beating convulsion. Gross or histological lesions are not present. Relative weights of internal organs from broilers dead from sudden death syndrome were compared to those of normal broilers to determine differences that might confirm a diagnosis of sudden death syndrome. Relative weights of lung, heart, liver, and intestine from normal broilers were determined at 9, 21, 30 and 42 days of age at various intervals after death. Organ weights stabilized approximately two hours postmortem and relative organ weight declined with age. A diagnosis of sudden death syndrome could not be made on the basis of relative organ weight.     

Dietary induction of sudden death syndrome in broiler breeders

Sudden death syndrome in broiler breeders at the point of lay was a serious problem in Australia for 18 months. This condition was reproduced by a combination of dietary and management practices. Chickens fed a diet low in potassium, phosphorus, protein, and energy had plasma potassium and phosphorus levels significantly lower than the levels seen in the controls. The plasma values of the test breeders were similar to levels seen in field cases. There was a significant difference (P less than 0.01) in the venous acid-base balance between the test chickens and controls. Test chickens were alkalotic and had a 6% mortality rate between 18 and 30 weeks of age.     

The effect of increased mineral levels in the feed on leg weakness and sudden death syndrome in broiler chickens

In two experiments with 98,000 and 40,000 broilers on commercial broiler farms, half of each flock were fed starter, grower and finisher diets with 0.2% added calcium, 0.2% added phosphorus and 0.2% added magnesium. This ration had no significant effect on the incidence of sudden death syndrome but the incidence of leg weakness in broilers on the increased mineral ration was higher in both flocks.

Approximately 28% of the mortality in both flocks was from sudden death syndrome, more than from any other condition. Approximately 20% of the mortality was associated with leg weakness.

     

Skeletal muscle sarcoplasmic calcium regulation and sudden death syndrome in chickens

1. Sudden Death Syndrome (SDS) is a disease of well‐developed, predominandy male broiler chickens where death appears to occur because of cardiovascular failure. The role of skeletal muscle sarcoplasmic calcium regulation as a potential cause of SDS has been investigated.

2. Calcium regulation of skeletal muscle sarcoplasmic reticulum was compared between broiler and Leghorn chickens. Calcium regulation matured from the 2nd to the 11 th week and, at any age, broiler chickens showed significandy lower calcium transport rates and transport efficiencies. The mechanism of calcium transport in broiler chickens was more energy‐consuming than that of the Leghorn chickens.

3. Sarcoplasmic calcium regulation is pivotal for muscle metabolism. As in porcine malignant hyperthermia, weaker calcium regulation might lead to hyperactivation of skeletal muscle, followed by elevated lactic acid concentrations and cardiovascular failure.     

水貂猝死综合征病原检测与分析

为探明水貂猝死综合征发生的病因,本研究对2012年~2014年间黑龙江省部分地区水貂养殖场出现的水貂猝死病例进行病原的检测和分析。结果显示,从猝死水貂体内分离得到10余种致病菌,包括7种革兰氏阴性菌和5种革兰氏阳性菌,大多数分离菌株可以致死小鼠,均具有高度耐药性。同时,PCR检测结果显示猝死水貂体内多数携带有阿留申病毒,其中部分样品还检出新城疫病毒和杯状病毒。综合分析结果表明,水貂猝死综合症的发生主要原因是由阿留申病毒和多种致病菌混合感染引起。本研究为水貂猝死综合症的诊治和预防提供有力的理论依据。     

鸡NLRC5基因启动子多态性分析

为了研究NLRC5基因启动子区的SNP及其对启动子功能元件的影响,采用目标捕获测序和PCR产物直接测序的方法对27个鸡品种和2种细胞的NLRC5基因启动子区进行SNP检测,总共检测到37个SNP位点,其中斗鸡未发现SNP存在,SNP9存在于除斗鸡以外的其他鸡种和细胞。生物信息学软件预测得到NLRC5基因启动子区转录因子结合位点和CpG岛,SNP位点对转录因子结合位点和CpG岛大小均有影响,表明NLRC5启动子区SNP可能通过不同方式影响基因表达调控。     

Observations on swollen head syndrome in broiler and broiler breeder chickens

Chickens on 14 broiler breeder farms were examined at various times throughout their laying cycle. Antibodies to the turkey rhinotracheitis virus were common although they were not always accompanied by clinical signs of the swollen head syndrome. Ninety-nine broiler flocks were tested of which only 20 were serologically positive to the virus. Some of these infections were subclinical. On nine farms where swollen head syndrome occurred several successive flocks were sampled; the syndrome occurred intermittently.     

An epizootiological study of acute death syndrome and leg weakness in broiler chickens in western Canada

In a survey of 51 broiler chicken flocks, the incidence of chickens dying from acute death syndrome and of those with skeletal deformities varied from 0.71 to 4.07% and from 0.46 to 4.08% among the flocks, respectively. The average incidence of those with skeletal deformities was 1.72%; 1.10% were culled in the field, and 0.62% were condemned or downgraded as carcasses. The major types of skeletal deformities were valgus deformation of the intertarsal joint (70%), varus deformation of the intertarsal joint (9%), tibial rotation (7%), and spondylolisthesis (14%). The strain and source of chickens and the management and nutritional practices were recorded for each flock. Statistical analyses were conducted in an attempt to identify factors that might correlate with the incidence of either chickens dying from acute death syndrome or those with skeletal deformities. Results of these analyses are discussed.     

Characterisation of glucose transporter (GLUT) gene expression in broiler chickens

1. Glucose transporter (GLUT) proteins, one of which is the major insulin-responsive transporter GLUT4, play a crucial role in cellular glucose uptake and glucose homeostasis in mammals. The aim of this study was to identify the extent of mRNA expression of GLUT1, GLUT2, GLUT3 and GLUT8 in chickens intrinsically lacking GLUT4. 2. GLUT1 mRNA was detected in most tissues of 3-week-old broiler chickens, with the highest expression measured in brain and adipose tissue. GLUT2 was expressed only in the liver and kidney. GLUT3 was highly expressed in the brain. GLUT8 was expressed ubiquitously, with expression in kidney and adipose tissue relatively higher than that of other tissues. 3. Expression levels of GLUT isoforms 1, 3 and 8 in skeletal muscle tissue were very low compared to the other tissues tested. 4. [3H]Cytochalasin B binding assays on tissue from 3-week-old chickens showed that the number of cytochalasin B binding sites in skeletal muscle plasma membranes was higher than in liver plasma membranes. These results suggest that GLUT proteins and/or GLUT-like proteins that bind cytochalasin B are expressed in chicken skeletal muscles. 5. It is proposed that GLUT expression and glucose transport in chicken tissues are regulated in a manner different from that in mammals.     

Studies on effect of lighting on "Sudden death syndrome" in broiler chickens.

Broiler chicken flocks were studied to determine the mortality from sudden death syndrome occurring in the flocks. The difference in the incidence of the syndrome in pullets and cockerels, and the age at which the most birds are affected were also studied. The weight of sudden death syndrome birds was compared with the flock average and the effect of continuous lighting as opposed to intermittent lighting was examined.The results suggest that; continuous lighting produces more sudden death syndrome deaths than intermittent lighting; that the incidence of sudden death syndrome is higher in cockerels than pullets; that the highest death rate occurred during the third and fourth weeks of life, and that sudden death syndrome birds on the average were heavier than the flock average.     

UK survey of broiler ascites and sudden death syndromes in 1993

1. The mean incidence of deaths from ascites in the UK in 1993 was 1.4% (0.7% in 1991 and 0.9% in 1992) and 0.8% from sudden death syndrome (SDS). In total, the economic loss to the UK Broiler Industry in 1993 as a result of these 2 conditions was 24M. 2. Clear geographical differences emerged in the occurrence of ascites, with, not only the lowest incidences being observed in Northern Ireland, but also the peak of the mortality from ascites occurring much later in the rearing cycle than in other regions on the mainland. 3. In all regions the incidence of SDS was lower than that of ascites but the reason for this disparity remains to be established. 4. Some of the variables associated with the road transportation of day-old chicks from the hatchery to the farm appeared to influence the incidence of ascites. These included distance or time travelled, stocking density, internal lorry temperature and the length of time the lorry was heated before transport as well as the time the shed was heated before chick arrival. Temperature was also an important factor during growth (brooding and finishing). 5. Negative pressure-powered ventilation was preferred in most organisations but more ascites was seen with positive pressure ventilation. However, the lowest incidence of ascites occurred with natural ventilation. There was more ascites relative to shed orientation when the wind direction was from the west compared to the east. 6. This survey identifies the extent of the problem of broiler ascites in the UK and also highlights the importance of good management control of day-old chicks, not only following placement, but even before their arrival on the farm.     

Kaempferol improves carcase characteristics in broiler chickens by regulating ANGPTL3 gene expression

1. The objective of this study was to examine the beneficial effects of kaempferol, a naturally occurring polyphenol, on carcase characteristics in broiler chickens and the mechanisms involved in this regulation.

2. Broiler chickens were randomly divided into 7 groups: control, carrier control, kaempferol (0·3%), kaempferol (0·6%), hypercholesterolemic (HLD), HLD and kaempferol (0·3%), HLD and kaempferol (0·6%).

3. Seven weeks after treatment, carcase characteristics, lipid levels in the blood and liver, expression of hepatic Angiopoietin-like protein 3 (ANGPTL3) mRNA, and expression of adipose lipoprotein lipase (LPL) protein were determined.

4. Treatment with kaempferol (0·3 or 0·6%) significantly increased plasma high-density lipoprotein cholesterol levels, decreased percentage of abdominal fat, thickness of subcutaneous fat, plasma and hepatic total cholesterol and triglyceride concentrations, muscle malondialdehyde level and down-regulated expression of ANGPTL3 mRNA concomitantly with up-regulated expression of LPL protein in normal and hypercholesterolemic broiler chickens.

5. Kaempferol (0·3 or 0·6%) treatment had no significant effect on the values of percentage of breast muscle, percentage of leg muscle, carcase weight and eviscerated percentage.

6. The results suggest that kaempferol improves carcase characteristics by decreasing expression of ANGPTL3 in broiler chickens.     

Use of electrocardiographic analysis for investigation of ascites syndrome in broiler chickens.

This study was conducted (at high altitude [1969 meters]) to determine whether chicks predisposed to cardiac failure and ascites could be identified and followed during growout with non-invasive electrocardiographic (ECG) techniques. ECG recordings were made on 40 chicks at 1 week of age. All recordings were analyzed by quantifying the amplitude in millivolts of the R-, S-, and T-waves in each of the recordings. During the study, ascites-related mortality was 40%, with the majority of the deaths occurring between 5 and 8 weeks of age. Chicks exhibiting moderate-to-severe right ventricular hypertrophy, as identified by ECG analysis at 1 week of age, were predisposed to development of ascites. Thus, the variability in ascites-related mortality observed in field cases may be directly related to the number of predisposed chicks at the time of placement in the broiler house.     

Occurrence of runting and stunting syndrome in broiler chickens in the Sudan

The first outbreak of reovirus infection in broiler chickens was observed in the Sudan in the largest poultry industry of the country. The disease was characterized clinically by growth retardation, lameness, poor feathering, shank depigmentation and occasionally retraction of the head. Grossly there was enlargement of the proventriculus, atrophy of the pancreas and bone abnormalities. Histopathologic changes included hepatitis, nephritis, myocarditis, pericarditis, catarrhal enteritis, pancreatic necrosis, encephalomalacia and ricketic changes. Details were described. Reovirus was isolated from affected birds and reisolated from experimentally infected chicks. Infection was confirmed by immunoelectrophoresis and agar gel precipitation tests.     

Echocardiographic study of pulmonary hypertension syndrome in broiler chickens

Echocardiography was used to study cardiovascular structure and function during the development of pulmonary hypertension syndrome (PHS) in broiler chickens. Body weight-normalized right and left ventricular diameters at both end-diastole (RVDD, LVDD) and end-systole (RVDS, LVDS) were determined weekly in broilers reared under either normobaric (altitude, 96.7 m) or hypobaric conditions (simulated altitude, 2900 m) until 5 wk of age. Hypobaric-exposed broilers had larger RVDD at 3 and 4 wk of age and larger RVDS at 3, 4, and 5 wk of age. Hypobaric-exposed broilers also had larger LVDD at 2, 3, 4, and 5 wk of age and larger LVDS at 4 wk of age. Right (RVFS) and left ventricular fractional shortening (LVFS) were smaller in hypobaric- vs. normobaric-exposed broilers at 3, 4, and 5 wk of age and at 4 wk of age, respectively. Among hypobaric-exposed birds, PHS-positive (+) broilers had larger RVDD and RVDS than PHS-negative (-) broilers on week 3 and on weeks 1 and 3 after hypobaric exposure, respectively. PHS-positive (+) broilers also had smaller RVFS on week 1 after hypobaric exposure. Electrocardiographic and post-mortem data indicated that PHS+ broilers also developed right ventricular hypertrophy when compared with PHS-negative (-) broilers. These results are consistent with the hypothesis that PHS develops as a result of pulmonary hypertension and cardiac overload and suggest that PHS+ broilers have a greater and more persistent reaction to hypoxia than PHS- broilers.     

肉仔鸡猝死综合征的防治

肉鸡猝死综合征是发展肉鸡养殖的大害 ,目前已成为肉鸡生产中一种常见的疾病 ,越来越引起了人们的重视。笔者就赤峰市种鸡场、内蒙古兴发集团、北京昌平、延庆等县的养殖小区、养殖场、养殖户几年发现的 AA肉仔鸡猝死综合征的报告 ,作如下论述。1　临床症状　多发于 8～ 2 1日龄的雏鸡 ,死亡率在0 .5 %～ 1 %。病程短 ,发病前没有任何异样。发病鸡的肌肉丰满 ,体重多超出日龄相应群体的标准体重。发病前的采食、活动、饮水、呼吸等均正常。有的猝死鸡只发病前比正常鸡只表现安静 ,对饲料采食量略低。常常在饲养员进舍喂料时 ,个别鸡只突然…     

肉鸡低血糖综合征的诊治

2005年8月以来，本市郊区乡村许多养鸡专业户饲养的肉鸡不断发病并出现死亡，多以肠炎症状为主，初期排出含未消化饲料的粪便，随后排出橘红色或白色米汤样带血粪便；病鸡运动失调、尖叫、头部震颤并在短时间（1—5 h）内出现高死亡率（大于0．5％）为特征的疾病，     

自由基与肉鸡肺动脉高压综合征

从病因、病理发生及防治方面阐述了自由基与肉鸡肺动脉高压综合征的相互关系。认为快速生长的肉鸡 ,其机体对氧的需要量剧增 ,导致机体相对性缺氧 ,缺氧的组织细胞将产生大量的氧自由基 ,不断攻击生物大分子物质 ,引发一系列自由基链锁反应 ,导致生物膜的结构和功能改变 ,引起血管收缩、血管重构、血栓形成和血管内皮细胞损伤 ,从而导致血流阻力增大 ,肺动脉血压升高。如果用一些自由基清除剂来增强机体抗氧化防御系统的防御功能 ,则可大大地降低肉鸡肺动脉高压综合征的发生。