肉鸡胫骨软骨发育不良研究进展

胫骨软骨发育不良(tibial dyschondroplasia,TD)是发生在多种禽类的一种发展迅速的疾病,而以快速生长的肉鸡最为普遍,给肉鸡生产带来严重的经济损失。该病以胫跗骨或跗趾骨近端生长板出现无血管的白色软骨楔为特征。本文结合国内外的最新研究成果,从临床症状、病因、病理变化、防治等方面对该病进行了综述。     

The development of tibial dyschondroplasia in broiler chickens.

Two strains of broiler chickens selected for a high and a low incidence of tibial dyschondroplasia were fed a standard broiler starter ration with and without added chloride. Development of tibial dyschondroplasia was studied by radiography and serial necropsies. Lesions of tibial dyschondroplasia were mild in the low-incidence strain, regardless of ratio. The defect was more severe in the high-incidence strain and most severe in those birds fed the high-chloride ration. An abnormal thickening of the growth plate was apparent in the high-incidence strain as early as 2 weeks of age and became progressively more severe with age. No significant differences were noted in serum calcium, phosphorus, alkaline phosphatase, pCO2, or bone ash between strains of birds or between birds of the same strain fed different rations. Birds fed the high-chloride ration had a higher serum chloride and a lower serum bicarbonate and blood pH than birds on the standard ration.     

肉鸡胫骨软骨发育不良分子机理的研究进展

对参与肉鸡胫骨软骨发育不良的酶、生长因子、维生素D及其受体，基因表达水平进行了综述，它们形成一个复杂的网络调控系统。阐述了它们在肉鸡胫骨软骨发育不良中所起的作用和变化。认为对参与干扰软骨细胞分化的各种基因的深入研究将为基因选择、消除机能紊乱、防治胫骨软骨发育不良的发生开辟新的途径。     

The influence of dietary calcium and phosphorus on tibial dyschondroplasia in broiler chickens

The incidence and severity of tibial dyschondroplasia in broiler chickens were increased by feeding rations containing high levels of phosphorus relative to the level of calcium. Tibial dyschondroplasia was not eliminated by feeding a ration containing 1.5% calcium and 0.5% available phosphorus. Before typical dyschondroplasia developed, chickens fed a high level of phosphorus had uniformly thickened growth plates at 2 weeks of age. The majority of this thickening was due to an increase in the zone of proliferation, identical to that which occurs in calcium-deficiency rickets.     

Effect of casein phosphopeptide and 25-hydroxycholecalciferol on tibial dyschondroplasia in growing broiler chickens

1. An experiment was conducted to investigate the influence of dietary casein phosphopeptides and 25-hydroxycholecalciferol on the incidence of tibial dyschondroplasia (TD) in 14-d-old commercial broiler chickens. 2. Three hundred and twenty broiler chicks (one day old) were randomly allocated to one of 4 dietary treatments. A standard broiler diet was used as the control with the three experimental treatments receiving the control diet supplemented with 10 g casein phosphopeptide/kg, 14 g casein phosphopeptide/kg or 69 microg 25-hydroxycholecalciferol/kg. 3. Those birds fed the diets supplemented with 14g casein phosphopeptide/kg or 25-hydroxycholecalciferol had a lower incidence of TD than both the control and 10g casein phosphopeptide/kg treatments when assessed grossly. 4. The body weight of birds fed the 10 g casein phosphopeptide/kg diet or the 25-hydroxycholecalciferol diet was higher than birds fed the control diet. Although not significant, the body weight of birds fed the 14 g casein phosphopeptide/kg diet was also greater than the control birds. 5. The current experiment demonstrated that both casein phosphopeptide and 25-hydroxycholecalciferol can reduce the incidence of TD in the young broiler chicken. More research is required to explain the unexpected increase in body weight described above.     

Effect of dietary selenium on the development of Fusarium-induced tibial dyschondroplasia in broiler chickens

A trial was conducted to determine the effects of dietary level of selenium on the pathogenesis of Fusarium-induced tibial dyschondroplasia (FITD) in broiler chicks, and to assess the applicability of FITD as an animal model of Kashin-Beck disease of humans. Day-old female broilers were fed diets that were deficient in selenium (0.02 ppm Se), adequate in selenium (0.15 ppm Se), or generous in selenium (0.50 ppm Se). TDP-1, the toxic component of the fungus, was administered to 15 of 26 chicks in each dietary group starting at 1 week of age and continuing until the chicks were killed at 24-30 days of age. Plasma selenium levels and hepatic glutathione peroxidase activity were significantly lower in the selenium-deficient group than in other dietary groups; these parameters were not affected by treatment with TDP-1. The mortality rate of the TDP-1-treated selenium-generous group was significantly less than that in the other TDP-1-treated groups, but there were no differences in the incidence, severity, or character of the FITD lesions among the groups. Thus, the interaction of selenium and TDP-1 did not include an effect on FITD.     

Morphogenesis of Fusarium sp-induced tibial dyschondroplasia in chickens

Tibial dyschondroplasia was induced in female broiler chicks by the incorporation of 2% Fusarium roseum "Alaska" culture into their starter ration. Chicks were placed on this diet at one day of age and maintained until they were killed at four days or one week. Proximal tibial physes were grossly thickened into cone-shaped masses of cartilage by one week of age. Microscopically, lesions were in both ages of treated chickens and were characterized by thickening of the transitional zone which was especially prominent in the center of the growth plate. This zone was unmineralized, avascular, and contained chondrocytes which were crenated and densely eosinophilic. The cartilage matrix was pale and contained some patchy eosinophilic foci. Four growth plates with tibial dyschondroplasia and four normal growth plates from each of the four-day and one-week-old age groups were evaluated based on the following parameters: number of metaphyseal vascular sprouts, distance between the proliferative/transitional junction and the tip of the metaphyseal vascular sprouts, width of the tips of the metaphyseal sprouts, distance between tips of adjacent metaphyseal vascular sprouts, and number of perforating vessels in the proliferative zone. The distance between the proliferative/transitional junction and the metaphyseal sprout tips was greatly increased (p less than 0.01) in the affected four-day and one-week-old chickens compared to age-matched controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Campylobacter succession in broiler chickens

The competitive ability of Campylobacter coli OR12 over C. jejuni OR1 has been examined in experimental broiler chickens following the observation that C. coli replaced an established C. jejuni intestinal colonisation within commercial chicken flocks reared outdoors [El-Shibiny, A., Connerton, P.L., Connerton, I.F., 2005. Enumeration and diversity of campylobacters and bacteriophages isolated during the rearing cycles of free-range and organic chickens. Appl. Environ. Microbiol. 71, 1259-1266]. Co-cultures of C. coli OR12 with C. jejuni OR1, revealed that the two species were able to grow together at similar growth rates in exponential growth phase but if the disparity of the inoculum ratios were >log(10)4 in favour of C. coli OR12, C. jejuni OR1 was observed to prematurely enter decline phase. Chickens were pre-colonised with C. jejuni OR1 at 21-days-old to examine succession in vivo. The birds were inoculated between 2 and 12 days later with C. coli OR12, to determine if the second isolate could efficiently colonise and compete with an established C. jejuni strain. C. coli OR12 were able to co-colonise before replacing C. jejuni OR1 as the dominant species when the birds were more than 27 days of age at the time of administration over a 4-day period. If these criteria were met C. coli OR12 became the dominant isolate otherwise co-colonisation occurred until they were met. C. coli OR12 was also found to displace three alternative C. jejuni strains from pre-colonised chickens challenged with C. coli OR12 at 30 days of age and tested at 40 days. These data raise the possibility of manipulating populations of Campylobacter colonising chickens through competition.     

Swollen-head syndrome in broiler chickens

Swollen-head syndrome is a disease seen in broiler chickens between 4 and 6 weeks of age in Southern Africa. It appears to be caused by a mixed coronavirus and Escherichia coli infection. The coronavirus appears to be of a hitherto unrecorded serotype. The disease is controlled by an attenuated live-virus vaccine and antibacterial medication.     

Salt poisoning in broiler chickens

The clinical signs of salt poisoning in young chickens are thirst, diarrhoea and weakness. When 13 500 broilers are simultaneously affected, the deterioration that occurs in their physical condition and in the litter beneath their feet is dramatic. Two flocks of meat chickens on a small unit in North Otago were affected in this way.     

Salt poisoning in broiler chickens

The incident occurred on a small, owner-operated broiler unit that used home-mixed feed. Two flocks of broilers, one aged 6 weeks and one aged 6 days, developed signs of watery diarrhoea, thirst and weakness. Over 3 days the mortality increased considerably and many birds were noticed to show laboured breathing. The majority of dead birds had an excess of clear fluid in the pericardial sac, oedematous lungs and pale swollen kidneys. Cystic dilation of the testes was conspicuous in several birds from the younger flock killed at 12 days of age. This lesion is a specific indication of sodium toxicity in young broilers. Histological lesions were those associated with cardiovascular collapse and hypoxia. Liver levels of sodium chloride were 4 g/kg of wet weight. Broiler feed samples contained more than 7% sodium chloride whereas the nutritional specifications were for 0.4%. The rations had been correctly mixed and the problem was traced to a faulty batch of meatmeal that had been contaminated by salt used for curing hides.     

表没食子儿茶素没食子酸酯对福美双诱导的肉鸡胫骨软骨发育不良的影响

旨在研究表没食子儿茶素没食子酸酯(EGCG)通过调控热休克蛋白HSP90的表达对肉鸡胫骨软骨发育不良(TD)的影响。试验将120羽1日龄健康AA肉鸡预饲1周后随机分成3组:对照组、TD发生组和EGCG处理组。通过向基础日粮中添加药物的方式,分别对TD发生组和EGCG处理组雏鸡饲喂25mg/kg的福美双,诱发TD。从第3日起,对EGCG处理组雏鸡每天腹腔注射10mg/kg的EGCG。14d后,全部扑杀试验鸡。形态学检查肉鸡胫骨生长板发育状况;HE染色法观察生长板软骨细胞分化和血管生成变化;Real-time PCR和Western blot法分别检测HSP90基因和蛋白表达差异。结果显示,TD发生组雏鸡TD症状明显,HSP90基因和蛋白表达量均明显上升。EGCG处理组雏鸡TD症状明显缓解,HSP90基因和蛋白表达量显著下降;生长板软骨细胞分化和血管浸润显著恢复。由此推测,EGCG可能通过下调HSP90基因和蛋白在TD肉鸡软骨细胞中的表达,恢复TD胫骨病变区软骨细胞分化和血管生成,抑制TD发生,提高肉鸡健康状况。