反刍动物瘤胃酸中毒的诊治体会

瘤胃酸中毒是反刍动物由于突然超量采食谷粒类富含可溶性糖类物质饲料,瘤胃急剧产生、积聚并吸收乳酸等物质所致的一种急性、消化性酸中毒疾病,严重影响了反刍动物的生产。对瘤胃酸中毒发病原因、临床症状、防治等方面进行了介绍,以期为反刍动物瘤胃酸中毒的防治提供参考。     

反刍动物瘤胃酸中毒的防治

瘤胃酸中毒是由于反刍动物突然超量采食谷粒等富含可溶性糖类物质,瘤胃内急剧产生、积聚并吸收大量乳酸等有毒物质所致的一种急性消化性酸中毒[1],以往均属于瘤胃积食的范畴。但从20世纪40年代开始,国外学者发现反刍动物过食谷物饲料(高碳水化合物饲料)后,可以导致瘤胃酸中毒。其后国内外许多学者先后对该病进行了研究,特别是20世纪70年代后,各国学者对该病的病因、发病机理和临床表现进行了更深入地探讨,把此病分别称为牛过食豆谷中毒、牛过食豆谷综合征、反刍动物过食症、乳酸中毒、右旋乳酸中毒等。根据酸中毒的临床表现,可分为急性酸中…     

山羊瘤胃酸中毒病的临床症状及防治措施

反刍动物的瘤胃酸中毒,是由于突然超量采食富含碳水化合物及谷类等精料,在瘤胃中积聚产生乳酸,并吸收大量乳酸等有毒物质的一种急性消化性中毒。在山羊发展的过程中,一些发展农户心疼山羊,饲喂了过多的精料,发生了这类疾病,在通过本病治疗中,根据草食动物的特点,不断摸索,收到了治疗山羊瘤胃酸中毒的防治措施。     

反刍动物瘤胃酸中毒研究进展

反刍动物瘤胃酸中毒是养殖过程中常见病之一,严重危害动物的健康生长,甚至导致死亡.因此,积极开展综合防治对策尤为重要.文章综述了瘤胃酸中毒的病理机制和瘤胃酸中毒的预防措施,为反刍动物提供科学合理的饲养管理方案和畜牧业的健康发展提供参考.     

反刍动物瘤胃酸中毒及其微生物学防治研究进展

瘤胃酸中毒是集约化养殖反刍动物的重要营养代谢病,给反刍动物养殖业造成了巨大的经济损失。在临床诊断上应注意对瘤胃酸中毒与瘤胃积食、瘤胃臌胀进行症状鉴别诊断。防治瘤胃酸中毒的瘤胃微生物途径包括两个方面:一方面促进乳酸的利用,如添加电子受体、乳酸利用菌以及酵母和曲霉等真菌;另一方面减少乳酸的产生,如给反刍动物接种牛链球菌和乳酸菌疫苗。通过调控乳酸利用菌群和乳酸产生菌群之间的平衡,控制乳酸的利用和产生,阻止瘤胃酸中毒的发生。     

反刍动物瘤胃酸中毒研究进展

瘤胃酸中毒是危害反刍动物常见的一种代谢病.其产生的主要原因是反刍动物日粮中含有大量的易发酵的碳水化合物饲料或者日粮纤维含量较低,导致瘤胃产生酸性物质过多,引起瘤胃微生物区系失调和瘤胃功能紊乱而造成的.笔者就瘤胃酸中毒的影响因素、类型及营养调控等几方面进行了论述.     

反刍动物发生瘤胃酸中毒的营养机制及其防治

瘤胃酸中毒是危害反刍动物常见的一种代谢病。其产生的主要原因是反刍动物日粮中含有大量易发酵的碳水化合物饲料或者日粮粗纤维含量较低,导致瘤胃产生乳酸过多,引起瘤胃微生物区系失调和瘤胃功能紊乱而造成的。本文就酸中毒的发病机理、防治措施等几方面进行了论述。     

反刍动物瘤胃酸中毒预防及治疗策略

反刍动物瘤胃酸中毒是反刍动物养殖过程中常见的的消化紊乱性疾病,它不仅会使得养殖户的养殖效益降低,而且一定程度上影响畜牧业的健康发展。文章综述了反刍动物瘤胃酸中毒的相关机制以及防治措施,以期为反刍动物的生产实践提供参考。     

反刍动物瘤胃酸中毒的发病机制及其营养调控

瘤胃酸中毒是反刍动物常见的一种代谢病。其产生的主要原因是日粮中含有大量易发酵的碳水化合物,饲料或者日粮粗纤维含量较低,导致瘤胃产生酸性物质过多,引起瘤胃微生物区系失调和瘤胃功能紊乱。本文就反刍动物瘤胃酸中毒的发病机制及其营养调控措施作一综述。     

饲用微生物缓解瘤胃酸中毒机理的研究进展

瘤胃酸中毒是反刍动物生产中常见的代谢疾病。本文阐述了反刍动物瘤胃酸中毒的发生机制和调控手段，并综述了饲用微生物缓解瘤胃酸中毒的机理。     

探讨牛瘤胃酸中毒的中西医结合治疗效果

现代牛养殖与生产中,牛瘤胃酸中毒是比较常见的一种消化性病症,该病发病急、病牛死亡快,所以很容易给奶牛行业带来巨大经济损失。本研究通过分析牛瘤胃酸中毒原因与症状,提出对牛瘤胃酸中毒实施中西医结合治疗方法,观察其治疗效果,以期能够为牛养殖提供有用的治疗建议。     

牛瘤胃酸中毒的血液学及生化指标变化

瘤胃酸中毒是由于牛过量采食含可溶性糖类物质的精饲料,瘤胃内急剧产生、积聚并吸收大量乳酸等物质所致的一种急性消化性酸中毒,危及牛的健康。本文分析了24例病牛的临床表现、血液学和生化指标变化情况。结果表明,病牛主要临床表现为轻症者食欲减退,瘤胃收缩力降低;中度病牛精神迟钝,食欲废绝,呼吸急促;重症病牛陷入昏迷状态,呼吸浅表而快,最后衰竭而死亡。血液学检测结果为病牛的RBC、Hb、Pcv均显著高于健康牛(P<0.05),且随着瘤胃酸中毒的加剧而升高;WBC总数上升,嗜中性白细胞增加而淋巴细胞减少。生化指标检测结果为随病情加重,其血浆二氧化碳结合力及钾、氯、钙等离子不同程度下降;尿素氮含量高于健康牛;轻度酸中毒阶段血糖含量不断增加,但病情严重时则下降。通过本研究,以期为反当动物瘤胃酸中毒的防治提供参考依据。     

瘤胃中乳酸的代谢及其调控机制

有关瘤胃酸中毒发生机制研究表明,瘤胃乳酸的累积可能对酸中毒诱导起重要作用,而高精料日粮下瘤胃乳酸累积主要取决于瘤胃乳酸产生菌和乳酸利用菌间的平衡程度。本文综述了瘤胃微生物对乳酸的代谢机制,包括主要乳酸产生菌[溶纤维丁酸弧菌(Butyrivibrio fibrisolvens)、牛链球菌(Streptococcus bovis)、乳酸杆菌(Lactobacillus)]和主要乳酸利用菌[反刍兽新月单胞菌(Selenomonus ruminantium)、埃氏巨型球菌(Megasphaera elsdenii)],并简要概述了酸中毒的调控方法,旨在为反刍动物瘤胃酸中毒的乳酸中毒机制深入解析提供参考。     

高精料饲粮条件下反刍动物瘤胃适应机制的解析

饲喂高能、高淀粉饲粮是集约化生产中提高反刍动物生产性能的常用策略,但高精料饲粮易引起一系列的营养代谢疾病,其中以瘤胃酸中毒最为常见。反刍动物瘤胃不仅具有消化、吸收营养物质的功能,瘤胃上皮亦是重要的免疫屏障,故瘤胃健康对反刍动物至关重要。本文主要从反刍动物采食高精料饲粮时其瘤胃组织形态、瘤胃上皮适应分子机制和瘤胃微生物区系3个方面的变化进行阐述,以期为高精料饲粮条件下瘤胃适应机制的研究提供参考。     

益生菌防治瘤胃酸中毒的研究进展

瘤胃酸中毒是一种严重的消化系统紊乱,对动物的健康及生产性能危害极大,益生菌进入瘤胃后可以通过稳定瘤胃内微生物群落的平衡,进而维持瘤胃液pH值的稳定,达到缓解瘤胃酸中毒的作用。此外,益生菌还通过刺激机体,恢复其正常的免疫机能,缓解由于酸中毒带来的症状。本文就目前的研究进展进行了综述。     

Induction of a transient acidosis in the rumen simulation technique

Feeding high concentrate diets to cattle results in an enhanced production of short‐chain fatty acids by the micro‐organisms in the rumen. Excessive fermentation might result in subclinical or clinical rumen acidosis, characterized by low pH, alterations in the microbial community and lactate production. Here, we provide an in vitro model of a severe rumen acidosis. A transient acidosis was induced in the rumen simulation technique by lowering bicarbonate, dihydrogen phosphate and hydrogen phosphate concentrations in the artificial saliva while providing a concentrate‐to‐forage ratio of 70:30. The experiment consisted of an equilibration period of 7 days, a first control period of 5 days, the acidosis period of 5 days and a second control period of 5 days. During acidosis induction, pH decreased stepwise until it ranged below 5.0 at the last day of acidosis (day 17). This was accompanied by an increase in lactate production reaching 11.3 mm at day 17. The daily production of acetate, propionate and butyrate was reduced at the end of the acidosis period. Gas production (methane and carbon dioxide) and NH₃‐N concentration reached a minimum 2 days after terminating the acidosis challenge. While the initial pH was already restored 1 day after acidosis, alterations in the mentioned fermentation parameters lasted longer. However, by the end of the experiment, all parameters had recovered. An acidosis‐induced alteration in the microbial community of bacteria and archaea was revealed by single‐strand conformation polymorphism. For bacteria, the pre‐acidotic community could be re‐established within 5 days, however, not for archaea. This study provides an in vitro model for a transient rumen acidosis including biochemical and microbial changes, which might be used for testing feeding strategies or feed additives influencing rumen acidosis.     

Chronic metabolic acidosis in dairy cows]

Complex clinical and clinico-biochemical examination of the blood, urine and rumen liquor in a herd of dairy cows revealed chronical metabolic acidosis accompanied by rumen dysfunction and by a reduced butterfat content of milk. During the first examination of the acid-base state of the blood was almost at a standard level. An increased level of urea in blood plasma and a higher GOT transaminase activity testified to an excessive load on the liver. Urine pH was considerably deviated towards the acidic side and inorganic phosphorus was present in urine in a greater concentration. The pH of rumen liquor was slightly shifted towards alkalinity owing to the release of NH3 from urea in the food ration. The diagnosis--suspect chronical metabolic acidosis--was determined on the basis of the first examination. Chronical metabolic acidosis was definitely proved by the second examination when urea had been excluded from the feed ration. Repeated examinations revealed chronical metabolic acidosis which had originally been accompanied by a higher rumen liquor pH. On the basis of case histories and mechanisms of chronical acidosis, measures were proposed, resulting in an increase of the butterfat content of milk. Chronical metabolic disorders often follow a long-lasting latent pattern, manifesting themselves as a reduced milk yield and lower resistance; the clinical form of disease appears only at a later stage. The system of preventive diagnostics provides information on the changes in the composition of internal medium and of the faeces before a drop occurs in milk and fat production. These measures prevent metabolic disorders and high losses of produce which otherwise remain hidden for a long time.     

牛瘤胃积食病因及防治

牛瘤胃积食又被称为瘤胃急性扩张,是牛养殖中最易发生流行的一种胃部疾病,主要是因为大量的纤维饲料或者易产生气体的膨胀饲料堆积在瘤胃中,不能正常向下运转,造成瘤胃容积显著扩大,内容物长期停滞发酵产生酸性物质,影响前胃机能,形成脱水和酸中毒的一种疾病。在牛养殖中,需要对饮食和饲养管理进行严格的要求,确保整个养殖环境清洁卫生,有效防止牛异食癖引发瘤胃积食的发生,保证牛健康生长。该文主要论述牛瘤胃积食的发病原因、临床症状和防治措施。     

Ruminal acidosis and the rapid onset of ruminal parakeratosis in a mature dairy cow: a case report

A mature dairy cow was transitioned from a high forage (100% forage) to a high-grain (79% grain) diet over seven days. Continuous ruminal pH recordings were utilized to diagnose the severity of ruminal acidosis. Additionally, blood and rumen papillae biopsies were collected to describe the structural and functional adaptations of the rumen epithelium. On the final day of the grain challenge, the daily mean ruminal pH was 5.41 ± 0.09 with a minimum of 4.89 and a maximum of 6.31. Ruminal pH was under 5.0 for 130 minutes (2.17 hours) which is characterized as the acute form of ruminal acidosis in cattle. The grain challenge increased blood beta-hydroxybutyrate by 1.8 times and rumen papillae mRNA expression of 3-hydroxy-3-methylglutaryl-coenzyme A synthase by 1.6 times. Ultrastructural and histological adaptations of the rumen epithelium were imaged by scanning electron and light microscopy. Rumen papillae from the high grain diet displayed extensive sloughing of the stratum corneum and compromised cell adhesion as large gaps were apparent between cells throughout the strata. This case report represents a rare documentation of how the rumen epithelium alters its function and structure during the initial stage of acute acidosis.     

Subclinical rumen acidosis as a cause of reduced appetite in newly calved dairy cows in Denmark: results of a poll among Danish dairy practitioners.

A questionnaire survey was conducted among Danish dairy practitioners to investigate reduced appetite and its relation to subclinical rumen acidosis in post partum dairy cows. The 115 practitioners who responded provided service to 325,300 cows representing 46% of the national herd. Results are presented and discussed in relation to the practitioners beliefs regarding occurrence and value of the diagnostic methods used and treatments applied. The most common diagnoses believed to occur were ketosis (26%), rumen acidosis (22%) abomasal disorders (16%), subclinical hypocalcaemia (15%) and milk fever (15%). Subclinical rumen acidosis was considered to be a commonly occurring underlying condition with significant importance as a cause of reduced appetite. Inadequate feeding strategies were considered to be a main cause of subclinical rumen acidosis. However, the veterinary practitioners were apparently reluctant to imply checking of feeding mangement in their diagnostic work. Possibel reasons for this are discussed. According to the national dairy health recording system subclinical rumen acidosis was rarely reported as a diagnosis among attended cases. Apparently, signs and manifestations of the condition were unclear to the practitioners. It is proposed that the discrepancy is partly due to a lack of precise diagnostic tools available to veterinary practitioners at present and partly due to a missing examination of farm specific feeding management.