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饲养场中的瘤胃酸中毒:从病因到预防

Ruminal acidosis in feedlot: from aetiology to prevention.

作者信息

Hernández Joaquín, Benedito José Luis, Abuelo Angel, Castillo Cristina

机构信息

Department of Animal Pathology, Faculty of Veterinary Science, University of Santiago de Compostela, Campus Universitario, 27002 Lugo, Spain.

出版信息

ScientificWorldJournal. 2014;2014:702572. doi: 10.1155/2014/702572. Epub 2014 Nov 12.

DOI:10.1155/2014/702572
PMID:25489604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4247954/
Abstract

Acute ruminal acidosis is a metabolic status defined by decreased blood pH and bicarbonate, caused by overproduction of ruminal D-lactate. It will appear when animals ingest excessive amount of nonstructural carbohydrates with low neutral detergent fiber. Animals will show ruminal hypotony/atony with hydrorumen and a typical parakeratosis-rumenitis liver abscess complex, associated with a plethora of systemic manifestations such as diarrhea and dehydration, liver abscesses, infections of the lung, the heart, and/or the kidney, and laminitis, as well as neurologic symptoms due to both cerebrocortical necrosis and the direct effect of D-lactate on neurons. In feedlots, warning signs include decrease in chewing activity, weight, and dry matter intake and increase in laminitis and diarrhea prevalence. The prognosis is quite variable. Treatment will be based on the control of systemic acidosis and dehydration. Prevention is the most important tool and will require normalization of ruminal pH and microbiota. Appropriate feeding strategies are essential and involve changing the dietary composition to increase neutral detergent fiber content and greater particle size and length. Appropriate grain processing can control the fermentation rate while additives such as prebiotics or probiotics can help to stabilize the ruminal environment. Immunization against producers of D-lactate is being explored.

摘要

急性瘤胃酸中毒是一种由瘤胃D-乳酸过量产生导致血液pH值和碳酸氢盐降低所定义的代谢状态。当动物摄入过量低中性洗涤纤维的非结构性碳水化合物时就会出现这种情况。动物会表现出瘤胃张力减退/无张力伴瘤胃积水,以及典型的角化不全-瘤胃炎-肝脓肿综合征,伴有大量全身症状,如腹泻、脱水、肝脓肿、肺部、心脏和/或肾脏感染、蹄叶炎,以及由于大脑皮质坏死和D-乳酸对神经元的直接作用而出现的神经症状。在饲养场,警示信号包括咀嚼活动、体重和干物质摄入量减少,以及蹄叶炎和腹泻患病率增加。预后差异很大。治疗将基于控制全身酸中毒和脱水。预防是最重要的手段,需要使瘤胃pH值和微生物群正常化。适当的饲养策略至关重要,包括改变日粮组成以增加中性洗涤纤维含量以及增大颗粒尺寸和长度。适当的谷物加工可以控制发酵速率,而益生元或益生菌等添加剂有助于稳定瘤胃环境。正在探索针对D-乳酸产生菌的免疫接种。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/f0d83efd88cd/TSWJ2014-702572.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/0d1ac4c09319/TSWJ2014-702572.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/c7e05663cb93/TSWJ2014-702572.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/f0d83efd88cd/TSWJ2014-702572.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/0d1ac4c09319/TSWJ2014-702572.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/c7e05663cb93/TSWJ2014-702572.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be9c/4247954/f0d83efd88cd/TSWJ2014-702572.003.jpg

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