Biochemical, clinical manifestation of vitamin D deficiency in calves

І. Ligomina, V. Sokolyuk, I. Sokulskyi, B. Gutyj, V. Dukhnytskyi
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引用次数: 1

Abstract

Today, one of the priority tasks in animal husbandry and veterinary medicine is the creation of a highly productive, stable herd with a stable level of metabolism. A large load on the animal's body reveals high milk productivity; in connection with this, metabolic processes slow down, directly reducing milk productivity and requiring a balanced diet and high-quality feed. An increase in milk productivity is often directly related to metabolic disorders and the appearance of diseases, including the intensity of physiological and biochemical metabolic processes associated with converting a significant amount of energy and nutrients from feed into milk. Metabolic pathologies in animals can be caused by hereditary defects in the metabolism of nucleic acids, congenital insufficiency of enzymes responsible for the synthesis and breakdown of amino acids, disorders of organic acid metabolism, fatty acid deficiency, etc. Timely diagnosis of rickets and rapid therapy in the initial period is essential in treatment because the earlier the diagnosis is made, the easier it is to treat the disease. This will lead to the termination of the further destructive process, the occurrence of bone deformations, and changes in internal organs. The article deals with the issue of vitamin D deficiency in young cattle from a modern perspective. Materials on the classification, etiology, and pathogenesis of vitamin D-deficient rickets in calves are covered. The role of vitamin D in the prevention of rickets and its importance for general animal health and welfare are summarized. It is noted that this disease's characteristic feature is mainly the course's hidden stages. Clinical symptoms of D-hypovitaminosis appear in the late stages of the disease when restoring the animal's health is impossible. The essence of the pathology is a violation of mineralization of the organic matrix of bone tissues (D-hypovitaminosis) or osteolysis of already formed structures. The work aimed to find out the distribution, etiology, biochemical and clinical manifestation of D-hypovitaminosis in calves in one of the farms of the northern districts of Zhytomyr region, which belongs to the natural-geographical zone of Zhytomyr Polissia. The material for the study was clinically healthy calves and calves with rickets aged 1–3 months. The conditions of keeping and feeding animals on the farm were studied. Diagnosis and spread of D-hypovitaminosis among calves 1–3 months old were carried out with the help of clinical and unique methods; first, preference was given to laboratory studies. Clinical manifestations are described, and laboratory features of the course of vitamin D deficiency in animals are presented. It has been established that vitamin D deficiency in calves is quite widespread on the farm. Thus, the subclinical (hidden) course was registered in 45.8 % of animals and the clinical – in 24.1 %. The disease was more often registered in the winter-spring period. The leading cause of the disease in calves is insufficient motor activity (hypodynamia) in the absence of insolation, as well as a low level of feeding: reduced provision of cholecalciferol (25.8 %), violation of the calcium-phosphorus ratio (2.7–4.2:1 versus 1.5–2.0:1), deficiency of microelements – cobalt, zinc, copper, the provision of which was, respectively, 57.6, 85.6 and 96.2 % of the need. Pathognomotic manifestations of the disease in calves are licking, allotriophagia, thickening of carpal joints, partial resorption of the last ribs and tail vertebrae, and loose teeth. Vitamin D deficiency prevents the efficient absorption of calcium and phosphorus in feed. With vitamin D deficiency, only 10–15 % of feed calcium and 50–60 % of phosphorus are absorbed. The most informative laboratory markers for diagnosing pathology are determining cholecalciferol content, total calcium, inorganic phosphorus, alkaline phosphatase activity, and its bone isoenzyme in blood serum.
犊牛维生素D缺乏的生化、临床表现
今天,畜牧业和兽医学的首要任务之一是创造一个具有稳定代谢水平的高产、稳定的畜群。动物身上的大负荷表明产奶量高;与此相关,代谢过程减慢,直接降低产奶量,需要均衡的饮食和高质量的饲料。牛奶产量的提高往往与代谢紊乱和疾病的出现直接相关,包括与将大量能量和营养物质从饲料转化为牛奶相关的生理和生化代谢过程的强度。动物的代谢病理可由核酸代谢的遗传缺陷、氨基酸合成和分解酶的先天不足、有机酸代谢障碍、脂肪酸缺乏等引起。佝偻病的及时诊断和早期快速治疗在治疗中至关重要,因为越早诊断,越容易治疗该病。这将导致进一步破坏过程的终止,骨骼变形的发生,以及内部器官的变化。本文从现代的角度探讨了小牛维生素D缺乏症的问题。资料的分类,病因学,和发病机制的维生素d缺乏性佝偻病犊牛覆盖。综述了维生素D在预防佝偻病中的作用及其对动物健康和福利的重要性。本病的特点主要是病程的隐性分期。d -维生素缺乏症的临床症状出现在疾病的晚期,此时动物的健康已无法恢复。病理的本质是骨组织有机基质矿化的破坏(d -维生素缺乏症)或已形成结构的骨溶解。本研究旨在了解日托米尔北部地区某农场犊牛d -维生素缺乏症的分布、病因、生化及临床表现,该地区属于日托米尔波兰自然地理区域。研究的材料是临床健康的犊牛和1-3个月的佝偻病犊牛。对该农场饲养动物的条件进行了研究。运用临床和独特的方法对1 ~ 3月龄犊牛d -维生素缺乏症进行诊断和传播;首先,优先考虑实验室研究。本文描述了动物维生素D缺乏症的临床表现和实验室特征。已经证实,小牛缺乏维生素D的情况在农场里相当普遍。因此,45.8%的动物出现了亚临床(隐藏)病程,24.1%的动物出现了临床病程。该病多发生在冬春季节。小牛患病的主要原因是缺乏日照时运动活动不足(动力不足),以及喂养水平低:胆钙化醇的供应减少(25.8%),钙磷比(2.7-4.2:1 vs 1.5-2.0:1)违反,缺乏微量元素——钴、锌、铜,其供应分别为需求的57.6%、85.6和96.2%。小牛的发病表现为舔食、异食症、腕关节增厚、最后一根肋骨和尾椎部分吸收和牙齿松动。缺乏维生素D会阻碍饲料中钙和磷的有效吸收。缺乏维生素D时,饲料中钙的吸收率只有10 - 15%,磷的吸收率只有50 - 60%。诊断病理最具信息性的实验室标记是测定血清中胆骨化醇含量、总钙、无机磷、碱性磷酸酶活性及其骨同工酶。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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