Abstract：
Measures of manganese (Mn) status in cattle vary among studies, and no single criterion accurately predicts or diagnoses Mn deficiency and pathologic outcomes. Mn deficiency causes congenital joint laxity and dwarfism (CJLD) when total dietary intake is <20 ppm Mn dry matter (DM) for most of the pregnancy. However, the recommended dietary intake of 40 ppm DM can also result in clinical Mn deficiency. Some studies have found that CJLD occurs in calves from cows fed red clover or silage but not in calves from cows fed hay. The concentration of Mn in the liver is the best indicator of Mn status in neonates and adults but cannot be interpreted in fetuses. Serum, plasma, and whole blood concentrations of Mn are unreliable indicators of bovine Mn status. The primary objective of our report is to present evidence linking CJLD to a primary or secondary Mn deficiency. To predict and diagnose Mn deficiency in cattle, we propose using a combination of clinical signs, dietary Mn, liver Mn at birth and beyond, positive response to Mn supplementation or the replacement of silage with other forages, and ruling out other causes of malformations. By following these recommendations, we expect that CJLD and gestational death will decrease as hepatic Mn concentrations increase at birth. Many publications we reviewed are not statistically sound, and future research should include a statistician from the initial discussions of the study through the final publication.
摘要：
在不同的研究中，牛的锰(Mn)状态的测量各不相同，没有一个单一的标准能准确地预测或诊断锰缺乏和病理结果。当大多数妊娠期的总饮食摄入量<20ppmMn干物质（DM）时，Mn缺乏会导致先天性关节松弛和侏儒症（CJLD）。然而,推荐的40ppmDM饮食摄入量也会导致临床锰缺乏.一些研究发现，CJLD发生在饲喂红三叶草或青贮饲料的奶牛的小牛中，但不发生在饲喂干草的奶牛的小牛中。肝脏中Mn的浓度是新生儿和成人Mn状态的最佳指标，但不能在胎儿中解释。血清,等离子体,和全血的Mn浓度是牛Mn状态的不可靠指标。我们报告的主要目的是提供将CJLD与原发性或继发性锰缺乏症联系起来的证据。预测和诊断牛锰缺乏，我们建议使用临床体征的组合，膳食锰，出生及以后的肝脏锰，对补充锰或用其他牧草替代青贮饲料的积极反应，排除畸形的其他原因。通过遵循这些建议，我们预计CJLD和妊娠死亡率将随着出生时肝脏Mn浓度的增加而减少。我们审查的许多出版物在统计上并不可靠，未来的研究应该包括从研究的最初讨论到最终出版的统计学家。
