Symptoms of vitamin and mineral deficiency vary depending on the deficiency. Serious conditions may arise in cattle after an extended period of consuming diet that lacks needed levels of key vitamins or minerals.
Selenium deficiency is commonly identified in ruminants, but rarely in dairy cattle. Selenium deficiency can lead to reduced growth rates, poor feed efficiency, poor immune function, impaired reproductive performance, and damage to muscle tissues. “White muscle disease,” a necrosis and scarring of cardiac and/or skeletal muscle, is linked to severe selenium deficiency; though, it can be caused by vitamin E deficiency as well. The recommended adequate liver selenium concentration range in adult cattle is 0.25 to 0.50 ppm. In comparison, late-term fetal or neonatal liver with 0.35 to 0.65 ppm selenium is considered normal.
Cattle can be diagnosed by analyzing liver tissue, whole blood, or serum for selenium content. The most specific analysis involves whole blood glutathione peroxidase, an enzyme that shows functional selenium status. Liver is the primary storage tissue, while serum reflects recent intake and whole blood reflects long-term intake. In order to properly diagnose selenium deficiency, the form of the selenium intake has to be taken into account. “Normal” concentrations in serum and whole blood differ depending on whether the dietary selenium is a natural form or an inorganic supplement.
Copper deficiency is one of the most commonly encountered nutritional problems in ruminants in the Intermountain West. Copper excess is also commonly encountered—especially in sheep. Clinical signs of deficiency can present as reduced growth rates, decreased feed conversion, abomasal ulcers, lameness, poor immune function, sudden death, achromotrichia, and impaired reproductive function. Copper deficiency is rare in non-ruminants.
The recommended adequate liver copper concentration range in adult cattle is 25 to 100 ppm. In comparison, normal late-term fetal or neonatal liver should have 65 to 150 ppm copper.
The best method for diagnosing copper status is analyzing liver tissue, although testing can be performed on serum. Deficiency within a herd will result in some animals that have low serum copper concentrations, but serum content does not fall until liver copper is significantly depleted. Thus, serum copper analysis should be viewed as a screening method only.
Cows will do all they can to ensure adequate copper and selenium are in calves when they are born. Cows’ bodies will actually deplete their own reserves to ensure neonatal adequacy. As such, neonates diagnosed with copper or selenium deficiencies are proof of maternal deficiencies. Since both minerals are essential components of the immune function, this maternal deficiency likely results in poor colostrum quality and inadequate neonatal protection even in calves that get adequate volumes of colostrum.
Manganese deficiency in ruminants is associated with impaired reproductive function, skeletal abnormalities, and less-than-optimal productivity. Cystic ovaries, silent heat, reduced conception rates, and abortions are reported reproductive effects. Newborn calves that are manganese deficient can be weak, small, and develop enlarged joints or limb deformities. Manganese deficiencies in beef cattle are most commonly seen in areas of highly alkaline soils, due to much poorer plant uptake of manganese.
Manganese deficiency, although not often reported, is identified routinely in tested dairy cattle. This may be due to high calcium and phosphorous content of dairy rations, which can decrease the bioavailability of manganese. Overall, response to supplementation has frequently been used as a means of verifying manganese deficiency, but it is critical that a bioavailable form be utilized. For more information, see https://digitalcommons.usu.edu/extension_curall/86/
Dr. Jeffery Hall, PhD email@example.com, Utah State University Department of Animal, Dairy, and Veterinary Sciences