Cattle Today

Cattle Today

cattle today (10630 bytes)

by: Stephen B. Blezinger

Part 2

In the last issue we reviewed and discussed steps and procedures to more accurately assess the status of a variety of minerals in cattle. Producers, veterinarians and nutritionists alike have found that it is important to sample and test the correct tissue (or fluid) in order to get the most accurate indication of what minerals may or may not be deficient in the animal. Previously we discussed the macro or major minerals. This part will elaborate on the trace minerals. One thing that nutritional research (and centuries of production) has shown us is that even the most minutely required nutrients can create huge problems if a deficiency or excess occurs (any type of imbalance).

As mentioned in Part 1, this discussion is based on recent work by Dr. Jeff Hall and the Utah State Diagnostic Lab which has shed some light on the fact that there are correct ways to pull samples and that different types of sampling may be necessary to more accurately assess the status of certain minerals in a given animal. Once again, the following discussion is taken from his paper and presentation at the Inter-Mountain Nutrition Conference held this past January in Salt Lake City.


Cobalt deficiency is associated with deficiency of Vitamin B12 (cobalamin) in ruminants. Deficiency is associated with decreased feed intake, lowered feed conversion, reduced growth, weight loss, hepatic lipidosis (build up of fat in the liver), anemia, immunosuppression, and impaired reproductive function. Cobalt deficiency can also lead to decreased copper retention in the liver. Tissue and serum concentrations of cobalt are generally quite small, as the B12 is produced in the rumen by the microflora. Since cobalt concentrations may not truly reflect the B12 concentrations, the most appropriate analysis for cobalt deficiency is the direct quantification of serum or liver Vitamin B12. However, there are numerous forms of cobalamins that ruminants produce with differing bioactivity, making interpretation of analytical results difficult. Cobalamin is absorbed into circulation and small amounts are stored in the liver. Of the tissues available, the liver cobalt concentration best reflects the animal's overall status, but it may not be truly reflective of Vitamin B12 content.


Copper deficiency is a commonly encountered nutritional problem in ruminants, but copper excess is also commonly encountered, especially in sheep. Clinical signs of deficiency can present as a large array of adverse effects. Reduced growth rates, decreased feed conversion, abomasal ulcers, lameness, poor immune function, sudden death and impaired reproductive function are commonly encountered with copper deficiency. The best method for diagnosing copper status is via analysis of liver tissue, although much testing is 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 fairly depleted. In herds that have tested livers and found a high incidence of deficiency, it is not uncommon for a high percentage of the animals to have “normal” serum concentrations. It is commonly recommended that 10 percent of a herd, or a minimum of 10-15 animals, be tested in order to have a higher probability of diagnosing a copper deficiency via serum quantification. Even with herd deficiency, low serum copper concentrations may only be seen in 20 percent or more of the individuals. Herds that may be classified as marginally deficient based on liver testing may have predominantly “normal” serum copper concentrations. Thus, serum copper analysis should be viewed as a screening method only. Another factor that can influence diagnosis of copper deficiency in serum is the presence of high serum molybdenum. As the copper-sulfur-molybdenum complex that forms is not physiologically available for tissue use, “normal” serum copper content in the presence of high serum molybdenum should always be considered suspect. In addition, the form of selenium supplementation can alter the normal range for interpretation of serum copper status, with selenite supplemented cows having a lowered normal range for serum copper.

Copper deficiency can be diagnosed via analysis of copper containing enzymes. The two most common enzymes that are utilized are ceruloplasmin and superoxide dismutase. Low concentrations of these enzymes in serum and whole blood, respectively, can be used effectively to diagnose for copper deficiency. However, ceruloplasmin concentrations can increase with inflammatory disease so these levels must be evaluated carefully. Finally, higher costs for analysis of these enzymes than that of liver copper analysis often limits their utilization.

Because of the interest over the last few years, excessive supplementation of copper in cattle is a relatively common finding, especially in dairy cattle. Liver copper concentrations greater than 200 ppm are routinely identified. In comparison, the recommended adequate liver copper concentration range in cattle is 25 to 100 ppm.


As an essential component of proteins involved in the electron transport chain and oxygen transport by red blood cells, iron is essential for normal cellular function of all cell types. Iron deficiency is associated with reduced growth, poor immune function, weakness, and anemia. Although offspring are typically born with liver reserves of iron, providing the mother had adequate iron reserves, milk has low iron content which results in iron deficiency over time in animals fed a diet of milk only, as is the case in veal animals.

Both liver and serum concentrations are commonly utilized to diagnose iron deficiency. When using serum to measure iron content, samples that have evidence of hemolysis should not be used, as they will have artificially increased iron content from the ruptured red blood cells. In addition, disease states can alter serum and liver iron concentrations as the body both tries to limit availability of iron to growing organisms and increases the availability of iron to the body's immune cells. Thus, interpretation of iron status should be made with consideration of the overall health of the animal.

Other factors that can be used to assist with diagnosis of iron status include serum iron binding capacity, serum iron binding saturation, red blood cell count, packed cell volume, serum hemoglobin concentration, and ferritin concentration. However, a variety of clinical conditions can cause these values to vary, including bacterial infections, viral infections, other types of inflammation, hemorrhage, bleeding disorders, and immune mediated disorders.


Manganese deficiency in ruminants is associated with impaired reproductive function, skeletal abnormalities in calves, and less than optimal productivity. Cystic ovaries, silent heat, reduced conception rates, and abortions are the typical reproductive effects. Calves that are manganese deficient can be weak, small, and develop enlarged joints or limb deformities. Manganese deficiency, although not reported often, is identified routinely in dairy cattle when tested. Of interest is the fact that most testing of beef cattle finds normal manganese concentrations in liver, blood, and serum. Of the samples available, liver is the most indicative of whole body status, followed by whole blood and then serum. As red blood cells have higher manganese content than serum, hemolysis (rupture of red blood cells due to mishandling) can result in increased serum content. Since the normal serum concentration of manganese is quite low, many laboratories do not offer this analysis because of inadequate ability to detect low concentrations. 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.


As an essential mineral, selenium is commonly identified as deficient in ruminants. Selenium deficiency in ruminants is associated with adverse effects on growth, reproduction, immune system function, offspring, and muscle tissues. “White muscle disease,” a necrosis and scarring of cardiac and/or skeletal muscle, is linked to severe selenium deficiency, although it can be caused by Vitamin E deficiency as well. Reduced growth rates, poor immune function, and impaired reproductive performance can be observed with less severe selenium deficiency.

Diagnosis of a deficiency can be made by analysis of liver, whole blood, or serum for selenium content or by analysis of whole blood for activity of glutathione peroxidase, a selenium-dependent enzyme. The most specific analysis is that of whole blood glutathione peroxidase, as it verifies true functional selenium status. Liver is the optimal tissue to analyze for selenium content, as it is a primary storage tissue. With serum and whole blood, the former better reflects recent intake, while the latter better reflects long term status. Since seleno-proteins are incorporated into the red blood cells when they are made and the cells have a long half-life, selenium content is a reflection of intake over the previous months. In order to adequately diagnose selenium deficiency, the dietary form of the selenium intake by the animals is important. Natural selenium, predominantly in the form of selenomethionine, is metabolized and incorporated into selenium dependent proteins, but can also be incorporated into non-specific proteins in place of methionine. This means that selenium from these sources can be deposited in muscle and other tissues. Inorganic selenium is metabolized and only incorporated into selenium dependent proteins but this does include the very important availability to the synthesis of glutathione peroxidase. Thus, “normal” concentrations in serum and whole blood differ depending on whether the dietary selenium is a natural organic form or an inorganic supplement.


Zinc is an essential mineral that is required by all cells in animals. Zinc plays a role in numerous enzymatic reactions. Deficiencies of zinc are associated with reduced growth, poor immune function, diminished reproductive performance, and poor offspring viability, as well as skin lesions in severe cases. Tissue zinc concentrations do not reflect body status well. Of the common samples tested, liver and serum are the best indicators of zinc status. But, serum and liver zinc can be altered by age, infectious diseases, trauma, fever, and stress. It has been suggested that pancreas zinc content is the best means of truly identifying zinc deficiency. Response to zinc supplementation has shown that some animals having low-end normal liver or serum zinc can still show improvement in some clinical conditions. Thus, liver and serum only verify deficiency when these samples have very low zinc content.


As you can see, obtaining an accurate “picture” of what an animal's actual mineral status is can be more complicated than just pulling blood samples. In many cases, based on this discussion and that in part 1, simple blood or serum samples are almost worthless. Considering this information and discussing with your veterinarian can save a great deal of time and following trails that may lead nowhere as you attempt to solve problems that can greatly affect your herd's health and productivity.

Finally, remember that appropriate diagnosis of mineral status involves thorough evaluation of groups of animals not just one or two. The evaluation should include a thorough health history, feeding history, supplementation history, and analysis of several animals for their mineral status.

Dr. Steve Blezinger is a nutritional and management consultant with an office in Sulphur Springs, TX. He can be reached at 667 CR 4711 Sulphur Springs, TX 75482, by phone at (903) 885-7992 or by e-mail at


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