Cattle Today

Cattle Today

cattle today (10630 bytes)

by: Stephen B. Blezinger

Part 1

Over the past few years we have discussed, at length, many of the factors related to mineral supplementation in beef cattle. We've looked at a variety of sources, discussed the differences between forms and mused over the contribution the forage base makes to providing for the animal's overall requirements. Even with all this, however, we still find herds that suffer from a variety of health issues that can be directly attributed to mineral deficiencies or imbalances. Every year we find producers who report the loss of animals to conditions such as milk fever or grass tetany. We hear reports of poor reproductive function or poor responses to vaccines or therapeutic antibiotic treatments. All of these, once again, can be tied to a problem with a producer's mineral program.

What this tells us is that certain situations call for a means of assessing the mineral status of an animal or herd of animals. We need to be able to take a look at what is going on “inside” the animal, at the tissue or blood/serum levels. This is the only way we can see what we are actually getting into the animal, or where the shortcomings may actually be occurring.

In considering this, our first inclination is to simply pull blood samples and send these off to the Vet diagnostic lab at your local land grant university. Some work done recently by Dr. Jeff Hall who is with the Utah State Diagnostic Lab 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. The following discussion is taken from his paper and presentation at the Inter-Mountain Nutrition Conference held this past January in Salt Lake City.


Testing for minerals has been commonly been performed on diets and/or dietary components to ensure “adequate” concentrations of specific minerals in the animal's diet. However, general mineral analysis does not identify the chemical forms of the variety of minerals used in the formulation or the form in which they exist in the plant or forage material. We know the form can dramatically alter their bioavailability and utilization by the animal. Although not possible for some of the minerals, the most specific means of diagnosing a mineral deficiency is by testing animals for unique functional deficits or deficiencies of specific mineral containing proteins or enzymes. This type of testing is often impractical or completely infeasible in the field. This due largely to individual test costs or rigorous sample handling requirements.

Mineral deficiencies can be suggestively diagnosed by the development of clinical disease or by post-mortem identification of tissue lesions. However, proof of deficiencies often requires analytical verification, since most do not have very unique clinical signs or symptoms. In some instances, circumstantial proof of a deficiency can be provided by positive response to supplementation of a suspected deficient mineral. However, positive response may have nothing to do with the supplementation and may be just a time responsive correction of some other clinical condition. An individual mineral may have multiple means of measurement for identification of deficiencies, but most have one that is more specific than the others. For example, dietary concentrations may or may not be reflective of the amount of bioavailable minerals, or an individual tissue concentration may or may not reflect functionally available mineral concentrations at the target or functional site. The age of the animal being tested also is important for proper interpretation of mineral status. For example, feti accumulate some minerals at different rates during gestation, necessitating adequate aging of the fetus for uses interpretation. In addition, some minerals, for which little is provided in milk, accumulate at higher concentrations during gestation in order to provide neonates with adequate body reserves for survival until they begin foraging. This is especially prevalent with copper, iron, selenium, and zinc. Thus, the “normal range” for these minerals in body tissue storage would be higher in early neonates than in an adult animal.

When individual animals are tested, the prior health status must be considered in interpreting mineral concentration of tissues. Disease states can shift mineral from tissues to serum or serum to tissues. For example, diarrhea can result in significant loss of sodium, potassium, and calcium from the body; acidosis will cause electrolyte shifts between tissues and circulating blood. It is known that infectious disease, stress, fever, endocrine dysfunction, and trauma can alter both tissue and circulating serum/blood concentrations of certain minerals and electrolytes. Thus, evaluation of multiple animals is much more reflective of mineral status within a group than testing individual animals that are ill or have died from other disease conditions.

Sampling Of Live Animals

A variety of samples are available from live animals that can be analyzed for mineral content. The most common samples from live animals are serum and whole blood. These samples are adequate for measurement of several minerals, but it must be recognized that some disease states, as well as feeding times, can result in altered or fluctuating serum concentrations. Other samples from live animals that are occasionally used for analyses include liver biopsies, urine, and milk. However, since milk mineral content can vary through lactation, vary across lactations, and be affected by disease it is not typically used to evaluate mineral status. Furthermore, hydration status (how much water has the animal had to drink) significantly affects urinary mineral concentrations, rendering it a poor sample for evaluation of mineral status.

Post-Mortem Animal Sampling

Obviously taking a tissue sample from an animal that has died is simpler than that of one that is still living and breathing. A variety of post-mortem animal samples are available that can be analyzed for mineral content. The most common tissue analyzed for mineral content is liver, as it is the primary storage organ for many of the essential minerals. In addition, bone is used as the primary storage organ for calcium, phosphorous, and magnesium. Other post-mortem samples that can be beneficial in diagnosing mineral deficiencies include urine and ocular fluid.

Evaluating Individual Mineral Status

Let's take a look at the individual minerals. We can break these into the macro or major minerals in the body which tend to be structural in their contribution and then the micro or trace minerals which are found in much lower concentrations but are critical to much if not all physiological function.


Analysis for calcium deficiency falls into two classes. The first of these is metabolic calcium deficiency, often referred to as “milk fever.” The second is due to a true nutritional deficiency, which is associated with long term dietary calcium deficits. Analysis for metabolic calcium deficiency is aimed at detection of low systemic or circulating calcium content. In live animals, testing is performed on serum to determine circulating calcium content. In dead animals testing is more difficult, as serum collected post-mortem will not accurately reflect true serum calcium content prior to death. However, circulating serum calcium content can be approximated from analysis of ocular fluid. True, nutritional calcium deficiency is associated with weak, poor doing animals that have swollen joints, lameness, weak bones, and a propensity for broken bones. Verification of calcium deficiency requires analysis of bone, since approximately 98-99 percent of the body calcium content is in bone, and serum concentrations are maintained by both diet and turnover of bone matrix. The bone analysis should be performed as fat-free, dry weight to remove the age variability of moisture and fat content.


Phosphorous status is somewhat difficult to measure in animal tissues. Serum and urine phosphorous concentrations can aid in diagnosing deficiency, but with mobilization of bone phosphorous to maintain serum content significant drops in serum and urine may take weeks to develop. Serum phosphorous measurement should be as inorganic phosphorous for adequate interpretation. Longer term phosphorous deficiency can be diagnosed post-mortem by measuring bone or bone ash phosphorous content. Dietary phosphorous and/or response to supplementation are better indicators of deficiency than tissue concentrations unless severe long term deficiency has occurred. The predominant effects of low dietary phosphorous are associated with diminished appetite and its resultant effects. Depressed feed intake, poor growth, and weight loss are common with phosphorous deficient diets. Longer term phosphorous deficiency resulting in impaired reproductive performance, diminshed immune function, bone abnormalities, and pica (depraved appetite – eating dirt, bones, etc.).


Tissue concentrations of potassium poorly correlate with dietary status. Of the animal samples available, serum potassium is the best indicator of deficiency; but disease states can cause electrolyte shifts that result in lowered serum potassium when dietary deficiency has not occurred. In addition, serum that is hemolyzed or left on the clot too long may have falsely increased potassium content due to loss from the red blood cells. Thus, dietary potassium concentrations are a better guide to potassium status. Dietary potassium deficiency affects intake, productivity, heart function, and muscle function. Common clinical signs of severe potassium deficiency include diminished feed intake, reduced water intake, pica, poor productivity and weakness.


As with calcium, analysis for magnesium deficiency falls into two distinct classes. The first is of which is metabolic magnesium deficiency often referred to as “grass tetany.” The second is due to a true nutritional deficiency, which is associated with long term dietary magnesium deficits. Analysis for metabolic magnesium deficiency is aimed at detection of low systemic or circulating content. In live animals, testing is performed on serum to determine circulating magnesium content. It must be noted that ruminants that are displaying recumbency or tetany may have normal serum magnesium, as tissue damage that occurs releases magnesium into the serum from the soft tissues. However, in dead animals testing is more difficult, as serum collected post-mortem will not accurately reflect true serum magnesium content prior to death. Circulating serum magnesium content can once again be approximated from analysis of ocular fluid. The Utah Veterinary Diagnostic Laboratory has been able to confirm clinical cases of hypomagnesemia in numerous post-mortem cases via vitreous fluid analysis. Urine is another post-mortem sample that can be analyzed, since at times of low serum magnesium, the kidneys minimize magnesium loss in the urine. True nutritional magnesium deficiency is not recognized in ruminants, except under experimental conditions. This syndrome is associated with weak, poor doing animals that have weak bones, low bone ash, and calcification of soft tissues. Analytical verification of true magnesium deficiency would require analysis of bone for verification, since approximately 70 percent of the body magnesium content is in bone. The bone analysis should be performed as fat-free, dry weight to remove the age variability of moisture and fat content.


Tissue concentrations of sodium poorly reflect actual dietary deficiency. Of the animal samples available, serum and urine are the best for measuring sodium deficiency, but disease states can cause electrolyte shifts that result in lowered serum or urinary sodium even when dietary concentrations are adequate. Thus, dietary sodium concentrations are a better guide to diagnosing a deficiency.

Dietary sodium deficiency affects feed intake and productivity. Common clinical signs of severe sodium deficiency include diminished feed intake, reduced water intake, poor productivity, and pica.


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, 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.

In Part 2 of this series we will consider the affect that trace minerals have in this situation and what we need to consider when assessing their 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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