by: Stephen B. Blezinger
Ph.D., PAS

Part 1

The management, nutrition and subsequent performance of calves is a topic of constant debate. In general this discussion begins with that period immediately after birth and continues on through the growing animal's life. It's interesting to note that how a young animal performs after birth, in many cases is tied directly to the dam carrying that calf. From conception on, the cow provides for the nutritional needs of the growing and developing fetus. Since this period of growth (from conception to birth) is the most rapid in the life cycle of the animal and since this is the period in which genetic mapping takes place, providing for the nutritional needs of the cow and subsequently the calf is critical.

One very specific area of focus in recent years has been on trace mineral status of the cow, the fetus and subsequently the newborn calf. The status (deficient, low, adequate) can have significant long term effects on how the calf performs. The focus of this article will be to discuss the effects and implications of trace mineral status of the cow and calf.

Mineral Concentrations in the Fetus and New-Born Calf

First, a little background: Both macro- and microminerals are essential nutrients necessary to support nearly all physiologic, metabolic and structural functions of the body. Macro-minerals such as calcium, phosphorus, potassium, magnesium, sodium, chlorine and sulfur, perform mostly structural, acid-base balance, nerve conduction and osmotic functions. Most macro-minerals are homeostatically regulated to various degrees. In other words, extensive mechanisms exist in the body which regulate and maintain proper macro-mineral levels.

Trace minerals are, however, not homeostatically regulated, but are more controlled through movement between “pools.” Micro-minerals such as cobalt, copper, iron, manganese, selenium, iodine and zinc can be found in the body as a component to one or more enzymes. This is known as the biochemical function pool. They are also transported on carrier proteins (transport mineral pool) or stored as metal complexes (storage mineral pool). While trace minerals are stored in a variety of tissues, in general, most storage takes place in the liver. The body makes every effort to maintain a necessary level of activity in the biochemical pool to ensure normal function. The storage pool holds a reserve of mineral and is sensitive to the nutritional status of the animal. If nutrient intake is in excess of requirements, excess intake will be stored until other regulatory processes, reduced absorption or increased excretion, modify mineral retention back into balance. Transport pool is ever changing in reflecting changes relative to both a deficient or sufficient nutrient status. In a situation of an inadequacy or deficiency, liver mineral storage will be mobilized and used to maintain biochemical pool activity until absorptive efficiency, reduced excretion or both can be enacted to raise mineral retention.

The developing fetus is totally dependent upon the availability of essential nutrients through the placenta from the dam's blood. As a result, fetal nutrient status is reflective of maternal nutrient status. Maternal nutrients available to the fetus would include those from the cow's diet as well as reserves mobilized from the cow's body, if needed. Numerous studies have observed the fetus's liver concentrating ability for minerals, i.e., fetal liver mineral concentrations, to exceed maternal values. As such, a decline in maternal liver copper concentration during late pregnancy would be consistent with maternal transfer of minerals to the fetus. In many situations, fetal liver mineral concentrations are twice that of their dams.

During the early periods after calving, almost all essential nutrients are adequately provided for by milk consumption. However, a number of critical micronutrients, namely Cu, Fe, Zn and Se are not provided well by milk consumption alone, thus requiring additional sources to meet daily needs. Because of this, fetal liver nutrient reserves play an important role in maintaining adequate concentrations of these trace elements to support the daily requirements in the milk-consuming, very young animal. Survey data from bovine newborns ranging from birth to three months of age showed significant declines in liver mineral concentrations during this time period. This is illustrated in Figure 1, taken from work by Branum (1999) showing the changes of copper (Cu), zinc (Zn) and iron (Fe) status in the calf from birth through weaning.

Liver mineral reserves are supported by consumption of colostrum, a highly concentrated source of most essential minerals. And, as would be expected, maternal mineral status will influence mineral concentration in colostrum. As colostrum production declines and stops, the availability of the trace minerals from this source also ceases.

Trace Minerals in Milk

Milk is in general a poor source of trace minerals. Trace mineral concentrations for bovine milk are given below (Table 1):

The selenium status of the calf at birth is a reflection of the status of the cow. Attempting to feed selenium through the cow to the calf is not extremely efficient as typical milk is not high in selenium. This can be modified somewhat through feeding of an organic form of selenium (selenomethionine) which has been shown to increase milk selenium content.

Trace Mineral Status and Calf Health

Trace minerals are indirectly or directly associated with a tremendous variety of metabolic processes in animals of all ages. Deficiency diseases affect almost every physiologic and metabolic function and include immune dysfunction (Cu, Zn, Se); developmental abnormalities (Cu, Mn, I); abortion (Cu, I, Se); retained placentas (Cu, Se, I); metabolic disturbances (Co, Fe, Zn, I); and poor growth (Co, Cu, Fe, Se, I, Zn).

Every calf is born with a certain amount of trace mineral deposited in body tissues prior to birth. Adequacy of nutrient reserves in the newborn might explain differences in time frame and severity of occurrences of specific nutrient deficiency disease. If a pregnant dam is severely deficient, mineral transfer to the fetus may be so limiting as to compromise normal functions, resulting in fetal death and abortion. If the deficiency is lessened but still serious, the fetus may die during birth or soon thereafter. If mineral status is sufficient to maintain fetal development, liver reserves may be limited to various degrees. This then may result in clinical deficiency signs in the new calf within only a week or two after birth. In other newborns where liver mineral reserves are slightly better, one might see clinical signs at one month or later or potentially may not see clinical signs at all. Instead this deficiency may result in poor growth and performance. One problem we have, though, as an industry, is that we don't know what mineral storage amount is necessary in the newborn calf's liver to minimize the occurrence of clinical and subclinical problems.

One area of particular interest to trace mineral status is the potential role they play in affecting immune function and response to stress. A study following beef calves to the feedlot found calves from mineral-supplemented cows had greater response to bacterial vaccines, lower morbidity and fewer sick pulls. Within this study, cows supplemented with metal-complex (chelated) minerals and inorganic sulfate minerals had higher liver mineral concentrations compared to no mineral supplementation. Improved health effects were seen primarily in the metal-complex mineral supplementation. It was found that healthy feedlot calves had higher serum zinc concentrations if compared to those experiencing bovine respiratory disease. Evidence is growing to support the belief that trace mineral requirements may be higher than currently recommended by the NRC to maintain adequate immune response, especially during periods of stress.

Trace Mineral Imbalances and Clinical Problems

The difference between sick or poor-doing, and healthy calves is often an optimal trace mineral status and, therefore, effective trace mineral functions. Sub-optimal trace mineral levels in calves can result in a multitude of clinical problems that could affect health/growth negatively as shown by Arthington (2008) and Underwood & Suttle (2001). Let's take a look at some specifics.


Selenium is an essential micronutrient for cattle. The primary role of selenium relates to its role as an essential component of glutathione peroxidase, the enzyme that protects cell and its components from damage that can result from normal immune system responses. Selenium deficiency has been linked to a variety of clinical disease manifestations in cattle. These include nutritional myodegeneration (degredation of nerve tissues), decreased reproductive performance, retained placenta, reduced immunity, and general poor performance. These clinical signs are not related to a specific disease they are often overlooked by producers and veterinarians.

Animals that are raised on diets that are low in selenium will develop selenium deficiency at some level. Soils upon which these forages and feedstuffs are grown play an integral part in selenium deficiency. This creates a geographical distribution which can explain the localized situations associated with disease outbreaks due to selenium deficiency. Many soils simply do not have an adequate amount of selenium present. In addition, factors such as a high soil pH and high sulfur content adversely affect selenium availability. Plant types may play a role as well. Some plants will concentrate selenium whereas others may fail to absorb selenium. For instance legumes tend to be lower in selenium concentration than do grasses. Seasonal variation in rainfall has also shown an effect on plant selenium concentration. As plants begin to dry in the summer and fall selenium concentrations decrease thereby limiting selenium available in feedstuffs.

The selenium status of the calf at birth is a reflection of the status of the cow. As mentioned earlier attempting to feed selenium through the cow to the calf is not extremely efficient as milk is not high in selenium. It is clear that as early as two to three months of age, calves can become marginal in selenium status. This is two to three months prior to the stress of weaning and one to two months prior to the start of vaccination programs.

Low selenium status in calves may cause:

• Weak calf syndrome

• Muscular dystrophy

• Impaired immune response

• Diarrhea

• Pneumonia

• Death in young calves

Selenium has been associated with immunological affects. Selenium deficiency has been shown to inhibit resistance to viral and microbial infections by reducing the number and activity of a variety of cells required for normal immune response.



Zinc is deposited in higher concentrations in the liver of the fetus. The zinc level of newly born calves is fairly well regulated and consistent and not quite as dependent on cow levels as in the case of selenium.

However, liver zinc levels in the calf decrease as it ages. One study reported that the liver zinc concentration in calves was 93 mg/kg (wet weight) at 30 days of age and that it decreased to 57 mg/kg (wet weight) at nine months of age, after which it began to increase. Calves could, therefore, approach weaning with decreasing or marginal zinc levels. This poses a risk where animals are expected to perform in a feedlot situation after weaning due to zinc's effect on appetite and immunity.

Zinc is involved in a variety of systems in the animal including enzyme systems, contributions to male fertility and improved hoof structural soundness.

Depressed zinc status in calves may cause:

• Swollen feet with open, scaly lesions

• Excessive salivation

• Alopecia – loss of hair

• Listlessness

• Reduced appetite

• Reduced feed intake

• Reduced feed efficiency

• Reduced growth

• Impaired immune response


As is obvious, trace mineral levels in the unborn and newborn calf can have significant implications for its growth and development. In Part 2 of this series we will continue this discussion, examining other trace minerals and evaluating strategies to increase the mineral status of the cow and subsequently the calf.

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


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