By Robert J. Van Saun
Lush spring pasture growth is upon us and given the change in our circumstances with the pandemic, this is a much welcome sight. Unfortunately, our beef cattle and potentially sheep and goats may not always take well to this lush pasture growth in the cool, wet spring season. Cool season grasses are known to be low in an essential mineral, magnesium (Mg), in plants growing under these conditions. Magnesium, like calcium (Ca), is essential to normal nerve and muscle function. When Ca is too low in the blood (i.e., hypocalcemia) we see clinical signs of muscle paralysis due to Ca’s role in muscle contraction. This is the disease “milk fever" most often seen in dairy cattle right after calving. When blood Mg concentration is too low (i.e., hypomagnesemia) then we observe clinical signs of “tetany" or stiffness to the muscles due to the role of Mg in stopping muscle stimulation. Death often is the outcome of this disease process if not properly treated in a timely manner (within hours). Ruminant animals are unique in their predisposition to this disease process and both feeding and agronomic management practices are needed to minimize the potential for this disease.
The Magnesium Challenge
Ruminants are not very efficient in their uptake of Mg from their diet. Unlike other species, ruminants only absorb Mg in the rumen through an exchange between potassium (K) and sodium (Na) at the cell level. Early, lush spring (or fall) grass growth is often associated with high plant tissue K concentrations (>2% of dry matter). In the rumen, the cells must push a K ion out into the rumen in exchange for a Na ion and this facilitates cellular Mg uptake. When the rumen contains grasses with high K this pump does not work well resulting in a low efficiency of Mg uptake. High dietary Ca and dietary fat can reduce Mg availability. The animal can reabsorb Mg at the level of the kidneys as the only means of maintaining blood Mg concentration in the face of inadequate dietary uptake. Excess Na intake (i.e., salt) can force more urinary Mg excretion. Although Mg can be found in bone, it cannot be readily released from bone to correct a dietary deficiency like for Ca.
The Forage Challenge
The dietary Mg requirement in ruminant species during pregnancy and lactation is 0.12-0.15% of dry matter. Legume plants, including alfalfa, clovers, birdsfoot trefoil, most often contain high Mg (>0.2% dry matter) and Ca in their tissues, which is protective against the disease. In contrast, grasses often are at or much below the required dietary Mg concentration leading to inadequate intake and increased potential for clinical disease. Higher levels of nitrogen and K (i.e., potash) fertilization will reduce plant Mg content. Excess Ca, sulfates, nitrates, and ammonia can also reduce grass plant tissue Mg content. Sulfates and nitrates can come from water sources or fertilization along with ammonia.
Calcium plays a unique role in this disease process. Excessive Ca in the diet can interfere with Mg uptake. Calcium liming can also lead to reduced plant Mg content. However, the ratio between plant tissue K content to the sum of plant tissue Ca and Mg can be used to define those forages at risk for causing hypomagnesemia. Unfortunately, plant tissue mineral content needs to be converted from % dry matter to a milliequivalents basis for the risk ratio equation to be useful. The table below provides two different examples of this calculation.
Some grasses, especially cereal grains, may contain sucrose compounds that are highly favored by specific rumen bacterial species. Additionally, these cereal grains may contain organic acids (cis-aconitic acid) that will be modified in the rumen by these favored bacteria to generate a chelating compound, tricarballylic acid. This compound will bind to Mg in the diet and prevent it from being absorbed.
Plant tissue needs to be evaluated for mineral content by wet chemistry methods. Near infrared (NIR) methods are not accurate for minerals. The plant K, Ca and Mg content need to be converted from a percent dry matter to millequivalents basis using the conversion variables for each element. Multiply the % dry matter by the conversion factor. Finally, the ratio can be calculated using the milliequivalent values by dividing K by the sum of Ca and Mg. Ratio values exceeding 2.2 are at increasing risk of inducing hypomagnesemia. In the table Forage A has high K, but also higher Ca and Mg resulting in a risk ratio of 1.52. In contrast, Forage B, has slightly higher K coupled with low Ca and Mg generating a risk ratio of 2.91. Forage B would be of concern in inducing hypomagnesemia and preventive measures should be in place if this forage were needing to be fed.
|Plant Mineral||Plant Content (% Dry Matter)||Conversion Factor||Milliequivalent Unit Value|
|Forage A|| || || |
|Forage Risk Ratio||K / (Ca + Mg)|| ||1.52|
|Forage B|| || || |
|Forage Risk Ratio||K / (Ca + Mg)|| ||2.91|
The Disease Challenge
Grass tetany is considered a serious emergency disease process as death can occur within hours of clinical sign presentation. In many cases, animals may be found dead in the morning becoming clinical during the overnight. Initial presentation shows a hyperexcitable animal, very nervous and tense, with excessive response to any loud noises. This hyperexcitability rapidly progresses into the animal becoming laterally recumbent with very stiff extremities. There may be evidence of leg paddling. The animal will expire within a couple of hours without treatment.
Treatment of these animals is an experience. The animal will be hypomagnesemic as well as hypocalcemic due to Mg’s effect on Ca homeostasis. Slow intravenous administration of a Ca-Mg solution to effect is needed. The heart rate should be monitoring as Ca administration can cause heart blockage. Relapses are very common with only intravenous treatment, thus subcutaneous administration of a saturated (50%) magnesium sulfate solution can be administered. Some will also provide oral Mg supplementation via magnesium hydroxide boluses for further protection against a relapse. Once the animal has been treated it is time to leave, quickly, very quickly. For some unclear reason, these animals become extremely aggressive following therapy. Most likely this has to do with changes in Mg concentration of the fluid bathing the brain. I have climbed trees and shown my high school high-jumping skills on numerous occasions fleeing an irate beef cow.
Focus on Disease Prevention
Animal management factors for hypomagnesemia prevention are to ensure adequate dietary Mg intake. This will require forage testing with calculation of forage risk ratio. Use of some legumes in late pregnancy into early lactation may help. Magnesium supplements are not very palatable so just adding them to forage may not be effective. Use of molasses-magnesium free choice licks has been used. You need to ensure these products have a minimum of 5% Mg. Another practical option for beef cattle is to mix equal parts of a trace mineralized salt, magnesium oxide (fine particle size), and distillers grains or soybean meal. The latter items are to improve palatability of the mix and encourage intake.
Agronomic management should focus on pasture plant species and soil management. Perform soil testing to provide the correct amount of nitrogen, phosphorus, and potassium. Phosphorus fertilization has been shown to improve plant Mg content. Applying dolomitic lime to adjust soil pH is preferred to traditional lime as this adds Mg, though dolomitic lime is more expensive. If one could interseed some legumes into a grass pasture, this could minimize hypomagnesemia risk, but may increase risk of bloat on the lush pasture. This interseeding may be minimized by the legume plants not germinating and growing as quickly in the cooler spring weather compared to grasses. The current interest in raising cereal grains as a secondary crop will increase the risk of hypomagnesemia. Watch fertilization practices and be sure to provide additional dietary Mg sources. Otherwise, get your running shoes ready!Source : psu.edu