Grass Tetany: A Disease of Many Challenges

Lush spring pasture growth is upon us, with April rains and warming temperatures bringing a new grazing season. Unfortunately, our beef cattle, sheep, and goats may not always adapt to this lush pasture growth in the cool, wet spring season. Cool-season grasses growing under these conditions are known to be low in an essential mineral, magnesium (Mg). Magnesium, like calcium (Ca), is essential for 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 in 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 cellular level. Early, lush spring (or fall) grass growth is often associated with high plant tissue K concentrations (>2% of dry matter) in addition to applied potash fertilizer to promote plant growth. In the rumen, the epithelial cells must push a K⁺ ion out of the cell into the rumen lumen 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 further reduce Mg availability. The animal can reabsorb Mg at 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 the bone mineral matrix to correct a dietary deficiency like 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, and birdsfoot trefoil, most often contain high Mg (greater than 0.2% dry matter) and Ca in their tissues, which is protective against the disease. In contrast, grasses often are at or 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 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 and 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 milliequivalent 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. Plant K, Ca, and Mg content need to be converted from a percent dry matter to millequivalent 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 and 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 needs to be fed.

The Disease Challenge

Grass tetany is considered a serious emergency disease as death can occur within hours of clinical signs. In many cases, animals may be found dead in the morning, becoming clinical during the overnight. The initial presentation shows a hyperexcitable, very nervous, and tense animal with an exaggerated response to 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 is needed to effect it. The heart rate should be monitored 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 relapse. Once the animal has been treated, it is time to leave quickly. For some unclear reason, these animals become extremely aggressive after therapy. This likely has to do with changes in the Mg concentration of the fluid bathing the brain. I have climbed trees and shown my high school high-jumping skills numerous times, 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 the calculation of the forage risk ratio. Using some legumes in late pregnancy and early lactation diets may help. Magnesium supplements are not very palatable, so just adding them to forage may not be effective. Molasses-magnesium-free choice licks have also 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 distiller grains or soybean meal. The latter items are to improve the 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 nitrogen, phosphorus, and potassium amounts. Phosphorus fertilization has been shown to improve plant Mg content. Applying dolomitic lime to adjust soil pH is preferred over traditional lime as this adds Mg, though dolomitic lime is more expensive. If one interseeds some legumes into a grass pasture, this could minimize hypomagnesemia risk but may increase the 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!