Grass tetany: It | Beef Magazine

2022-06-18 18:28:14 By : Ms. Laura Melody

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Dr. Jeff Lehmkuhler, and Dr. Michelle Arnold, University of Kentucky | May 11, 2022

Classic “grass tetany” is a rapidly progressing and potentially fatal disorder caused by low magnesium level in the blood, also known as “hypomagnesemia”. It is usually seen in older, lactating beef cows when grazing young, succulent grass in early spring, particularly during cool and rainy weather.

Other common names for this disorder, including spring tetany, grass staggers, wheat pasture poisoning, and lactation tetany, reflect the season of the year, symptoms seen, types of forage, or physiology of the animals most often involved.

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Magnesium is an essential mineral as its presence is vital for many enzymes of major metabolic pathways, in normal nerve conduction and muscle contraction, and in bone mineral formation. Approximately 60-70% of total magnesium in the body is bound up in the bones.

Grass tetany occurs when the magnesium (Mg) level in blood decreases rapidly, resulting in less than adequate Mg reaching the cerebrospinal fluid surrounding the brain and spinal cord. Without Mg present in spinal fluid, there is uncontrolled activation of the nerves supplying muscles throughout the body. This causes constant overstimulation and contraction of muscles, appearing first as nervousness then muscle stiffness and rigidity (“tetany”), that can progress to convulsions then death.

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Maintenance of normal blood magnesium depends on daily absorption of enough Mg from the rumen to meet the amount required for milk production, soft tissue and bone growth, fetal development during pregnancy, and the small amount lost in feces.

Any excess dietary Mg is excreted by the kidneys in the urine (see Figure 1). Hypomagnesemia results when magnesium absorption is less than the daily Mg lost. Cattle have no effective tissue Mg reservoir so a shortage cannot be compensated for by removal from bones or increasing Mg²⁺ ion absorption from other sites in the body. In addition, Mg is not under direct hormonal control to keep it in balance as with other major minerals. Although a simple lack of Mg intake in the diet can happen as in cases of starvation or if off feed, deficiencies are most often due to interference with Mg absorption in the rumen. Absorption basically depends on 1) the amount of soluble Mg²⁺ ions available (“in solution”) in the rumen fluid and 2) the performance of the transport mechanisms that move Mg²⁺ ions across the rumen wall to the bloodstream.

1. High potassium (K⁺) in rumen fluid. High K⁺ is consistently cited as the most important factor in development of hypomagnesemia. The movement of magnesium across the rumen wall depends on an active transport mechanism (or “pump”) driven by an electrical potential created at the cell membrane. High potassium along with low sodium conditions alters the ion gradient required for active transport. If this active transport mechanism fails due to high K⁺, there is a secondary pathway, but it requires a much higher rumen magnesium concentration (4X higher) to enable Mg²⁺ ions to override the pump and passively flow down a concentration gradient to the blood.

High K⁺ levels in rumen fluid (Figure 2) are expected in any of the following situations: 1) cattle naturally high in K 2) cattle graze pastures fertilized with excessive potash or when high nitrogen fertilizer is added when soil phosphorous is low; 3) when cows are deficient in sodium (salt) and 4) when the diet changes suddenly from hay/dry feed to lush pasture. Small grain forages, including wheat, oats and rye, ryegrass and cool season perennial pastures in spring are often high in potassium (K⁺) and nitrogen (N⁺) ions and low in magnesium (Mg²⁺) and sodium (Na⁺) ions; these forage factors collectively reduce absorption of dietary magnesium.

2. Sudden increase in rumen ammonia. Lush grass is often high in soluble nitrogen and rumen degradable protein which allows for an increase in rumen ammonia levels. A rapid change from low-nitrogen to a high-nitrogen diet and rapid increase of ruminal ammonium ions (NH4+) impairs ruminal Mg²⁺ absorption, although the effect is transient and lasts for just a few days.

3. Insoluble Form of Magnesium. Magnesium must be present in soluble form (ionized) to be absorbed through the rumen wall. Solubility declines as the rumen fluid pH rises above 6.5. Grazing beef cattle often have higher rumen pH due to buffers present in saliva and slower production of volatile fatty acids from forage fermentation compared to grain diets. In addition, Mg²⁺ ion binders within forages, such as unsaturated fatty acids, can form insoluble Mg²⁺ salts reducing availability for absorption in the rumen.

4. Lack of dietary energy (fermentable carbohydrates)- In rumen fluid, a lack of fermentable carbohydrates results in fewer short-chain fatty acids (SCFA), a higher rumen pH, and an increase in ammonia concentration which decreases Mg²⁺ ion absorption. This is an important factor in development of winter tetany, an underlying form of hypomagnesemia that most often occurs when feeding harvested forages high in K⁺ but low in Mg²⁺, calcium (Ca²⁺), sodium (Na⁺) and energy throughout the winter. Cattle will have borderline low Mg and Ca blood levels but do not show tetany symptoms until triggered by a stressor such as severe weather, a new feed or environment, or after shipping. The stress hormone adrenaline rapidly shifts Mg²⁺ ions to the inside of cells, making it unavailable to the spinal fluid of the animal. If blood calcium is concurrently low, Mg levels in the spinal fluid decline even more quickly.

The classic grass tetany cow is most often found dead with disturbed soil around her hooves due to paddling and seizures before death. The interval between first symptoms and death may be as few as 4-8 hours. However, if noticed in the beginning stage, the earliest signs are twitching of the ears, facial muscles, shoulder, and flank and a stiff gait.

The affected cow separates from the herd and may show a variety of symptoms including excitement, teeth grinding, aggression, galloping, bellowing, staggering and may appear blind. As the fall in magnesium progresses, sustained muscle spasms eventually cause the cow to stagger and fall, legs outstretched, stiff and paddling. Convulsions and seizures follow with the head arched back and the legs paddling. The heart rate may reach 150 beats per minute (approximately twice the normal rate) and can often be heard without the use of a stethoscope.

Respiratory rates of 60 breaths per minute (normal is 10-30 breaths per minute) and a rectal temperature as high as 105°F may result from the excessive muscle activity. Animals may get up and repeat these convulsive episodes several times before death.

The diagnosis is made based on history, symptoms, and low magnesium concentration measured in the blood, urine or cerebrospinal fluid prior to death. After death, postmortem samples of spinal fluid that test below 1 mg/dL of magnesium or vitreous humor, fluid within the eye, below 1.34 mg/dL are reliable indicators of grass tetany if collected within 1-2 days after death.

Cattle exhibiting symptoms of grass tetany need immediate veterinary treatment; preferably 1.5-2.25 grams of magnesium intravenously for an adult cow. If unable to treat in the vein, a 10% magnesium sulfate solution given SQ or as an enema is a useful alternative therapy until a veterinarian arrives. Response to therapy depends on the length of time between onset of symptoms and treatment.

Cattle that do recover take at least an hour to return to normal. Many of these cows will relapse and require additional Mg treatment within 12 hours. Administering oral magnesium gel or drenching with magnesium oxide or magnesium sulfate once the animal has regained good swallowing reflexes will reduce the rate of relapse. A magnesium sulfate enema can be administered because the large intestine can absorb Mg rapidly. If grass tetany has occurred within a herd, an effort should be made to immediately increase the intake of magnesium to other members of the herd to prevent further losses.

Prevention of grass tetany is based on maintaining consistent intake of soluble magnesium to be absorbed in the rumen of susceptible cattle when conditions for grass tetany exist.

In the long term, prevention of disease is based on instituting management changes that decrease K⁺ and increase Mg²⁺ and Ca²⁺ in the forage.

Source: University of Kentucky, which is solely responsible for the information provided and is wholly owned by the source. Informa Business Media and all its subsidiaries are not responsible for any of the content contained in this information asset. 

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