Nutritional Muscular Dystrophy (NMD)
Also known as
White muscle disease , Stiff lamb disease, Nutritional myodegeneration.
White muscle disease is a muscular dystrophy (wasting) caused by a deficiency of selenium (Se) or vitamin E, or both, in young ruminants. Selenium and vitamin E function together as antioxidants that protect cell membranes from oxidative damage. Lack of one or both nutrients results in loss of membrane integrity in muscles, including the heart.
Calves affected by the congenital form of white muscle disease (when the dam was short on selenium and/or vitamin E) usually die within 2 to 3 days of birth due to cardiac muscle degeneration.
On necropsy examination, the heart has white, chalky plaques just beneath the outer surface that are most noticeable in the left ventricle. The result is damage to muscle cells and fibers in the heart.
Nutritional myodegeneration (NMD) can also occur in young, rapidly growing calves, lambs, and kids. Their dams usually had selenium-deficient diets during gestation. Selenium supplementation seems to be more important than vitamin E in preventing NMD.
The disease occurs worldwide in areas where the soil (and therefore the grains and forages grown there) is deficient in selenium. Many soils in the northeastern, eastern and northwestern regions of the U.S. are deficient in selenium. Vitamin E deficiency occurs most commonly when animals are fed poor-quality hay, straw, or root crops.
Newborn, and young, rapidly growing animals 3 to 8 weeks of age are most often affected, although the disease has also been reported in yearling and adult cattle. When the heart muscle is primarily affected, the animal may have respiratory distress, cardiac arrhythmias (beating too slowly, too fast, or irregularly), or die suddenly.
In cases affecting the heart, the clinical course is frequently short, with death occurring in less than 24 hours despite medical therapy.
When skeletal muscle is affected, signs of muscle weakness, stiffness, and difficulty rising are seen. Most affected animals can only remain standing for short periods, and the muscles of the limbs may be firm and painful when touched.
This condition can be observed in the tongue before it is seen anywhere else. In a young calf, the muscle with the highest metabolic activity is the tongue, so the calf can suckle. If the tongue is flaccid and nonresponsive to touch, this is a major clue. A calf with white muscle disease will waste away if it has trouble nursing.
Young animals may appear lame or weak, walking with arched back, spending most of their time lying down and resting their chin on the ground. They may have diarrhea and be unthrifty.
If respiratory muscles are affected, the animal may show respiratory distress and increased abdominal effort when breathing. If muscles of the tongue are involved, the animal has trouble eating and swallowing.
Animals with skeletal NMD often respond favorably to treatment and rest. Improvement is seen within 3 to 5 days; these animals can often stand and walk again.
Signs of weakness may be brought on by vigorous exercise. Chronically affected cattle may have splayed toes. If a calf is affected severely it may die of starvation due to weakness and inability to nurse properly.
The skeletal muscle lesions associated with the delayed from of white muscle can affect one or more muscle groups. At necropsy the muscle will have white strips and feel dry and chalky due to abnormal calcium deposits.
- Muscle stiffness and tremors
- Motor disturbances
- Hind-end paralysis
- Heart failure
White muscle disease is most often caused by selenium deficiency. The muscles of affected animals have white streaks, particularly in the heart. The damaged tissue gets replaced with fibrous connective tissue—scar tissue—and scar tissue in muscle is white.
The tongue, heart, diaphragm, and major muscles in the hind legs are key sites for these white lesions. Excessive damage to the diaphragm and heart can lead to labored breathing and heart failure.
Some soils are deficient in selenium, and different types of plants take up selenium at different rates. Soil pH can also alter how available soil selenium is to plants. Acidic soil (lower pH) decreases plant uptake of selenium, whereas alkaline conditions (higher pH) increase selenium uptake. Other minerals in the soil, such as sulfur, also may lower selenium bioavailability in growing plants.
The two forms of the disease are cardiac and skeletal. The cardiac form occurs most commonly in newborn animals and typically has rapid onset; these young animals may be found severely debilitated or dead.
Respiratory difficulty is a sign of damage to heart, diaphragm, and intercostal muscles, which are groups of muscles between the ribs. Those muscles help expand and contract the size of the chest cavity to facilitate breathing.
In older animals, locomotor impairment and/or circulatory failure may accompany respiratory signs. These animals may have muscle weakness and partial paralysis, stiffness or inability to stand, rapid but weak pulse, and often die suddenly. With the skeletal form, affected animals are stiff and reluctant to move, with painful muscles. Young animals may be reluctant to get up, and may have difficulty nursing.
Definitive diagnosis is based on checking blood levels of selenium and plasma levels of vitamin E. Necropsy lesions include petechial hemorrhages (tiny spots of bleeding under the skin) and muscle edema (swelling due to fluid seepage), along with pale white streaking of affected heart and skeletal and muscles, diaphragm, and tongue.
In young ruminants with signs of respiratory and cardiac dysfunction, differential diagnosis possibilities include congenital cardiac abnormalities and pneumonia.
Calves may be severely deficient but show no clinical signs unless they are subjected to stress. Nursing beef calves may be at risk of deficiency if dams are not supplemented.
Awareness of regional selenium deficiencies is important, since this disease is frequently subclinical. Prevention involves vitamin E and selenium supplementation, particularly to pregnant dams and/or young animals in deficient areas. Injectable selenium supplements are necessary to prevent clinical disease in animals in regions with severely deficient soil.
The U.S. Food and Drug Administration limits supplemental selenium in ruminant diets to 0.3 parts per million (no more than 0.7 mg per day for adult sheep and 3 mg per day for adult cattle) because excess selenium is toxic.
However, this level of supplementation often is not adequate in deficient regions and the use of injectable sources is necessary to prevent clinical deficiencies.
Under most conditions, white muscle disease of calves and lambs can be prevented by providing selenium and vitamin E in the diets of cows or ewes during pregnancy. If possible, supplementation should be continued during lactation to provide a continuous source of selenium to their calves and lambs.
Young, rapidly growing cattle, particularly beef cattle that are eating hay and straw deficient in selenium, and those that are fed high-moisture grain should receive supplementation. If selenium-supplemented concentrates are used as part of a feeding program for dairy cows, it is not necessary to provide additional selenium by injection.
NMD can be prevented in suckling beef calves and lambs by including selenium (14.8 mg/kg) and vitamin E (2700 IU/kg) in the mineral supplement for pregnant cows and ewes on a selenium-deficient ration during the latter two-thirds of gestation and for the first month of lactation.
Providing sodium selenite in a salt–mineral mixture for 3 months can bring selenium levels up into normal ranges in beef cows, even when fed to extremely deficient animals.
To prevent white muscle disease in the first month of life in calves, pregnant cows can be given 15 mg of selenium, usually as sodium selenite, four weeks before calving.
To prevent the delayed type, calves can be given 5 mg of selenium at two to four weeks of age and two more doses at monthly intervals. A selenium and vitamin E mixture is recommended in some regions.
Other procedures for selenium supplementation include oral administration of selenium pellets, use of selenium-fortified salt or mineral mixtures, subcutaneous implantation of selenium pellets. Some farmers apply selenium to deficient soils, via fertilizer.
When adding selenium to grain mixes, proper amounts and thorough mixing is crucial because of the minute quantities needed and the toxicity of excess intake. In some countries, including the U.S, addition of selenium to feeds is controlled by law.
The use in ruminants of selenium boluses (given orally, to lodge in the rumen), which release a precise amount of selenium daily, is common in many countries, but not in the U.S.—due to FDA regulations.
These slow-release boluses can replace supplementation by salt mixtures or by injections and can be very valuable in extensive grazing systems.
Alternatively, individual animals can be supplemented by periodic injections (every 30 to 60 days) of selenium/vitamin E preparations to help maintain body concentrations and delivery of selenium to the fetus in pregnant animals.
Regardless of the method of supplementation used, periodic blood (or tissue) sampling of animals at risk is recommended to monitor levels of selenium.
Selenium alone is protective against a greater spectrum of diseases than is vitamin E, but there are situations in which vitamin E is more important. Both should be provided when the diets are deficient in both nutrients, but this may not apply in every situation.
NMD can occur in ruminants with vitamin E deficiency and adequate selenium status. Most injectable preparations are adequate in selenium but insufficient in vitamin E.
Affected animals may be treated by administering vitamin E and selenium injections.
Cattle affected by white muscle disease can be treated with sodium selenite and vitamin E in sterile emulsion. This can be administered subcutaneously or intramuscularly at a rate of 1 mg selenium and 50 mg (68 IU) of vitamin E per 40 pounds of body wt.
If necessary, the treatment may be repeated two weeks later, but no more than four doses total should be given. In calves affected with simple vitamin E deficiency, treatment with dietary supplementation or substances rich in vitamin E can be used. Polyunsaturated fats should be removed from the diet as these may be causing the vitamin E deficiency.
The cardiac form of NMD is often fatal, but the skeletal form may respond to injectable selenium products. Follow label dosage recommendations and don’t give more than what is recommended since overdose can be toxic.
When using vitamin E/selenium combinations, the amount of vitamin E may be insufficient for treatment; it is present only as a preservative for the solution. Injectable vitamin E products that contain 300 and 500 IU vitamin E per mL as d-α-tocopherol are available.
Oral supplementation can provide additional dietary levels of vitamin E. Recommended levels of supplementation for calves range from 15 to 60 mg of dl-α-tocopherol acetate per kg of dry feed.
If the deficient animal is suffering from respiratory problems, antibiotics may be needed to combat secondary pneumonia. Providing adequate energy intake and paying attention to fluid and electrolyte balance are also crucial for recovery.