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Aina Meducci 2012


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White muscle disease (WMD)

Assalam, Hello people!! Dr Meducci is back! Geez, I really miss blogging!! I've been stressed up for the whole month for final examination and it was AWEEEEso.... erm actually, no target to be shoot this time, I just hope the result will be as good as the previous semester.

Damn! My surgery and pathology T.T


Today i would like to share regarding White Muscle Disease. The reason why I choose WMD because this topic was often discussed in my class. Let's get a review of it

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White muscle disease

White muscle disease (WMD) is a degenerative muscle disease found in all large animals. Commonly it is found in grazing lamb or sheep It is caused by a deficiency of selenium and/or vitamin E. Generally, it is not known which. Selenium (Se) deficiency is associated with selenium deficient soils and the inadequate uptake of selenium by forages grown on these soils.

So it is all about the NUTRITIONAL problem

Cause of disease

Pasture, hay, grain, and other supplements can be analyzed to determine the amount of selenium to be added to supplemental feeds. Grazing sheep usually consume adequate amounts of vitamin E. Fresh legumes and pasture are good sources of vitamin E whereas silage, oil seeds, root crops, cereal grains, and dry hays tend to be poor sources of vitamin E. Prolonged storage of feedstuffs results in a degradation of Vitamin E content.

In addition to white muscle disease, selenium and vitamin E deficiencies can produce symptoms of ill thrift and reproductive losses. They can cause poor rate of growth or ill thrift in young lambs throughout the growing period. Selenium and vitamin E also play key roles in the animal's normal immune response.

White Muscle Disease

Lameness of lamb

While the leg muscles are generally affected first, any muscle area including cardiac muscle may be affected. Chronic or borderline deficiencies may result in lung edema resulting in increased pneumonia problems. It is quite common for the disease to show up after forced exercise, vaccination procedures, sorting, weaning, fitting or being chased by dogs or children.

Normal heart (left) vs WMD heart (right)

Clinical signs

All breeds of sheep and goats are suceptible to WMD, and the condition may develop under extensive or intensive management systems. WMD is most commonly found in newborns or fast growing animals. Kids are believed to be more susceptible than lambs, possibly because they have a higher requirement for selenium. The disease can affect both the skeletal and cardiac muscles.

When the skeletal muscles are affected, symptoms vary from mild stiffness to obvious pain upon walking, to an inability to stand. Lambs/kids may tremble in pain when held in a standing position. A stiff gait and hunched appearance are common. Affected lambs/kids may remain bright and have normal appetites, but eventually they become too weak to nurse. When the problem occurs in newborns, they are born weak and unable to rise. Sudden exercise may trigger the condition in older lambs and kids.

When the disease affects the heart, the animal shows signs similar to pneumonia, including difficult breathing, a frothy nasal discharge (may be blood stained), and fever. The heart and respiratory rates are elevated and often irregular. Skeletal and cardiac muscle disease may occur concurrently.

The congenital type of white muscle disease may result in sudden death within 2-3 days of birth, usually with involvement of the myocardium. The delayed type is associated with cardiac or skeletal muscle involvement and may be precipitated by vigorous exercise. Affected animals may move stiffly with an arched back and frequently become recumbent.

If the condition is severe enough to prevent nursing, either from dysfunction of the muscles of the legs or the tongue, death may result from starvation. Sometimes, there is profuse diarrhea. In chronic cases, there may be relaxation of the shoulder girdle and splaying of the toes. In progressive cardiac failure, dyspnea results. Signs vary with dietary selenium status; in some areas, general unthriftiness may be the only sign associated with selenium deficiency.

Hunched appearance is affected sheep

Stiff gait


Selenium deficiency can be confirmed by measuring selenium levels in whole blood or tissues. A diseased animal will have less than 0.04 ppm of selenium in its blood. Breeding ewes require more selenium, and their blood levels should be over 0.5 ppm. At necropsy, the muscles of affected animals appear paler than normal and may show distinct longitudinal striations or a pronounced chalky appearance due to abnormal calcium deposition.

Paler flesh of dead affected sheep

Histolopath finding: necrosis of muscle

Review pathology: how does it occur???

Deficiency in vitamin E and/or Selenium → peroxidation of membrane lipids (sometimes exacerbated by stress) → Ca 2+ enters cytoplasm and mitochondria, damaging respiratory mechanisms → cell death → symmetrical necrosis of the most active skeletal muscle (like postural muscles)


Lambs and calves may be given sodium selenite and vitamin E in sterile emulsion, SC or IM, at 1 mg selenium and 50 mg (68 IU) of vitamin E per 18 kg (40 lb) body wt. This may be repeated after 2 wk, but no more than 4 doses should be given. Larger dosages are sometimes advocated, but caution is advised because they approach the toxic level. In practice, several products are available for use with designated animal species. When simple vitamin E deficiency is apparent, dietary supplementation with α-tocopherol or substances rich in vitamin E should be instituted. Minimum dosages have not been established.

When the causative diet contains substances antagonistic to vitamin E, such as unprotected, polyunsaturated fats, these must be removed or stabilized by addition of an appropriate antioxidant. Dry concentrates of vitamins A and D may substitute for cod-liver oil, thus removing a potential source of oxidative damage.


To prevent white muscle disease within 4 wk after birth, ewes are given 5 mg and cows 15 mg of selenium, PO or SC, usually as sodium selenite 4 wk before expected parturition. To prevent the delayed type, lambs are given 0.5 mg and calves 5 mg of selenium at 2-4 wk of age and twice more at monthly intervals. A selenium and vitamin E mixture is advocated in some areas. Other procedures for selenium supplementation include administration of intraruminal selenium pellets, use of selenium-fortified salt or mineral mixtures, SC implantation of selenium pellets, or soil application of selenium at 4 g/acre (10 g/hectare) in fertilizer.

Adding selenium to feed for breeding animals or their young is useful in areas of known deficiency. The recommended supplemental level is 0.3 ppm selenium, calculated on the basis of total dry-matter intake. It is added as sodium selenite, which contains 45.65% selenium. Because of the minute quantities involved and the toxicity of excess intake, premixing and thorough subsequent mixing is necessary. In some countries, caution in the use of selenium is indicated.

Sources: Barbados Blackbelly Sheep Association, University of Maryland;white disease in sheep and goat, Merck Veterinary Manual., WMD; purdue.edu

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