Nutritional Muscular Dystrophy (Nutritional Myopathy or White Muscle Disease) is a disease caused by a deficiency of selenium and vitamin E in dietary intake. Soils that contains low levels of selenium produce forages and grains that are deficient in selenium. Similarly, if the forage is of low quality or is not stored properly it may be deficient in vitamin E. If an animal consumes this type of diet without additional supplementation they become susceptible to this disease. This condition often affects young ruminants, such as calves and lambs.Selenium and vitamin E are antioxidants. Therefore, deficiencies of these nutrients lead to oxidative damage to cells within the body. The muscle cells are the most vulnerable to damage in livestock species. Clinical symptoms
The oxidative damage causes degeneration of muscles, in particular those within the skeletal and cardiac systems. If the cardiac muscles are impaired the animal may exhibit signs of respiratory distress. While deterioration of skeletal muscles results in stiffness, weakness, and recumbency. Treatment & Prevention
If the diet is deficient supplement with selenium and/or vitamin E. Injections can be given to treat the condition or as a preventative measure. Horses
In equids, it is most common in the first twelve months of life. Neonatal foals born to dams that are selenium-deficient often develop the condition. There are two forms: peracute, and subacute. The peracute form is characterized by recumbency, tachypnea, dyspnea, myalgia, cardiac arrhythmias, and rapid death.
Progressive osseous heteroplasia is a cutaneous condition characterized by cutaneous or subcutaneous ossification.According to the Progressive Osseous Heteroplasia Association:

Progressive Osseous Heteroplasia (POH) is a rare genetic condition in which the body makes extra bone in locations where bone should not form. Extra bone develops inside skin, subcutaneous tissue (fat tissue beneath the skin), muscles, tendons, and ligaments. This ”out of place extra bone formation” is commonly referred to as heterotopic ossification. In people with POH, nodules and lace-like webs of extra bone extend from the skin into the subcutaneous fat and deep connective tissues, and may cross joints. Extra bone formation near the joints may lead to stiffness, locking, and permanent immobility.”
It is associated with GNAS.A telltale symptom of POH is osteoma cutis under the skin of a newborn. It was discovered in 1994 by physician Frederick Kaplan. Diagnosis
Patients with POH have a distinctly different manifestation of symptoms than those with fibrodysplasia ossificans progressiva (FOP), though heterotopic ossification appears in both diseases. They lack the congenital abnormality of the big toe that is a diagnostic feature for FOP. People with POH also have ossification of the skin during infancy, which does not occur in FOP. Also, the pattern of ossification differs in POH, spreading in an intramembranous fashion rather than endochondral. See also
Fibrodysplasia ossificans progressiva
Punctate porokeratosis
List of cutaneous conditions
Pseudopseudohypoparathyroidism

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