3-week-old female miniature donkey, Equus asinusFound in recumbency, treated with IV fluids and antibiotics. Brown urine was discharged shortly before death.

Gross Description:  

The lungs were edematous. Several ulcers up to 5mm length were present in the squamous mucosa of the stomach. The urinary bladder contained brown urine.

Histopathologic Description:

There is diffuse to segmental degeneration and necrosis of skeletal muscle fibers, characterized by fragmentation of fibers and condensation of the sarcoplasm into hypereosinophilic coagulum with loss of cross striations(Fig. 3-1). There is eosinophilic, granular to fibrillary debris within the fibers and extending into the interstitium around the affected fibers. Rarely, macrophages or satellite cells surround affected fibers.

Morphologic Diagnosis:  

Skeletal muscle myofiber degeneration

Lab Results:  

Liver selenium concentration was 0.7 ug/g (reference range 0.7-2.0 ug/g); liver Vitamin E concentration was < 2.5 ug/g (reference range 15.0-25.0 ug/g).


Vitamin E deficiency

Contributor Comment:  

Nutritional myopathy was diagnosed in this donkey foal based on the muscle lesions and extremely low concentration of vitamin E in the liver. Selenium concentration in the liver was in the low normal range. Nutritional myopathy usually occurs in young animals on diets deficient in selenium and/or vitamin E, with or without the conditioning factors such as an excessive quantitiy of polyunsaturated fatty acids in the diet.(5) Vitamin E is an antioxidant that prevents oxidative damage to sensitive membrane lipids by decreasing hydroperoxide formation.(3) Selenium is an essential component of the enzyme glutathione peroxidase (GSH-PX). GSH-PX catalyzes the breakdown of hydrogen peroxide and other organic hydroperoxides produced by glutathione during the process of redox cycling.

Microscopic lesions similar to those in skeletal muscle were also present in the heart of this donkey, but were more mild. Granular eosinophilic material compatible with hemoglobin or myoglobin was present in tubular lumens of the kidney. This material is most likely myoglobin released from the affected skeletal muscle fibers. Although gross lesions were not detected in the heart or skeletal muscle of this foal, pale areas in the heart and skeletal muscle can be observed in cases of nutritional myopathy of foals, however is not always observed.(7) Degenerate muscle may be very difficult to detect grossly when it is uncalcified, and is likely to escape detection.(3) Mineralization of muscle fibers is not always present in cases of nutritional myodegeneration in foals.(7)

There were approximately 50 female donkeys in this herd, with this being the only donkey diagnosed with nutritional myopathy, although foals had died in previous years with similar signs. The female donkeys were fed brome grass hay year-round, never being pastured on green grass, or supplemented with vitamins or minerals. Green, growing forages should provide adequate vitamin E as α-tocopherol, but the vitamin E content is greatly reduced in grass that is dried for hay. Mature plants contain less α -tocopherol than younger plants, and mature grass cut for hay can have loss of up to 80% of the tocopherols when dried in the sun for 4 days.(1) Plasma vitamin E status of horses is highest from May to August when fresh grass is being grazed and lowest when horses are fed harvested or stored feed during the same period.(2)

JPC Diagnosis:  

Skeletal muscle: Degeneration and necrosis, multifocal, moderate

Conference Comment:  

Differentials for this lesion in horses were discussed during the conference and included white muscle disease, capture myopathy, exertional rhabdomyolysis, and toxic myopathy due to toxic plants and ionophores. Nutritional myopathy causes a polyphasic, multifocal lesion in affected muscle while ionophore toxicity causes monophasic, multifocal lesion thus allowing for microscopic differentiation of these two conditions.(6)

Nutritional myopathy is common in calves, lambs, swine, and foals.(6) It can be caused by a lack of dietary intake of vitamin E or selenium or from competitive binding of selenium by copper, zinc, silver, or tellurium. Foods high in polyunsaturated fats such as fish require intake of more vitamin E to minimize oxidative damage from the metabolic processing of these foods.(6)

Vitamin E and selenium are important in preventing damage from free radicals from both within and from outside the cell. Free radicals are molecules with an odd number of electrons produced during normal cell functions or from tissue radiation, drug reactions, or inflammation. Free radicals are highly reactive molecules that can cause damage to mitochondria, endoplasmic reticulum, or the cytosol via damage to important cellular proteins or peroxidation and damage of cellular lipid membranes. When cellular membranes are damaged, ion gradients can not be properly maintained. Extracellular calcium moves into the cytosol and the cell responds by attempting to protect calcium-sensitive myofilaments by pushing calcium into mitochondria. Mitochondria quickly accumulate excess calcium and lose their ability to produce energy for the cell. Myofibrils exposed to leaking calcium hypercontract leading to degeneration and necrosis of myofibers.(6)

The attached table provides a non-comprehensive list of diseases considered to be associated with an imbalance or deficiency in either selenium or vitamin E.
CattleNutritional myopathy
Retention of fetal membranes
HorseNutritional myopathy
Swine Mulberry heart disease
Hepatosis dietetica
Exudative diathesis
Iron hypersensitivity
Nutritional myopathy
Sheep Nutritional myopathy
Poor growth potential
Dogs Intestinal liposfuscinosis
Cats; mink; birds;
pigs; rabbits;
Steatitis (yellow fat disease)
Chickens and Turkeys Encephalomalacia (superficial cerebellar hemorrhage crazy chick disease)


1. Ballet N, Robert JC, Williams PEV: Vitamins in forages. In: Forage Evaluation in Ruminant Nutrition, eds., Givens DI, Owen E, Axford RFE, Omed HM, pp. 399-43. CABI Publishing, New York, NY, 2000
2. Blakley BR, Bell RJ: The vitamin A and vitamin E status of horses raised in Alberta and Saskatchewan. Can Vet J 35: 297-300, 1994
3. Hulland TJ: In: Pathology of Domestic Animals, eds., Jubb JVF, Kennedy PC, Palmer N, pp. 228-234. Academic Press, Inc. San Diego, CA, 1993
4. Jones TC, Hunt RD, King NW: Nutritional deficiencies. In: Veterinary Pathology, 6th ed, pp. 789-794, Williams and Wilkins, Baltimore, MD, 1997
5. Radostits OM, Gay CC, Blood DC, Hinchcliff KW: Veterinary Medicine. In: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses, pp. 1515-1533. WB Saunders Company, London, 2000.
6. Van Vleet JF, Valentine BA: Muscle and tendon. In: Jubb, Kennedy, and Palmer's Pathology of Domestic Animals, vol 1 ed. Maxie MG, pp. 236-243. Elsevier Limited, Philadelphia, PA, 2007
7. Wilson TM, Morrison HA, Palmer NC, Finley GG, van Dreumel AA: Myodegeneration and suspected selenium/vitamin E deficiency in horses. J Am Vet Med Assoc 169: 213-217, 1976

Click the slide to view.

3-1. Skeletal muscle, donkey.

Back | VP Home | Contact Us |