Vitamin E and Selenium Deficiency

By Deb Haines

Clinical Description

The clinical signs of vitamin E deficiency typically develop in chicks between 15 and 30 days old. Nervous signs may include ataxia, opisthotonus, torticollis, myoclonus, paresis, and eventually prostration. These nervous signs are caused by encephalomalacia of the cerebellum and cerebrum.

If vitamin E deficiency is identified and treated in its early stages, some birds do respond to treatment. In the encephalomalacia form of the disease however, birds do not always respond to therapy. This adult chicken continues to exhibit torticollis, a neurologic sign consisting of an abnormal twisting of the head and neck.

Similar edema and discoloration of the neck region, as seen here, can also occur. Swelling and discoloration of the unfeathered skin of the head of this chick. Edema and discoloration of the legs and feet caused by exudative diathesis, a manifestation of vitamin E deficiency. Exhibiting a characteristic leg posture associated with exudative diathesis. The accumulation of subcutaneous edema along the ventrum may cause birds to stand with their legs spread apart. Affected birds may also have difficulty walking. Edema and skin discoloration is also evident. Discoloration of the skin proximal to the hock joint, associated with exudative diathesis. In the muscular dystrophy form of vitamin E deficiency, skeletal, smooth, and cardiac muscles can all develop lesions resulting in clinical signs.

Vitamin E and Selenium Deficiency


Vitamin E plays multiple roles in poultry nutrition and is an essential dietary vitamin required for the normal embryonic development of birds. Diets deficient in vitamin E can lead to a variety of disorders in poultry including encephalomalacia, exudative diathesis, and muscular dystrophy.

Host Range

Vitamin E deficiency may cause clinical disease in young chickens and turkeys raised in confinement. Clinical signs usually manifest in the first few weeks of life. In adults, no outward signs of illness occur. However, the hatchability of eggs from vitamin E-deficient chickens and turkeys is reduced.


Most cases of vitamin E deficiency occur in birds that are fed rations high in polyunsaturated fats (e.g. cod liver oil and soy bean oil). When vitamin E in these diets becomes oxidized (rancid), the vitamin is no longer bio-available.

  • Clinical Signs In encephalomalacia, nervous signs typically begin between 15-30 days of age. However, the onset of clinical signs has been observed in chicks as young as 7 days old and as late as 56 days old. Signs may include ataxia (loss of balance and falling backward), opisthotonus, torticollis, myoclonus (repeated muscle contractions of the legs), paresis, and prostration. Birds showing neurologic signs often continue to eat. In exudative diathesis in chicks, capillary walls become abnormally permeable and subcutaneous edema develops. This edema is often located along the ventrum of the thorax, abdomen, and under the mandible. The edema may appear to have a slightly greenish-blue color, due to the hemoglobin breakdown of the leaking red blood cells. If extensive edema develops, birds may have difficulty walking and may stand with their legs spread apart. In turkeys fed vitamin E deficient diets, abnormalities may develop in their legs. Enlarged hocks and bowing may develop at 2-3 weeks of age. The signs may disappear by 6 weeks of age. However if the deficiency is not corrected, the disorder will reappear in a more severe form by 14-16 weeks of age.

Post-mortem Lesions

  • On post-mortem examination, vitamin E deficiency associated with the encephalomalacia form may produce grossly visible lesions in the central nervous system. The most common lesions that are visible occur in the cerebellum. The cerebellum may appear softened and swollen and may extend into the foramen magnum. Hemorrhages, ranging from petichiae to ecchymotic, may be visible on the surface of the cerebellum. Lesions in the cerebrum are less common. One to two days after the onset of clinical signs, necrosis may be observed grossly within the brain tissue. Areas of necrosis appear as green to yellow opaque lesions. As the condition progresses, the cerebellum may become pale and small. In the exudative diathesis form of the disease, subcutaneous edema is usually present under the ventral skin region. In the muscular dystrophy form of the disease, muscle fibers can undergo degeneration, resulting in pale areas or streaks that may be found within smooth muscles (e.g., gizzard), skeletal muscles (e.g. pectoral/breast), and cardiac muscles. These lesions are more commonly observed in turkeys.

Differential Diagnosis

Nutritional encephalomalacia must be differentiated from avian encephalomyelitis, Newcastle disease, and vitamin B1 deficiency. Exudative diathesis should be differentiated from gangrenous dermatitis.


Analysis of the feed ration may indicate rancidity or deficiency of vitamin E and/or selenium. Care should be taken to submit truly representative feed samples. Microscopic examination of tissue lesions can be used to confirm suspected cases of vitamin E deficiency, especially for encephalomalacia and exudative diathesis.

Prevention and Control

The relationship between vitamin E and selenium is not fully understood, however selenium appears to play a critical role in protecting capillary membranes from oxidative damage. The prevention and treatment of vitamin E deficiency disorders therefore is closely tied to selenium. If clinical signs are identified early in the course of exudative diathesis and nutritional myopathy, they are often treated successfully by administering vitamin E and selenium in the feed. Encephalomalacia does not always respond to therapy. Each of these disorders can be prevented by proper dietary supplementation with vitamin E and selenium. Synthetic antioxidants can prevent encephalomalacia, inorganic selenium can prevent exudative diathesis, and cystine can help in the prevention of muscular dystrophy.

Reference and by clicking on this link you may see pics of this illness.

Selected References

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Klasing, K.C. 2008. Nutritional diseases. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  3. World Organization for Animal Health (OIE) website. 2008.

Thank you to the following individuals for reviewing these materials: Richard Chin

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