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Vitamin E and Selenium Deficiency

Submitted by admin on Wed, 09/17/2008 - 19:29
Vitamin E and Selenium Deficiency
Etiology
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.

Epidemiology
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
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12/24/21, 12:16 AM Vitamin E and Selenium Deficiency | Partners in Animal Health

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.

Diagnosis
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.

Selected References
Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road,
Athens, Georgia 30602-4875.
Klasing, K.C. 2008. Nutritional diseases. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
World Organization for Animal Health (OIE) website. 2008. www.oie.int
Thank you to the following individuals for reviewing these materials:

Richard Chin
Jaime Ruiz
Jose Bruzual

Differentials:
Avian Encephalomyelitis
Gangrenous Dermatitis
Newcastle Disease
Vitamin B1
Etiology:
Vitamin E and Selenium Deficiency

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