Vitamin Deficiency in Poultry with Special Reference to Vitamin E

Vitamin Deficiency in Poultry with Special Reference to Vitamin E

 V.K.Varun^1*, M.V.Jithin¹, Jeny K john¹, Ajit Kumar Singh¹, Shubham Kumar²

¹Assistant Professor Department of Veterinary Clinical complex, COVAS, SVPUAT, Meerut, UP-250110

² PhD Scholar, Division of Pharmacology and toxicology, ICAR-IVRI, Bareilly, UP-243122

*corresponding author: drvarun15487@gmail.com

Key words: Poultry, vitamins, encephalomalacia, chick, egg production,

Vitamins are a group of substances which are required for normal cell function, growth, and development. Vitamins have a very important role in healthy and economical poultry farming. Poultry require all the vitamins except vitamin C. deficiency of vitamins can leads to serious health issue and low egg and meat production. In this article we will know the various condition/disease caused by vitamin deficiency with special reference to vitamin E.

Vitamin E 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 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

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. www.oie.int

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