vitamin E deficiency (Crazy chick disease, encephalomalacia)

Occurrence: Worldwide.

Species affected: All.

Age affected: Young chicks, usually between 15th and 30th day of life.
Causes: Deficiency of Vitamin E in the diet. Vitamin E is heat labile. It can also be caused by deficiency of selenium. As selenium levels in the soil are very variable, cereal grains are often suboptimal in selenium.

Effects: Incoordination, tremors, rapid contractions and relaxation of the legs results in the name "crazy chick disease".

Detailed causes:

Vitamin E is required for reproduction and normal integrity of central nervous and muscular system. Vitamin E is also an effective antioxidant. It is an important protector of essential fatty acids, Vitamin A and D3. Young chicks, usually between 15th and 30th day of life are most susceptible.


Mode of transmission
Vitamin E is heat labile. A deficiency of selenium will result in a deficiency of Vitamin E. Selenium levels in some areas are very variable, which may result in suboptimal levels in cereal grains.

Clinical signs:

Incoordination, tremors, rapid contractions and relaxation of the legs results in the name "crazy chick disease".

Postmortem lesions
The cerebellum is softened and oedematous which may progress to haemorrhage and/or necrosis.

Diagnosis:

Histopathology reveals diagnostic lesions in the brain, which includes ischemic necrosis, demyelination and neuronal degeneration.

It simulates Avaian encephalomyelitis (AE), Newcastle disease and vitamin B1 deficiency.

Treatment and control:

Prevention
Proper storage of premixes and finished feed and proper amount of selenium in feed will prevent the disease.

Treatment
Add the dietary ingredient to reduce clinical signs. Selenium is involved in vitamin E metabolism. A deficiency of selenium will cause a deficiency of E. A deficiency in vitamin E will also result in testicular degeneration in adult males and increase embryonic mortality.