Vitamin-A Deficiency in Chicken

Dr. K. Merina Devi, Dr. Bhupamani Das, Dr. Aashiq Hussain Dar and Dr. Derhasar Brahma


Vitamin A is a generic name that refers to a fat soluble compounds recognized as preformed vitamin A (retinol) in animal products and as provitamin A carotenoid in vegetables and fruits. Carotenoids (structurally similar to vitamin A) have around 600 compounds and only 50 of these compounds have provitamin A activity. Recent evidences have shown that all these compounds can be used as an effective antioxidant for inhibiting the development of heart related diseases. Vitamin A can be obtained from green and yellow vegetables, dairy products, fruits and organ meats are some of the richest sources.

Vitamin A deficiency is occasionally seen in chickens of 1-7 weeks of age. The deficiency seldom occurs in commercially raised flocks but it is commonly seen in small, backyard flocks where the rations compounded by owner is likely to be deficient of vitamin A. The deficiency of vitamin A in birds is termed as NUTRITIONAL ROUP or AVITAMINOSIS A. This vitamin deficiency can affect an entire flock. It is not spread from bird to bird, but it can lead to other communicable infections rather. There are 3 forms of vitamin A, viz,

  1. Retinol (vitamin A in alcohol form)
  2. Retinal (vitamin A in aldehyde form
  3. Retinoic acid (vitamin A in acidic form).Some of their stereoisomers form also present in chicken and other animals.               

Role of vitamin A in body           

  1. Vitamin A functions in normal growth and development of various body organs and bones and also in other hard tissues of body.
  2. It is essential for the maintenance of normal integrity of the epithelial lining of all body canals and cavities like alimentary canal and its accessories, respiratory, genitourinary tracts, corneal epithelium and other soft tissues around eyes. Thus it protects the body from various invaders and also from keratinization.
  3. Vitamin A is required for the normal vision of eyes. Severe vitamin A deficiency not only causes blindness due to deficiency of retinene but also causes structural damage to the eyes.
  4. Vitamin A plays an important role in reproduction in both male and female. Improper supply of vitamin A leads to atrophy of germinal epithelium.
  5. Vitamin A in diet prevents keratosis of skin (dryness and roughness) and hair follicles.  
  6. Vitamin A also prevents severe ataxia in young growing chicks by preventing the elevation of CSF(Cerebrospinal Fluid) pressure which might have occurred due to cell damage leading to decrease fluid absorption.
  7. Also, vitamin A involves in carbohydrate metabolism i.e., it plays an important role for the glucose formation from triose sugar.


The main role of vitamin A in the body is to maintain the normal integrity of epithelial lining of the body (the mucous membranes of GIT, respiratory, urogenital and epithelium lining of eyes and skin). When there is deficiency of vitamin A, the normal epithelial cells become atrophy, disappear and is replaced by keratinised, stratified squamous epithelium. The keratinisation lowers the resistance of epithelial tissue to the entrance of infective organisms. When Vitamin A is low or absent from the diet, these cells undergo changes that prevent the secretion of mucous, thus destroying a critical line of defence against microbial invasion. The microorganisms can enter inside the body and begin multiplying. Mostly, the respiratory system is the primarily affected followed by the other systems of the body. Thus, the individual is susceptible to various infections.     


  1. a)Chicken being a mono gastric animal, derives little or no benefit from microbial synthesis of vitamins in the gastrointestinal tract. The intestinal microorganisms compete with the host for dietary vitamins rather than synthesizing leading to deficit of nutrients.
  2. B) Any type of stresses on the birds may increases the vitamin requirements.
  3. Predisposing factors
    1. Most poultry ration contains alfalfa and yellow corn which are the excellent sources of vitamin A. If the rations do not contain alfalfa meal and if stored(depleted) corn is fed then the flocks is likely to suffer from vitamin A deficiency.
    2. Chicks hatched out from layer breeders with low vitamin A reserve in the body; if the chicks are reared on deficiencies ration, they soon will suffer the vitamin A deficiency
  4. Birds raised on free range system derived vitamin A from green vegetables. During confinement, this source of vitamin A is not available and deficiencies may develop unless the formulated ration includes sufficient vitamin A source.
  5. In case of chronic diseases of intestine, vitamin A cannot be synthesized by the body causing avitaminosis A.
  6. Excess inorganic Phosphorus in the diet diminishes vitamin A storagein the body leading to its deficiency.
  7. A diseased liver is unable to store vitamin A; and also in absence of bile, vitamin A cannot be absorbed by the body resulting to its deficiency.                                                                           

Clinical signs    

a) In recently hatched chicks:                    

In newly hatched chicks, the deficiency signs appear in 1-7 weeks of age according to the amount of vitamin A present in the diet, stored in the egg and also received from maternal source. If the chicks are the progeny of hens receiving high source of vitamin A, symptoms of deficiency may not appear until the chicks are 6-7 weeks of age. Initially, there is cessation of growth, drowsiness, mild anorexia, weak, ruffled feathers. The yellow pigment in the shanks and beaks is lost, combs and wattles may be pale. In severe case, there is ataxia (unlike that of vitamin E deficiency that is Crazy Chick Disease).The cause of ataxia was better understood that one of the earliest sign of vitamin A deficiency is the increase in cerebrospinal fluid pressure. Xerophthalmia is the definite sign of chronic vitamin A deficiency but it is not often manifested in chicks because in acute they may die due to some other causes before the eyes are affected.

Vitamin A deficient chicks are infected significantly with larger numbers and longer intestinal round worms compared with chicks receiving with an adequate vitamin A. The recovery of the affected chicks can be enhanced with increasing levels of vitamin A up to 10 times the minimal requirement under normal conditions. The affected chicks develop a crusty material in the nostrils and eyelids, progressing to the accumulation of a cheesy material. In the initial stages, it mimics respiratory diseases. Similarly, in young chicks suffering from chronic deficiency, shows the presence of pustules in the mucous membrane of mouth, esophagus, crop, respiratory tract etc. The infection progresses and becoming so painful that the bird ceases to eat. In extreme case, there is accumulation of urates in renal tubules and blood uric acid level increases from a normal level (5mg) to as high as 44mg per 100ml of whole blood. Deposition of urates have been found in heart, pericardium, liver, bursa of fabricius and spleen. The renal tubules show epithelial hyperplasia leading to dilation and fibrosis to certain extent. Deficient chicks fail to grow, are severely depressed and die of organs failure. 

b) In adult birds :

In adult birds, severe deficiency of vitamin A over a period of 2-5 months is necessary before the signs develop depending upon the amount of vitamin A stored in liver.Adult hens experience a drop in egg production, decrease fertility andhatchability rates due to interference in the reproduction system.

Blood spots are seen on eggs incertain strains of chicken and also there is occulonasal discharges along with sinusitis.

In adult chickens, vitamin A deficiency lesion first appears in upper alimentary tract (pharynx) and are largely confined to mucus glands and ducts. The normal epithelium is replaced by stratified squamous, keratinising epithelium which blocks the ducts of the mucous membrane causing them to be distended with secretions and necrotic materials. There is presence of small white pustules in the nasal passage, mouth, esophagus pharynx and it may extend into the crop. It is called as Nutritional Roup. The size of pustules may vary from microscopic lesions to 2mm in diameter. As the deficiency progresses, the lesions enlarge and are raised above the surface of the mucous membrane and have a depression in the center. Due to the breakdown of the original epithelial lining of mucous membrane, there may be invasion of bacteria, virus and other pathogenic microorganisms and enter into the body producing infections which are secondary to the original vitamin A deficiency signs.

Other symptoms may include:

There is unthriftness, sneezing, wheezing, lethargy, depression, diarrhoea, egg binding (dystocia), tail-bobbing, lack of appetite, emaciation (severe weight loss), poor feather colour, gagging, foul-smelling breath, lower resistance, white patches or a “slimy” appearance in the mouth, poor feather growth .In chronic case, xerophthalmia is developed which is characterised by accumulation of milky white exudates in eyes in such extent that it becomes impossible for the birds to see unless the mass is removed and often the eyes are destroyed.


  1. A careful study of the ration formulation may reveal the likelihood of deficiency of vitamin A.
  2. The characteristic sign and symptoms and the present of roup indicated the deficiency of Vitamin A.
  3. Microscopic examination of squamous metaplasia in nasal passage may assist in diagnosis. Low level of vitamin A in liver is an indicative of vitamin A deficiency.
  4. Differentiation diagnosis with infectious coryza, chronic respiratory disease, influenza and vitamin E deficiency is a must.

Differentiation of ataxia between vitamin A and vitamin E deficiencies:

Adamstone (1947) differentiated between the ataxia of vitamin A and vitamin E deficiencies in chicken by histologic means. Both the deficiencies are characterised by in coordination and imbalance of central nervous system origin. But in vitamin A deficiency, there is no presence of gross lesions in brain and upon microscopic examination, deficient cells lose their chromaticity but do not shrink. In contrast vitamin E deficient chicks show haemorrhage, edema and degeneration of Purkinje cells in the cerebellum. Also the livers of ataxic vitamin A deficit chicks contain little or no vitamin A.


  1. Vitamin A supplementation should be provided to the birdsas soon as the symptoms appear.
  2. Since the major problem and most threatening condition is usually the secondary microbial infections, the infection must also be treated immediately.
  3. If diagnosed and treated early, the severe birds can usually be cured without long-lasting effects.
  4. Vitamin A deficient birds can be treated by adding water dispersible vitamin A supplement to the drinking water.
  5. Adding a stabilized vitamin A supplement to the ration 2-4 times the normal levels for about 2 weeks may improve the condition.


  1. Prevention is easily achieved by feeding a ration with adequate vitamin A.
  2. Avoid long storage of prepared feed ingredients
  3. Adding antioxidant to feed at the time of preparation so as to protect the loss of vitamin A or adding stable form of vitamin A in the feed is recommended.
  4. Hypovitaminosis A is easily preventable in companion birds if they are fed with fruits and vegetables high in vitamin A.

In general, most birds should be fed a diet that consists of 65-80% formulated foods, 15-30 % vegetables, and the remainder fruits and nuts.

Following are listings of the vitamin A content of poultry feed ingredients with Vitamin A.