Vitamin A Deficiency in Avian

Dr.Nasih H Ali
Roles of Vitamin A in diets
• Vitamin A is involved in vision, reproduction, immunity, growth,
embryogenesis and the maintenance of epithelial cells, vascular development,
adrenal hormone production and the formation of red and yellow pigments
in feathers.
• Vitamin A is of animal origin and does not occur in plant tissues. Some
carotenoids can be converted to vitamin A in the intestinal wall via a specific
enzyme.
Corn has moderately high levels of beta‐carotene, which is converted to
retinol
Approximately 90% of total-body vitamin A is contained in the liver.
Rates of Vitamin A in avian diets
Vitamin A is usually supplemented to poultry diets as retinyl‐esters of
acetate or palmitate at a level of 4,000 to 12,000 IU/kg.
Dietary requirements of psittacine birds at maintenance are 2000-4,000
IU/kg
Normal Physiological functions of Vitamin A
Retinol and retinal must be converted to retinoic acid for their required function. Retinoic
acid binds to specific nuclear receptors and induces the expression of more than 500 genes
that regulate cell replication, differentiation, and death.
The retinal aldehydes are incorporated in rhodopsin and influence dim light vision
Although retinoic acid appears to play a role in testosterone synthesis
Retinoic acid is among the most important signaling molecules in ontogenesis and early‐
stage embryo formation.
Retinoic acid induces the differentiation of epithelial basal cells into the cubodial,
columnar, and goblet cells characteristic of a soft, moist epithelia. When vitamin A is
deficient, the basal cells differentiate into squamous cells (squamous metaplasia), which may
become stratified and keratinized to form a hard, dry epithelia characteristic of the skin.
Bone modeling and leukopoiesis.
Vitamin A Deficiency
Clinical Signs
Chicks and poults:
Poor growth.
Poor feathering.
Nasal and ocular discharge.
Drowsiness.
Pale comb and wattles.
Eyelids stuck shut with thick exudate.
Clinical Signs..
Chickens and Turkeys
Vitamin A can be stored in relatively large amounts as retinyl‐fatty acid esters in
the liver. it usually takes 2–5 months for deficiency signs to develop in adult
chickens or turkeys.
weakness, weight loss, ruffled feathers.
 sharp drop in egg production,
increased incidence of blood spots in eggs
time between two clutches increases
Hatchability Decrease
Nasal and ocular discharge
Swallow of face and stuck eyelid with thick exudate.
Clinical Signs..
Pet Bird:
Pet birds that eat only seeds (especially sunflower seeds and peanuts) are most prone to this
problem because an all-seed diet is low in vitamin A.
cockatiels can be maintained on a diet devoid of vitamin A for up to two years before demonstrating
clinical signs.
skin loses its suppleness and becomes dry and flakey.
The feathers may develop abnormal coloration--for example, a dark green Amazon parrot may
appear a light yellowish-green or have streaks of white or yellow throughout its feathers.
 It is very common for a parrot with a vitamin A deficiency to have broken and frayed tail feathers.
sneezing, wheezing, nasal discharge.
Diarrhea, pneumonia and blunted immune response are characteristic of vitamin A deficiency in
cockatiels.
nose starts to have a discharge that may be thick or crusty.
Pathology
1- Epithelial Tissues
Vitamin A‐deficiency lesions first appear in the esophagus and pharynx and are confined
largely to mucous glands and their ducts. The original epithelium is replaced by a
keratinizing epithelium that blocks ducts of the mucous glands, causing them to become
distended with secretions and necrotic materials. Small, white nodules may be found in
the nasal passages, mouth, esophagus, and pharynx and may extend into the crop. As the
deficiency progresses, lesions enlarge, are raised above the surface of the mucous
membrane, They may be removed easily without bleeding

2- Eyes
milky white, caseous material accumulates in the eyes and eyelids may become stuck
together. Chronic infection of the eye results in necrosis and irreversible blindness.
Pathology..
3- Reproduction
Vitamin A deficiency in the embryo often results in death during the first week of incubation. decreased survival time of
progeny, decreased testes size. Those embryos that survive to term may be too weak to hatch or die shortly thereafter.

 4- Immune Function

Vitamin A deficiency in chicks lea Deficiencies lead to decrease phagocytic activity in macrophages and neutrophils, and
impair intestinal IgA responses to a rapid loss of lymphocytes.
Deficiencies of vitamin A are deleterious for development of the cloacal bursa and thymus.

5- Bones 
A deficiency results in reduced activity of osteoclasts, leading to excessive deposition of periosteal bone by the
unchecked function of osteoblasts.

6- Others
Chronic vitamin A deficiency causes damage to the kidney tubules, Excessive urate in kidneys and ureters…
Histopathology
Atrophy and deciliation of columinar-cilated epithelium of respiratory
tract.
Stratified Sq. Keratinized Epithelium in glands of palate, tongue and
esophagus.
Vitamin A deficiency in young chicks and ducks causes marked
retardation and suppression of endochondral bone growth. The
proliferating zone is reduced.
Diagnosis
Signs.
Lesions
Examination the levels of Vitamin A in the diet for definitive diagnosis
Treatment of Deficiency
Poultry found to be severely deficient in vitamin A should be given a
stabilized vitamin A preparation at a level of approximately 10,000 IU
vitamin A/kg of ration. It also may be provided in the water or via
injection.
Absorption of vitamin A is rapid; therefore, chickens or turkeys not in
advanced stages of deficiency should respond promptly.
Prevention
The best and safest way to ensure that a bird will not suffer from a
vitamin A deficiency is to provide it with adequate nutrition. Birds that
prefer seeds should be given a commercial vitamin supplement,
administered on the food or in the water. All birds should also be
provided with foods that are rich in vitamin A, In addition, beta-carotene
supplementation is effective. Readily converted by birds to the active form
of vitamin A.
Food rich in vitamin A and vitamin A precursors include fruits like
cantaloupe and papaya, vegetables like chili peppers, leaves of broccoli,
turnip and flowers, sweet potato, carrots, beetroot, spinach, dandelion,
collards, endive, egg yolks, butter and liver.
Toxicity
Mistakes in formulation of vitamin premixes can result in toxicity at vitamin A
levels between 35,000 and 60,000 IU/kg. Reduced bone growth and
mineralization is caused by reduced osteoblastic cell activity and inhibited
expression of calcium binding protein excretion.
In breeders, doses of 45,000 IU/kg and above significantly decreased egg weight,
yolk color, eggshell thickness and strength, andreproductive performance.
In broilers, signs of toxicity include slow growth, an unsteady gait, reluctance to
walk, reduced bone mineralization
Cockatiels at maintenance are more susceptible to vitamin A toxicity than
deficiency, Perhaps ß-carotene would be a superior source of vitamin A in some
psittacine diets.
Differential Diagnosis
Infectious Coryza.
Wet Pox
Trichomoniasis
Candidiasis
Infectious sinusitis