Deficiency of vitamin -A (hypovitaminosis-A)

Vitamin A deficiency develops due to insufficient supply of the vitamin or its defective absorption from alimentary tract. The deficiency is manifested by night blindness, corneal keratinisation, hoof defects, loss of weight and infertility in adult animals, and signs of compression of brain and spinal cord in young animals.

Aetiology: Primary hypovitaminosis-A occurs due to absolute deficiency of the vitamin or its precursor carotene in the diet. The condition develops most commonly in young growing animals fed vitamin A deficient diet. Feeding of dried, poor quality roughage for prolonged period is associated with vitamin-A deficiency in horses. Housed cattle fed a ration lacking in green fodder develop hypovitaminosis-A.Grains, except yellow corn, contain very low amount of carotene and cattle fed on carotene grains such as barley and barley straw with vitamin supplement are likely to suffer form vitamin A deficiency. Long storage of feed and grains, and hay bleached by sun significantly reduces carotene content. Heifers produce vitamin A in corpus luteum and are therefore less likely to develop vitamin A deficiency than the steers fed on similar vitamin A deficient.

Secondary vitamin A deficiency may be associated with chronic liver diseases, or intestinal disorder. Phosphorous deficiency lowers efficacy of conversion of vitamin A and vitamins C and E check the loss of Vitamin A. High nitrate content of the feed, and high environmental temperature reduce the conversion of carotene to vitamin A and thus enhance  chances of vitamin A deficiency.

Clinical findings: Vitamin A is necessary for night vision, bone growth and maintenance of normal epithelial tissues. The clinical signs found in vitamin A deficiency are attributable to disturbances of these functions. Deficiency of vitamin A is associated with the thickening of the connective tissue matrix of cerebral dura matter leading to reduced permeability of the arachnoids villi and subsequently increases in the pressure of cerebrospinal fluid (CSF), which is clinically marked by syncope and convulsions.Night blindness (inability to see in dim light) is the foremost clinical finding of vitamin. A deficiency in all species, except in pigs. The sign of night blindness in pigs appear when plasma vitamin A level is very low. Calves show thickening and clouding of cornea, whereas serous mucoid discharge from eyes is noted in other species, changes in the skin include rough, dry coat with shaggy appearance and splitting of the bristle lips in pigs; and heavy deposits of bran like scales on skin in cattle. Scaly hooves with  the unevenly laid down horny layer are noticed in horses.  General effects of vitamin A deficiency are manifested by loss of body weight, emaciation, and stunted growth, loss of reproductive functions and abortion, and increased susceptibility to infections. Signs related to nervous system damage include paralysis of skeletal muscles, abnormality of gait, convulsions and blindness. Dilated pupils, optic disc oedema and varying degrees of peripapllary retinal detachment are also noticed depending on severity of the disease.

Hypovitaminosis-A also induces congenital blindness due to optic nerve constriction and encephalopathy in calves and piglets. Corneal dermoid, microphthalmos and aphakia (absence of lens) are noticed in calves born to vitamin A deficient cows. Congenital defects found in piglets include anophthalmos or microphthalmos, degenerative changes in lens and retina, cleft palate and harelips, accessory ears and malformed hind legs.

Diagnosis: Deficiency of vitamin A should be suspected on presence of the characteristic clinical signs. Detection of papilloedema and testing for night blindness are the simplest tests, which can be used for diagnosis of vitamin A deficiencies in ruminants. Plasma level of vitamin A is a good diagnostic indicator. Normal levels of vitamin A in serum of cattle and pigs are 25-60 µl/dl and 23-29 µl/dl, respectively, which decline to 18 µl/dl in cattle and 11 µl/dl in pigs. CSF pressure also indicates vitamin A status. Marked increase in pressure >200 mm of saline in cattle and pigs, and 70-150 mm in sheep occurs in hypovitaminosis-A. The disease should be differentiated from polioencephalomalacia, hypomagnesaemic tetany, lead poisoning and rabies, which are associated with signs of convulsion. Central blindness also occurs in lead toxicity and polioencephalomalacia. However, vitamin A deficiency is characterized by loss of body condition in addition to convulsions and blindness.

Treatment and Prevention: Parenteral administration of vitamin A @ 440 IU/kg body weight provides quick response in acute conditions. However, chronic cases, particularly with ocular form in cattle, fail to respond. Such cases are recommended for elimination. Heavy dosing of vitamin A should be avoided as it may cause lameness, ataxia, paresis, exostosis, and reduced growth in calves.Daily minimum maintenance requirement of vitamin A for all species is 40 IU per kg body weight. The requirement increases during pregnancy, lactation or rapid growth. The recommended daily dietary allowances of vitamin A for farm animals are, growing calves- 40 IU/kg body weight; lactating cows-80 IU/kg; sheep (growing and early pregnancy)- 30-40 IU/kg; sheep in late pregnancy and lactation- 70-80 IU/kg; growing pigs and pregnant sows 40-50 IU/kg; lactating sows- 70-80 IU/kg, working horses-20-30 IU/kg; growing horses- 40 IU/kg and pregnant and lactating mares- 50 IU/kg body weight. Parenteral or oral administration of vitamin A preparations are also used to prevent its deficiency. Intramuscular administration of vitamin A @ 3000-6000 IU/ kg body weight at 50-60 day intervals is an effective preventive measure.