VITAMIN – A

Vitamin A deficiency is caused by an in sufficient supply of the Vitamin in the ration or its
defective absorption from the alimentary canal. In young animals manifestations of deficiency
are compression of brain and spinal cord. As Vitamin A deficiency results in ↑CSF pressure. In
adult animals the syndrome produces – Night blindness, Corneal Keratinization, Pityriasis,
defects in the hooves, loss of B.W. and infertility. Congenital defects are common
manifestations. Congenital defects are common in off springs in deficient dam.
ETIOLOGY:
• Primary deficiency: absolute deficiency of Vitamin A or its precursor carotene in the diet.
• Secondary deficiency: digestion, absorption or metabolism is interfered
• Chronic disease of liver (poor storage) or Intestine( poor absorption)
• Poisoning with chlorinated naphthalene’s. It interrupts conversion of carotene to Vit A.
• Deficiency of P may lower the efficiency of carotene conversion.
• Long term ingestion of mineral oil hinders absorption of carotene from intestine.
• Lack of carotene in diet due to confined housing with feed limited to poor quality hay,
wheat pulp, grains.
• Commercial mixed feed may loose carotene of original feed during processing/storage.

PATHOGENESIS: Vitamin A is essential for the regeneration of the visual purple necessary for
dim light vision, essential for normal bone growth and for maintenance of normal epithelial
tissues.
Deprivation of the vitamin produces effects largely on the following :
– Night Vision: Ability to see in dim light is reduced.
– An Increase in Cerebrospinal fluid pressure: First abnormality to occur in hypo
vitaminosis –A in calves. It is more sensitive indicator than ocular changes.
– Bone growth – Vitamin A maintain normal position and activity of osteoblasts
and osteoclasts. It’s deficiency leads to incoordination of bone growth and
shape of bones.
– Epithelial tissues – Vitamin A deficiency atrophy of all epithelial cells, but
important effects are limited to those types of epithelial tissue which have a
secretary as well as covering function. In deficiency – Secretary cells
gradually replaced by stratified, keratinized epithelial cells common to non-
Secretary epithelial tissues. Ex : Salivary glands urogenital tract including
placenta, paraoccular glands and teeth. The Secretion of thyroxin is markedly
reduced.
– Embryological development : Vitamin A is essential for organ formation during
growth of faetus. Its deficiency causes multiple congenital defects in pig,
rabbits and rats
Clinical signs :
(1) Occular signs –
• Congenital xerosis, Biot’s spot, conjuctival and corneal xerosis.
• Secondary ocular signs – Night blindness, Corneal scar
• Xerophthalmia : Thickening and clouding of the cornea due to abnormal dryness
of conjunctiva. It is due to non secretary a goblet cells. It is seen in dog and
calves.
• Blindness - The ocular form of hypovitaminosis-A occurs usually in yearling
Cattle (12-18months) Blindness in both eyes during day light, pupils are dilated
and fixed, menance reflex is absent, Palpebral and corneal reflexes are present .
• Congenital defects – Observed in Piglets and calves. In Calves the defects are
limited to congenital blindness due to optic nerve constriction and
encephalopathy.
• In Piglets – Anophthalmos - Complete absence of the eyes or microphtholmos
–Small eyes, Presence of cleft palate and harelip.
(2) Change in the skin – A rough, dry coat with a shaggy appearance and splitting of the bristle
tips in pigs. Keratinization, Heavy deposits of bran like scales on the skin in the affected cattle.
Dry, scaly hooves with multiple vertical cracks are seen in horses.
(3) Body Weight – Loss of body weight because of loss of epithelium of GIT and secretion →
poor absorption.
(4) Reproductive efficiency – Both male and female are affected. In Male-Libido is retained but
degeneration of the terminative epithelium of the semniferous tubules causes reduction in the
number of motile spermatozoa. In Female – Placental degeneration lead to abortion and the
birth of dead or weak young. Retention of Placenta is common.
(5) Nervous System : Due to damage of CNS Paralysis of skeletal muscles damage of peripheral
never roots. Encephalopathy due to ↑d intracranial pressure. Blindness due to constriction of
the optic never canal. In Paralytic from- Disturbance in gait due to weakness and in
coordination in hind legs first and forelimbs later. In pigs, there may be Stiffness of the legs,
silted gait or Flaccidity, Knuckling of the Fetlocks and sagging of hind quarters. In terminal
stage complete limb paralysis occurs.
• Convulsions – Encephalopathy associated with an increase in CSF pressure, is
manifested by convulsions. it is common in calves at 6-8months of age.
DIAGNOSIS :-
• (1) Clinical Signs
• (2) Clinical Pathology :
• (1) Plasma Vitamin A level 20 µg/dl is the minimal concentration of Vitamin A.
• (2) Plasma carotene : In cattle 150 µg/dl are optimum, Clinical signs develop the level
fall to 9 µg/dl.
• (3) Hepatic Vitamin A – Liver Vitamin A critical level 2 µg/g of liver
• Liver Vitamin A Normal level 60 µg/g of liver
• Liver carotene Normal 4 µg/g of liver, critical 0.5µg/g of liver
• (4) CSF Pressure: In calves Normal Pressure 100 mm of saline H2O
• In deficiencay ↑ pressure 200 mm of saline H2O
• In Sheep Normal Pressure 55-66 mm of saline H2O
In deficiency ↑ Normal Pressure 70-150 mm of saline H2O

DIFFERENTIAL DIAGNOSIS:
Convulsive form of Vitamin A deficiency in cattle must be differentiated from
Hypomagnesemiatetany, polioencephalomalacia, Lead Poisoning, Rabies,
Paralytic form :Pseudo Rabies, Viral encephalomyelitis, Salt Poisoning, Organic Arsenic
poisoning

TREATMENT : Parentral injection of an aqueous rather than oily 440 IU/kg BW I/M
• Calves with clinical signs due to ↑CSF pressure will return to normal with in 48 hrs
after treatment.

CONTROL :
• Provide minimum Vitamin A requirement in feed i.e. 40 IU/Kg BW
• Commonly supplied level 60-80IU /kg BW but 50% extra added during pregnancy
and lactation.
• Supplementation may be daily or weekly by grain or concentrate feed. Injection at an
interval of 60 days, In late pregnancy @ 3000-6000IU/kgBW protect calf.
• Proper colostrum feeding
• Green fodder should be given regularly

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 VITAMIN – D DEFICIENCY

DISCUSSED IN DETAIL UNDER BONE DISEASE OSTEODYSTROPHY, RICKETS,

OSTEOMALASIA

• Clinical signs –
• Reduced productivity,
• ↓ Appetite, poor weight gain in growing animals,
• Reproductive efficiency may be reduced.
• In late stage lameness, particularly in fore legs.
• In young animals bending of the long bones and enlargement of the joints may be
noticed.
• Treatment
• Calf: 150000-225000 IU Total dose
• Other ruminants young ones: 20000-40000 IU Total dose
• Dog: 20-275 IU/Kg
• Control
• Sun dried (cured) hay should be given to farm animals kept indoor.
• Calciferol @ 11000 IU /kg BW gives protection for 3-6 months in ruminants.
• Administration of Vitamin D3 3 lakh – 6 lakhs IU/ml to pregnant ewes before 2
months of lambing. 3,00,000 IU – protects lambs for further deficiency.

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VITAMIN E DEFICIENCY
ANTI STERILITY FACTOR
DISCUSSED IN DETAIL IN MINERAL DISEASE UNDER SE DEFICIENCY

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 VITAMIN K DEFICIENCY

A primary deficiency of vitamin K is unlikely under natural conditions in domestic animals

because of the high content of substances with vitamin K activity in most plants and the
substantial synthesis of these substances by microbial activity in the alimentary canal.

• Vitamin K, as a fat-soluble vitamin, impairment of the flow of bile reduces the digestion
and absorption of this fat-soluble vitamin.
• Antibiotic in feed may reduce microflora of gut leading to decreased Vit K production
• Neonates are relatively vitamin K deficient
• Prothrombin time (PT) and activated partial thromboplastin time (aPTT) are prolonged,
along with decreased levels of vitamin K–dependent factors II, VII, IX, and X.

PIGLETS: Hypersensitivity, anemia, anorexia, weakness, and a marked increase in prothrombin

time. Affected pigs fail to grow, become pale, develop large subcutaneous hematomas, and
exhibit lameness and epistaxis.
Vitamin K, or vitamin K2, given at a dose of 3 mg/kg BW IM as a single dose,
Vitamin K3 added to the feed at a rate of 25 mg/kg for 4 days was also shown to be effective

FOAL: Vitamin K–dependent bleeding evident as multiple hemorrhages or hemarthroses.

Administration of vitamin K (2 mg/kg SC q 12 h for 2 days and then 0.5 mg/kg SC q 12 h for 17
days). Vitamin K3 administered parenterally to horses causes kidney failure.

POISONING
• Sweetclover poisoning: Toxic quantities of coumarin severely depress the prothrombin
levels of the blood and interfere with its clotting mechanism.

• Warfarin poisoning: Industrial poisons used in rodent control that contain

anticoagulants of the coumarin type cause fatal hypothrombinemia; vitamin K is an
effective antidote.

As antidote Vit K1 @ 5-10 mg/kg SC every 4 to 6 hours until the PT returns to baseline values is
recommended.

For warfarin-induced anticoagulation in the horse, the administration of 300 to 500 mg (5-
10mg/kg) of Vitamin K1 (only Vit K1) SC every 4 to 6 hours until the PT returns to baseline
values is recommended.

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