11. Deficiencies of certain antioxidants (beta carotene, vitamin E) in cattle.

Question 1

Vitamin A Cause(primary and secondary)?

Answer 1

Vitamin A and beta-carotene deficiencies

Cause

• Primary: absolute deficiency in supply (prolonged droughts on pasture, dried sugar beet pulp, poor quality hay

and concentrate, high level of PUFAs in food, lack of colostrum in calves)

• Secondary: maldigestion, malabsorption, interfered conversion of beta-carotene to vitamin A in intestinal

epithelium or lack of storage in the damaged liver

Question 2

Signs of Vit A deficiency?

Answer 2

Signs

• Clinical signs are not common (liver stores vitamin A is high)
• There’s two ways maternal deficiency can to it, either:
• Maternal deficiency leads to constriction of the optic nerve canal which leads to necrosis of the optic nerve

which leads to blindness in calf

• Maternal deficiency leads to increased intracranial pressure which leads to increased susceptibility to infections

(E. coli)

• Adult: loss of reproductive functions, retained placenta, night blindness (due to lack in regeneration of visual

purple), papillary oedema

Question 3

Early diagnosis of Vit A deficiency?

Answer 3

Early diagnosis

• Monitoring cow’s plasma for beta-carotene (check the colour of plasma) - Treatment: beta-carotene

supplementation, vitamin A 400-500 IU/kgbw IM

Question 4

Prevention of Vit A deficiency?

Answer 4

Prevention

• Turning to green vegetation if possible
• B-carotene supplementation
• Vitamin A 400-500IU/Kgbw IM

Question 5

Vitamin B1 deficiency cause?

Answer 5

Vitamin B1 (aneurin, thiamine) deficiency

Cause:

• Primary

o Lack of vitamin in diet (rare)

• Secondary

o Due to increased thiaminase activity (clostridia)

o Amprolium (coccidiostat - thiamine antagonist)

o Due to intensive, concentrate-rich ratio

o Diets high in sulphates

Question 6

Signs and Treatment of CCN?

Answer 6

Signs

• Cerebrocortical necrosis (CCN, polioencephalomalacia)
• Mainly in young beef cattle and lambs
• Blindness, muscle tremor, champing of jaws, salivation
• Recumbency, opisthotonos, clonic-tonic convulsion, UMN signs
• Menace (threatening) reflex is absent, frequently nystagmus

Treatment of CCN

• Thiamine hydrochloride 10 mg/bwkg repeat 3-5X (effective only within a few hours after onset)

Question 7

Vitamin E causes?

Answer 7

Vitamin E

• The delayed form of selenium/ Vitamin E deficiency is usually seen in calves between 1 and 4 months old
• Signs are usually precipitated by sudden unaccustomed exercise typically following turn out to pasture in the

spring

• The clinical appearance varies according to the muscles affected

Question 8

Clinical signs of Vitamin E?

Answer 8

Clinical signs

• Skeletal muscles

o There is a sudden onset stiffness and inability to stand

o Otherwise, the calf is bright and alert with a normal appetite

• Respiratory muscles

o The calf presents with respiratory distress

• Cardiac muscles

o There is sudden death without previous signs of illness

Question 9

Diagnosis of vit E deficiency?

Answer 9

Diagnosis

• Haematology
• Enzyme concentrations

o Muscle damage and/or identify typical changes at post mortem examination

• Whole blood glutathione peroxidase (selenium containing enzyme)

o Standard biochemical test for selenium deficiency

Question 10

Treatment of vit E deficiency?

Answer 10

Treatment

• Sodium selenate or selenite may be given by injection, usually combined with vitamin E and will provide

adequate selenium supplementation for up to 3 months

• The response to treatment may take 4-7 days

Question 11

Prevention/control measure of Vit E deficiency?

Answer 11

Prevention/ control measure

• SC injections of barium selenate
• Oral dosage 0.1mg/kg sodium selenate
• Intraruminal soluble glass boluses provide slow release of selenium
• Selenium and vitamin E are frequently added to concentrate rations for feeding