VITAMINS

Only the fat-soluble vitamins A, D and E have any major importance in ruminant diseases. Vitamin E and selenium are discussed in Chapter 3.

Vitamin A

Cattle obtain their vitamin A from carotene, which is the yellow pigment present in abundance in all green plants.

Provided the animals are grazing or are receiving well-made forage, deficiency is unlikely to occur, although maize silage can be deficient in carotene. Drying, bleaching and weathering of grass will reduce carotene levels, however, and there is relatively little in cereal grains. Overheating of hay and prolonged storage also reduce the vitamin A content. Cattle fed on poor-quality hay in winter or on a straw and cereal diet will need additional supplementation, and levels of 10 million i.u./ton are usually recommended. Provided that the feeding of the dry cows is adequate, colostrum will be rich in vitamin A and give the calf the reserves it will need during its suckling period. This is often not the case, however, and winter-born calves may be deficient, leading to an increased susceptibility to scouring, pneumonia and other diseases. This is why many farms inject vitamins A, D and E to all winter-born calves and consider they get a response.

Deficiency of vitamin A produces a variety of symptoms. There is decreased appetite leading to reduced growth and, even in the early stages, night vision is impaired. Reproductive function may be affected and there may be an increase in the number of stillborn calves. This could be especially relevant when the dry cows are being fed only very poor-quality fodder. Fainting fits may also be seen: the calf collapses as if in a deep sleep, and a few minutes later it gets up and walks away quite normally. In the later stages of deficiency bone growth becomes affected. This can cause pressure on the nerve to the eye and eventually leads to total blindness.

Most of the changes (apart from total blindness) are reversed when the deficient animal is injected with vitamin A. Vitamin A assists in maintaining the membranes of the body in a healthy state and deficient animals are more susceptible to diseases such as ringworm, calf pneumonia and scouring.

A diagnosis of vitamin A deficiency is made from an investigation of the history of the animal, especially the diet, from an analysis of blood and/or liver samples, and from response to treatment.

Vitamin D

Vitamin D is involved with the absorption of calcium and phosphorus from the intestine, the absorption and deposition of minerals in bone and the maintenance of normal blood levels. Details of its action in conjunction with parathyroid hormone are discussed in the milk fever section in Chapter 6, which should be read in conjunction with the following.

There is relatively little vitamin D in plants, and cattle obtain the majority of their requirements by synthesising the vitamin in the skin under the influence of ultra-violet light from the sun. Milk contains only low levels, and calves fed solely on milk may develop a deficiency. However, deficiency is most likely to occur in young growing cattle in dimly lit buildings during the winter, especially when only poor-quality hay is being fed. A similar syndrome, involving non-specific lameness and multiple spontaneous fractures, has been seen in rapidly growing beef calves on a diet of maize silage and maize gluten which had no mineral or vitamin supplementation and has been referred to as metabolic demineralisation.

The symptoms are those of rickets: growth rates are reduced, the legs may be bent and have abnormal swellings and many animals show stiffness and lameness. The teeth may be pitted and out of line and the jawbone deformed. Treatment is by injecting vitamin D and by correcting the ration, which may include oral supplementation with vitamin D.

Vitamin K

Vitamin K is involved in blood clotting mechanisms.

It is synthesised by the ruminal micro-organisms and there are also ample supplies in leafy forages. Primary deficiency does not occur therefore, although deficiency may be induced by poisoning with dicoumarols, compounds which prevent the action of vitamin K. Sources of dicoumarol include warfarin rat poison and mouldy clover hay. The latter is sometimes known as sweet clover poisoning. Symptoms are caused by a failure of blood clotting and include bleeding excessively from cuts, the appearance of large red haemorrhagic areas on the membranes of the mouth, eyes or nose, abdominal pain and lameness. The latter is due to haemorrhage into the joints. The treatment is to give vitamin K by mouth or by injection and to try to identify and remove the source of the poison.

B Vitamins

The B vitamins are all synthesised by the micro-organisms in the rumen and the excess is absorbed by the cow. They are also present in ample quantities in milk, so primary dietary deficiency is never seen. Induced deficiencies can occur however, for example with CCN (Chapter 3), where there is a factor preventing the action of thiamine (vitamin B₁), and with cobalt deficiency which leads to inadequate vitamin B₁₂. There is evidence that supplementation with biotin (vitamin B₆) will improve the quality of the hoof and reduce the incidence of sandcracks and of white line lesions.

Although all B vitamins are synthesised in the rumen, there is very little storage in the body. Temporary deficiencies can therefore occur during illness and anorexia, for example following a toxic mastitis, and particularly following severe ruminal upsets such as acidosis (Chapter 6) and overeating (Chapter 13). Injection of B vitamins would be a sensible supplementary therapy for such animals.

Vitamin C

Vitamin C is produced in the tissues of all farm livestock. A dietary supply is therefore unnecessary and deficiency is never seen. Only man and guinea pigs are unable to synthesise vitamin C.

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Source: Blowey R.W.. A Veterinary Book for Dairy Farmers. 3rd Edition. — Old Pond Publishing,1999. — 480 p.. 1999

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