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This article was published in 1993
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Hypovitaminosis A and E in a Cattle Feedlot
B.A. VANSELOW, Regional Veterinary Laboratory, NSW Agriculture, Armidale, NSW 2351 & R.J. HUNTER, Glen Innes Veterinary Clinic, 233 Ferguson Street, Glen Innes, NSW 2370
The association of clinical disease in grazing animals with a prolonged lack of fresh green feed is age old. Jeremiah Ch.14, verse 6 describes wild asses whose 'eyes did fail because there was no grass'. Perhaps these were the observations of an ancient D.V.!
In the feedlot situation, grain and silage based diets contain inadequate amounts of β-carotene (the precursor of vitamin A) and vitamin E to maintain rapidly growing animals, and therefore supplementation is essential.
When grazing animals ingest green feed, the β-carotene is split into two molecules of vitamin A in the small intestine. The vitamin A is carried in the bloodstream and stored in the liver. Some ß-carotene is also absorbed and has been recently shown to have antioxidant properties. Vitamin A is necessary for the development of epithelial cells, for normal bone growth, and for the production of visual purple (rhodopsin), the retinal pigment required for adaptation to poor light. Both vitamin A and β-carotene are easily oxidised and destroyed particularly in the presence of oxygen, heat, light and moisture. Vitamin A (whether stabilised or not) is more rapidly oxidised when trace minerals are mixed with it as a concentrate. Excessive nitrates, deficiency of phosphorus, deficiency of vitamin E, infectious disease, parasitic infestations, and diarrhoea may all affect the availability of vitamin A from the intestine. Vitamin A storage is principally in the liver and the level in blood changes little until the liver stores are virtually depleted and then a rapid fall in blood values occurs.
Vitamin E is an antioxidant produced by plants which is particularly abundant in seeds in association with their high content of polyunsaturated fatty acids (PUFAs). Various formations exist but α-tocopherol is the most important biologically in mammals (Greek tocos = childbirth, phero = to bear - related to the early discovery of the role of vitamin E in fertility). Prior to absorption, vitamin E is emulsified by bile in the small intestine. Pre-intestinal destruction can occur e.g. microbial action in the rumen, high levels of PUFA in the diet or absorption may be impaired e.g. in lipid malabsorption or in association with excess vitamin A in the diet. Little tissue storage occurs - the liver is not a specific storage organ as it is with vitamin A. Proportionally more vitamin E is present in fat than in other tissues. α-tocopherol fits into the membranes of organelles (microsomes, mitochondria) where it acts as a lipid soluble antioxidant protecting adjacent polyunsaturated phospholipids and sulphydryl groups that play a major role in maintaining membrane integrity and permeability. The vitamin E requirements of ruminants partly depends on the amount of PUFA in the diet. Hydrogenation of PUFA in the rumen is not complete and in an acid environment (acidosis), hydrogenation would not occur. PUFAs are easily oxidised. The resultant free radicals produced, may in turn oxidise polyunsaturated phospholipids and sulphydryl groups in membranes causing membrane damage. Glutathione peroxidase is also an intracellular antioxidant but it acts in the cytoplasm while α-tocopherol acts in the membranes. In situations of marginal deficiency of either vitamin E or selenium, adequate levels of the other antioxidant will prevent disease. Gross deficiency of either antioxidant will result in oxidative damage. The clinical manifestations of vitamin E deficiency are related to membrane damage with the organs and tissues affected varying between species. This may be related to the genetic makeup of membranes and their susceptibility to oxidative damage.
A combined deficiency of vitamin A and E was diagnosed in finisher cattle in a 12,000 head feedlot producing beef for the Japanese market. It was estimated that approximately 2,000 cattle were affected at any one time (i.e. cattle between 220 and 300 days in the feedlot). The diet was based on grain and corn silage and although each animal had been injected with 1,000,000 IU vitamin A and 100 IU Vitamin E at the time of entry, there was no additional supplementation.
The clinical condition became obvious in the summer months. Animals were noticed to be suffering from clear ocular and nasal discharges, swollen hind legs, varying degrees of lameness and incoordination, exophthalmus, 'glazed' bluish appearance to the eyes, poor adaptation to dull light with pupils more dilated than normal and occasional cases of complete blindness, with no pupillary light reflex. In advanced cases the swelling or oedema in the hind legs progressed to include oedema of all four legs, and extended to the shoulder and under the jaw. A number of affected animals were also seen to have corneal ulcerations, possibly as a result of injuries incurred through poor vision. Affected animals also showed a poor tolerance of hot weather. Their body temperatures were above normal in the middle of the day (ambient temperature 23.8°C and no wind) when compared with unaffected cattle. This was associated with increased respiration, drooling of saliva and occasionally panting. When observed in the cool evening these same animals showed no evidence of hyperthermia. Deaths of clinically affected animals occurred during hot weather and during prolonged transportation.
Pathological findings consistent with vitamin A deficiency included squamous metaplasia of the parotid salivary duct and papillo-oedema of the optic nerve. Grossly and histopathologically oedema occurred in subcutaneous tissue, within muscle bundles and within nerve bundles. Microangiopathy was identified in association with and probably as a cause of the oedema. It has yet to be ascertained as to whether the microangiopathy was due to low vitamin A or E, or both.
From severely affected animals both serum and liver levels of vitamin A and E were below normal. Serum levels of both vitamins were measured in relation to 'days on feed'. Both levels dropped with time, with vitamin A dropping to its critically low level at approximately 180 days and vitamin E not dropping to its accepted low level. From liver samples collected at slaughter, vitamins A and E were deficient. That is, vitamin A levels appeared to be critically depleted first with vitamin E levels becoming critically depleted in the clinically ill animals. CPK and LDH values were elevated in severely affected animals.
Following the commencement of oral supplementation at a rate of 40,000 IU Vitamin A, 11.2 IU Vitamin E per head per day, the clinical condition disappeared and serum vitamin A levels rose above the critical level. The vitamin E level has since been increased to 100 IU per head per day.
Vitamin A and E requirements are high for rapidly growing animals and may be particularly high when the preference is for marbled meat with a high fat content. The requirement for vitamin A is greater in hot weather and it is conceivable from our observations that either vitamin A or E or both are required for effective thermoregulation.
SAMPLE COLLECTION FOR DIAGNOSIS
Serum or plasma - at least 2 ml, protected from light and heat. Can be stored frozen. Liver - approx. 2 cm cube, protected from light and heat. Can be stored frozen.
[Note - these tests are expensive with approx. costs of $40.00 per serum sample and $100.00 per tissue sample for vitamins A and E together.]
Parotid Salivary gland (not mandibular), plus parotid duct if possible, for histopathology.
CONVERSION FACTORS FOR VITAMIN A AND E
VITAMIN A RECOMMENDATIONS FOR FEEDLOT CATTLE
| TYPE OF ANIMAL | ANIMAL WEIGHT lb | DAILY INTAKE/ANIMAL* | ||
|---|---|---|---|---|
| CAROTENE mg | OR | VITAMIN A IU | ||
| CALVES FINISHING AS SHORT YEARLINGS | 400 | 75 | 30,000 | |
| 600 | 78 | 35,000 | ||
| 800 | 100 | 40,000 | ||
| 1,000 | 125 | 50,000 | ||
| FINISHING YEARLINGS | 600 TO 1,100 | 125 | 50,000 | |
| FINISHING 2-YR. OLDS | 800 TO 1,200 | 125 | 50,000 | |
* In addition each animal may be given 0.5 to 1 million IU of injectable vitamin A at the time of entry
VITAMIN E RECOMMENDATIONS FOR FEEDLOT CATTLE
20-50 IU supplementary oral Vitamin E/head/day especially during the finishing period. Recent studies have shown beneficial effects on meat keeping quality with oral supplementation at 500 IU per head/day. These higher levels have also been associated with a lowered incidence of infectious disease.
BOVINE VITAMIN A & VITAMIN E LEVELS
| VITAMIN A (µmol/l) | VITAMIN E (µmol/l) | ||
|---|---|---|---|
| SERUM | Deficient | <0.9 | <4.6 |
| Normal | 0.9-2.1 | 4.6-20 | |
| VITAMIN A (µmol/kg) | VITAMIN E (µmol/kg) | ||
| LIVER | Deficient | <17 | <11.6 |
| Normal | 20-1000 | 21-102 |