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This article was published in 1983
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Nutritional Myopathy Due to Vitamin E Deficiency in Merino Weaners

G. Timmins, B.V.Sc., Veterinary Inspector, COOMA

A Vitamin E deficiency in 4 - 8 month old Merino weaners that have been hand fed prior to and after weaning on a cereal grain and lucerne hay ration (a suspected case has also occurred on a Barastock nut (containing Vitamin E) and lucerne hay ration). A few, to virtually all the skeletal muscles have been affected. I feel that the problem may be exacerbated by marginal Selenium levels. During the month, after 15th Feb., 1983, - 20 properties - 16,000 weaners experienced losses to greater or lesser extent.

INTRODUCTION

The Cooma P.P. Board district has been continuously drought declared since 1/12/79 and the pasture situation has been declining over the past three years and four months to the stage now where there is virtually nil paddock feed available.

In the spring, summer and autumn period of 1980 and 1981, even though the pasture feed available was very low, most graziers had something aside after weaning in the form of lucerne, oat crops or a saved pasture paddock to put their weaners onto after weaning.

Unfortunately, there was no meaningful rain forthcoming in the spring, summer or 1st 3 wks. autumn of 1982 - 1983 such that a lot of graziers were faced with the decision of either virtually giving weaners away in the saleyard or putting them into a survival feeding situation, whether it be in a very small area or in the paddock. If they didn't hand feed them they were faced with the stark reality that they would die from malnutrition.

EARLY PROBLEMS

The main early problems run into were grain/concentrate poisoning, or malnutrition from shy feeders and lambs that were either too young or in too light a condition with no body reserves when first put into the lot feed situation.

Losses ranged from 3% to 25% depending upon the standard of management and the weight and age of the lambs when they were introduced to the total hand feeding situation.

The losses so far appear to be reasonably similar whether they are locked up in a very small area or put in a paddock with a minimal amount of paddock feed available.

The losses from such things as worms, coccidiosis, pink eye and E. ovis were minimal and to my knowledge there were no losses from lack of water which was mainly available from troughs.

At this stage the above problems have been more or less ironed out and now the main concern is to keep the remaining viable lambs alive. The next thing to crop up was a Nutritional Myopathy.

TYPICAL CASE HISTORY

MAY JUNE 1982

Ewes fed May/June to mid-August on a ration of 300g to kg of cereal grain (corn/nuts/wheat/barley) per head per day, plus lucerne fed out 3 times per week.

MID-AUGUST TO LATE SEPTEMBER

Lambing began mid-August to late September, Lambed in paddocks containing adequate pasture. Feeding ceased for 1 - 2 months.

NOVEMBER

Feeding recommenced when lambs were 4 - 6 weeks old to ewes and lambs. Cereal grain/nuts 3009 to 600g per ewe/lamb unit per day, fed out 3 times per week.

JANUARY/FEB

Weaned January/Feb. into mobs containing 100 - 800 weaners in each mob. Put into lot feed or paddock situations with very little green pick. NM has been seen within 2-6 weeks of going into a virtually total hand feeding situation.

A BRIEF REVIEW OF NUTRITIONAL MYOPATHIES

1. Congenital White Muscle Disease

2. Delayed White Muscle Disease

3. Nutritional Myopathy in South West NSW

Nutritional Myopathy in sheep in South Western NSW was reported by Mr. Dave Kennedy, Veterinary Officer at the Veterinary Officers' Conference in August, 1981. Twenty reported instances in the 4 years from July 1977. The quality of the feed in these cases was noted on 14 occasions:

It was also reported that:

Dave Kennedy felt that probably the lack of green feed in dry pasture and stubbles may lead to Vitamin E deficiency in weaners.

4. Mr. Ned Buckley, Veterinary Inspector, Wagga, at the Veterinary Inspectors' Conference, 1980, reported losses of 1% - 3% on several properties where long term grazing on cereal stubble had occurred. In one instance, lambs were being fed cereal stubble plus oats in self-feeders. Most outbreaks responded to Vitamin E - one did not, but immediately responded to Selenium.

5. Nutritional Myopathy in the Cooma/Bombala Area

Acute Nutritional Myopathy in the 4 - 8 month age group after long term feeding cereal grain/nuts and lucerne hay. A generalised paling of some to all of the skeletal muscles is seen.

PRESENTING PROBLEM

Reasonably to particularly healthy and reasonable to very well grown weaners become affected and die over a 24 to 48 hour period. The losses seem to occur in twos and threes in a dribbling type every few days or so. It usually takes the grazier a while to either, (a) become concerned, or (b) recognise that reasonably healthy lambs are dying under unexplained circumstances.

CLINICAL SIGNS

Some of the lambs were found either down or dead. From other cases it seems they were initially lethargic, inclined to lie down, showed a slight stiffness of gait; within a very short time lambs go down, become prostrate and can't lift their heads. They exhibit short, rapid abdominal breathing. Some dribbling of clear saliva from the mouth was noted in quite a few instances.

POST-MORTEM FINDINGS

Post-mortems were carried out on both dead and affected cases The post-mortem findings in general were very similar -

The lesions were not typical of what I have seen in delayed WMD in good years, though I guess the position presented here is (a) basically a Vitamin E deficiency, and (b) so acute there is no time for calcium deposition to produce chalky white areas.

CAUSE OF DEATH

SPECIMENS TO COLLECT

RESULTS TO DATE

PLASMA

NB - Normal levels - Vitamin E > 1.5 µM/l.

1. ASF

2. HPL

3. LEI

4. ILI

5. ASC

HISTOPATHOLOGY RESULTS

All sections of affected leg muscles

LEI, Adaminaby

Very severe hyalinisation of 90% of muscle fibres. These changes were non-inflammatory in origin.

ASC, Berridale

Widespread degeneration of muscle fibres - many groups of fibres showing severe liquefactive necrosis. Individual fibres within these affected groups showed hyaline degeneration. No inflammatory response was seen apart from macrophage infiltration.

NWA, Cooma

Varying stages of degeneration affecting most groups of muscle fibres. Advanced liquefactive necrosis was evident within many fibres and some individual fibres showed hyalinisation. These changes were non-inflammatory in origin.

DIAGNOSIS: NUTRITIONAL MYOPATHY

N.B. No gross heart lesions seen. Awaiting Histopathology results for heart muscle.

TREATMENT OF AFFECTED ANIMALS

Administer 3 thousand international units (iu's) of Vitamin E. If not too acutely affected the animal should recover in about 3 days. To ensure adequate Selenium levels, 2 mg of Selenium is also administered in the form of an oral drench, because marginal Se levels have been found in blood samples analysed to date. You could also try giving 1 mL of Selenium/Vitamin E injection per day for 4 days, but I don't feel that enough Vitamin E can be made available to the animal by this method of administration to elicit a response. The two types of injectable I have on hand are marketed by Essex Laboratories, (a) B0-SE containing 1 mg of Selenium and 68 iu's of Vitamin E per ml, (b) E-SE containing 2 mg of Selenium and 68 iu's of Vitamin E per ml. Of course, by this method of administration all the vitamin E injected should become available to the animal because there are no ruminal factors knocking out the Vitamin E, and/or interfering with its absorption.

PRODUCTS AVAILABLE

1. Vitamin E - water miscible 10% - made by Roche.
Comes in 1 litre containers and is a yellowish/green liquid: which contains 100 iu's per ml. Cost: $15-00 per litre or 1.5c per ml.

Dose Costs:
250iu - 3.75 cents
500iu - 7.5 cents
1000iu - 15 cents

2. Feed Grade Vitamin E - distributed by Colburn-Dawes, wagga - (purchased from Roche)

Feed grade Vitamin E containing 50% Vitamin E that is, 5 hundred thousand iu's per kilogram. Cost: $24-00 per kg or 4.8c per 1,000 iu dose.

I did a feeding trial to see if weaners would eat treated grain. They don't like it, but will eat it over a two hour period. Of course, the intake per animal with this method of administration is very questionable. It does not mix with water very well because an oily fraction sets on top.

3. Rovimex E. Type 20 W

200 iu x-Tocophenyl per gram.
Dose of 1000 iu's - require 5 grams.

But its dispersibility in water is only 100 mg in 10 ml therefore to give a weaner 1000 iu's you would have to give 100 ml/weaner!

PREVENTION DOSE REQUIREMENTS

At this stage I am hoping that a 250 iu dose will control the problem for two weeks, but since the condition, when it arises is so acute, and it appears that the vitamin E levels of the animal are so low, it may well be that a dose of 1,000 iu's or more may be required to give a reasonable measure of control (say 2 weeks) especially if adverse climatic conditions or other stress factors are imposed on the weaners. Basically the limited supply of easily administrable Vitamin E is limiting me to this dose, e.g. 10 days after 250 iu's Vitamin E/2mg Se one ex 1300 died Acute NM. But, did it miss the drench?

Of course, the ultimate means of prevention is to place the animals onto green pasture.

PROPERTIES AND LOSSES

During the month after 15 February when the first case showed up on a property in the Berridale district, 20 properties, involving 16 thousand weaners from varied and widespread areas of the Cooma district had the problem of unexplained Merino weaner deaths to a greater or lesser extent.

The presenting problem, clinical sign and post-mortem lesions were all very similar.

During this period the weather was unseasonably hot - we experienced several days during March which were hotter than we had experienced for 15 years. We also received occasional showers and cold nights during this period which meant that the weaners were subjected, even though it never got extremely cold, to a wide variation in temperatures.

LOSSES

Approximately 2½% of viable lambs, that is, we had already lost the shy feeders grain poisoning, weaker, lighter lambs due to malnutrition, misadventure, or smothering, so that lambs we have lost over the last month have basically been unexpected deaths of viable lambs.

Listed below are some of the losses experienced:

L. Platts

LPH 12 x 2000
36 x 1900 ram weaners
4 x 1400 ewe weaners
TL 6 x 1200 mainly wethers
PL 6 x 300
NW 9 x 270 all ewe weaners
BL (?)30 x 550 nuts and luc. hay
AS 6 x 250
AF 30 x 1200
RB 20 x 250
TB 12 x 100
CM 20 x 600
PR 8 x 1000 c
LM 4 x 130

ECONOMIC IMPORTANCE

1. By this stage a tremendous amount of grazier's time and effort has been put into keeping the lambs going. We are now talking about viable lambs that have had an estimated $5-00 - $6-00 per head spent on them after all rebates have been received. We want to keep these lambs alive.

2. Future breeders/wool-cutters.

3. Since this sort of problem had not been envisaged a lot can be learnt from the present experience with regard to keeping animals alive, healthy and growing well in a lot feed situation, dose rates required, clinical responses to treatment and methods of administration of Vitamin E.

OBSERVATION ON SHEARING

Due to animals being in close contact, and the fact that it does not make a lot of difference in the long term with regard to weight gain, we have not advised for any of the weaners to be shorn. With regard to confinement, I was worried about infection of shearing cuts.

Unbeknown to me, one property did shear 700 odd weaners that were in a lot feed situation at a stocking rate of about 500 per acre and even the smallest shearing cuts developed tremendous infections and many lambs were lost. This property was also experiencing losses due to N.M. So, maybe, the Vitamin E deficiency played a role in these massive infections.

DISCUSSION

Normal Sources of Vitamin E:

Supposedly abundant in natural foods such as cereal grains, green leaves, legumes, nuts and particularly the oil from wheatgerm.

It has been found that if none of the above are incorporated into the diet of rats, reproductive deficiencies in both males and females occur. No such problems appear in to occur in ruminants.

Absorption

It is a fat soluble Vitamin and apparently is absorbed from the intestinal tract and stored to some extent in body fats and muscles.

Types

Vitamin E comes from a group of compounds called Tocopherols. There are several Tocopherols, but Alpha Tocopherol has by far the greatest biological potency. Beta and Gamma tocopherol have between 10% - 20% the activity of Alpha.

1 mg of Alpha-Tocopherol - one international unit of Vitamin E.

Alpha-tocopherol content of feedstuffs

Feedstuff mg/kg
Lucerne Hay
   Dehydrated, 17% protein 28-121 Illustrates the extreme variation in α-Tocopherol content of various typical feedstuffs
   Dehydrated, 20% protein 38-141
   Sun-cured, 13% protein 18-61
   Hay 52-53
Corn 11-35
Barley 22-43
Linseed meal 3-10
Soybean meal, 44% protein 2-5

Bunnell et al. 1968. Journal Agricultural Food Chemicals.

Tocopherol content of feedstuffs

Feed evaluation done Glenfield years ago - Vitamin E.

α-Tocopherol Content mg/kg
Wheat 6.42
Corn 1.60
Barley 4.70
Dried Lucerne Leaves 160
Beta & Gamma Content
Wheat 7.93
Corn 14.40
Barley 16.60
Lucerne No figure

Considering Beta and Alpha have 10-20% the biological activity of Alpha-Toc. then the Alpha-toc. Equivalent

per lb
Wheat 8.80 iu/kg 4
Corn 6.40 3
Barley 10.23 4.6
Dried Lucerne leaves 160 72
Source of Feed Wheat Trangie
Corn V.R.S.
Barley Wagga
Lucerne V.R.S. Shed

A comparison of the Vitamin E levels in the feed stuffs with the requirement suggests that most typical production rations contain adequate Vitamin E far cattle and sheep.

We are not looking at production feeding here. We are looking at Survival Feeding.

Even so, for an average ration, say ¾lb wheat (340gm) & ¼lb luc. hay (113gm) per day at 72 i.u./lb for luc. hay & 3 i.u./lb for wheat = 3 i.u. from wheat & 18 i.u. from luc. hay = 21 i.u. Vit. E/day

BUT if only

9 i.u./lb for luc. hay = 3 i.u. from wheat & 2¼ i.u. from luc. hay = 5¼ i.u. Vit. E/day

The fact that a deficiency is occurring is good evidence that either tremendous losses occur or other factors are inhibiting its utilisation.

Either way, the fact that a deficiency is occurring etc. as above in the three lines enclosed in black.

SUGGESTIONS

  1. Cut lucerne left in the paddock for four days may lose as much as 60%.
  2. A further 50% of the balance can occur after 1 month's storage.
  3. Mouldy hay - any mould present helps to knockout Vitamin E.
  4. When grain or green feed is mixed with minerals, ground as peed and pelleted you could increase oxidation of Vitamin E.
  5. Corn: The total Vitamin E content of corn may contain only 5 to 40% of Alpha-tocopherol plus mould and moisture.
  6. Low Selenium rations could result in high requirement for Vitamin E. Wheat is traditionally low in Selenium.
  7. Lucerne Hay: There may be an antagonist in lucerne hay which further decreases Vitamin E.
  8. Placental Barrier: We know a pre-lambing Selenium dose is transferred to lambs and protects them from congenital WMD. With regard to Vitamin E there appears to be a placental barrier.
  9. Storage: It appears that although ruminants will absorb Vitamin E and store it in muscle and fats, they are not able to store large amounts.
  10. When lucerne is at high levels in a young ruminant diet storage of Vitamin A in the liver is decreased and serum levels are lowered. This may also apply to Vitamin E.

CONCLUSION

This is basically Vitamin E deficiency with the situation probably being made worse by marginal Selenium deficiency.

Cause: Long term feeding cereal grain/hay ration.

Treatment: 3,000 iu's Vitamin E plus 2 mg Se.

Prevention: when the problem arises 1,000 iu's Vitamin E and 2 mg Se/weaners.

REFERENCE MATERIAL

Se/Vit E findings, trialsetc., ROCHE.

The Therapeutic Jungle Proc. 39. 1978.

Hungerford's Diseases of Livestock' 9th Edit.

Sheep Course Notes, Proc. 58. 1981.

Puch & Patton 'Physics & Biochem.' 9th Edit.

Harrow & Mayur 9th Edit.

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