ARCHIVE FILE
This article was published in 1992
See the original document
Myopathy due to Vitamin E Deficiency and Associated With Heliotrope Poisoning
James Godwin, District Veterinarian, Gundagai
Introduction
According to Caple (1990) there are four circumstances under which myopathy due to Vitamin E deficiency has occurred in sheep in Australia. The case presented here is unusual in that it fits into none of these. Caple lists them as:
1. Lambs less than 6 weeks of age in flocks where ewes have been fed mainly wheat with little roughage during pregnancy and lactation.
2. Lambs, 6 to 12 months old being fed on stubble or dry pasture for several months and then introduced to grain feeding with wheat, lupins or oats.
3. Adult housed 'Sharlea sheep' fed oats: lupins (90:10) with minimal roughage.
4. Adult ewes fed on dry pasture for 4 to 6 months, and then introduced to wheat feeding in late pregnancy. As well as myopathy affected ewes have shown myoglobinuria and haemoglobinuria.
Chapman (1990) discusses another form of myopathy called Lupinosis associated myopathy. In this disease Lupinosis leads to liver damage, and subsequently interference in the 'metabolism and distribution of selenium and possible Vitamin E.'
History
The property upon which the myopathies occurred runs up against the Murrumbidgee River approximately 30 kilometres west of Gundagai.
It comprises 420 hectares of flat to gently undulating country. Pastures comprise of crops - oats for feeding, lucerne flats and native pasture.
There are 1200 sheep and 200 beef cattle run on the property.
Responding to enquiries from the owner regarding an outbreak of lice in his ewes, with 5 months of wool growth, I dropped off a dutjet hand-piece and advisory material on 20/1/92. That day at 1 pm he began jetting the sheep using diazinon at 200 ml/100 litres of water and 150 PSI. Five litres of fluid was applied over 13 seconds.
The sheep had been mustered at 8:30 am by motor bike. They had been walked approximately 600/800 metres. Upon questioning after the deaths, the owner insisted that the sheep had been mustered and walked at a gentle pace.
The temperature on the day was 40°C and had been for approximately 2 days prior.
350 ewes were jetted in that afternoon. The gate out of the yards was opened and the sheep allowed to make their own way back to the paddock.
On the morning of 21st January, 1992 the owner rang to report 5 deaths in the ewes. One of the animals was found within a few metres of the yards. They appeared to have dropped dead without struggle.
I collected 2 animals for post-mortem. They appeared to have been dead for approximately 4 to 6 hours. Upon post-mortem of one animal no gross lesions were noted apart from a brown discoloured liver with a slightly rounded border and multiple focal pinpoint lesions of uniform distribution over the surface and cut surface, yellow in colour and 1/2 mm in diameter consistent with the normal pyrrolizidine alkaloidosis seen on this property in the past.
Samples of organs were collected for Histopathology and aqueous humour for nitrate/nitrite poisoning. At this stage the owner was blaming the Diazinon and I was suspicious of Pyrrolizidine Alkaloids coupled with stress.
Over the day of the 21st and the 22nd approximately another 15 animals died. I was able to attend the property on the afternoon of the 22nd, at which stage I injected Atropine IV into 3 recumbent animals to rule out organophosphate poisoning. No response was seen. Pupillary light response was normal and no other OP poisoning signs noted.
Animals showed sternal recumbency and weakness and were not able to rise. Approximately 10 others showed signs of weakness when approached. But when chased they were able to run away at 'Phar Lap' speed.
One of those animals was pursued and eventually caught. It died within seconds. We decided to retreat immediately working on the premise of stress inducing death from Chronic copper poisoning/Pyrrolizidine Alkaloids.
The next day I was unable to attend the property, but approximately 10 animals died. On the 24th I again attended the property intending to post-mortem further animals and also to rule out Ca & Mg deficiency, approximately 15 animals died.
For the first time we observed weakened animals, able to walk, that had severe hind limb weakness. This was a consistent feature of those animals in a weakened state - approximately 5. One of these animals was captured and taken to the Regional Veterinary Laboratory - the rain at the time making a field post-mortem difficult. None of the other animals responded to IV Calcigol.
At the laboratory a diagnosis of possible nutritional myopathy was rapidly made when incised hind limb muscle was examined.
The owner was advised immediately and the next morning all sheep were drenched with a Selenium drench and placed onto lucerne. Deaths that day were approximately 10.
Deaths tapered immediately and approximately 5 animals died over the next week.
Questioning of the owner post diagnosis revealed that blood coloured urine was commonly seen in the recumbent animals.
The owner advised me that the only time that the sheep had gone without access to green feed was December 1 to January 15.
Rainfall for January was;
| 1st | 12.5 mm |
| 9th | 32 |
| 10th | 23 |
| 23rd | 1 |
| 25th | 23 |
The summer of 1991 - 1992 was one of the most consistently wet for some time. Straight out Vitamin E deficiency seemed an impossibility.
Laboratory Results:
1. Gross Pathology (John Glastonbury)
Extensive areas of fish flesh coloured skeletal muscle obvious in adductor muscles of the pelvic limbs and the psoas and cranial cervical muscles.
The changes in the pelvic limbs were 1-3 cm in diameter as viewed on the cross sectioned surface.
The liver was firm of orange yellow hue and had a knobby surface.
There was an excessive volume of straw coloured pleural fluid.
2. Biochemistry
| Sample | Calcium | Magnesium |
|---|---|---|
| 1 | 1.91 | 1.49 |
| 2 | 1.77 | 1.40 |
| 3 | 2.59 | 2.15 |
(from 3 animals live in the field and recumbent on 24th January, 1992).
| GSH Px 262 | post-mortemed animal |
| Vit A 813.80 moles/kg | post-mortemed animal |
| Vit E 8.66 moles/kg | post-mortemed animal |
| Normal Vit E 15 moles/kg. |
3. Histopathology Findings
1. Severe acute nutritional degenerative myopathy.
2. Chronic degenerative hepatopathy - nodular regenerative hyperplasia.
3. Chronic suppurative bronchopneumonia.
4. Myoglobinuric nephrosis.
5. Mild degenerative myelopathy.
Discussion
Jeremy Allen, from the Department of Agriculture in WA, reported to me by phone conversation that well over 50% of lupinosis cases in Western Australia have muscle damage associated with them.
Discussion by phone with Ivan Caple and Jeremy Allen has led me to believe that the liver damage associated with pyrrolizidine alkaloids could explain the Vitamin E associated Myopathy in these sheep. Both Ivan and Jeremy explained that this could be through either disturbances to the normal metabolism of Vit E or to a reduction in storage of the same, or to a combination of the two.
These sheep were subjected to; (a) Liver damage, (b) exercise - mustering, (c) high environmental temperatures and (d) Copper toxicity - copper is an oxidant. This could all add up to a crisis in which the demand for the metabolism of oxidants could not be met.
No more significance can be drawn from this case than to raise these possibilities. It would be interesting if more muscle was examined histologically, in association with livers, from pyrrolizidine alkaloid cases. Perhaps even Vit E levels with the same.
References
Caple I, Myopathies: Selenium and Vitamin E, in Sheep Medicine, Proceedings 141, Post Graduate Committee in Veterinary Science, pp 359 - 367, July 1990
Chapman H, Myopathies - Non Selenium Responsive, in Sheep Medicine, Proceedings 141, Post Graduate Committee in Veterinary Science, pp 483-492, July 1990