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This article was published in 1981
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Nutritional Myopathy in Sheep
E.P. Buckley, B.V.Sc., Veterinary Inspector, Wagga Wagga
Recorded are several property histories where Myopathy has been recorded in sheep in the Wagga district during 1980. Similar conditions have been encountered in Jerilderie district on several properties and in Gundagai, Young, Albury and Hay. During 1980 spring and since trials were instituted to regularly weigh and sample lambs on properties where the disease had previously occurred, but the measured parameters tend to indicate that repeat outbreaks are unlikely on those properties.
Literature indicates that similar outbreaks have been occurring in western Victoria and Western Australia. L
Traditionally 'White Muscle Disease' has been associated with Selenium deficiency on lush clover dominant spring pastures, but in all of the cases here recorded the early occurrence was in animals subject to long term grazing on cereal stubbles. One or two outbreaks may have then continued in untreated stock into the following spring.
(Property) 1. Experimental ewes on stubble grazing trial. 8.2.80 4 ex 400 dead - 3 on previous day, one in transit to laboratory. Lupin stubbles had also been grazed and main diagnostic effort was directed at confirmation that this was not responsible (no hepatitis apart from old pyrrolizidine alkaloidosis - no fungus in stubble). The reason I suspect myopathy was the reported marked haemosiderosis in kidneys from both ewes examined. 21.2.80 - ewes yarded for treatment and 2 dropped dead, 2 more down that night were bled and showed marked suspect haemoglobinuria. These were later showed to have SGOT levels in excess of 2000 µ/litre (normal less than 100 µ/litre). The pigment in the urine was confirmed as myoglobin.
On 13.5.80 a sudden death in a sucker lamb was undiagnosed.
On 5.8.80 staggers in a dorset horn ram was undiagnosed.
On 9.9.80 a downer lambed ewe was presented at the lab. Serum calcium was 8.0 mg/100 ml, magnesium 3.7 mg/100ml. Hypocalcaemia was the diagnosis offered but Histopath. did reveal some degenerative myopathy and haemoglobin or myoglobin casts in kidneys.
Property 2. Downer lambs were a problem in a line of shorn carry over lambs being fed on oat self feeders in a stubble paddock. A blood sample was taken for mineral estimation. Calcium was marginally deficient (8.4 mg/100ml) but S.G.O.T. at 4000 µ/litre and S.C.P.K. at 495 µ/litre were markedly elevated. The condition was controlled by Vitamin A, D & E dosing.
Property 3. A Poll Dorset Stud was suffering quite heavy losses in weaner ram lambs on 14.4.80. 5 of 200 had died and 2 were stilty gaited and inappetent. Sera was collected and the mob injected with 'Janajec 500' Vitamins A, D3 & E. The lab reported one lamb deficient in calcium (4.3 mg/100ml). On 24.4.80 8-10 lambs had died and 10 or so were stiff and tucked up. A ram lamb was removed to the laboratory. P.M. revealed slightly pale muscles and myoglobinuria later S.C.O.T. of 5300 µ/L and S.C.P.K. of 31,000 µ/L revealed very severe leaking of muscle enzymes. A week later a report came to hand that G.O.T. & C.P.K. levels were similarly severely elevated in sera collected on 14.4.80.
This outbreak had not responded to Vitamin E treatment but immediately cleared up after Selenium drenching.
Property 4. Polwarth aged ewes had reported 40 ex 500 deaths over lambing maybe with pregnancy toxaemia symptoms early, but later just stiff, stilty gait and sudden death.
Histopathology only mentioned oedema of interstitium in skeletal muscles but no more died after selenium drenching.
On 9.10.80 I was called out to a 2 Y. old ewe (which age group were not previously supplemented) which were then suffering occasional stilty staggers and losses particularly when yarded. One downer showed marked degeneration in Quadriceps muscles. S.G.O.T. 610 µ/litre and S.C.P.K. 121 µ/litre.
However this ewe showed a blood glutathione peroxidase level of 238/µmoles/gHb and kidney selenium level of 4980 mg (dry weight basis) both of which are normal levels.
DISCUSSION
Probably both Selenium deficiency and Vitamin E deficiency would appear to be involved in outbreaks of myopathy in sheep in the Riverina in the autumn of 1980. At least two of these outbreaks were still affecting some animals in the following spring. Veterinary Inspector Jerilderie has also recorded some further outbreaks in the spring of 1980.
The condition is not easily differentiated from other conditions. I have been requested to confirm this disease in one outbreak of grain engorgement in recently shorn lambs for example. However the condition in all cases recorded here followed a considerable period of grazing on cereal stubbles. These of course are subject to heavy sulphate application during cropping.
Second point of some significance in the aetiology of this condition is the failure of one of these cases to respond to Vitamin E supplements, but immediate response to Selenium. Reports from Western Victoria and indications from other outbreaks in this state are that Vitamin E response may be better than response to Selenium.
Thirdly the number of unanswered queries warrants further investigation. Is this an emerging condition or a result of dry summer pasture growth? Is the occurrence the result of changed stubble flora as a result of changed agronomic management?
A closer and more widespread surveillance of animals at risk may help to provide answers to some of these questions, but the occurrence in diverse regions over recent seasons may indicate an emerging problem. The severe myoglobinuria has not been a previous lesion which has been overlooked.