Muscular Dystrophy, also known as White Muscle Disease or Stiff Lamb Disease, has been known for many years, and was diagnosed clinically in America in the early 1920's.
A similar condition in many breeds of animals has been called by varying names, such as Dietary Hepatic Necrosis in rats, Multiple Dietary Necrotic Degeneration in mice, Exudative Diathemis in chicks and many others. All apparently respond to treatment with Vitamin E and/or selenium and most workers consider them allied pathologically.
Originally, Muscular Dystrophy in lambs was considered to be due to a Vitamin E deficiency, but subsequently Vitamin E was found not to prevent entirely the condition when ewes were fed on a ration deficient in alpha-tocopherol and selenium, but supplementation with selenium gave much better protection than supplementation with Vitamin E (Muth et al. 1959). The same workers showed that Muscular Dystrophy could be present without clinical signs of macroscopic lesions, but macroscopically, muscle tissue could show degeneration, and the normal procedure was to examine heart muscle and the proximal portion of the semitendinosus muscle of all lambs in their experiments.
In New Zealand considerable investigations have been carried out over the last 10 years, and a condition known as Hogget Ill Thrift appears to be associated with White Muscle Disease (Clarke and Filmer, 1958). Workers in New Zealand have been experimenting with dosing ewes and lambs to prevent the disease.
An optimum dose of 2.5-5 mgs. to lambs is suggested by Jolly (1960), to be repeated twice to check unthrifty lamb mortalities and result in the best weight gains. It is also suggested that a high number of empty ewes could be associated with congenital White Muscle Disease (Grant, Hartley and Drake, 1960).
Selenium was shown to give some protection against perinatal deaths in lambs due to White Muscle Disease, if given to ewes during pregnancy, while alpha-tocopherol did not; selenium almost completely prevented White Muscle Disease and alpha-tocopherol gave some protection when given to lambs 2-3 weeks of age (Drake, Grant and Hartley, 1960, Part 1).
The same workers also found that selenium administered to unthrifty lambs after weaning gave significant weight gains on 15 out of 22 properties and in the more severely affected flocks mortalities were markedly reduced (Drake et al. 1960, Part 2).
Hartley (1953) points out the stress factor of moving ewes and lambs, and thus precipitating outbreaks of the disease. This has been noted in some outbreaks in N.S.W.
Muscular Dystrophy in lambs was first recognised in Australia on the Northern Tablelands of N.S.W. in 1955, and widespread outbreaks occurred in the spring of 1959. At the same time it was recognised on the Southern Tablelands of N.S.W. at Cooma and Goulburn (Walker et al. 1961).
The disease is characterised clinically by leg weakness in both front and hind legs and arched back. The lamb is first noticed walking stifly, and as the condition progresses over a day or so the legs will suddenly give way and the animal will lie down for a short time, and then rising walk stifly again, soon to collapse as before. Finally, the lamb is unable to rise and death usually results, probably from starvation, after a few days, although some lambs do recover without treatment. Cases are uncommon in lambs less than one week old, and occur mostly at 2-4 weeks of age.
There appears to be no relationship in regard to sex or the type of country. Out of 19 properties where the disease has been diagnosed on the Northern Tablelands, 13 were on basalt, three on granite and three on trap, which is really granite formation. All properties have been highly improved and sown to pastures, and regularly top-dressed with superphosphate.
On postmortem examination the skeletal muscles of both hind and front legs are affected most commonly, usually bilaterally symmetrically. The psoas, intercostal muscles and, occasionally, the diaphragm are affected. Heart lesions, although common in New Zealand, have been found here in four cases only. These lesions are seen most often beneath the endocardium of the ventricles and are of a splash nature.
The muscles are pale and the lesions may involve the whole or portion of the muscle bundle. On histopathological examination, up to 90 per cent of muscle fibres show necrosis with hyaline degeneration, fibrosis and even calcification (Walker et al.. 1961). As stated before, muscle which may appear normal macroscopically can show significant change microscopically, up to 20 per cent of cells showing degeneration.
The most reliable diagnostic method is by glutamate oxalacetate transaminase (G.O.T.) test of blood serum, positive cases being greater than 100 units/ml, while showing a normal bilirubin concentration up to 4.6 ug/ml.
Response to selenium has been spectacular and most lambs recover after dosing with 1 ml. of a solution containing 1 mg. of sodium selenite per ml. Selenium may also be injected subcutaneously. In some flocks 100 per cent recovery has been noted. An incidence of 50 per cent of lambs affected in a mob, which had been subjected to stress when the flock was brought in for shearing. was seen this year. From one paddock on this property half of 94 lambs out of 91 Merino ewes showed evidence of being affected when mustered for shearing. Treatment resulted in all lambs except three recovering within 24 hours. In a mob from another paddock, 63 lambs from 82 young ewes again showed about 50 per cent incidence, and all lambs had recovered within 24 hours. These lambs were between four and 10 weeks of age. On another property, 16 affected lambs were treated in the paddock, and next day only one stiff lamb could be found and it was improved.
During 1960, experiments were conducted to endeavour to prevent Muscular Dystrophy by dosing ewes before lambing with selenium and also dosing the lambs when 2-3 weeks of age. Vitamin E dosing was also included in some experiments. Little Muscular Dystrophy was seen during 1960 when these experiments were conducted, as the season was much drier and apparently not conducive to outbreaks of the disease. However, on one property in the Glen Innes district an outbreak did occur and eight cases were seen in lambs from the control ewes, one lamb in the Vitamin E group and none in the selenium dosed group (Setchell et al. 1961).
During the spring of 1961, further outbreaks of this disease occurred and pasture conditions in certain parts of the Glen Innes district were more favourable than in 1960. It has been noted that on one property where all ewes were dosed with selenium, prior to lambing, cases have been seen and treated in the lambs. This was on the property previously mentioned when 16 cases were detected. The mob consisted of 300 young crossbred ewes and lambing had not been completed, although nearly 100 per cent was expected.
Experiments to determine if there is any weight gain, due to dosing lambs with selenium, have been generally inconclusive, and on only two properties in the Armidale district has there been any significant response (Setchell et al. 1961, unpublished). Further trials are being conducted this year and are now in progress. One trial in the Glen Innes district does not appear to be showing any significant difference.
DISCUSSION
White Muscle Disease appears now to be well established in N.S.W., and especially on the Northern Tablelands. Under good seasonal conditions it is probable that there will be a higher incidence. Experiments confirm the fact that selenium is efficient in treating the condition.
The lack of general growth response in lambs could be due to the fact that our experiments have not been conducted on similar lines to those in New Zealand. Trials on the Northern Tablelands have been on properties with a history of Muscular Dystrophy in the previous year, but there has not been any evidence of clinical cases in the flock either before or during the trials themselves. The dose of selenium has been 1 mg, repeated each four weeks.
Jolly (1960) used unthrifty lambs and not normally healthy lambs, and also the dosage, and frequency of dosage, were much higher, even up to 5 mg, of selenium at two-weekly intervals. He suggests that 2.5 mg. or 5 mg. should be used at each dosing. McLean et al. (1959) administered 1 mg. each 10 days and showed growth responses in six out of nine trials varying between 12 per cent and 40 per cent.
SUMMARY
The history of Muscular Dystrophy and its incidence in N.S.W. is mentioned.
Trials to determine what protection was afforded to lambs by treating ewes with selenium and Vitamin E have been carried out. Treatment of affected lambs with selenium has proved apparently highly successful.
The reasons for the lack of weight gains in selenium dosed lambs when compared with results in New Zealand are discussed.
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