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Bruce Watt (Tablelands Livestock Health and Pest Authority, Bathurst) and Patrick Staples (State Veterinary Diagnostic Laboratory, Menangle)

Posted Flock & Herd December 2012


The manager of a cattle property in the Peelwood district (north of Goulburn and southeast of Bathurst) noticed that a one-month-old Angus calf became lethargic then died on 8 September 2012. Subsequently two more large well-grown calves were noticed to be lethargic and suffered respiratory distress when mustered. Both died and one was presented for autopsy. All calves were from a mob of 22 first-calf Angus heifers that commenced calving on 1 August 2012.


A well-grown calf weighing approximately 80 kg was presented for autopsy on 12 September 2012. The moderately autolysed carcass showed no evidence of dehydration or diarrhoea. The lungs were dark red, heavy and wet especially ventrally but there was no line of demarcation as might typify pneumonia. The trachea contained white froth and the heart appeared enlarged and spherical. The right ventricle was similar in size to the left. There was a diamond-shaped, white patch about 4 cm in diameter on the epicardial surface. It did not appear to extend into the myocardium. There were petechial haemorrhages on the epicardial surface. The bowel contents were pasty and yellow.

Samples were forwarded to the State Veterinary Laboratory for histopathological examination.

Image of post-mortem view of bovine heart
Figure 1. Heart showing right-sided enlargement and white discolouration, presumably due to myonecrosis and mineralisation


The myocardium contained extensive areas of necrosis and fibrosis. Necrotic myofibres were shrunken and stained hypereosinophilically. Mild to moderate infiltrates of macrophages, fewer lymphocytes and scattered, regenerative myoblasts were present. Von Kossa stain revealed numerous, fine granules of calcium (mineralisation) within the cytoplasm of necrotic myofibres. The histopathological diagnosis was of severe subacute to chronic, myocardial necrosis and replacement fibrosis.

The lungs showed changes consistent with heart failure. They were congested and oedematous with protein-rich oedema fluid present within alveolar lumina and interlobular septa. Alveoli also contained some fibrin casts and mild infiltrates of macrophages and fewer neutrophils. Focal haemorrhages were present.


On 19 September 2012, the mob and pastures were examined. The mob of first calf heifers with 1-2 month old calves at foot appeared well grown and clinically normal. Five calves and five heifers selected at random were blood tested to establish selenium status and CK levels.

GAHPX (40-300 u/gHb) CK (0-300 U/L)
Calf 1 9 257
Calf 2 6 343
Calf 3 10 7209
Calf 4 5 450
Calf 5 4 210
Heifer 1 1 252
Heifer 2 3 382
Heifer 3 2 271
Heifer 4 3 955
Heifer 5 4 371
Table 1. GSHPx and CK levels from heifers and calves in the affected mob
Image of black cows with calves
Figure 2. A sample of the mob of heifers with calves at foot
Image of paddock
Figure 3. The clover dominant pasture


In view of the severe lesion of myocardial necrosis, accompanying pulmonary congestion and oedema and exceptionally low GSHPx levels, a diagnosis of acute nutritional muscular dystrophy (white muscle disease with myocardial involvement) was made.


The soils and pastures of the central and southern tablelands of NSW are well known to be selenium deficient (Watt 2007, Parkinson et al. 2010), however clinical nutritional muscular dystrophy (NMD) or ‘white muscle disease’ is rare. Parkinson et al. (2010) suggest that ‘selenium is not the only moderator of risk of NMD and that the presence of other antioxidants, especially vitamin E, modify the risk of clinical disease.’

Subacute NMD involving the skeletal muscles occurred during 2011 in the Tarana district of the central tablelands (Watt and Rajkumar 2011) although the owner reported that some calves had also died suddenly, perhaps from myocardial disease. In this case, the primary manifestation was exercise intolerance followed by death, due to NMD of the myocardium.

The 2011 and 2012 cases share some interesting similarities. Both occurred in well-grown 6-8 week old calves in September on exceptionally well fertilised, clover dominant pastures. In both cases, the dams of the calves had remarkably low GSHPx levels (ranging from 0-1 u/gHb in the Tarana case and 1-4 u/gHb in the Peelwood case) and yet appeared healthy, in excellent body condition with no evidence of impaired fertility or retained foetal membranes. While ill thrift is described as a manifestation of selenium deficiency, it was not evident in either of these two cases.

One of five calves had a moderately increased CK level. This suggests a sub-clinical myopathy. Nonetheless, this level was an order of magnitude lower than those seen in the clinically affected calves in 2011.


  1. Parkinson, TJ, Vermunt, JJ and Malmo, J 2010, Diseases of Cattle in Australasia: a comprehensive textbook, The New Zealand Veterinary Association Foundation for Continuing Education, Wellington
  2. Watt BR. (2007) A Serological and Trace Mineral survey of Beef Heifers in Central NSW Australian Cattle Veterinarian's Conference, Townsville
  3. Watt BR and Rajkumar T (2011) A case of subacute nutritional muscular dystrophy in calves. www.flockandherd.net.au accessed 15 December 2012


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