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Bruce Watt (Tablelands LHPA, Bathurst) and Steven Hum (State Veterinary Diagnostic Laboratory, Menangle)

Posted Flock & Herd December 2012


While a range of infectious, toxic, nutritional, genetic and neoplastic agents can cause cardiomyopathy in cattle, in the experience of the authors it is rare in beef cattle. This report describes a case of spontaneous cardiomyopathy of unknown aetiology in a 15-month-old Angus heifer.


One of 120 August 2011 drop Angus heifers was observed with a marked swelling of the brisket. The heifer was weaned in late March, when the mob was treated with moxidectin and injected with 5-in-1 vaccine and barium selenate. They were then drenched with triclabendazole and oxfendazole in late May and given a 5-in-1 booster, and treated with ivermectin plus clorsulon in late August. The mob ran on improved pastures dominated by Currie cocksfoot (Dactylis glomerata), Australian phalaris (Phalaris aquatica), Demeter fescue (Festuca arundinacea), Ladino or Haifa white clover (Trifolium repens) and Woogenellup subterranean clover (Trifolium subterraneum) and was supplemented with safflower meal from July until early September. While the meal was availablead lib., on average 1.5-2.0 kg was consumed per head per day.

Clinical findings

The heifer, examined on 20 November 2012 was bright, alert and responsive and while in moderate body condition was judged to be about 80 kg lighter than her cohort. The swelling below the mandibles, in the caudal neck and brisket and ventral abdomen pitted, suggesting that it was oedema fluid. The heart was audible on both sides of the chest cavity with a rapid beat of approximately 100 bpm. No lung sounds were audible. Respiration was rapid (about 40 bpm), laboured on inspiration and occasionally open-mouthed.

The owner decided to attempt treatment with antibiotics for a few days followed by euthanasia if the heifer deteriorated. However, she died overnight on 22 November and was autopsied on the morning of the 23 November.

Image of bovine showing lower neck swelling
Figure 1. Affected heifer showing anasarca

Laboratory Findings

Blood and urine were submitted to the laboratory with the aim of determining if hypoproteinaemia was the cause of the oedema. Blood protein levels (and both the albumin and globulin fractions) were within the normal range. Fibrinogen levels were low (1 g/L, normal 3-7) but GGT and AST levels were mildly elevated (98 compared to normal of 0-35 U/L and 158 compared to 0-120 U/L respectively). Urine protein levels were normal. Other blood parameters were unremarkable.


The autopsy revealed anasarca in the ventral neck, left foreleg, brisket and ventral abdomen. The thoracic cavity contained an estimated 5 litres of straw-coloured fluid. The lungs appeared compressed and atelectic. However, there was no evidence of inflammation of the lungs or pleura. The heart appeared larger and more rounded than normal with a white, thickened, corrugated epicardial surface. On cut surface, the myocardium appeared normal. The liver appeared to be normal in size but the cut surface showed a ‘nutmeg’ pattern. No abnormalities were detected in the mediastinum.

Image of post-mortem view of bovine thorax
Figure 2. Thoracic cavity showing hydrothorax, heart enlargement and atelectic lungs
Image of post-mortem view of bovine heart
Figure 3. Heart in situ, pericardial sac removed

Laboratory Findings

Histologic examination revealed a diffuse interfibrillary oedema and multifocal areas of myofibrillar degeneration associated with interstitial fibrosis. The liver was diffusely congested with dilation and severe congestion around central venules, findings typical for congestive heart failure.

histopathology image of heart tissue
Figure 5. Heart - Oedema, fibrillar degeneration and fibrosis
histopathology image of liver tissue
Figure 4. Liver showing dilated and congested central venule


This heifer, at 15 months, is beyond the age when most inherited cardiomyopathies, gossypol poisoning and vitamin E/selenium deficiency (and foot-and-mouth disease) might be included in the differential diagnosis of cardiomyopathy. However, mature Holstein Friesians suffer an inherited dilated cardiomyopathy. Poisoning by ionophores, sodium fluoro acetate, plants containing cardiac glycosides and neoplastic infiltrations remain possibilities. Neither the history nor subsequent findings support these possibilities. Staphylococcus aureus, Histophilus somni and Mycobacterium spp are all known to cause myocarditis with subsequent cardiomyopathy (Radostits et al. 2007, Vermunt et al. 2010). Vermunt et al. (2010) however commented that ‘myocarditis can also occur after a bacteraemia (or) septicaemia regardless of the aetiological agent.’

Since the original definition, the term cardiomyopathy has been used loosely to describe any abnormality of the myocardium for which aetiology cannot be defined. It remains essentially a diagnosis by exclusion. In the absence of a plausible explanation as listed above and the fact that inherited cardiomyopathy has not been reported in Angus cattle the condition remains an ‘idiopathic primary myocardial disease’.


  1. Vermunt JJ, Malmo J and Parkinson. Respiratory conditions, chapter 5 in TJ Parkinson TJ, Vermunt JJ and Malmo J. Diseases of Cattle in Australasia. A comprehensive textbook (New Zealand Veterinary Association Foundation for Continuing Education, Wellington, 2010)
  2. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. Veterinary Medicine, 10th Edition, 2007
  3. Jubb KVF, Kennedy PC and Palmer NC. Pathology of Domestic Animals. 5th edn. Vol 3, Elsevier Limited; 2007:44-50


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