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This article was published in 1981
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Congenital Cardiomyopathy in the Poll Hereford Breed

I.R. Harradine, B.V.Sc., Veterinary Inspector, Grafton

INTRODUCTION

The finding of calves aged three days to six weeks with typical lesions of nutritional cardiomyopathy on post-mortem prompted investigation into tissue and blood selenium levels from specimens submitted. The presence of acute necrosis and mineralisation in the left ventricle of the heart was suggestive of nutritional myopathy. However, the apparently normal blood and tissue selenium levels and the correlation between lesions and the calves having a woolly haircoat prompted the suspicion of a heritable condition.

CASE HISTORY

The property concerned is a typical North Coast beef cattle enterprise comprising one hundred acres with eighty breeders carried. In April, 1980 the owner reported the loss of approximately ten (10) calves all less than six weeks of age over the last five months. Calving on the property is all year round with the majority dropped between spring and late summer.

The first calf post-mortemed on 29th April, 1980 was the tenth such calf lost and indeed had a woolly hair coat. The hair coat is characterised by curly, woolly hair about two to four centimetres in length extending over the entire body but particularly noticeable around the tail and legs. The owner recalled the other calves lost to have had similar hair coats. This calf had been apparently healthy the day before and was found dead first thing in the morning. All calves were given a proprietary selenium drench and an injectable copper compound was given to both cows and calves. Prior to this the herd was blood sampled on 16th May, 1980 for serum copper, magnesium, calcium and selenium. Glutathione Peroxidase was also assayed.

On 2nd July, 1980 three further calves were found dead. Post-mortem on one of the least decomposed carcases revealed Blackleg as the cause with Clostridium chauvoei isolated on anaerobic culture. The herd was then vaccinated and given a further selenium drench.

Results of the herd blood sampling received 22nd July, 1980 showed apparently normal blood selenium and glutathione peroxidase. Copper deficiency was however confirmed.

On 17th December, 1980 another woolly coated calf aged four days in excellent condition died suddenly. Post-mortem revealed the type and distribution of the cardiac lesion to be almost identical to the calf seen on 29th April, 1980. The dam of this second calf post-mortemed had lost a calf in a similar way in December, 1979 having been mated to the same sire, according to the owner.

Selenium drenching ceased when the results of blood sampling arrived but the owner is continuing with copper, vaccination and strategic drenching.

Post-mortem

Gross heart pathology involved the left ventricle, and intraventricular septum. There were multiple confluent pale areas of myocardial mineralisation often forming bands up to 4mm wide particularly on the epicardial surface.

Splash haemorrhages throughout the carcase and marked liver congestion with a zonular pattern was suggestive of acute passive venous congestion. Cardiac failure was the cause of death.

HISTOPATHOLOGY

Heart: Within the left ventricle and left ventricular septum there were multiple confluent cellular areas replacing normal myocardium and composed of histiocytes and proliferating sarcoblasts. There was granular mineralisation of cells within these areas, which frequently contain one or more central foci of coarse calcium deposition. There was no mineralisation of the surrounding myocardial cells which gave way abruptly to the zone of proliferative cellular reaction.

Fibrosis was not prominent but there were some branching areas of loose collagen deposition. These were most obvious in the right ventricular wall which is relatively free of cellular reaction and mineralisation, (Gross lesions were confined to the left ventricle). Myolysis without mineralisation appears to have occurred with minimal inflammatory reaction and minimal evidence of myofibre regeneration.

Liver: Diffuse marked periacinar congestion and degeneration indicating acute passive venous congestion.

Tongue, Diaphragm, Multiple Sections of skeletal Muscles: No evidence of fibre mineralisation or degeneration.

In Summary

Severe multifocal fibrosis and necrosis with mineralisation of the left ventricle. Severe epicardial myolysis and fibrosis (with minimal calcification) of the right ventricle. The gross distribution and microscopic appearance of the myocardial lesion is typical of nutritional myopathy (cardiac 'white muscle disease'). However, the myocardial fibrosis confirms that the changes were present in utero: Congenital cardiomyopathy (four day old calf).

CHEMISTRY

Herd blood sampling of both adults and calves gave a mean selenium of 150 ng/ml and a mean glutathione peroxidase of 270 I.U./gHb. The respective ranges were for selenium 89 - 198 ng/ml and glutathione perodide 167 - 377 I.U./gHb. The normal range for New South Wales cattle will be determined as more samples are tested at Glenfield Veterinary Research Laboratory. New Zealand results for deficient cattle herds are:

Blood Selenium
Deficient less than 10ng/ml
Normal greater than 20ng/ml

Tissue selenium levels from the two calves post-mortemed revealed apparently normal amounts:

CALF SAMPLE SELENIUM ng/g DRY WEIGHT BASIS
1 Heart 930
Kidney 2370
2 Left Ventricle 1466
Septum 1306
Liver 3840
Kidney 3560
3 (Blackleg victim) Heart 1350

Selenium estimations on a group of cattle (age unspecified) used in a parasite trial at Glenfield: Selenium, ng/g, dry weight basis.

KIDNEY CORTEX LIVER SEPTUM LEFT VENTRICLE
MEAN 3805 4697 711 695 672
RANGE: LOW 3078 4026 582 526 508
RANGE: HIGH 4321 5573 843 889 885
(Courtesy Peter Healey)

So the two calves I post-mortemed were found to have much higher Se tissue levels than the Glenfield Veterinary Research Station cattle.

Hartley (1967) quoted normal liver selenium levels to be 400 - 1000 ng/g.

Dr. B.L. Munday, at Mt. Pleasant Laboratories in Tasmania observed that in sporadic cases of 'cardiac white muscle disease' diagnosed in Tasmania, liver selenium levels were not depressed. They were low in calves with skeletal lesions, and in sheep with nutritional myopathy.

Perhaps these calves with apparently normal selenium tissue levels and classical white muscle disease lesions had woolly hair coats. There is a need to establish tissue Selenium levels in 'typical' cases of white muscle disease in cattle.

HERITABILITY

The finding of woolly hair coated poll hereford calves affected with typical cardiac white muscle disease lesions exclusively is suggestive of an inherited condition. This is supported by other herds experiencing similar mortalities (notably a Lismore herd).

Perhaps the gene for a woolly hair coat is associated with an inability to utilise available selenium.

Unfortunately the percentage of the affected calves is unclear.

The second calf post-mortemed was from a cow which lost a calf in a similar way the year before. A bull introduced in 1974 gave rise to the cow which had the first calf post-mortemed. Another poll hereford bull introduced in 1977 was the sire of the second calf post-mortemed.

CONCLUSION

Although we have no concrete evidence to suggest that congenital cardiomyopathy in the poll hereford breed may, in sporadic cases, be a heritable condition, the absence of depressed blood and tissue selenium levels and the association with a woolly hair coat supports the heritable hypothesis.

There is a need to establish tissue selenium levels from all cases of white muscle disease in cattle with particular attention drawn to those sporadic cases seen where a poll hereford woolly hair coat calf is involved.

ACKNOWLEDGEMENTS

1. Special thanks to Roger Cook O.I.C. at the R.V.L. Wollongbar for histopathology and slides.

2. Peter Healey for V.R.S. cattle selenium levels.

REFERENCES

Hartley, W.J. (1967) Symposium: Selenium in Biomedicine. Ed. 0.H. Muth.

Munday, B.L. (1978) Senior Veterinary Pathologist, Mt. Pleasant Laboratories. 'Selenium in Tasmanian Agriculture'


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