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CASE NOTES


BLACKLEG CAUSING ACUTE MYOCARDITIS IN A HEREFORD CROSS CALF

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

Posted Flock & Herd December 2012

Introduction

Blackleg is an acute myositis caused by the activation of latent intramuscular Clostridium chauvoei spores. It commonly kills unvaccinated cattle between 3 months and two years of age especially in higher rainfall areas such as the coast of NSW. Blackleg usually commences in skeletal muscles but occasionally the heart or diaphragm is affected. This is a report of a case in which the myocardium was considered the primary site of infection.

History

A single well-grown bull calf, described as ‘one of the best,’ of 350 calves was noticed to be dull on the afternoon of 7 December. The calf died about 6:00 pm and was autopsied about 6:30 am next morning. The calf had not yet been marked or vaccinated. The cows were not vaccinated pre-calving against clostridial diseases.

Image of dead bovine
Figure 1. The affected well-grown unvaccinated 3-month-old bull calf

Background

The calf was a well-grown Hereford cross bull that had been dead about 12 hours. There was blood from the nose and mouth and gas was palpable under the skin of the trunk. The carcass was moderately autolysed. Small patches of dark muscle were detected through the lumbar muscles. The heart was adhered to the pericardium and when separated diffuse small fibrin tags could be seen on the endocardial surface. There was a dark red patch of myocardium approx 3 X 2 cm on the right ventricle (Figure 2).

Image of bovine right ventricle
Figure 2. Right ventricle showing dark red patch of myonecrosis and fibrin tags.
Image of cut surface of bovine right ventricle
Figure 3. Cut surface, wall of right ventricle showing foci of myonecrosis, emitting gas bubbles.
Image of bovine musculature post-mortem
Figure 4. Small foci of myonecrosis in lumbar musculature

Laboratory Findings

Sections of the heart revealed severe diffuse congestion, multifocal haemorrhages, extensive coagulative myofibrillar necrosis, abundant fibrinopurulent exudate and occasional intralesional clostridial organisms. There were similar but more acute and less developed inflammatory changes in the skeletal muscle with extensive haemorrhages and large number of organisms.

Fluorescent antibody test conducted on impression smears of skeletal muscle was positive for Cl. chauvoei but negative for Cl. novyi, Cl. septicum and Cl. sordelli.

Image of bovine epicardium histopathology
Figure 5. Severe congestion, necrosis and fibrinopurulent exudate, epicardium
Image of bovine myocardium histopathology
Figure 6. Coagulative myofibrillar necrosis (left) and fibrinopurulent exudate (right), heart
histopatholgy section of bovine epicardium
Figure 7. Cl. chauvoei organisms in the heart (centre)

Discussion

Blackleg can cause severe financial losses in endemic areas. Risk factors include unvaccinated, rapidly growing cattle on a high plane of nutrition. It is usually thought of as a disease of cattle and occasionally of sheep but outbreak of disease has also been recorded in deer. Necropsy findings are quite characteristic and consist of severe gangrenous myositis usually confined to the upper part of one limb, but occasionally lesions can be seen at the base of the tongue, in heart, diaphragm, psoas muscles, brisket and udder. Gangrenous change may be small, to escape cursory examination and can be present in more than one location. Changes in muscle are often accompanied by copious oedema, emphysema, haemorrhage and a sweet butyric smell, like rancid butter.

Differential diagnosis should include ‘Malignant oedema’, ‘Anthrax’, ‘lightning strike’ ‘bacillary haemoglobinuria’, and other causes of sudden unexpected death. Blackleg can be confirmed by histologic examination of suspected muscle lesion and demonstration of the organism by fluorescent antibody test on air-dried impression smears as described in this case.

Reference

  1. Radostits OM, Gay CC, Hinchcliff KW and Constable PD, Veterinary Medicine, 10th Edition 2007

 


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