Difference between revisions of "Black Leg"
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(New page: right|thumb|100px|<small><center>Blackleg myositis (Image sourced from Bristol Biomed Image Archive with permission)</center></small> *Causative agent: ''...) |
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− | + | [[Image:Black leg myositis.jpg|right|thumb|100px|<small><center>Blackleg myositis (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | |
− | + | *Causative agent: ''[[Clostridium chauvoei]]'' | |
− | + | *May affect the fattest cattle at pasture in the summer | |
− | + | *Rapid toxaemia -> death | |
− | + | *If clinical signs observed: | |
− | + | **Toxaemia -> pyrexia, depression, [[Lungs Circulatory - Pathology#Pulmonary oedema|pulmonary oedema]], circulatory collapse | |
− | + | **Muscle lesions -> lameness, swollen hot muscles later becoming cool as necrosis sets in | |
− | + | *Pathogenesis: | |
− | + | **Spores gain entry to GI tract -> blood -> muscle -> lie latent | |
− | + | **Under right conditions (usually anaerobic following injury) they germinate and bacilli grow | |
− | + | **Toxin damages capillaries -> serosanguinous exudate | |
− | + | **Muscle necrosis due to gas producing bacteria -> emphysaema and crepitus | |
− | + | *Grossly: | |
− | + | **Early stages | |
− | + | ***At muscle periphery | |
− | + | ***Dark red | |
− | + | ***Distended by serous or serosanguinous exudate | |
− | + | ***Wet cut surface | |
− | + | **Old stages | |
− | + | ***Centre of lesion is full of gas bubbles, porous, dry, reddish black | |
− | + | ***Rancid odour | |
− | + | *Histologically: | |
− | + | **Early stages | |
− | + | ***Separation of myofibres by exudate | |
− | + | ***[[Necrosis - Pathology#Coagulation Necrosis|Coagulative necrosis]] | |
− | + | ***No nuclei | |
− | + | **Old stage | |
− | + | ***Fragmented muscle fibres separated by gas bubbles | |
− | [[ | + | ***Gram positive bacilli may be found in clumps |
− | + | [[Category:Sheep]][[Category:To_Do_-_Clinical]] | |
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Revision as of 10:34, 1 July 2010
- Causative agent: Clostridium chauvoei
- May affect the fattest cattle at pasture in the summer
- Rapid toxaemia -> death
- If clinical signs observed:
- Toxaemia -> pyrexia, depression, pulmonary oedema, circulatory collapse
- Muscle lesions -> lameness, swollen hot muscles later becoming cool as necrosis sets in
- Pathogenesis:
- Spores gain entry to GI tract -> blood -> muscle -> lie latent
- Under right conditions (usually anaerobic following injury) they germinate and bacilli grow
- Toxin damages capillaries -> serosanguinous exudate
- Muscle necrosis due to gas producing bacteria -> emphysaema and crepitus
- Grossly:
- Early stages
- At muscle periphery
- Dark red
- Distended by serous or serosanguinous exudate
- Wet cut surface
- Old stages
- Centre of lesion is full of gas bubbles, porous, dry, reddish black
- Rancid odour
- Early stages
- Histologically:
- Early stages
- Separation of myofibres by exudate
- Coagulative necrosis
- No nuclei
- Old stage
- Fragmented muscle fibres separated by gas bubbles
- Gram positive bacilli may be found in clumps
- Early stages