Black Leg

Blackleg myositis (Image sourced from Bristol Biomed Image Archive with permission)

Also known as:

Blackquarter '''''

Description

A bacterial disease affecting cattle and sheep caused by Clostridium chauvoei. Latent spores of this organism are deposited in the muscle and liver of ruminants via the circulation resulting in oedematous and crepitant swellings of the muscles.

Signalment

In cattle it is typically beef breeds who are affeceted particularly animals in good health and gaining weight quickly. More frequently occurs in cattle between 6-24 months old but can affect animals of any age. In some animals lesions occur following muscle trauma, which is thought to activate latent spores In cattle, blackleg infection is endogenous, in contrast to malignant edema ( Malignant Edema). Lesions develop without any history of wounds, although bruising or excessive exercise may precipitate some cases. Commonly, the animals that contract blackleg are of the beef breeds, in excellent health, gaining weight, and usually the best animals of their group. Outbreaks occur in which a few new cases are found each day for several days. Most cases are seen in cattle from 6-24 mo old, but thrifty calves as young as 6 wk and cattle as old as 10-12 yr may be affected. The disease usually occurs in summer and fall and is uncommon during the winter. In sheep, the disease is not restricted to the young, and most cases follow some form of injury such as shearing cuts, docking, crutching, or castration. Endogenous blackleg in sheep is uncommon in the USA; it is much more common in New Zealand where blackleg is seen more frequently in sheep than in cattle.

History and Clinical Signs

• 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
• 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