Blackleg is an acute, febrile, highly fatal, worldwide disease of cattle and sheep caused by Clostridium chauvoei and characterized by emphysematous swelling and necrotizing myositis that commonly affects large muscles (clostridial myositis)
C chauvoei is found naturally in the intestinal tract of animals. Spores remain viable in the soil for years and are purported to be a source of infection. Outbreaks of blackleg have occurred in cattle on farms in which recent excavations have occurred, or after flooding. The organisms probably are ingested, pass through the wall of the GI tract, and, after gaining access to the bloodstream, are deposited in muscle and other tissues (spleen, liver, and GI tract) and may remain dormant.
In cattle, blackleg infection is endogenous. Lesions develop without any history of wounds, although bruising or excessive exercise may precipitate disease in some cases. Commonly, the animals that contract blackleg are of the beef breeds, in excellent health, and gaining weight. Outbreaks occur in which a few new cases are found each day, sometimes for several days. Most cases are seen in cattle 6–24 months old, but thrifty calves as young as 6 weeks and cattle as old as 10–12 years may be affected. The disease usually occurs in summer and fall and is uncommon during the winter. In sheep, the disease is almost always the result of a wound infection and often follows some form of injury such as shearing cuts, docking, crutching, or castration. The case fatality rate approaches 100%. In New Zealand, blackleg is seen more frequently in sheep.
Usually, onset is sudden, and a few animals may be found dead without premonitory signs. Acute, severe lameness, more commonly affecting the hind legs, and marked depression are common. Initially, there is a fever, but by the time clinical signs are obvious, body temperature may be normal or subnormal. Characteristic edematous and crepitant swellings develop in the hip, shoulder, chest, back, neck, or elsewhere. At first, the swelling is focal, hot, and painful. In some very rare cases, the tongue can be affected and may protrude. As the disease rapidly progresses, the swelling enlarges, there is crepitation on palpation, and the skin becomes cold and insensitive, with decreased blood supply to affected areas. General clinical signs include prostration and tremors. Death occurs within 12–48 hours. In some cattle, the lesions are restricted to the myocardium and the diaphragm. Clinical signs include abnormal breathing and pericardial friction rub.
A rapidly fatal, febrile disease in well-nourished young cattle, particularly in beef breeds, with crepitant swellings of the large muscles suggests blackleg. The affected muscles are dark red to black and dry and spongy, have a sweetish odor, and are infiltrated with small bubbles but little edema. The lesions may be seen in any muscle, even in the tongue or diaphragm. In sheep, because the lesions of the spontaneously occurring type are often small and deep, they may be overlooked. If available, ultrasonography of affected muscle could support a presumptive diagnosis (irregular muscle tissue, little edema, with gas present).
Occasionally, the tissue changes caused by C septicum, C novyi, C sordellii, and C perfringens may resemble those of blackleg. At times, both C septicum and C chauvoei may be isolated from blackleg lesions, particularly when the carcass is examined ≥24 hours after death, which allows time for postmortem invasion of the tissues by C sordellii.
Field diagnoses are confirmed by laboratory findings of C chauvoei in affected muscle tissue (standard methods: anaerobic culture and biochemical identification). Muscle tissue samples should be collected as soon as possible after death. The fluorescent antibody test for C chauvoei is rapid and reliable. Immunohistochemical testing is performed on formalin-fixed tissue samples. A PCR assay is available and has been reported to be reliable for clinical samples but not for environmental samples.
A multivalent vaccine containing C chauvoei, C septicum, and, where needed, C novyi antigens is safe and reliable for cattle and sheep. Calves 2 months old should be vaccinated twice, 4 weeks apart, followed by annual boosters before the anticipated danger period (usually spring or early summer). In an outbreak, all susceptible cattle should be vaccinated and treated prophylactically with administration of penicillin (10,000 IU/kg, IM) to prevent new cases for as long as 14 days. Cattle should be moved from affected pastures. Vaccine failure has been observed locally and attributed to a deficient spectrum of antigens in the vaccine. In such instances, a bacterin vaccine is produced with local, previously identified clostridial strains of C chauvoei.
Naive ewes should be vaccinated twice, with the second dose 1 month before lambing and then with yearly boosters. In outbreaks in flocks of ewes, administration of prophylactic penicillin and antiserum treatments are recommended. Young sheep should be vaccinated before going to pasture. Immunity in young sheep is relatively short. Clostridial vaccines are reported to create a weaker immune response in sheep and goats than in cattle. Carcasses should be destroyed by burning or deep burial in a fenced-off area to limit heavy spore contamination of the soil.
Useh NM, Nok AJ, and Esievo KAN. (2003) Pathogenesis and pathology of blackleg in ruminants: The role of toxins and neuraminidase. A short review. Vet Quar 25(4):155-159,
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