Blackleg is an acute, febrile, highly fatal disease of cattle and sheep caused by Clostridium chauvoei and characterized by emphysematous swelling, commonly affecting heavy muscles (clostridial myositis). It is found worldwide.
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 alimentary tract) and may remain dormant indefinitely.
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 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. Interestingly, 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 cattle may be found dead without premonitory signs. Acute, severe lameness 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 small, hot, and painful. 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 signs include prostration and tremors. Death occurs within 12–48 hr. In some cattle, the lesions are restricted to the myocardium and the diaphragm.
A rapidly fatal, febrile disease in well-nourished young cattle, particularly of the beef breeds, with crepitant swellings of the heavy 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. 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 hr after death, which allows time for postmortem invasion of the tissues by C sordellii. Field diagnoses are confirmed by laboratory demonstration of C chauvoei in affected muscle (standard methods: culture and biochemical identification). The samples of muscle should be taken as soon after death as possible. The fluorescent antibody test for C chauvoei is rapid and reliable. A PCR is available and reported to be very good 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 3–6 mo of age should be vaccinated twice, 4 wk 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 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 1 mo before lambing and then with yearly boosters. In outbreaks in flocks of ewes, 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 buried deeply in a fenced-off area to limit heavy spore contamination of the soil.