PROFESSIONAL VERSION

Blackleg in Animals

(Black Quarter, Clostridial Myositis)

Full Review: Sept 2026 ByErin L. Goodrich, DVM, DACVPM, Cornell University, College of Veterinary Medicine | Peer reviewed byAngel Abuelo, DVM, PhD, DABVP, DECBHM, FHEA, MRCVS, Michigan State University, College of Veterinary Medicine
Last updated: Sept 2026
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Blackleg is an acute, highly fatal disease of cattle (and, rarely, other ruminants) caused by Clostridium chauvoei. In cattle, characteristic lesions of emphysematous swelling of the musculature often develop without a history of wounds. In contrast, the disease in sheep is almost always the result of a wound infection, such as after shearing cuts, docking, or castration. The disease is highly fatal. Control is via a multivalent vaccine containing antigens for multiple clostridial organisms.

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).

Etiology of Blackleg

Spores of C chauvoei, the cause of blackleg, can remain viable in soil for long periods of time. They are ingested by cattle from contaminated pastures or feed. They are thought to be absorbed from the intestinal tract and to travel in the bloodstream and lymphatic system to skeletal and cardiac muscle, where they are phagocytosed by macrophages and can remain latent for long periods of time. Once an anaerobic environment in this tissue is created, by trauma or hypoxia, the spores can germinate, reproduce, and release toxins, resulting in clinical disease.

Outbreaks of blackleg have also occurred in animals soon after they have been moved to new pastures or when they have been fed feedstuff believed to be heavily contaminated with C chauvoei spores, suggesting that active infection might be possible without trauma, if cattle are exposed to a very large pathogen load.

In sheep, blackleg is almost always the result of a wound infection and often follows some form of injury, so it is best characterized as C chauvoei–associated gas gangrene.

Epidemiology of Blackleg

Outbreaks of blackleg have occurred in cattle after changes in feedstuff or movement to new pastures (1).

In cases of blackleg in which cardiac lesions are the only clinical sign, underlying problems such as stress-induced increases in catecholamine and cortisol concentrations, cardiac toxicants, or selenium or vitamin E deficiency are thought to have predisposed the animal to the disease.

Most cases of blackleg occur in unvaccinated cattle 6–24 months old that are in good nutritional condition; however, thrifty calves as young as 6 weeks and cattle as old as 10–12 years can be affected.

Blackleg usually occurs in the wet season, and incidence of the disease is strongly correlated to annual rainfall.

Blackleg is nearly always fatal (1).

Clinical Findings and Lesions of Blackleg

Usually, the onset of blackleg is sudden. Acute, severe lameness (more commonly affecting the hindlegs) and marked depression are common. Initially, there is fever, but by the time clinical signs are evident, the body temperature can be normal or subnormal.

In cases of blackleg, 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 might protrude.

Blackleg progresses rapidly. The swellings become larger, there is crepitus on palpation, and the skin becomes cold and insensitive, with decreased blood supply to affected areas. General clinical signs include prostration and tremors. If the myocardium or diaphragm is affected, clinical signs can include abnormal breathing or pericardial friction rub. Death occurs within 12–48 hours.

Occasionally, animals with blackleg are found dead without premonitory signs.

Lesions of Blackleg

Many animals with blackleg have lesions in both skeletal muscle and cardiac muscle (see ). In some cattle, the lesions are restricted to the myocardium and the diaphragm.

Grossly, red to black discoloration of the skeletal muscle is evident on cut section (see , sometimes with gas bubbles present and a sweet, rancid odor. When the heart is affected, similar lesions can occur in the myocardium and pericarditis.

Diagnosis of Blackleg

  • Clinical signs

  • Postmortem examination

  • Identification of Clostridium chauvoei on anaerobic culture, fluorescent antibody testing, PCR assay, or immunohistochemistry of affected tissues

Diagnosis of blackleg can be suspected on the basis of compatible clinical signs. A rapidly fatal, febrile disease in well-nourished young cattle, together with crepitant swellings of the large muscles, suggests blackleg.

On postmortem examination, muscles affected by blackleg are dark red to black and dry and spongy, have a sweetish odor, and are infiltrated with small bubbles, but little edema is present. The lesions can occur in any muscle, even in the tongue or diaphragm.

In sheep, the lesions of the spontaneously occurring type of blackleg are often small and deep, so they can be overlooked. Ultrasonography of affected muscle that shows irregular muscle tissue, little edema, and the presence of gas can support a presumptive blackleg diagnosis.

Occasionally, the tissue changes caused by Clostridium septicum, Clostridium novyi, Clostridium sordellii, and Clostridium perfringens resemble those of blackleg. At times, both C septicum and C chauvoei can 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 of blackleg are confirmed by laboratory findings of C chauvoei in affected muscle tissue; the standard method is anaerobic culture, followed by identification via matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF). Muscle tissue samples should be collected as soon as possible after death to avoid the isolation of gut microbes that invade the tissues post mortem.

Pearls & Pitfalls

  • Muscle tissue samples should be collected as soon as possible after death from blackleg, to avoid the isolation of gut microbes that invade the tissues post mortem.

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.

Treatment and Control of Blackleg

  • Antimicrobial therapy

  • Vaccination

  • Removal of animals from affected pastures

Because of the rapid progression of blackleg, treatment is rarely successful; when indicated, however, high doses of penicillin (44,000 U/kg, IM or SC, every 12 hours, or IV, every 4–6 hours) can be effective (2).

In blackleg cases, antimicrobials can be effective at reaching organisms in the body where there is still healthy circulation; in affected tissue, however, effective levels might not be reached. Fenestration of affected muscle with lavage enables oxygenation and can minimize further pathogen replication.

Control measures include administration of a multivalent vaccine containing antigens (C chauvoei, C septicum, and, where needed, C novyi) that prevail in the region where blackleg occurs. A commercial polyvalent vaccine containing C chauvoei 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), or even biannual boosters, if regional incidence is high.

Vaccines against blackleg are nearly 100% effective in preventing disease (1).

Cattle should be moved out of pastures infected with C chauvoei.

Key Points

  • Rapidly fatal disease in well-nourished cattle suggests blackleg.

  • Blackleg in sheep is associated with wound infections.

  • Disease is controlled by administration of a multivalent vaccine containing antigens that prevail in the region where blackleg occurs.

For More Information

References

  1. Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.

  2. Peek SF, Divers TJ. Rebhun's Diseases of Dairy Cattle. 3rd ed. Elsevier; 2018.

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