(Blackleg, Malignant edema, False blackleg, Gas gangrene, Gangrene)
Clostridial infection of skeletal muscle is a noncontagious cause of acute myonecrosis. Clostridium chauvoei, C septicum, C sordellii, occasionally C novyi type B, C perfringens type A, C carnis, or mixed infections involving several agents are common (see Clostridial Diseases). Clostridia or their spores are ubiquitous in the environment, feces, intestinal tract, and other internal organs of a variety of species. Clostridial myonecrosis may develop after introduction of spores via an IM injection or penetrating wound or through sporulation of organisms already present in muscle when suitable anaerobic conditions are created with muscle trauma. Any skeletal muscle group in the body can be involved, but most infections affect the limb or trunk muscles. Occasionally, muscles such as those around the vulva, tongue, and diaphragm can be involved, or the udder in a cow may be the primary site of sepsis. The release of powerful exotoxins by multiplying clostridia is responsible for the local tissue damage, systemic toxemia, and widespread organ dysfunction. The toxins of C sordelli are the most potent of all the clostridial species, and myonecrosis caused by this organism is fatal.
Infections are characterized by a rapid clinical course, fever (104°–106°F [40°–41°C]), lameness, systemic toxemia, tremors, ataxia, and dyspnea, often followed in 12–24 hr by recumbency, coma, and death. Mortality may approach 100%. Initially, the skin over the area may be swollen, hot, and discolored; however, as the disease progresses, the skin over the area may become cool and insensitive with progressive sloughing. Crepitus may be detectable, indicating subcutaneous gas production. If a wound is present, malodorous, serosanguineous discharge may be seen. Hematology and serum biochemical analyses usually reflect hemoconcentration and a stress/toxic leukogram with increased activities of serum CK and serum AST that often do not reflect the toxicity of clostridial myonecrosis. A definitive diagnosis is made from direct smear examination, fluorescent antibody testing, or anaerobic bacterial culture of aspirates of affected tissues. Differential diagnoses include other fulminant disease processes in which there is rapid debilitation or death of the animal.
Clostridial myonecrosis generally has characteristic pathologic lesions that are absent in most other conditions, making diagnosis relatively straightforward. Swelling and autolysis are rapid in animals that have died from clostridial myonecrosis, and the carcass usually has a foul odor similar to that of rancid butter. This odor is a characteristic of most cases of clostridial myonecrosis. C chauvoei infection is characterized by engorgement of the subcutis and adjacent tissues with bloodstained fluids and gas bubbles. Cut tissue from the affected area reveals moist, dark-colored muscle in the periphery of the lesion, with lighter-colored, drier muscle with gas bubbles between the separate bundles of muscle toward the center. Lesions are similar in sheep and cattle, except that there is usually less gas and the muscles are not as dry in affected sheep. Myonecrosis resulting from C sordelli is most often associated with lesions of the neck or brisket area of cattle; death is frequently so rapid that subcutaneous gas accumulation is rare. In addition to local myonecrosis, animals often have massive subendocardial hemorrhages in the left ventricle of the heart and hemorrhage in the trachea, bronchi, and thymus. Extensive perirenal edema and hemorrhagic renal calyces and severe congestion of the lungs are common findings.
Antibiotic therapy and aggressive surgical debridement may be attempted in the individual animal; however, most cases are usually fatal. Penicillin at a dosage of 44,000 U/kg, IV, every 2–4 hr is given until the animal is stable (1–5 days). Use of specific antitoxins is recommended when possible. Supportive fluid therapy and use of analgesics and anti-inflammatory agents for control of pain and swelling are recommended. Short-acting corticosteroids may be used for initial therapy of systemic and toxic shock, but continued use is contraindicated in the face of overwhelming sepsis.
Vaccination beginning at 4–6 mo in cattle with bacterins containing antigens against two or more clostridial species, including C chauvoei, C septicum, C novyi, C sordelli, and C perfringens is recommended. For all clostridial species except C chauvoei, two doses of vaccine are necessary to establish good protection. Booster vaccinations should be administered every 6–8 mo if protection is to be maintained.
Cysts of Sarcocystis are common in the heart, esophageal, and skeletal muscle of cattle, sheep, goats, and other species but rarely cause disease. Heavy infestations of sarcocystis may cause fever, mild anemia, chronic myositis, and muscle wasting. S cruzi, S hirsuta, and S hominis are known to infect cattle, whereas S ovicanis and S capracanis infect sheep and goats. The most common mechanism for natural infection in cattle is by ingestion of feeds contaminated with infected carnivore feces. (For complete discussion of sarcocystosis, see Sarcocystosis.)