Blackleg

Blackleg is chiefly a disease of pastured animals and tends to occur in the summer when pastures are moist and growing. The disease occurs most often in cattle that are between 9 months to 2 years of age and that appear to be in good condition and are the best fattened. Blackleg is caused by Clostridium chauvoei when latent spores within the muscle are activated by areas of hypoxia. The source of the Clostridium chauvoei organism appears to be persistent in certain fields. Once a field has experienced an infection, the Clostridium chauvoei will always be present in the environment.

Detailed pathogenesis of blackleg is still uncertain, but many of the following proposed life cycle have been confirmed in the natural disease and in experimental infections. The infection is acquired by ingestion of spores. These spores undergo germinative cycles in the gut and produce additional spores which are then transported to various tissues where they are stored for prolonged periods of time in phagocytic cells. Latent spores in muscle are stimulated to germinate when a local event creates muscle damage or low oxygen tension. Symptoms of blackleg can include lameness, swelling, and crepitation under the skin over the site of the lesion.

Affected animals subsequently show depression and circulatory collapse. Death ensues rapidly and seldom does an animal survive more than 24-36 hours after the onset of lameness. Animals that die due to blackleg usually swell and bloat rapidly, but upon incision, the odor is not as putrid as the external appearance of the carcass would indicate. The lesions can be quite localized and, in some cases, easily escape detection (Figure 1). Clinical manifestations of blackleg are often not observed due to the rapid clinical course and animals are often found dead.Affected muscles appear slightly different at varying distances from the center of the lesion. Toward the periphery of the lesion, the muscle is dark red and moist with edema fluid. Toward the center, it is red or black, and occasionally has putty colored islands of dry, porous tissue where gas bubbles separate muscle bundles. If this tissue is squeezed, it crepitates as a small amount of thin red fluid is expressed. The affected skeletal muscle may have the odor of rancid butter. Clostridial Fluorescent Antibody (FA) tests are used to detect the causative agent. Fresh portions of muscle which are necrotic and exuding serosanguinous fluid should be submitted for testing. If the FA is negative, histology on similar fixed tissue can diagnose the disease by looking for muscle necrosis and inflammation. The toxin always affect the heart muscles causing cardiovascular collapse and death. Upon gross examination, the heart can appear normal. The heart may have a fibrinous plaque, and/or be diffusely darkened, this is characteristic of blackleg. Thus, fresh heart can also be submitted for clostridial FA testing. Histologically, similar lesions are observed in the myocardium as are observed in the affected skeletal muscle. Scattered muscle fibers are necrotic, shrunken, or vacuolated. The interstitium contains localized hemorrhage and sparse suppurative infiltrates.