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Etiology
Clinical Findings and Lesions
Diagnosis
Control

Blackleg is an acute, febrile disease of cattle and sheep caused by Clostridium chauvoei (feseri) characterized by emphysematous swelling, usually in the heavy muscles. It is found worldwide.
Etiology:
C chauvoei is found naturally in the intestinal tract of animals. It probably can remain viable in the soil for many years, although it does not actively grow there. Contaminated pasture appears to be a source of organisms. Outbreaks of blackleg have occurred in cattle on farms in which recent excavations have occurred, which suggests that disturbance of soil may activate latent spores. 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.
In cattle, blackleg infection is endogenous, in contrast to malignant edema ( Malignant Edema). Lesions develop without any history of wounds, although bruising or excessive exercise may precipitate some cases. Commonly, the animals that contract blackleg are of the beef breeds, in excellent health, gaining weight, and usually the best animals of their group. Outbreaks occur in which a few new cases are found each day 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. In sheep, the disease is not restricted to the young, and most cases follow some form of injury such as shearing cuts, docking, crutching, or castration. Endogenous blackleg in sheep is uncommon in the USA; it is much more common in New Zealand where blackleg is seen more frequently in sheep than in cattle.
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Clinical Findings and Lesions:
Photographs

Blackleg, cow

Blackleg, cow
Usually, onset is sudden, and a few cattle may be found dead without premonitory signs. Acute 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 as the blood supply to the area diminishes. General signs include prostration and tremors. Death occurs in 12-48 hr. In some cattle, the lesions are restricted to the myocardium and the diaphragm, with no reliable antemortem evidence of the localized lesion.
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Diagnosis:
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 muscle is dark red to black and dry and spongy; it has a sweetish odor and is infiltrated with small bubbles but with little edema. The lesions may be 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 septicum . Field diagnoses are confirmed by laboratory demonstration of C chauvoei in affected muscle. The samples of muscle should be taken as soon after death as possible. The fluorescent antibody test for C chauvoei is rapid and reliable.
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Control:
A bacterin containing C chauvoei and C septicum is safe and reliable for both cattle and sheep. Calves should be vaccinated twice, 2 wk apart, at 2-6 mo of age; in high-risk areas, revaccination may be necessary at 1 yr and every 5 yr thereafter. When outbreaks are encountered, all susceptible cattle should be vaccinated and treated prophylactically with penicillin to prevent new cases, which may develop for up to 10 days, at which the bacterin provides protection. In some areas, multicomponent clostridial vaccines are warranted. Treatment of clinical cases with parenteral and multiple local injections of penicillin may be attempted but is frequently unsuccessful.
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See Also
Introduction
Bacillary Hemoglobinuria
Big Head
Infectious Necrotic Hepatitis
Malignant Edema
Botulism
Clostridia-associated Enterocolitis in Horses
Clostridium difficile in Swine
Enterotoxemias
Overview
Enterotoxemia Caused by Clostridium perfringens Type A
Enterotoxemia Caused by Clostridium perfringens Types B and C
Type D Enterotoxemia
Tetanus
Clostridial Vaccines