Malignant Edema

C septicum is found in soil and intestinal contents of animals throughout the world. Infection ordinarily occurs through contamination of wounds containing devitalized tissue, soil, or some other tissue debilitant or through activation of dormant spores. Wounds caused by accident, castration, docking, insanitary vaccination, and parturition may become infected. Potent clostridial toxins cause local and systemic signs, often resulting in death. Local exotoxins cause excessive inflammation, resulting in severe edema, necrosis, and gangrene. Risk factors include IM injections in horses; shearing, docking, and lambing in sheep; and traumatic parturition and castration in cattle. Horses and probably cows have dormant spores present in muscle tissues.

General signs, such as anorexia, intoxication, and high fever, as well as local lesions, develop within 6–48 hr after predisposing injury or activation of dormant spores. The local lesions are soft swellings that pit on pressure and extend rapidly because of the formation of large quantities of exudate that infiltrate the subcutaneous and intramuscular connective tissue of the affected areas. The muscle in such areas is dark brown to black. Accumulations of gas in subcutaneous tissue and along muscle fascias may or may not be present. These muscle infections are extremely painful, and systemic toxemia may evolve. Extensive local sloughing of skin and tissues is often seen in progressed states of malignant edema. Severe edema of the head of rams develops after infection of wounds inflicted by fighting. Malignant edema associated with lacerations of the vulva at parturition is characterized by marked edema of the vulva, severe toxemia, and death in 24–48 hr.

Similarity to blackleg (see Blackleg) is marked, and differentiation made on necropsy is unreliable; laboratory confirmation is the only certain procedure. Horses and pigs are susceptible to malignant edema but not to blackleg. An important differential diagnosis in these species is anthrax (see Anthrax).

C septicum also causes braxy in sheep, a highly fatal infection characterized by toxemia and inflammation of the abomasal wall. This disease seems to be confined mostly to European sheep fed on “frosted” pasture.

Diagnosis can be confirmed rapidly on the basis of fluorescent-antibody staining of C septicum from a tissue smear. However, C septicum is an extremely active postmortem invader from the intestine, and its presence in a specimen taken from an animal that has been dead for ≥24 hr is not significant. PCR can be used for direct identification and differentiation of clostridia associated with malignant edema. The presence of type III echinocytes or spheroechinocytes in blood smears may help diagnose immune-mediated hemolytic anemia associated with clostridial infections in horses. Fine-needle aspirates and Gram stain may confirm the presence of gram-positive rods before confirmation by anaerobic culture.

Bacterins are used for immunization. C septicum usually is combined with C chauvoei in a blackleg/malignant edema vaccine and is available in multivalent vaccines. In endemic areas, animals should be vaccinated before they are castrated, dehorned, or docked. Calves should be vaccinated at ~2 mo of age. Two doses 2–3 wk apart generally give protection. In high-risk areas, annual vaccination is indicated, as is revaccination after severe trauma.

Treatment with high doses of parenteral penicillin, tetracyclines, or broad-spectrum antibiotics is indicated early in the disease. Although injection of penicillin directly into the periphery of the lesion may minimize spread of the lesion, the affected tissues usually slough. Supportive therapy with NSAIDs (flunixin meglumine for cattle and horses) is recommended. Local treatment includes surgical incision of skin and fascia to allow drainage. Animals with systemic toxic signs will need supportive treatments such as IV perfusion.