Gas gangrene is a necrotizing soft tissue infection that affects ruminants, horses, pigs, and other mammals and birds worldwide. It is caused by pathogenic clostridial species found in soil and in the intestines of healthy animals and humans. Infection generally occurs via contamination of wounds; however, "spontaneous" gas gangrene is possible in rare instances. Clinical signs include systemic signs (eg, fever), localized swelling and erythema, subcutaneous edema, emphysema, and fatal toxemia. Diagnosis is confirmed via laboratory testing. Antimicrobial treatment is rarely effective; treatment consists mostly of supportive care, including draining exudates and gas over affected tissue by making incisions and washing the wounds with hydrogen peroxide and iodine solution. Control is via vaccination using a multivalent product containing bacterins and toxoids that target the causative agents.
Gas gangrene (formerly called malignant edema) is an acute, generally fatal toxemia affecting all species and ages of animals. It is usually caused by one or more of the following: Clostridium septicum, Clostridium chauvoei, Clostridium novyi type A, Clostridium perfringens type A, and Paraclostridium sordellii. The disease occurs worldwide.
Etiology and Pathogenesis of Gas Gangrene
The pathogenic clostridia that cause gas gangrene are found in soil and intestinal contents of animals throughout the world. Infection ordinarily occurs via contamination of wounds that contain devitalized tissue, soil, or another tissue debilitant, or via activation of dormant spores. Wounds caused by accident, castration, docking, insanitary vaccination, fighting, and parturition can 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 for gas gangrene include intramuscular injections, shearing, docking, and lambing in sheep; fighting in rams; and traumatic parturition and castration in cattle. Although they are less common, some cases lacking previous trauma have been described (1). The pathogenesis of these "spontaneous" gas gangrene cases is not fully understood; however, it is thought that the organism gains access to the bloodstream through damaged GI mucosa or that the pathogenesis might be similar to that of blackleg.
Survival rates in gas gangrene cases are < 50% for ruminant species and < 80% for horses (1).
Clinical Findings of Gas Gangrene
General clinical signs of gas gangrene, such as anorexia and high fever, as well as local lesions, usually develop within hours after the injury. Rare cases are subacute to chronic.
Chronic cases of gas gangrene can result in extensive tissue loss. In more typical acute cases, local lesions include swellings and erythema (see ) that progress over time, and the affected area develops crepitus on palpation because of emphysema.
Gas gangrene in a pig. Note the swelling in the neck, as well as the blue color that is typical of gangrene.
Courtesy of the Department of Pathobiology, University of Guelph.
More specific clinical signs of gas gangrene depend on the location of the lesion; examples include the profound lameness and eventual recumbency that often accompany limb involvement. Later-stage lesions become cold, and death from toxemia typically occurs 2–4 days after the onset of clinical signs, if signs are observed. Some affected animals die without premonitory signs.
There are some more specific forms of gas gangrene, such as the type that occurs in rams secondary to fighting, in which lesions occur on the head, face, and neck (referred to as "big head disease"). Big head is an acute form of gas gangrene that is caused by C novyi type A, Paraclostridium sordellii, or, rarely, C chauvoei. In young rams it is characterized by nongaseous, nonhemorrhagic, edematous swelling of the head, face, and neck.
Clostridial infection that leads to gas gangrene is initiated in young rams via fighting or continual butting of one another. The bruised and battered subcutaneous tissues provide conditions suitable for the growth of pathogenic clostridia, and breaks in the skin offer an opportunity for entry of the pathogens.
Gas gangrene can also occur after calving, especially in primiparous individuals. Clinical signs in these cases are necrotizing vulvovaginitis and metritis, including vulvar swelling, that begins 1–3 days after parturition. As with other forms of the disease, these cases often result in fever, recumbency, and death.
Avian gas gangrene is usually caused by C septicum and is characterized by anorexia, ataxia, and death from toxemia. Omphalophlebitis due to P sordellii, C chauvoei, or C novyi can occur in neonates, with characteristic edema surrounding the navel and fetid peritoneal fluid.
Mastitis due to gas gangrene has been described in cattle and sheep, typically manifesting as a clear line of demarcation between healthy and diseased skin on the overlying mammary tissue, along with edema and hemorrhage of the subcutaneous tissue (see ).
A dairy cow with gangrenous mastitis and dermatitis. Note the sharp demarcation on the mammary gland between normal skin and dark, purple, discolored skin.
Courtesy of Cornell University College of Veterinary Medicine.
Lesions of Gas Gangrene
Gas gangrene results in hemorrhagic tissue with gelatinous subcutaneous edema and emphysema, with the exception of the specific form of gas gangrene known as big head, which is characterized by nongaseous, nonhemorrhagic edema of the head and face in rams secondary to fighting. The gross lesions in affected muscle tissue are similar to those described for blackleg (see ).
Right caudal thigh of a foal that received an intramuscular injection of flunixin meglumine at this site and became non-weight-bearing on that limb within 48 hours. Ultrasonographic examination of the area revealed gas dissection through fascial planes. Incisions were made, blunt dissection was performed, the area was lavaged, and a drain was placed. This photograph was taken 1 week later.
Courtesy of Dr. Toby Pinn-Woodcock.
In cases of gas gangrene, toxemia can result in more disseminated disease, including congestion and edema of the spleen, lungs, and liver. The inflammatory exudate is typically neutrophilic, and gram-positive bacilli with central, subterminal, or terminal spores can be evident in these diseased tissues. Necrosis in surrounding tissue might also be present (as in blackleg).
Diagnosis of Gas Gangrene
Clinical signs
Gram stain on impression smears
Confirmatory testing
A presumptive diagnosis of gas gangrene is based on clinical signs and lesions. However, clinical signs of gas gangrene are similar to those of anthrax, bacillary hemoglobinuria, and other intoxications.
Gram stains performed on impression smears of affected tissues can provide additional supportive evidence. However, confirmation requires laboratory testing.
Diagnostic specimens in cases of gas gangrene must be collected as soon as possible after death to avoid the detection of clostridial species from the GI tract that invade the tissues quickly post mortem. 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 hours is likely not significant.
Pearls & Pitfalls
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Confirmatory diagnosis of gas gangrene relies on the detection of clostridia in fresh tissue or in swabs of affected tissue via anaerobic culture, with subsequent identification of isolates via biochemical techniques, PCR assay, or matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF).
Fluorescent antibody testing is another rapid testing modality that can be performed on smears of fresh tissue made at the time of death, to avoid C septicum overgrowth.
Histological examination and subsequent immunohistochemistry can be performed on formalin-fixed tissue with compatible lesions.
Treatment and Control of Gas Gangrene
Antimicrobial therapy
Supportive care
Vaccination and other preventive measures
Treatment with penicillin is indicated early in the course of gas gangrene, when possible. For horses, such treatment may include sodium or potassium penicillin at 44,000 IU/kg, IV, every 2–4 hours until the patient is more stable (for 1–5 days). The dosage can then be decreased to every 6 hours, or metronidazole (15 mg/kg, PO, every 6–8 hours) may be considered instead. Similar treatment is recommended for ruminants (2).
Supportive care for gas gangrene can include anti-inflammatory medications and fluid therapy. In addition, incisions should be made in the skin overlying affected muscles to enable the drainage of accumulated exudates and gas.
Survival rates in cases of gas gangrene, even when treatment is initiated early, are reported to be < 80% for horses and < 50% for ruminants (1).
Strict surgical hygiene, proper navel care in neonates, and avoidance of wound contamination are all crucial measures for preventing gas gangrene. Proper carcass disposal helps to prevent soil contamination. However, vaccination is the main tool to prevent gas gangrene.
Combinations of bacterins and toxoids against C septicum, C chauvoei, C novyi type A, C perfringens type A, and P sordellii are used for vaccination. Administration of two doses of vaccine 2–3 weeks apart for animals < 6 months old, followed by annual boosters, generally gives protection. Revaccination is recommended after severe trauma or invasive procedures such as castrations, dehorning, or tail docking.
Key Points
Gas gangrene, caused by one or more of five clostridial species, is an acute, generally fatal toxemia that can affect all species and ages of animals.
Infection ordinarily occurs via contamination of wounds containing devitalized tissue, soil, or another tissue debilitant.
Proper carcass disposal and vaccination prevent gas gangrene.
For More Information
Odani JS, Blanchard PC, Adaska JM, Moeller RB, Uzal FA. Malignant edema in postpartum dairy cattle. J Vet Diag Invest. 2009;21(6):920-924.
Peek SF, Semrad SD, Perkins GA. Clostridial myonecrosis in horses (37 cases 1985–2000). Equine Vet J. 2003;35(1):86-92.
Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.
References
Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.
Valberg SJ, Spier SJ, Parish SM, Murphy M, Carlson GP. Diseases of muscle. In: Smith BP, Van Metre DC, Pusterla N, eds. Large Animal Internal Medicine. 6th ed. Elsevier; 2020:1421-1455.e5. doi:10.1016/B978-0-323-55445-9.00042-2
