Clostridial Myonecrosis (Gas Gangrene)

How to Cite This Chapter: Bociąga-Jasik M. Clostridial Myonecrosis (Gas Gangrene). McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed December 04, 2023.
Last Updated: January 31, 2022
Last Reviewed: January 31, 2022
Chapter Information

Etiology and PathogenesisTop

1. Etiologic agent: Clostridium spp bacilli (most frequently C pefringens, less frequently C novyi, C septicum, C histolyticum, C sordellii, C bifermentans), gram-positive anaerobes. C perfringens usually causes clostridial myonecrosis associated with traumatic wounds; C septicum infection occurs in patients with neutropenia or gastrointestinal (GI) cancers; C sordellii, in postpartum women or after at-home abortion. C perfringens, C novyi, or C sordellii may cause clostridial myonecrosis in illicit IV drug users.

2. Pathogenesis: Exotoxins produced by the bacteria play a key role in the pathogenesis. Alpha-toxin (lecithinase), which causes cell membrane destruction, is produced by all strains of C perfringens as well as by C sordellii, C novyi, and C bifermentans. In addition to a local effect, alpha-toxin also causes hemolysis of red blood cells. The bacilli that cause clostridial myonecrosis also produce a variety of other exotoxins, including hemolysins, proteases, collagenase, hyaluronidase, DNase, neuraminidase, and perfringolysin O (theta-toxin). As a platelet antagonist, alpha-toxin causes thrombosis that leads to ischemia and severe pain. C perfringens theta-toxin causes cell lysis and modulates the inflammatory response to infection.

3. Reservoir and transmission: C perfringens colonizes the human and animal colon and is widespread in the environment. Clostridial myonecrosis most often develops as a complication of severe injury, with wound contamination with soil or other foreign matter containing C perfringens spores. Although wound contamination with C perfringens is common, clostridial myonecrosis develops only in 1% to 2% of cases. Occasionally the infection may develop without a visible wound. In such cases the causative agent is usually C septicum, which leads to bacteremia.

4. Risk factors: Trauma with wounds contaminated with soil or feces, surgical treatment within the abdominal cavity (most commonly the GI tract, gallbladder, and bile ducts). The risk of clostridial myonecrosis is higher in the presence of factors reducing the amount of oxygen in tissues such as wound infection with mixed bacterial flora or ischemia (among others, in diabetes, burns, or neoplastic diseases).

5. Incubation and infectious period: The incubation period is 2 to 3 days, but it may be as short as ~6 hours. Cases of recurrent clostridial myonecrosis have been described. C perfringens spores may survive in tissues for up to 20 years following an episode of clostridial myonecrosis and, in minor wounds that favor anaerobic conditions, may cause recurrence. The disease is not spread through human-to-human contact.

Clinical Features and Natural HistoryTop

Sudden onset of acute, severe pain at the site of the wound. Pale edema and local tenderness are observed initially, followed by muscular swelling with hemorrhagic blisters filled with sweet-smelling brownish contents and by subcutaneous emphysema. The affected areas are crimson or brown colored.

Body temperature usually does not exceed 38.3 degrees Celsius. The patient's overall condition deteriorates towards shock and multiorgan failure.


The clinical picture is crucial.

Diagnostic Tests

1. Identification of the etiologic agent: Identification of Clostridium bacilli in the blister discharge (Gram-stained direct smear, culture) with nearly complete absence of white blood cells (WBCs) (the presence of WBCs indicates another concomitant bacterial infection). Bacteremia secondary to clostridial myonecrosis is present only in 15% of cases.

2. Other tests: Imaging studies may reveal gas in tissues and muscle necrosis.

Differential Diagnosis

Necrotizing fasciitis, wound infection with other pathogens, for example, Aeromonas (water/soil) or Vibrio vulnificus (sea water, crustaceans, oysters).


Start surgical and antibiotic treatment as soon as possible. A suspicion of clostridial myonecrosis warrants urgent surgical consultation.

1. IV antibiotics: Clindamycin 600 to 900 mg every 8 hours in combination with benzylpenicillin 3 to 4 million IU every 4 hours. In cases with no microbiologic confirmation of infection, the Infectious Diseases Society of America (IDSA) recommends vancomycin in combination with any of the following antibiotics: piperacillin with tazobactam, ampicillin with sulbactam, or carbapenem.

2. Surgical treatment: Removal of necrotic tissues or amputation.

3. Hyperbaric oxygen therapy (HBOT): There is no strong scientific data confirming the effectiveness of HBOT. The therapy can be used as an ancillary treatment but should not delay surgery.


The mortality rate is 20% and increases to 40% if shock develops. In myonecrosis caused by C septicum the mortality rate is as high as 100%, with the majority of patients dying within 24 hours from symptom onset.


Specific Prevention

1. Immunoprophylaxis: None available.

2. Pharmacoprophylaxis: The same as for contaminated wounds in individuals with risk factors—use a broad-spectrum antibiotic active against Clostridium spp.

Nonspecific Prevention

Urgent surgical wound cleaning and debridement, ensuring proper perfusion and oxygenation of damaged tissues (do not close the wound if there is high risk for clostridial myonecrosis, eg, if there are signs of infection or in open fractures).

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