Necrotizing fasciitis is a life-threatening surgical emergency. Immediate wide surgical incision, drainage, and debridement is the cornerstone of therapy. Broad-spectrum intravenous antibiotics should be instituted as soon as the diagnosis is suspected. At operation, tissue cultures should be obtained and antibiotic coverage should be tailored to culture growth. The most common causative agents of necrotizing fasciitis are Staphylococcus aureus, Clostridium species, group A Streptococcus, enterococci, and Bacteroides species. Many necrotizing infections are mixed aerobic/anaerobic in origin. Controversy still remains about the use of hyperbaric therapy in these cases. However, if it is utilized, hyperbaric treatment should never delay aggressive surgical treatment.

Infections caused by group A Streptococcus (e.g., S. pyogenes, aka “flesh-eating bacteria”) deserve special mention. Group A Streptococcus is responsible for a range of skin and soft-tissue infections, including impetigo, erysipelas, cellulitis, and necrotizing fasciitis. Group A Streptococcus necrotizing fasciitis is commonly associated with septic shock and multiorgan failure—the streptococcal toxic shock syndrome. This is secondary to the presence of M protein, a virulence factor present on the bacterial surface that is highly antigenic and inhibits phagocytosis. In addition, streptococcal pyrogenic exotoxins cause fever and contribute to organ failure and shock by stimulating host synthesis of tumor necrosis factor α, interleukin-1 β, and interleukin-6.