Excerpt from Necrotizing Fasciitis

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Background

Necrotizing fasciitis (NF) is an insidiously advancing soft tissue infection characterized by widespread fascial necrosis. A number of bacteria in isolation or as a polymicrobial infection can cause NF. The organisms most closely linked to NF are group A beta-hemolytic streptococci, although the disease may also be caused by other bacteria or different streptococcal serotypes.

NF was first described in 1848. In 1920, Meleney identified 20 patients in China in whom hemolytic streptococcus was the sole organism. Wilson coined the term necrotizing fasciitis in 1952 and found no specific pathologic bacteria related to the disease.

A few distinct NF syndromes should be recognized. The 3 most important are type I, or polymicrobial; type II, or group A streptococcal; and type III gas gangrene, or clostridial myonecrosis. A variant of NF type I is saltwater NF, in which an apparently minor skin wound is contaminated with saltwater containing a Vibrio species.

NF may occur as a complication of a variety of surgical procedures, including cardiac catheterization.¹ Familiarity with NF may facilitate earlier diagnosis and initiation of appropriate therapy.

A related Medscape CME course that may be of interest is The New York Course 2007: Developments in Infectious Diseases—Community-Acquired Methicillin-Resistant Staphylococcus aureus Infections. A related eMedicine article is Necrotizing Fasciitis (emergency medicine focus). Finally, an article available through Medscape that may be helpful is Maggot Debridement Therapy in Necrotizing Fasciitis Reduces the Number of Surgical Debridements.

Pathophysiology

Organisms spread from the subcutaneous tissue along the superficial and deep fascial planes, presumably facilitated by bacterial enzymes and toxins. This deep infection causes vascular occlusion, ischemia, and tissue necrosis. Superficial nerves are damaged, producing the characteristic localized anesthesia. Septicemia ensues with systemic toxicity.

Important bacterial factors include surface protein expression and toxin production. M-1 and M-3 surface proteins, which increase the adherence of the streptococci to the tissues, also protect the bacteria against phagocytosis by neutrophils.

Streptococcal pyrogenic exotoxins (SPEs) A, B, and C are directly toxic and tend to be produced by strains causing NF. These pyrogenic exotoxins, together with streptococcal superantigen (SSA), lead to the release of cytokines and produce clinical signs such as hypotension. The etiological agent may also be a Staphylococcus aureus isolate harboring the enterotoxin gene cluster seg, sei, sem, sen, and seo but lacking all common toxin genes, including Panton-Valentine leukocidin.² The poor prognosis associated with NF has been linked to infection with certain streptococcal strains. Community-acquired methicillin-resistant S aureus has also been associated with NF.³

Mortality/Morbidity

The mortality rate can be as high as 25%. Cases of NF with sepsis and renal failure have a mortality rate as high as 70%.

Age

Approximately one half of the cases of streptococcal NF occur in young and previously healthy people.

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