Necrotizing fasciitis is most commonly caused by the pathogenic bacteria Streptococcus pyogenes, also known as group A Streptococcus, of which there are more than 80 types in existence. The bacteria enter the body through a wound, such as a pinprick, needle puncture, bruise, blister, or abrasion, or through a traumatic injury or surgical incision. They can also enter through a breach in a mucous membrane barrier. Other aerobic and anaerobic pathogens, including Staphylococcus aureus, Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella, may also be present. These pathogens can proliferate in an environment of tissue hypoxia caused by trauma, recent surgery, or medical compromise. The end product of this invasion is necrosis of the surrounding tissue, which accelerates the disease process by creating an even more favorable environment for the organisms.

Complications include renal failure, septic shock with cardiovascular collapse, scarring with cosmetic deformities, myositis, and myonecrosis.

Pain that is out of proportion to the size of the wound or injury is usually the first symptom of necrotizing fasciitis. The infective process begins with a mild area of erythema at the site, changing in color from red to purple to blue, with the formation of fluid-filled blisters and bullae within 48 hours. By days 4 and 5, multiple patches of this erythema form, producing large areas of gangrenous skin. By days 7 to 10, dead skin begins to separate at the margins of the erythema, revealing extensive necrosis of the subcutaneous tissue. Other clinical symptoms include fever and hypovolemia. In later stages, hypotension, respiratory insufficiency, and overwhelming sepsis requiring supportive care ensue. In the most severe cases, necrosis advances rapidly until several large areas of the body are involved and the patient becomes less alert, delirious, or even unresponsive.