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- Patient Comments: Necrotizing Fasciitis - Cause
- Patient Comments: Necrotizing Fasciitis - Treatments
- Patient Comments: Necrotizing Fasciitis - Signs and Symptoms
- Patient Comments: Necrotizing Fasciitis - Diagnosis
- Patient Comments: Necrotizing Fasciitis - Experience
- Necrotizing fasciitis (flesh-eating disease) facts
- What is necrotizing fasciitis?
- Do different types of necrotizing fasciitis exist?
- What causes necrotizing fasciitis?
- What are necrotizing fasciitis symptoms and signs?
- How is necrotizing fasciitis diagnosed?
- What is the treatment for necrotizing fasciitis?
- How is necrotizing fasciitis prevented? Is necrotizing fasciitis contagious?
- Who is at risk to get necrotizing fasciitis?
- What is the prognosis (outcome) for patients with necrotizing fasciitis? What are complications of necrotizing fasciitis?
- What are some additional sources of information on necrotizing fasciitis?
Quick GuideBacterial Infections 101: Types, Symptoms, and Treatments
What are necrotizing fasciitis symptoms and signs?
The majority of infected individuals who develop necrotizing fasciitis begin with an existing infection (cellulitis, abscess, or wound), most frequently on an extremity or in a wound or surgical site. The initial infection can be from almost any cause (for example, cuts on the skin, puncture wounds, surgical incisions, or rarely, insect bites [spiders, biting flies]). Instead of healing, the infected site can show erythema (redness) and swelling. The site may be very sensitive to pain, even past the area of erythema and may tingle. A classic finding is the presence of pain far in excess of what would be expected based upon physical findings. At the same time, patients often experience fever and chills. Early symptoms resemble those of cellulitis, but progressive skin changes such as skin ulceration, bullae (thin-walled fluid-filled blisters) formation, necrotic scars (black scabs), gas formation in the tissues, and fluid draining from the site can occur rapidly as the infection progresses. Some patients can become septic (meaning the infection has spread to the bloodstream and throughout the body) before the skin changes are recognized, especially when flesh-eating disease begins in deep facial planes. Type 1 often occurs after trauma or surgery and may form little or undetectable amounts of gas. Type 2 usually occurs after more simple skin trauma (cuts, abrasions, and insect bites) and infects more superficial facial planes with almost no gas formation. Type 3 usually occurs after trauma or after wounds become contaminated with dirt that contains Clostridium bacteria, which produce gas in tissues (gangrene) and necrotic eschars. However, symptoms for types 1-3 are not definitive, and symptoms vary widely which is why some investigators prefer to define individual patients' disease by the organism(s) isolated from the patient rather than assigning a type label.
One set of patients that is being recognized with a more specific set of symptoms and health history are those infected with Vibrio vulnificus. The organisms occur in the warmer waters in the U.S. (Gulf of Mexico and southern coastal states) and elsewhere in the world with similar water conditions. Either ingesting the organisms or getting Vibrio vulnificus from contaminated seawater into skin abrasions or cuts can cause necrotizing fasciitis. The majority of those affected is either immunosuppressed or has chronic liver problems (for example, alcoholic liver disease, hepatitis, or cirrhosis). Bullae formation and rapid progression of the disease (within hours) on the extremities are hallmarks of Vibrio vulnificus wound infections. Even though a single type of bacteria causes this infection, some investigators classify it as a variant of type 1 necrotizing fasciitis.
Necrotizing enterocolitis (also termed NEC; necrosis of gastrointestinal tissue) occurs mainly in premature or sick infants and may be another variant of necrotizing fasciitis. Although investigators suggest that bacterial infection causes this disease, there is no definitive data to prove this and others attribute the disease to a dysfunction of the intestinal tissue.