Read more about this disease, some with Classification – Types – Signs and symptoms – Genetics – Pathophysiology – Diagnosis – Screening – Prevention – Treatment and management – Cures and much more, some including pictures and video when available.
Necrotizing fasciitis (NF) or fasciitis necroticans, commonly known as flesh-eating disease or flesh-eating bacteria, is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. Type I describes a polymicrobial infection, whereas Type II describes a monomicrobial infection. Many types of bacteria can cause necrotizing fasciitis (eg. Group A streptococcus (Streptococcus pyogenes), Staphylococcus aureus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis).
Historically, Group A streptococcus made up most cases of Type II infections. However, since at least 2001, another serious form of monomicrobial necrotizing fasciitis has been observed with increasing frequency.[1] In these cases, the bacterium causing it is methicillin resistant Staphylococcus aureus (MRSA), a strain of S. aureus which is resistant to methicillin, the antibiotic used in the laboratory that determines the bacterium’s sensitivity to flucloxacillin that would be used for treatment clinically.
The infection begins locally, at a site of trauma, which may be severe (such as the result of surgery), minor, or even non-apparent. Patients usually complain of intense pain that may seem in excess given the external appearance of the skin. With progression of the disease, tissue becomes swollen, often within hours. Diarrhea and vomiting are common symptoms as well. Inflammation does not show signs right away if the bacteria are deep within the tissue. If they are not deep, signs of inflammation such as redness and swollen or hot skin show very quickly. Skin color may progress to violet and blisters may form, with subsequent necrosis (death) of the subcutaneous tissues. Patients with necrotizing fasciitis typically have a fever and appear very ill. Mortality rates have been noted as high as 73 percent.[2] Without surgery and medical assistance, such as antibiotics, the infection will rapidly progress.[3]
“Flesh-eating bacteria” is a misnomer as the bacteria do not actually eat the tissue. They cause the destruction of skin and muscle by releasing toxins (virulence factors), which include streptococcal pyogenic exotoxins. S. pyogenes produces an exotoxin known as a superantigen. This toxin is capable of activating T-cells non-specifically, which causes the overproduction of cytokines.
Patients are typically taken to surgery based on a high index of suspicion, determined by the patient’s signs and symptoms. In necrotizing fasciitis, aggressive surgical debridement (removal of infected tissue) is always necessary to keep it from spreading and is the only treatment available. Diagnosis is confirmed by visual examination of the tissues, and by tissue samples sent for microscopic evaluation. Early medical treatment is often presumptive; thus, antibiotics should be started as soon as this condition is suspected. Initial treatment often includes a combination of intravenous antibiotics including penicillin, vancomycin and clindamycin. Cultures are taken to determine appropriate antibiotic coverage, and antibiotics may be changed when culture results are obtained. As in other maladies characterized by massive wounds or tissue destruction, hyperbaric oxygen treatment can be a valuable adjunctive therapy, but is not widely available.[4] A recent study demonstrated excellent clinical outcomes from the use of topical negative pressure, a technology which is portable and readily available.[5] Amputation of the affected organ(s) may be necessary. Repeat explorations usually need to be done to remove additional necrotic tissue. Typically, this leaves a large open wound which often requires skin grafting. The associated systemic inflammatory response is usually profound, and most patients will require monitoring in an intensive care unit.
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