Necrotizing Fasciitis


by Erica Nagel 


Necrotizing fasciitis, or the “flesh eating bacteria, is a skin disease which can be caused by several bacteria, but the most common and deadly causative agent is Streptococcus pyogenes, or group A streptococcus, from here on denoted as GAS (Tortora 591). GAS is the causative agent for several diseases and is “among the most common human pathogens (Tortora 590).”  This bacterium also causes scarlet fever, impetigo, cellulitis, and sepsis.

“The only known natural reservoir of S. pyogenes is the skin and mucous membranes of humans (Luckman 1).” Transmission is spread by person-to-person contact with the mucus of infected persons or through contact with infected wounds or sores on the skin (Luckman 2).

There are over 80 immunological types of GAS. Thisbacteriais grouped according to the antigenetic properties of the M protein, external to their cell wall, found in some strains of the bacteria (Tortora 590). GAS is Gram-positive, non-motile, round to ovoid coccus shaped bacteria, occurring in chains or pairs. GAS is fermentative, it is catalase negative, and it is a facultative anaerobe.  Enriched medium containing blood is needed in order to grow the bacteria in the lab and it exhibits Beta hemolysis (Todar).

            Necrotizing fasciitis is difficult to diagnose in the early stage because symptoms, such as tenderness, swelling, redness, and pain at the affected site, are similar to other, less threatening skin diseases such as cellulitis and erysipelas. The chief symptom, unique to necrotizing fasciitis, is severe pain disproportionate to physical findings (Shimizu 1052). The diagnosis of necrotizing fasciitis is a clinical one but lab findings can be used in conjunction with physical findings; these include a raised white cell count as well as raised levels of glucose, urea, and creatinine in samples taken. Hypoalbuminaemia, acidosis, and an altered coagulation profile may also be present. CT Scans and MRIs can also be used and are useful in delineating the extent of the infection and showing soft tissue gas (Hasham). The Finger test is another adjunct method for diagnosing the disease. “The finger test is a bedside procedure in which, under local anesthesia, a 2-cm incision is made down to the deep fascia and gentle probing of the index finger is performed at the level of the deep fascia. Lack of bleeding, presence of characteristic “dishwater pus” and lack of tissue resistance to blunt finger dissection are features of a positive finger test and indicate NF (Shimizu 1053).”

As stated earlier, the symptoms of necrotizing fasciitis can be similar to those of other skin diseases such as redness, swelling and pain at infection site. At the first sign of infection, a small, reddish, painful spot or bump appears on the skin. The spot quickly grows to a very painful bronze or purple colored patch that grows rapidly. The center of the infection may become black and necrotic and the skin may break open and weep fluid. The wound quickly grows, frequently in less than an hour. Other symptoms may include a general ill feeling, fever, sweating, chills, nausea, dizziness, profound weakness, and shock. Without treatment, death is likely and can occur rapidly (A.D.A.M.).

The earliest known report of necrotizing fasciitis dates back to Hippocrates’ description of a complication of cellulitis in the 5th century B.C. “…The erysipelas would quickly spread widely in all directions. Flesh, sinews and bones fell away in large quantities...Fever was sometimes present and sometimes absent...There were many deaths.The course of the disease was the same to whatever part of the body it spread (Green 220)." In 1871, Joseph Jones, who studied more than 2,600 cases of the disease during the Civil War described the disease, whichwas common among soldiers due to the conditions at the front. In 1883 Jean-Alfred Fournier described a condition he coined Fournier’s Gangrene; necrotizing fasciitis when it attacks the genital area. He noted that diabetic patients might be at a higher risk of developing this disease. Dr. B. Wilson was the first used the term "necrotizing fasciitis" in 1952.  This term is still generally considered to be the most accurate and concise description of the disease (Cummings).

Many factors contribute to the virulence of GAS. The M protein in the cell wall prevents antigenic complement and allows the microbe to evade phagocytosis by neutrophils. Its capsule, composed of hyaluronic acid, also aids GAS’ virulence. Hyaluronic acid is immunogenic and therefore few antibodies are produced against the capsule. GAS also produces enzymes that promote the rapid spread of infection through tissue. These enzymes include streptokinases, an enzyme that dissolves blood clots, hyaluronidase, an enzyme that dissolves the hyaluronic acid in connective tissue, and deoxyribonucleases, which degrades DNA (Tortora 590).

Treatment of necrotizing fasciitis can be painful and often results in severe disfigurement.  Patientsbelieved to be infected with necrotizing fasciitis should be immediately put on broad-spectrum antibiotics. The length of antibiotic therapy generally ranges from four to six weeks but six weeks is recommended. Intravenous immunoglobulin is an additional treatment option, which helps to neutralize the exotoxins created by the bacteria. “Surgical debridement is the mainstay of treatment of NF and results in significantly improved mortality compared to cases in which surgery is delayed for even a few hours (Shimizu 1054-55).” When Necrotizing fasciitis is believed to be the cause of infection, patients, as soon as possible, should be operated on for a “search and destroy” mission of vigorous and extensive debridement. Infected tissue should be removed until there is no evidence of further infection. Early surgery is the most important factor in increasing survival rates (Shimizu 1055). Skin grafts are often used to repair the damage to the skin after debridement but occasionally amputation is the only sure way to remove the disease (A.D.A.M.).

There is no sure prevention for necrotizing fasciitis. The disease has even been known to appear spontaneously. The best method of prevention is keeping the skin intact, as said before; all it takes is a minor cut or abrasion to become infected. Hand washing, use of prophylactics, and avoiding contact with infected peopleshould also be implemented (Batdorff). Vaccine development for GAS faces several significant obstacles. Firstly, the widespread diversity of GAS strains and their M protein types is a major obstacle. Secondly, immunological cross-reactivity has been demonstrated between M proteins and several human tissues. Finally, as humans are the only hosts for GAS, no animal model is available (WHO).

For 2009, according to the Center for Disease Control, the estimated US national outbreak of GAS infections was 11,000, of which, and estimated 5.9% were necrotizing fasciitis (USA CDC). From December 1997 through May 1998, the Texas Department of Health received reports of 232 invasive GAS cases. Sixteen percent of patients during the outbreak were diagnosed with necrotizing fasciitis. For children, varicella infection during the two weeks prior to their GAS infection was a significant risk factor for developing necrotizing fasciitis. Health experts say they do not know what caused the outbreak or why it affected individuals differently (Texas Department of Health 1-8).

According to the World Health Organization, GAS also is an important cause of severe infection such as streptococcal toxic shock syndrome and necrotizing fasciitis. Severe GAS infection can reach 2.5 to 3/100 000 of populations in the northern European countries. It has been estimated that there are currently more than 18 million cases of severe GAS disease in the world, with more than 500,000 deaths each year. These statistics are for the bacteria GAS and are not specific to necrotizing fasciitis (WHO).

            In conclusion, necrotizing fasciitis is difficult to diagnose, its etiology is hard to discover, and treatment is frequently painful and disfiguring. Vaccine development has proven unsuccessful and with a death rate of forty percent upon contracting the disease, the outlook is dim. Fortunately the disease is very rare with less than 1,000 deaths occurring in the US each year. This, coupled with education and early treatment, can be and effective tool in combating this disease.

Works Cited

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Batdorff, Donna. "NNFF - Prevention." Welcome to the National Necrotizing Fasciitis Foundation. Web. 06 Dec. 2010.

Cummings, Tucker. "The History of Necrotizing Fasciitis |" EHow | How To Do Just About Everything! | How To Videos & Articles. Web. 06 Dec. 2010.

Green, R. J., D. C. Dafoe, and T. A. Raffin. "Necrotizing Fasciitis." Chest 110.1 (1996): 219-29. Print.

Hasham, Salidy, Paolo Meteucci, Paul Stanley, and Nick Hart. "Necrotising Fasciitis -- Hasham Et Al. 330 (7495): 830 --" British Medical Journal, 7 Apr. 2005. Web. 05 Dec. 2010.

Luckman, Emily, and Alexandra Hristov. The John's Hopkins Microbiology Newsletter 26 (3 Apr. 2007): 7. Print.

Luckman, Emily, and Alexandra Hristov. The John's Hopkins Microbiology Newsletter 26 (3 Apr. 2007): 7. Print.

Shimizu, Taro, and YasuharuTokuda. "Necrotizing Fasciitis." Internal Medicine 49.12 (2010): 1051-057. Print.

Texas Department of Health, and Mike Burr. "Group A Streptococcus Cluster in Central Texas." Disease Prevention News 58.5 (1998): 1-8. Print.

Todar, Keneth. "Streptococcus Pyogenes and Streptococcal Disease." Online Textbook of Bacteriology. 2008. Web. 05 Dec. 2010.

Tortora, Gerard J., Berdell R. Funke, and Christine L. Case. Microbiology: an Introduction. San Francisco: Pearson Benjamin Cummings, 2007. Print.

USA. Center for Disease Control and By Center for Disease Control and Prevention. 2010. Web. 06 Dec. 2010.

USA. Department of Health and Human Safety.Center for Disease Control.Group A Streptococcal (GAS) Disease. National Center for Immunization and Respiratory Diseases: Division of Bacterial Diseases, 3 Apr. 2008. Web. 5 Dec. 2010.

"WHO | Bacterial Infections." World Health Organization. Web. 06 Dec. 2010.