Necrotizing fasciitis• Rapidly spreading destructive disease of the

fascia.• Deep-seated infection of the subcutaneous tissue

that progressively destroys fascia and fat but may spare the skin and muscle

• Usually attributable to Group A Streptococci• Other etiologies: Mixed aerobe and anaerobe

(Clostridium perfringens, Peptostreptococcus, Burkholderia and Bacteroides spp.)

• Risk factors: Surgeries, Diabetes, Peripheral vascular disease

Harrison's Principles of Internal Medicine, 17th ed.

Necrotizing fasciitis

• 61-year-old Chinese man with a history of psoriasis and alcoholic liver cirrhosis sought treatment for left ankle swelling, erythema, and tenderness

• could not recall any antecedent trauma to the affected limb• Febrile• Progression to formation of blisters, extensive subcutaneous

tissue and fascial necrosis, loss of resistance of the normally adherent superficial fascia to blunt dissection, and foul-smelling “dishwater” pus

Necrotizing fasciitis

• Culture: Burkholderia pseudomallei. (Endemic to Southeast Asia, Taiwan, China, Central and South America, and northern Australia)

• sporadic infections occur throughout the world

Yi-Shi Wang, Chin-Ho Wong, and Asok Kurup. Cutaneous Melioidosis and Necrotizing Fasciitis Caused by Burkholderia pseudomallei. 2003

Necrotizing fasciitis

(Group A Streptococci)A. Definite case1. Necrosis of soft tissues with involvement of the

fasciaPLUS2. Serious systemic disease, including one or more

of the following:a) Deathb) Shock (systolic blood pressure <90 mm of Hg).c) Disseminated intravascular coagulopathy

Necrotizing fasciitis

d) Failure of organ systemsa. respiratory failureb. liver failurec. renal failure3. Isolation of group A Streptococcus from a

normally sterile body site

Necrotizing fasciitis

B. Suspected case1 . 1 + 2 and serologic confirmation of group A

streptococcal infection by a 4-fold rise against:a) streptolysin Ob) DNase B2. 1 + 2 and histologic confirmation:Gram-positive cocci in a necrotic soft tissue

infection

Usual Clinical Course

• 24 hours of the initial lesion— mild erythema, swelling, heat

• Next 24 to 48 hours-the erythema changed from red to purple and then to blue, and blisters and bullae, which contained clear yellow fluid

• Days 4 and 5- the purple areas became gangrenous.• Day 7 to day 10- the line of demarcation became

sharply defined, and the dead skin began to separate at the margins or breaks in the center, revealing an extensive necrosis of the subcutaneous tissue.

Necrotizing fasciitis

• More severe cases: the process advancedrapidly until several large areas of skin becamegangrenous, and the intoxication rendered the patient dull, unresponsive, mentally cloudy, or even delirious.

Streptococcal Toxic-Shock Syndrome:Spectrum of Disease, Pathogenesis, and NewConcepts in TreatmentDennis L. Stevens, Ph.D., M.D.Emerging infectious Diseases Vol.1 No.3 July-Sept 1995