Cellulitis is a local inflammation of the skin characterized by pain, induration, warmth, and erythema. It is caused by invasion of the tissues with bacteria, most commonly staphylococci or streptococci in adults and Hemophilus influenzae in children. In diabetic patients, additional consideration needs to be given to Enterobacteriaceae and rarely clostridia. Lymphangitis and lymphadenopathy are seen occasionally in previously healthy patients, but purely local inflammation is much more common. Systemic involvement with fever, leukocytosis, and bacteremia is seen most typically in patients with underlying immunosuppressive diseases. Traditional thought has been that the symptoms of cellulitis are related to the effects of the bacteria and their proliferation on local tissues. This has been poorly substantiated in that efforts at isolating these organisms from infected tissue have had a very poor yield. Needle aspiration of the leading edge of an area of cellulitis produces organisms in less that 10 percent of cultures, and even punch biopsy from the same area yields organisms in only around 20 percent of cultures. Only areas with suppuration or abscess formation have significantly higher yield. Recent studies now suggest that although bacterial invasion is what triggers the inflammation, the organisms are largely cleared from the site within the first 12 h, and the infiltration of lymphoid and reticular cells and their products is what produces the majority of symptoms.4 Cells such as Langerhans cells and keratinocytes release the cytokines interleukin-1 and tumor necrosis factor that enhance infiltration of the skin by circulating lymphocytes and macrophages. The net effect of this is much more rapid clearing of bacteria but at the price of a significantly larger inflammatory response. Theoretically, the addition of anti-inflammatory agents to the treatment regime of cellulitis would be beneficial. Further study needs to be done to identify what specific role, if any, such agents should play.

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