History
Patients often cannot recall an inciting event, but a history of recent trauma or pharyngitis may be elicited. Prodromal symptoms, such as malaise, chills, and high fever, often begin before the onset of the skin lesions and usually are present within 48 hours of cutaneous involvement. Pruritus, burning, and tenderness are typical complaints.
Physical
Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque, as shown in the image below.
Facial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders. The lesion classically exhibits raised, sharply demarcated, advancing margins. This is in opposition to the slightly deeper involvement seen in cellulitis, with which lesions present with limited edema and less well-defined borders. Local signs of inflammation, such as warmth, edema, and tenderness, are universal. Lymphatic involvement often is manifested by overlying skin streaking and regional lymphadenopathy. More severe infections may exhibit numerous vesicles and bullae along with petechiae and even frank necrosis. With treatment, the lesion often desquamates and can resolve with pigmentary changes that may or may not resolve over time.
Causes
Streptococci are the primary cause of erysipelas. Most facial infections are attributed to group A streptococci, with an increasing percentage of lower extremity infections being caused by non–group A streptococci. Streptococcal toxins are thought to contribute to the brisk inflammation that is pathognomonic of this infection. No clear proof has emerged that other bacteria cause typical erysipelas, although they clearly coexist with streptococci at sites of inoculation. Recently, atypical forms reportedly have been caused by Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Yersinia enterocolitica, and Moraxella species, and they should be considered in cases refractory to standard antibiotic therapy.
The role of Staphylococcus aureus, and specifically methicillin-resistant S aureus, remains controversial. No conclusive evidence demonstrates a pathogenic role for staphylococci in typical erysipelas. The infection's predictable response to penicillin, even when S aureus is present, argues against S aureus as an etiologic agent. However, analogous to what occurs in bullous impetigo or staphylococcal scalded skin syndrome, exotoxins from coexisting S aureus may account for the clinical presentation of bullous erysipelas.[6]
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