A blistering disease: bullous erysipelas
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* Janet Edwards
* Peter Green
* David Haase

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![Figure1](http://www.cmaj.ca/https://www.cmaj.ca/content/cmaj/175/3/244.2/F1.medium.gif)

[Figure1](http://www.cmaj.ca/content/175/3/244.2/F1)

Figure. A 57-year-old man with type 2 diabetes with blistering on his lower limb, which began 4 days after he was treated with cefazolin and probenecid for acutely painful erythema (accompanied by fever and nausea) that had been diagnosed as cellulitis.

This patient with non–insulin-dependent diabetes mellitus had initially come to the emergency department. His diagnosis at that time was cellulitis, which was treated with a course of intravenous cefazolin and oral probenecid. By 4 days afterward his systemic symptoms had resolved, but he was referred to us for assessment of severe blistering that had erupted within the erythema.

We ruptured and drained the patient's bullae; a culture of the contained fluid grew only normal skin flora. He was provided a regimen of wound care, and his doses of cefazolin and probenecid were increased and continued for 14 days, followed by a 4-week course of cephalexin (by mouth). His edema and erythema resolved with no recurrence; graduated compression stockings were prescribed.

We diagnosed bullous erysipelas, which is a clinical diagnosis that indicates superficial cellulitis with lymphatic involvement; it is typically caused by group A β-hemolytic streptococci. It typically appears on the legs and face as sharply demarcated, tender erythema and edema, with an indurated border. Accompanying signs and symptoms include lymphangitis, fever and chills. Eryisipelas generally responds robustly to antibiotic therapy with β-lactams (*Dermatology* 2006;212:31-5).

In a few cases, the clinical course is complicated by local appearance of bullae, necrosis or hemorrhage. This may represent a synergistic superinfection with *Staphylococcus aureus* or anaerobic microbes. These more aggressive forms of erysipelas respond less well to therapy and have a protracted course of disease (*Dermatology* 2006;212:31-5).

Bullous involvement complicates erysipelas in some 5% of cases, with flaccid intraepidermal sterile blisters. The bullous form tends to occur more frequently among women and people with liver or renal disease. Those with bullous lesions have increased rates of infection with MRSA, the methicillin-resistant strains of *S. aureus* (*Dermatology* 2006;212: 31-5). Diagnosis involves the differential exclusion of cellulitis, allergic contact dermatitis, bullous pemphigoid, necrotizing fasciitis and varicella– zoster.

Management of bullous erysipelas includes appropriate empiric antibiotic therapy, with consideration given to local rates of MRSA. Bullous fluid may be cultured, but the yield is generally low. Suggested adjuvant therapy includes rupture of the bullae, débridement of sloughed tissue and compression stockings. Recurrence, attributed to lymphatic obstruction, occurs in 30% of patients within 3 years.