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James Studdiford, MD, and Bullous eruption Amber Stonehouse, MD Thomas Jefferson University on the posterior thigh Hospital, Department of Family and Community Medicine, Philadelphia, Pa healthy 11-year-old girl visited her (FIGURES 1 AND 2). A thick, honey- family physician with a lesion on yellow adherent crust covered the erod- A her right posterior thigh. The ed center of the lesion. The girl’s lesion was a 1-cm plaque that was tender, temperature was 37.1°C, and she firm, erythematous, and indurated, with a reported no burning, pain, or pruritus. central pustule. It had been present for 3 She had full range of motion of her right days; it was noticed by the patient after hip and knee, and no lymphadenopathy returning from a camping trip in south- was detected. Her white blood cell eastern Pennsylvania. The pustular area count was normal; blood and wound was incised, drained, and cultured, and the cultures were taken. patient was started on cephalexin. Two days later, the lesion did not improve, showing increased induration, ■ What is the most likely , and blistering. The patient went diagnosis? to the emergency department with an 8 cm by 6 cm coalescence of thin-walled vesicles ■ How would you empirically and bullae with surrounding erythema treat this condition?

FIGURE 1 Bullous eruption on the thigh FIGURE 2 Close-up

FEATURE EDITOR Richard P. Usatine, MD University of Texas Health Sciences Center at San Antonio

CORRESPONDING AUTHOR Richard P. Usatine, MD, University of Texas Health Science Center at San Antonio, Department of Family and Community Medicine, MC 7794, 7703 Large coalescence of thin-walled bullae on an Large coalescence of thin-walled bullae with a Floyd Curl Drive, San Antonio, erythematous base located on the right posterior thick, honey-yellow adherent crust covering the TX 78229-3900. E-mail: thigh. eroded center of the lesion. [email protected]

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■ Diagnosis: Bullous , matous, edematous base distributed along caused by methicillin- a dermatome constitutes the classic resistant S aureus appearance. This was not the case with Impetigo is a highly contagious superfi- this patient. cial , with peak incidence foliaceous is an autoim- among children aged 2 to 6 years.1,2 mune intraepidermal blistering disease Nonbullous impetigo (70% of cases) is with lesions occurring on the face, scalp, caused by Staphylococcus aureus or beta- chest, and upper back.5 Intact are hemolytic Streptococcus.3 Bullous impeti- not commonly seen. The vesicle roof is go is almost always caused by S aureus. very thin and ruptures easily, forming Epidermolytic toxins produced by phage broad areas of crust. Skin biopsy reveals group II strains cause loss of cell adhe- intraepidermal bulla or acantholysis in the sion in the stratum granulosum due to upper . proteolytic attack of desmoglein 1, is also an autoim- resulting in bullae.4 mune blistering disease that affects the Bullous impetigo may occur after skin and mucous membranes. It is gener- minor skin injury, such as an insect bite, ally seen among patients aged >40 years. abrasion, or dermatitis. Lesions generally is an autoimmune start as small vesicles on the face, but- disorder presenting with chronic eruption tocks, extremities, or perineum, and may of erythematous, papular, urticaria lesions progress to a coalescence of thin-roofed often evolving into bullae. Childhood bullae. The flaccid bullae rupture easily, cases are rare. Biopsy of the lesions draining serous or purulent fluid. demonstrates subepidermal bulla with an Lesions are usually painless, and sys- infiltration of eosinophils within the der- temic findings are rare. Lymphadenopathy mis.5 is rare in bullous impetigo but common in with central vesicu- nonbullous impetigo. The disease is gener- lation must be considered given the ally self-limited and complications are patient’s camping trip. Recent evidence FAST TRACK uncommon. However, ecthyma (ulcerative shows that erythema migrans with central Risk factors impetigo) may result from an untreated redness accounts for most cases in areas impetigo infection.5 endemic for . Only 10% of for community- the patients with early Lyme disease show acquired MRSA the classic bulls-eye lesion with concentric infections include ■ Differential diagnosis erythematous rings and central clearing. The differential diagnosis for bullous Vesiculation can occur in up to 30% of attending day impetigo is broad, and may include allergic lesions.6 care, recent , , herpes hospital visit or zoster, pemphigus foliaceus, bullous pem- ■ use, or phigoid, pemphigus vulgaris, and (in this Staphylococcus aureus case specifically) erythema migrans. and antibiotic resistance chronic illness Allergic contact dermatitis is a delayed As many as 61% of community-acquired hypersensitivity reaction, usually caused methicillin-resistant S aureus (MRSA) by skin contact with an allergen. Lesions infections are initially treated only with can be vesicular, edematous, erythema- beta-lactam , to which they are tous, and pruritic. In this case, the patient resistant.7 Risk factors for community- did not have allergen exposure or a acquired MRSA infection include day-care pruritic lesion. attendance, recent hospitalization, recent Herpes zoster is a reactivation of the antibiotic use, chronic illness, and frequent varicella zoster virus, characterized by health care visits.8 A growing number of stabbing, neuritic pain in a dermatomal cases are reported among patients without distribution. Clear vesicles on an erythe- risk factors.

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Bullous eruption on the posterior thigh ▲

Community-acquired MRSA isolates ■ Empiric treatment are usually genetically different from of impetigo: Consider nosocomial isolates, and have been rela- a culture for MRSA tively susceptible to non–beta-lactam For localized impetigo, topical therapy antibiotics. These strains vary substantial- with mupirocin 2% ointment 3 times a ly, however, and it is important to check day for 10 days is usually adequate. A the susceptibility of the isolate. 10-day course of oral antibiotic therapy Virulent new strains of S aureus are with dicloxacillin or cephalexin is indi- infecting children—these strains have a cated in more widespread impetigo novel transpeptidase, which offers them presumed to be methicillin-sensitive S a mechanism of resistance to beta-lactams aureus. Azithromycin (Zithromax) or different from hospital- and community- clarithromycin (Biaxin) may be given to acquired types. patients allergic to penicillin. Awareness of the local antimicrobial However, it is becoming increasingly susceptibility patterns of community S important to consider community- aureus isolates is also helpful. Oral antibi- acquired methicillin-resistant S aureus otics that have been successful include species in cases such as this that do not clindamycin, minocycline, , respond to traditional therapy. Hence, and trimethoprim-sulfamethoxazole. culture and sensitivity of all suspicious Cephalexin has no therapeutic value in lesions is highly suggested. treating community-acquired MRSA. ■ Patient’s treatment ■ Preventing disease spread and recovery in the patient and contacts In this case, the patient was diagnosed Preventive efforts should be directed at with bullous impetigo and admitted to patients with recurrent episodes of MRSA the hospital. She was started on intra- skin . Metabolic and immuno- venous clindamycin at 380 mg (30 mg/kg) logic screening should be performed to every 8 hours. Clindamycin was chosen FAST TRACK rule out underlying disease processes because most cases of community- It is important causing increased risk for infection. acquired MRSA in this geographic area In most cases these test results are are resistant to trimethoprim- to consider normal, and patients with recurrent sulfamethoxazole and susceptible to methicillin- MRSA skin abscesses should also be clindamycin. resistant S aureus empirically treated for presumed nasal Although doxycycline would have carriage of MRSA. covered both community-acquired in cases that Mupirocin ointment (Bactroban) MRSA and Lyme disease, we were less do not respond to should be applied to the nares twice daily suspicious of Lyme given the physical traditional therapy for 5 days in an effort to prevent recur- exam of the patient, and we were reluc- rent self-inoculation and lateral transmis- tant to start this patient on doxycycline sion of MRSA. due to the fact she did not have complete Patients and families should also be maturation of her dentition. instructed in hygienic measures such as Within 24 hours of intravenous clin- daily changing of underwear and damycin, the lesion was markedly personal use only of towels, washcloths, improved and the culture confirmed that and sleepwear. Fingernails should be the MRSA was sensitive to clindamycin. kept short and clean. Open insect bites She was discharged on oral clindamycin at or superficial skin abrasions should be 375 mg 3 times daily, to complete a 14- kept clean and covered. Benefit from day course of therapy. The lesion was the daily use of antimicrobial soaps is completely resolved without recurrence controversial. within 2 weeks. ■

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REFERENCES 1. Dagan R. Impetigo in children: changing epidemiology and new treatments. Pediatric Annals 1993; 22:235–240. 2. Bruijnzeels MA, van Suijlekom-Smit LW, van der Velden J, van der Wouden JC. The child in general practice. Dutch national survey of morbidity and inter- ventions in general practice. Rotterdam: Erasmus University Rotterdam, 1993. 3. Allen CH, Patel M, Endom, E. Primary bacterial infec- tions of the skin and soft tissues changes in epidemi- ology and management. Clin Ped Emerg Med 2004; 5:246–255. 4. Amagai, M, Matsuyoshi, N, Wang, ZH, et al. Toxin in bullous impetigo and staphylococcal scalded skin syn- drome targets desmoglein 1. Nat Med 2000; 6:1275. 5. Habif TP. Skin Disease Diagnosis and Treatment. 2nd ed. Philadelphia, Pa: Elsevier-Mosby, 2005:136–141. 6. Smith RP, Schoen RT, Rahn DW, et al. Clinical charac- teristics and treatment outcome of early Lyme disease in patients with microbiologically confirmed erythema migrans. Ann Intern Med 2002; 136:477–479. 7. Naimi, TS, LeDell, KH, Como-Sabetti, K, et al. Comparison of community- and health care-associat- ed methicillin-resistant Staphylococcus aureus infec- tion. JAMA 2003; 290:2976. 8. Cohen, P. Community-acquired methicillin-resistant staphylococcus aureus: skin infection presenting as an axillary with cellulites in a college athlete. Skin Med 2005; 4:115–117.

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