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Bullous eruption on the posterior thigh by iav17490



Bullous eruption                                                                                        James Studdiford, MD, and
                                                                                                        Amber Stonehouse, MD

on the posterior thigh                                                                                  Thomas Jefferson University
                                                                                                        Hospital, Department of Family
                                                                                                        and Community Medicine,
                                                                                                        Philadelphia, Pa
        healthy 11-year-old girl visited her        (FIGURES 1 AND 2 ). A thick, honey-

A       family physician with a lesion on
        her right posterior thigh. The
lesion was a 1-cm plaque that was tender,
                                                    yellow adherent crust covered the erod-
                                                    ed center of the lesion. The girl’s
                                                    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
erythema, 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

                                                                                                        F E AT U R E E D I T O R
                                                                                                        Richard P. Usatine, MD
                                                                                                        University of Texas Health
                                                                                                        Sciences Center at San

                                                                                                        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.              

w w w. j f p o n l i n e . c o m                                        VOL 54, NO 12 / DECEMBER 2005                              1041

                     ■   Diagnosis: Bullous impetigo,                    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 skin infection, with peak incidence                 Pemphigus 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 blisters 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 epidermis.
                     proteolytic attack of desmoglein 1,                      Pemphigus vulgaris 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               Bullous pemphigoid 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                Erythema migrans 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
                     impetigo) may result from an untreated              redness accounts for most cases in areas
Risk factors         impetigo infection.5                                endemic for Lyme disease. 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         contact dermatitis, herpes simplex, herpes
hospital visit or    zoster, pemphigus foliaceus, bullous pem-
                     phigoid, pemphigus vulgaris, and (in this           ■   Staphylococcus aureus
antibiotic use, or   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 antibiotics, 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.

   1042              VOL 54, NO 12 / DECEMBER 2005 THE JOURNAL OF FAMILY PRACTICE
                                                                       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, doxycycline,          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 abscesses. 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-
causing increased risk for infection.           acquired MRSA in this geographic area
                                                                                                  It is important
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. ■

w w w. j f p o n l i n e . c o m                                  VOL 54, NO 12 / DECEMBER 2005                1043
                                       PHOTO ROUNDS
                                       1. Dagan R. Impetigo in children: changing epidemiology
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                                       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;
                                       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
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