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A 13-year-old boy with a worsening neck, arm rash
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A 13-year-old boy presented with a 10-day history of a rash that started on his left arm after receiving his influenza vaccine. Following vaccination, the patient noted small red bumps around the injection site, leading to his presentation at an urgent care facility. He was treated empirically for an allergic reaction with a 1-week course of oral prednisone.
The patient’s rash proceeded to spread to his neck and face, as well as his left hand and thigh, where he had healing abrasions from a recent fall. He developed pruritic and tender bullae with oozing crusts on his neck, yet denied having a similar rash or vaccine reaction in the past. The patient had a history of eczema, seasonal allergies, and asthma but exhibited no other associated symptoms, and no one in his family experienced a similar rash. The patient denied a personal and family history of recurrent skin infections.
On exam, the patient had a few pink, serous-crusted papules on his nasolabial folds and cheeks, a small intact vesicle on his forehead, and pink papules with peripheral scale on his left lateral upper arm. On his neck, he had numerous round, coalescing, eroded, erythematous plaques with golden crusts, and heaped skin at the borders. Additionally, he had healing eroded papules with peripheral scale on his left dorsum fourth finger and left thigh.
Source: Boulos S
Can you spot the rash?
A. Pemphigus foliaceus
B. Eczema herpeticum
C. Rhus dermatitis
D. Bullous impetigo
E. Pemphigus vulgaris
Click to the next page to confirm your answer.
Case Discussion
Bullous impetigo (D) is the most common primary superficial infection in children, and it is most commonly caused by Staphylococcus aureus and group A beta-hemolytic Streptococcus pyogenes. The bullous form of impetigo is primarily caused by S. aureus — phage group 2-types 71 and 55 — which produces exfoliative toxins that cleave desmoglein 1 in the subcorneal layer to form superficial blisters. Nonbullous impetigo presents with honey-colored crusted, erythematous plaques.
Bullous impetigo is characterized by single or clustered flaccid vesicles and bullae that easily rupture — intact vesicles and bullae are rarely seen due to their fragility — to reveal shallow erosions with collarettes of scale. The lesions often lack surrounding erythema. Both forms of impetigo tend to favor moist, intertriginous, and periorificial areas. Lesional skin from recent trauma or other diseases like atopic dermatitis can become impetiginized and lead to more widespread disease. Among neonates, a healing umbilical cord or circumcision site is a possible nidus of infection often leading to lesions in the periumbilical region or suprapubic skin. Bullous impetigo heals without scarring and leaves behind post-inflammatory hyperpigmentation that can last weeks to months, depending on the severity of the eruption. The infection is very contagious, and it easily spreads among school children and patients involved in contact sports.
The diagnosis is made clinically, however, obtaining bacterial cultures is imperative to guide appropriate therapy. The most high-yield cultures are obtained from swabbing fluid from a vesicle, pustule or the area beneath the edge of a crusted plaque. A skin biopsy is not usually warranted unless the diagnosis is in question. The histopathology shows a subcorneal pustule with mixed dermal inflammation, and bacteria can be noted within the crust. Localized forms of impetigo are self-limiting or can be treated with topical antibiotics like mupirocin or retapamulin.
Oral antibiotics are reserved for more diffuse eruptions or resistant organisms. Antibiotic treatment like cephalexin, cloxacillin or dicloxacillin should cover penicillinase-resistant S. aureus. These options also cover S. pyogenes in cases of nonbullous impetigo. Empiric treatment for methicillin-resistant S. aureus (MRSA) may also be required based on local epidemiology of MRSA infection rates, but the condition is seen less often in children with bullous impetigo. Clindamycin is a good empiric treatment for MRSA; however, clindamycin resistance among methicillin-susceptible S. aureus and MRSA is increasing. Because of changing resistance patterns, following culture sensitivities are important to ensure optimal treatment. In some cases, bullous impetigo requires parenteral therapy such as in infants, in whom the infection can rapidly progress.
The differential diagnosis of bullous impetigo includes pemphigus foliaceus, pemphigus vulgaris, eczema herpeticum, rhus (poison ivy) dermatitis, and linear IgA bullous dermatosis (LABD). Pemphigus foliaceus and pemphigus vulgaris are autoimmune bullous disorders that target desmoglein 1, the same cell adhesion molecule cleaved in bullous impetigo. Additionally, pemphigus vulgaris has autoantibodies to desmoglein 3.
Pemphigus foliaceus presents with superficial, crusted, eroded, and erythematous plaques or flaccid blisters that usually start on the trunk, and spread to the face and scalp. Pemphigus vulgaris is characterized by flaccid bullae and erosions commonly on the mucous membranes, trunk, face, and extremities. Both conditions should improve with oral steroids, but if the course is too short, it may lead to rebound.
Eczema herpeticum is the widespread infection of herpes simplex virus (HSV) in a patient with atopic dermatitis. The condition presents with hemorrhagic punched-out erosions, vesicles and pustules that favor lesional skin. The erosions are painful and can further ulcerate to form a scalloped border. Unlike bullous impetigo, which tends to make lesions of different sizes, the individual lesions in eczema herpeticum are monomorphic and tend to be all the same size. The diagnosis can be confirmed with a Tzanck smear, direct fluorescent antibody testing, HSV polymerase chain reaction, viral culture and bacterial culture if there is a concern about impetiginization. Systemic acyclovir or valacyclovir treatment is indicated, and in more severe cases, parenteral therapy is required.
Bullous impetigo is a common superficial cutaneous infection with erosions of variable sizes with crusting, and early recognition can expedite appropriate workup and treatment.
- References:
- Eichenfield LF, et al. Neonatal and Infant Dermatology. 3rd ed. London: Elsevier; 2015.
- Koch E, et al. Pediatr Dermatol. 2016; doi: 10.1111/pde.12982.
- Paller AS, et al. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. 5th ed. London: Elsevier; 2016.
- For more information:
- Scarlett Boulos, MD, is a pediatric dermatology fellow at The Children’s Hospital of Philadelphia. She can be reached at bouloss@email.chop.edu.
- Marissa J. Perman, MD, is an attending physician at The Children’s Hospital of Philadelphia.
Disclosures: Boulos and Perman report no relevant financial disclosures.