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Diagnosis: Bullous impetigo
Bullous impetigo is a superficial skin infection that is most commonly seen in children (especially under the age of 2 years). It accounts for 10% of all pediatric skin disease and 25% of all impetigo.
Bullous impetigo is a variant of impetigo that produces exfoliative or epidermolytic toxins (ETA and ETB) in response to a staphylococcal infection. ETA and ETB are glutamate-specific serine proteases that bind and cleave desmoglein-1, a glycoprotein integral to intraepidermal keratinocyte adhesion. ETA and ETB produced at the site of a staphylococcal infection drive a cutaneous blistering response caused by intraepidermal cleavage below or within the stratum granulosum. While toxins typically act locally, they can spread systemically and produce generalized blistering. Therefore, lesions may be few and localized, or numerous and widespread.
A patient with bullous impetigo typically presents with a history of vesicular lesions that progress to flaccid bullae with little/no surrounding erythema. The color of the fluid contents can change from clear to cloudy/yellow. These bullae can easily rupture and leave a moist, erythematous base with surrounding honey-colored crust. Sometimes only the central portion of the bullae will drain, leaving a surrounding rim that retains fluid for days. Bullous impetigo most commonly affects moist, intertriginous areas. Most bullae heal without scarring, although hyperpigmentation has been reported in patients with darker skin types. Fever and other constitutional symptoms are uncommon.
The differential diagnosis of bullous impetigo includes contact dermatitis, bullous insect bites, thermal burns, pemphigus vulgaris, bullous pemphigoid, erythema multiforme, and dermatitis herpetiformis. It is especially important to rule out herpes simplex, varicella, bullous tinea, bullous fixed drug reaction, bullous drug eruption, and staphylococcal scalded skin syndrome.
The diagnosis of bullous impetigo is usually based upon clinical presentation. However, the diagnosis can easily be confirmed through bacterial culture of blister fluid that isolates Staphylococcus. Nikolsky’s sign is usually negative.
Bullous impetigo is self-limiting and, if left untreated, will typically resolve in weeks to months. The treatment of choice includes topical mupirocin ointment, along with local cleansing and crust removal. Oral antistaphylococcal drugs for 7-10 days are prescribed in the setting of widespread or complicated disease. Penicillinase-resistant penicillins and cephalosporins are effective against methicillin-susceptible Staphylococcus aureus. It is also important to consider methicillin-resistant S. aureus and treat with trimethoprim-sulfamethoxazole, clindamycin, or linezolid. Intravenous vancomycin should be reserved for patients with severe, widespread disease.
This patient was treated with cephalexin and mupirocin. Her lesions began drying up 2 days after the initiation of antibiotics. Bacterial culture results were positive for Staphylococcus.
Diagnosis: Bullous impetigo
Bullous impetigo is a superficial skin infection that is most commonly seen in children (especially under the age of 2 years). It accounts for 10% of all pediatric skin disease and 25% of all impetigo.
Bullous impetigo is a variant of impetigo that produces exfoliative or epidermolytic toxins (ETA and ETB) in response to a staphylococcal infection. ETA and ETB are glutamate-specific serine proteases that bind and cleave desmoglein-1, a glycoprotein integral to intraepidermal keratinocyte adhesion. ETA and ETB produced at the site of a staphylococcal infection drive a cutaneous blistering response caused by intraepidermal cleavage below or within the stratum granulosum. While toxins typically act locally, they can spread systemically and produce generalized blistering. Therefore, lesions may be few and localized, or numerous and widespread.
A patient with bullous impetigo typically presents with a history of vesicular lesions that progress to flaccid bullae with little/no surrounding erythema. The color of the fluid contents can change from clear to cloudy/yellow. These bullae can easily rupture and leave a moist, erythematous base with surrounding honey-colored crust. Sometimes only the central portion of the bullae will drain, leaving a surrounding rim that retains fluid for days. Bullous impetigo most commonly affects moist, intertriginous areas. Most bullae heal without scarring, although hyperpigmentation has been reported in patients with darker skin types. Fever and other constitutional symptoms are uncommon.
The differential diagnosis of bullous impetigo includes contact dermatitis, bullous insect bites, thermal burns, pemphigus vulgaris, bullous pemphigoid, erythema multiforme, and dermatitis herpetiformis. It is especially important to rule out herpes simplex, varicella, bullous tinea, bullous fixed drug reaction, bullous drug eruption, and staphylococcal scalded skin syndrome.
The diagnosis of bullous impetigo is usually based upon clinical presentation. However, the diagnosis can easily be confirmed through bacterial culture of blister fluid that isolates Staphylococcus. Nikolsky’s sign is usually negative.
Bullous impetigo is self-limiting and, if left untreated, will typically resolve in weeks to months. The treatment of choice includes topical mupirocin ointment, along with local cleansing and crust removal. Oral antistaphylococcal drugs for 7-10 days are prescribed in the setting of widespread or complicated disease. Penicillinase-resistant penicillins and cephalosporins are effective against methicillin-susceptible Staphylococcus aureus. It is also important to consider methicillin-resistant S. aureus and treat with trimethoprim-sulfamethoxazole, clindamycin, or linezolid. Intravenous vancomycin should be reserved for patients with severe, widespread disease.
This patient was treated with cephalexin and mupirocin. Her lesions began drying up 2 days after the initiation of antibiotics. Bacterial culture results were positive for Staphylococcus.
Diagnosis: Bullous impetigo
Bullous impetigo is a superficial skin infection that is most commonly seen in children (especially under the age of 2 years). It accounts for 10% of all pediatric skin disease and 25% of all impetigo.
Bullous impetigo is a variant of impetigo that produces exfoliative or epidermolytic toxins (ETA and ETB) in response to a staphylococcal infection. ETA and ETB are glutamate-specific serine proteases that bind and cleave desmoglein-1, a glycoprotein integral to intraepidermal keratinocyte adhesion. ETA and ETB produced at the site of a staphylococcal infection drive a cutaneous blistering response caused by intraepidermal cleavage below or within the stratum granulosum. While toxins typically act locally, they can spread systemically and produce generalized blistering. Therefore, lesions may be few and localized, or numerous and widespread.
A patient with bullous impetigo typically presents with a history of vesicular lesions that progress to flaccid bullae with little/no surrounding erythema. The color of the fluid contents can change from clear to cloudy/yellow. These bullae can easily rupture and leave a moist, erythematous base with surrounding honey-colored crust. Sometimes only the central portion of the bullae will drain, leaving a surrounding rim that retains fluid for days. Bullous impetigo most commonly affects moist, intertriginous areas. Most bullae heal without scarring, although hyperpigmentation has been reported in patients with darker skin types. Fever and other constitutional symptoms are uncommon.
The differential diagnosis of bullous impetigo includes contact dermatitis, bullous insect bites, thermal burns, pemphigus vulgaris, bullous pemphigoid, erythema multiforme, and dermatitis herpetiformis. It is especially important to rule out herpes simplex, varicella, bullous tinea, bullous fixed drug reaction, bullous drug eruption, and staphylococcal scalded skin syndrome.
The diagnosis of bullous impetigo is usually based upon clinical presentation. However, the diagnosis can easily be confirmed through bacterial culture of blister fluid that isolates Staphylococcus. Nikolsky’s sign is usually negative.
Bullous impetigo is self-limiting and, if left untreated, will typically resolve in weeks to months. The treatment of choice includes topical mupirocin ointment, along with local cleansing and crust removal. Oral antistaphylococcal drugs for 7-10 days are prescribed in the setting of widespread or complicated disease. Penicillinase-resistant penicillins and cephalosporins are effective against methicillin-susceptible Staphylococcus aureus. It is also important to consider methicillin-resistant S. aureus and treat with trimethoprim-sulfamethoxazole, clindamycin, or linezolid. Intravenous vancomycin should be reserved for patients with severe, widespread disease.
This patient was treated with cephalexin and mupirocin. Her lesions began drying up 2 days after the initiation of antibiotics. Bacterial culture results were positive for Staphylococcus.
This case and photo were submitted by Tanya Greywal and Dr. Brooke Resh Sateesh. Dr. Resh Sateesh is in private practice in San Diego, Calif. A 2-year-old girl presented with a 1-week history of papules on her left abdomen. She had no systemic symptoms. However, the patient returned 2 days later with diffuse lesions on her trunk and legs.
