A 12-year-old adolescent presents with the chief complaint of a burning pruritic rash on her legs, which was diagnosed 4 days prior as contact dermatitis. At the time of diagnosis, she was started on triamcinolone 0.1% cream as well as mupirocin ointment but the rash has spread. Physical examination of the patient shows annular patches with central pustules located on the thighs.
Submit your diagnosis to see full explanation.
Approximately 10% of pediatric skin complaints are due to impetigo, which includes both bullous and nonbullous types; 90% of bullous impetigo cases are seen in children younger than 2 years.1 Impetigo is an infection of the epidermis that is most commonly caused by Staphylococcus aureus and group A Streptococcus species. It is a highly contagious condition and can be passed on through contact with lesions or by direct contact with colonized nares, pets, or fomites such as towels, sheets, and nasal grooming devices.1-3
Bullous impetigo is almost always caused by the local release of exfoliative toxin by toxin-producing strains of S aureus. Release of toxin causes damage to desmogleins in the epidermis, specifically desmoglein 1, which leads to acantholysis.1,2,4 Interestingly, desmoglein 1 is the same target for autoantibodies in pemphigus vulgaris. The targeting of desmoglein 1 by exfoliative toxin causes a local production of vesicles surrounded by an erythematous base that are limited to the superficial epidermis. This affords the bacteria easy transmissibility through skin contact.2,5
Clinically, bullous impetigo often presents initially with vesicles without surrounding erythema and is typically found around skin folds including on the neck, axillae, and thighs. Lesions can also be found on buccal mucosa. These vesicles ultimately evolve into flaccid bullae and change from being filled with clear fluid to more dark and purulent fluid. Since these bullae are located at the surface of the epithelium, rupture commonly occurs leaving shallow erosions with erythematous borders.6 Systemic symptoms may be present but are not typical. Lymphadenopathy is not often associated with bullous impetigo.1,6
Diagnosis of bullous impetigo is made by clinical history and culture of lesions. Culture of lesions should be performed to determine the pathogen and specific antibiotic coverage options for each case. For patients whose lesions are caused by methicillin-resistant S aureus (MRSA), clindamycin and doxycycline are commonly used. Both nonbullous and bullous impetigo may be managed with bleach baths along with topical antibiotics that cover staphylococcal and streptococcal species such as mupirocin, retapamulin, and ozenoxacin.
Some severe and systemic bullous impetigo cases, as well as diffuse cases of nonbullous impetigo, may also be treated with oral antibiotics; however, oral antibiotics have been shown to be similar in efficacy to properly used topical antibiotics.6,7
Treatment will also reduce complications that might arise from prolonged infection with these pathogens, including osteomyelitis, endocarditis, toxic shock syndrome, and staphylococcal scalded skin syndrome.
Individuals should also be tested for asymptomatic colonization of their nares by S aureus and counseled on proper handwashing and wound coverage to prevent spread of the disease to other individuals. Clothing and bedding should be washed.1,6,7 Affected individuals should refrain from group sports and make sure they do not share equipment such as knee pads, helmets, and eye guards.
Differential diagnosis of bullous impetigo should include herpes and varicella virus infections, staphylococcal scalded skin syndrome, bullous pemphigoid, bullous erythema multiforme, pemphigus vulgaris, Stevens-Johnson syndrome, and toxic epidermal necrolysis.8
The patient in this case was originally diagnosed as having contact dermatitis. Upon proper diagnosis of bullous impetigo and culture of the lesions (both skin and nose), steroid treatment was stopped, bleach baths were started, and topical mupirocin was used on open sores and in the nose. The patient achieved a full recovery within 4 weeks.
Note: When patients have staphylococcal infections, it is important that they alert their primary care doctors. If any surgeries are planned in the future, preoperative cultures are warranted from the nose and any nonhealing open wounds. Family members and pets should be cultured and treated appropriately to eradicate the infection from the family unit.
Cooper Tye, MD, is a resident physician at John Peter Smith Hospital in Fort Worth, Texas. Cynthia Trickett, PA-C, is a physician assistant at North Dallas Dermatology Associates in Dallas, Texas. Alyssa Spiegel, PA-C, is a physician assistant at Mindful Dermatology in Dallas, Texas. Jennifer Cather, MD, is the practicing physician at Mindful Dermatology in Dallas, Texas.
1. Nardi NM, Schaefer TJ. Impetigo. In. StatPearls. Treasure Island, FL: StatPearls Publishing; 2021.
2. Stanley JR, Amagai M. Pemphigus, bullous impetigo, and the staphylococcal scalded-skin syndrome. N Engl J Med. 2006;355(17):1800-1810. doi:10.1056/NEJMra061111
3. Occelli P, Blanie M, Sanchez R, et al. Outbreak of staphylococcal bullous impetigo in a maternity ward linked to an asymptomatic healthcare worker. J Hosp Infect. 2007;67(3):264-270. doi:10.1016/j.jhin.2007.08.023
4. Mahoney MG, Wang Z, Rothenberger K, Koch PJ, Amagai M, Stanley JR. Explanations for the clinical and microscopic localization of lesions in pemphigus foliaceus and vulgaris. J Clin Invest. 1999;103(4):461-468. doi:10.1172/JCI5252
5. Amagai M, Matsuyoshi N, Wang ZH, Andl C, Stanley JR. Toxin in bullous impetigo and staphylococcal scalded-skin syndrome targets desmoglein 1. Nat Med. 2019;6(11):1275-1277. doi:10.1038/81385
6. Cole C, Gazewood J. Diagnosis and treatment of impetigo. Am Fam Physician. 2007;75(6):859-864.
7. Johnston GA. Treatment of bullous impetigo and the staphylococcal scalded skin syndrome in infants. Expert Rev Anti Infect Ther. 2004;2(3):439-446. doi:10.1586/14787188.8.131.529
8. Duggal SD, Bharara T, Jena PP, et al. Staphylococcal bullous impetigo in a neonate. World J Clin Cases. 2016;4(7):191-194. doi:10.12998/wjcc.v4.i7.191