CASE #2: Bullous impetigo

The two classic forms of impetigo are bullous and nonbullous. Bullous impetigo is sometimes considered a localized form of SSSS. Although found in groups of all ages, impetigo is most commonly seen in infants and children. Adults usually contract the disease through contact with infectious children.7,8 Impetigo was first described by Dunn and Fox in the 1860s. It is best portrayed as a superficial skin infection that is extremely contagious, thus easily spread amongst children via direct person-to-person contact. Nonbullous impetigo accounts for 70% of the cases, and bullous impetigo accounts for the other 30%.3

Bullous impetigo is nearly always caused by Staphylococcus aureus. S. aureus is also the most common cause of nonbullous impetigo; however, infection with Group A beta-hemolytic streptococcus (Streptococcus pyogenes) is also seen. The infection is more common in the summer and fall months, primarily due to the increase in heat and humidity. Other predisposing factors are poor hygiene, skin trauma, and atopic diathesis. If the pathogen colonizes the pharyngeal, axillary, and nasal areas, there is an increased chance of developing impetigo. Lesions may occur all over the body but are most commonly seen on such exposed areas as the hands, neck, face, and extremities. Bullous impetigo is also commonly noted in the diaper area.

In the early stages, bullous impetigo can be seen as small vesicles that grow into 1- to 2-cm superficial bullae containing a yellowish or slightly turbid fluid. In the later stages, flaccid, transparent bullae measuring up to 5 cm in diameter appear on the skin.4 Thick crust and erythema are not appreciated in the surrounding area. Once ruptured, the bullous lesions decompress, leaving a shallow and tender erosion surrounded by the roof of the former bullae. Systemic symptoms are rare, but fever, diarrhea, and weakness may be seen. If the infection progresses further or the host is immunodeficient, such complications as septic arthritis, osteomyelitis, sepsis, cellulitis, lymphadenitis, and progression to SSSS may arise.3

In bullous impetigo, blister formation is mediated by the binding of exfoliative toxin to a desmosomal protein known as desmoglein 1. This leads to cleavage that typically occurs within the epidermal granular layer. Secondary acantholysis may be observed, mimicking pemphigus foliaceus.2 Most commonly, few inflammatory cells are present, and no bacteria are found within the blister. In the upper dermis, neutrophils may be present.

History, visual examination, and ancillary tests are usually sufficient to make the diagnosis of bullous impetigo. Dermatopathology or Gram stain and culture of the blister fluid will confirm the diagnosis. The Gram stain may reveal neutrophils with Gram-positive cocci. Bacterial culture will yield S. aureus.7 Common differential diagnoses include insect bites, HSV infection, and thermal burns. Autoimmune bullous dermatoses, bullous erythema multiforme, Stevens-Johnson syndrome, and subtypes of epidermolysis bullosa must also be considered.

If left untreated, the disorder may last for three to six weeks, with continuous spread and development of new lesions. Pay special attention to local wound care. This includes gentle cleansing, removal of crusts, and drainage of blisters and vesicles. In an otherwise healthy patient, localized disease attributable to S. aureus may be treated with such topical antibiotics as bacitracin, polymyxin, gentamicin, and erythromycin.1 Mupirocin (Bactroban) has also shown a high level of bactericidal activity against a broad spectrum of Gram-positive organisms, including both S. aureus and group A beta-hemolytic streptococci. Reduction in colonization of S. aureus may be achieved by the application of intranasal mupirocin in those who are known carriers with recurrent impetigo or in the setting of epidemic outbreaks. In more severe cases or in those who are immunocompromised, oral or IV antibiotics may be necessary. Penicillin has been shown to be inferior to treatment with erythromycin and penicillinase-resistant penicillins. Macrolides may also be effective. Local drug-resistance patterns and cost must be taken into consideration when choosing appropriate antibiotic therapy.

When one fails oral antibiotics or if the infection is severe, a skin swab for bacterial culture and sensitivity may be necessary, and the possibility of infection with community-acquired methicillin-resistant S. aureus must be considered.1

Follow-up is important to ensure complete clearing of lesions and to make certain that the infection is not progressing. Scarring is not usually a consequence; however, post-inflammatory pigment alterations may occur.

Since this child was otherwise healthy and the disease was localized, he was treated with topical mupirocin. All lesions cleared with no further complications.

Kerri Robbins, MD, is a resident in the department of dermatology at Baylor College of Medicine in Houston. The author has no relationships to disclose relating to the content of this article.



References

1. Paller AS, Mancini AJ. Hurwitz Clinical Pediatric Dermatology. 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2006:350-352, 366-368.

2. Fitzpatrick TB, Johnson RA, Wolff K, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology, 5th ed. New York, N.Y.: McGraw-Hill; 2005:94-96, 587-592.

3. JL Bolognia, JL Jorizzo, RP Rapini, eds. Dermatology, 2nd ed., St. Louis, Mo.: Elsevier-Mosby; 2008:457-466, 1075-1077.

4. RP Rapini. Practical Dermatopathology. Philadelphia, Pa.: Elsevier-Mosby; 2005:95-96, 155-156.

5. Christiano AM, Uitto J. Molecular diagnosis of inherited skin diseases: the paradigm of dystrophic epidermolysis bullosa. Adv Dermatol. 1996;11:199-213.

6. Gedde-Dahl T Jr. Epidermolysis Bullosa. A Clinical, Genetic and Epidemiologic Study. Baltimore, Md.: Johns Hopkins University Press; 1971:1-180.

7. Shriner DL, Schwartz RA, Janniger CK. Impetigo. Cutis. 1995;56:30-32.

8. Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol. 1994;11:293-303