Fragile, bullous lesions on the trunk of a child - Clinical Advisor

Fragile, bullous lesions on the trunk of a child

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An 8-year-old African-American boy presents with a 3-day history of fever, pain, and a rash on his trunk. On examination, the patient has several fragile, bullous lesions on his trunk, many of which have eroded, exposing erythematous, annular lesions. The patient is febrile and shaking in the office, and he appears to be in pain. He has no other relevant social or family history and does not take any medications. His mother is very concerned about her son.

Bullous impetigo is a highly contagious infection of the epidermis caused by the bacterium Staphylococcus aureus that is most commonly seen in neonates. It typically presents with fragile, flaccid bullae that easily rupture, leaving annular erosions with an erythematous base...

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Bullous impetigo is a highly contagious infection of the epidermis caused by the bacterium Staphylococcus aureus that is most commonly seen in neonates. It typically presents with fragile, flaccid bullae that easily rupture, leaving annular erosions with an erythematous base and central healing.1 Limited infections typically resolve in 2 to 3 weeks without scarring.2

Although bullous impetigo can present in any individual, it most commonly occurs during the neonatal period, and to a lesser degree in children (especially those under age 5).1 Some cases of bullous impetigo have also been reported during pregnancy, and should be included in the differential diagnosis for blistering conditions in pregnant women.3,4

Several risk factors can increase the risk or severity of infection. Factors such as poor hygiene, high humidity, warm temperatures, atopic diathesis, and  Staphylococcus aureus colonization can all predispose individuals to impetigo infections.5 In adults, pharmacologic immunosuppression, AIDS, and lymphoma chemotherapy have been shown as risk factors for bullous impetigo.6,7

Bullous impetigo is most often found in intertriginous areas of the body, such as diaper areas, as well as axilla and neck folds; it can often be found on the buttocks of infants. Initial presentation of the disease typically involves small vesicles that develop into flaccid blisters.8 Their contents are initially clear but, over time, become more purulent.9 The roof of the blister eventually ruptures, revealing an erythematous base that may appear shiny or wet.8 Rupture may also result in a peripheral collarette and lead to confluence of lesions.8

The bacterial skin infection of impetigo can be subcategorized into two types: nonbullous impetigo (or impetigo contagiosa), which comprises approximately 70% of cases, and bullous impetigo, which comprises approximately 30% of cases.9 Although nonbullous impetigo may be caused by Streptococcus or S aureus infection, bullous impetigo is almost solely caused by S aureus, which produces exfoliative toxin A and B.8 Exfoliative toxin A, a serine protease produced by the bacteria, binds and destroys desmosomes in the granular layer of the epidermis through cleavage of the desmosomal cadherin desmoglein-1.8,9 The thin epidermal barrier of the stratum corneum is left intact, resulting in bullae formation in the superficial epidermis.9

Diagnosis of bullous impetigo is predominantly clinical. Skin swabs are not helpful due to their inability to differentiate between normal colonization of the skin and the pathogenic cause of infection.1 However, drainage and inoculation of pustule fluid for Gram stain and culture can aid in the diagnosis.1,5

The appearance of epidermal infections similar to bullous impetigo contains a broad differential diagnosis. It is important to rule out bullous erythema multiforme and Stevens-Johnson syndrome, as early identification of both hypersensitivity reactions can have a significant impact on prognosis.10,11 Autoimmune bullous dermatoses should also be ruled out, although some of these conditions, such as bullous pemphigoid, usually occur in older adult populations. Often, bullous insect bite reactions and potential viral infection by herpes simplex virus are highest on the differential diagnosis when considering bullous impetigo.11 In these cases, obtaining a thorough medical history, along with close examination of the blisters, can aid in differentiating these disorders. When fluid-filled vesicles are present, culture of fluid from vesicles can be used to differentiate the disorders.

Bullous impetigo is often self-resolving when the infection is limited, but numerous options are available for treatment. Oral antibiotics, such as penicillin derivatives or clindamycin, may be utilized in cases of severe or systemic infection.1,8 For mild or moderate cases, topical antibiotic therapy is safe and optimal.6 Mupirocin 2% is a common topical treatment option that is highly effective against S aureus as well as most Streptococcus species.1,8  Retapamulin 1% ointment has also been shown to be clinically effective; however, it may cause localized pruritus.8,12

It should be noted that some children appear to have recurrent flares of bullous impetigo. This may be caused by colonization of S aureus. In these cases, the acute bought of impetigo should be treated, as discussed above, and the child should undergo decolonization treatment over time. Decolonization can occur via extended treatment of the nares and intertriginous regions with mupirocin spray and ointment, respectively.

Our patient in this case was diagnosed with a severe case of bullous impetigo. Due to systemic symptoms and widespread lesions, the patient was treated with a course of oral clindamycin, which led to the resolution of his symptoms.

Sirus Jesudasen, BS, is a medical student at the Baylor College of Medicine, Christopher Rizk, MD, is a dermatology resident at the Baylor College of Medicine in Houston.

References

  1. Hartman-Adams H, Banvard C, Juckett G. Impetigo: diagnosis and treatment. Am Fam Physician. 2014;90:229-235.
  2. Koning S, van der Sande R, Verhagen AP, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2012;1:CD003261.
  3. Piechowicz L, Garbacz K, Budzyńska A, Dąbrowska-Szponar M. Outbreak of bullous impetigo caused by Staphylococcus aureus strains of phage type 3C/71 in a maternity ward linked to nasal carriage of a healthcare worker. Eur J Dermatol. 2012;22:252-255.
  4. Cohen PR. Bullous impetigo and pregnancy: case report and review of blistering conditions in pregnancy. Dermatol Online J. 2016;22: pii: 13030/qt7533z2m0.
  5. Duggal SD, Bharara T, Jena PP, et al. Staphylococcal bullous impetigo in a neonate. World J Clin Cases. 2016;4:191-194.
  6. George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract. 2003;53:480-487.
  7. Bukowski M, Wladyka B, Dubin G. Exfoliative toxins of Staphylococcus aureus. Toxins (Basel). 2010;2:1148-1165.
  8. Pereira LB. Impetigo—review. An Bras Dermatol. 2014;89:293-299.
  9. Bangert S, Levy M, Hebert AA. Bacterial resistance and impetigo treatment trends: a review. Pediatr Dermatol. 2012;29:243-248.
  10. Brown J, Shriner DL, Schwartz RA, Janniger CK. Impetigo: an update. Int J Dermatol. 2003;42:251-255.
  11. Ki V, Coleman R. Bacterial skin and soft tissue infections in adults: a review of their epidemiology, pathogenesis, diagnosis, treatment and site of care. Can J Infect Dis Med Microbiol. 2008;19:173-184.
  12. Koning S, van der Wouden JC, Chosidow O, et al. Efficacy and safety of retapamulin ointment as treatment of impetigo: randomized double-blind multicentre placebo-controlled trial. Br J Dermatol. 2008;158:1077-1082. 
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