Two-month-old boy with erythroderma

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A healthy 2-month-old boy presents with a 4-day history of diaper dermatitis unresponsive to barrier creams. The infant has developed “red spots” that started on his cheeks, then spread to his trunk and diaper area. He is a bit fussy but feeding well.

THE CASE

A healthy 2-month-old boy presents with a 4-day history of diaper dermatitis unresponsive to barrier creams. The infant has developed “red spots” that started on his cheeks, then spread to his trunk and diaper area. He is a bit fussy but feeding well. FOR MORE ON THIS CASE, SEE NEXT PAGE.

 

 

Dermcase diagnosis: Staphylococcal scalded skin syndrome

Clinical findings and etiology

Staphylococcal scalded skin syndrome (SSSS) is a toxin-mediated infection caused by Staphylococcus aureus, leading to an exfoliative dermatitis because of activity of epidermolytic toxins A and B. These toxins bind to and cleave an adhesion molecule desmoglein-1, which causes disruption of the desmosomes in the subgranular layer of the epidermis close to the surface of the skin.1,2,3

The syndrome typically affects newborns and children aged younger than 5 years. It often presents with a prodrome of conjunctivitis or sore throat.4 The rash is preceded by irritability, fever, malaise, and tenderness of the skin.1,2 Erythematous crusted patches develop in areas of minor trauma such as the perineum, axilla, face, and neck and progress to flaccid blisters that rupture, leaving a wet, red “scalded “ appearance.4 The Nikolsky sign is positive (with rubbing, sloughing of the skin appears). Mucous membranes are not affected, which differentiates SSSS from Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), in which the split in the skin is full thickness and multiple mucous membranes are involved.1,2,3

Evaluation

The clinical diagnosis of SSSS can be confirmed by a skin biopsy that will show a blister or erosion with a split high in the epidermis at the level of the zona granulosa. The syndrome can be quickly distinguished histologically from SJS and TEN, in which the split occurs at the dermoepidermal junction.1

More: Alternative medicine for atopic dermatitis

Although bacterial cultures from the areas of blistering are usually negative, superficial foci of infection such as the nasopharynx, nostrils, conjunctivae, or umbilicus often will demonstrate positive cultures for exotoxin producing S aureus.1

Treatment

Treatment for generalized SSSS may require hospitalization for children who are not taking fluids well, who are immunologically compromised, and/or who have a systemic source of infection. Patients also may require careful monitoring of fluids and electrolytes.

Empiric antibiotic coverage should include a penicillinase-resistant penicillin or first- or second-generation cephalosporin until adjustments can be made based on local resistance patterns and culture sensitivities.1,5 

Although clindamycin has been favored for its excellent skin penetration and inhibition of toxin production, recent reports suggest that the organisms associated with SSSS are increasingly resistant to this antibiotic.5

In addition to antibiotic therapy, skin care should include bland emollients. There is no role for topical antibiotics because they add little to systemic antibiotic therapy and might be associated with the development of contact dermatitis and potential toxicity from systemic absorption

The patient

Based on the patient’s presentation, the diagnosis of SSSS was highly suspected based on clinical findings. He was admitted to the general pediatric service and treated with intravenous cefazolin as well as clindamycin. Culture of the skin around the nose and eyes grew S aureus sensitive to oxacillin, erythromycin, clindamycin, cephalosporin, sulfamethoxazole/trimethoprim, and doxycycline. 

The infant was treated with parenteral antibiotics for 5 days and then transitioned to oral cephalosporin to complete a 10-day course of treatment after discharge.

 

REFERENCES

1. Berk DR, Bayliss SJ. MRSA, staphylococcal scalded skin syndrome and other cutaneous bacterial emergencies. Pediatr Ann. 2010;39(10):627-633.

2. Handler MZ, Schwartz RA. Staphylococcal scalded skin syndrome: diagnosis and management in children and adults. J Eur Acad Dermatol Venereol. 2014;28(11):1418-1423.

3. Bukowski M, Wladyka B, Dubin G. Exfoliative toxins of Staphylococcus aureus. Toxins (Basel). 2010;2(5):1148-1165.

4. Patel GK, Finlay AY. Staphylococcal scalded skin syndrome: diagnosis and management. Am J Clin Dermatol. 2003;4(3):165-175.

5. Braunstein I, Wanat KA, Abuabara K, McGowan KL, Yan AC, Treat JR. Antibiotic sensitivity and resistance patterns in pediatric staphylococcal scalded skin syndrome. Pediatr Dermatol. 2014;31(3):305-308.

Dr Clark is a third-year pediatric resident, University of Nevada School of Medicine, Las Vegas. Dr Das is director, pediatric residency program, and vice chair of pediatrics for education, University of Nevada School of Medicine. The authors have nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article. Dr Di John is associate professor of pediatrics and section chief, pediatric infectious diseases, University of Nevada School of Medicine. He reports that he is a speaker for Sanofi Pasteur. Dr Cohen, section editor for Dermcase, is professor of pediatrics and dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland. Vignettes are based on real cases that have been modified to focus on key teaching points. Images also may be edited or substituted for teaching purposes.

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