FIGURE 66.3 Bullous impetigo (Reprinted with permission from Goodheart HP Goodheart’s Photoguide of Common Skin Disorders 2nd ed Philadelphia, PA: Lippincott Williams & Wilkins; 2003.) Staphylococcal-Scalded Skin Syndrome Staphylococcal-scalded skin syndrome (SSSS) is a severe infection resulting from dissemination of the exfoliative toxin produced by SA SSSS is most common in children under years of age and can present in neonates The clinical appearance is diffuse redness that parents commonly liken to a sunburn The skin then peels most characteristically around the mouth, nose, and eyes Although the crusting and peeling is most prominent in these periorificial areas and can be exuberant, the actual conjunctiva and oral mucosa are not affected Peeling is also typically prominent in the neck, axillary, and inguinal folds ( Fig 66.4 ) If the red skin is rubbed, a blister can often be induced (Nikolsky sign) The main clinical differential is Stevens–Johnson syndrome (SJS), which by definition must affect two mucous membranes In the mucosa, desmoglein (DSG3) is more important in keratinocyte cell–cell adhesion than DSG1 The exfoliative toxin only targets DSG1 and so the mucosa is spared in SSSS Therefore, the most reliable way of differentiating SSSS from SJS is the lack of mucosal involvement in SSSS Kawasaki can also cause peeling skin, especially on the hands and feet, but the peeling occurs at least 10 to 14 days after the initial febrile episode, while the exfoliation in SSSS occurs within the first few days of the onset of the illness FIGURE 66.4 Staphylococcal-scalded skin syndrome Note the scalded appearance of the skin under the ruptured bullae of the chest and axilla in this child with staphylococcal-scalded skin syndrome (Reprinted with permission from Lippincott Nursing Assessment Philadelphia, PA: Wolters Kluwer; 2014.) The primary site of the staphylococcal infection is often unknown but recent surgeries (umbilical cord or circumcision in neonates) or other breaks in the skin should be evaluated and cultured If no clear source of infection can be found, the nares and anus and most heavily crusted areas should be cultured in order to establish antibiotic sensitivities of the SA that is colonizing the child Therapy for SSSS is with systemic antistaphylococcal antibiotics, typically oxacillin or other beta lactamase–resistant antibiotics Clindamycin is often added because it inhibits bacterial ribosomal function, thus decreasing toxin formation In critically ill patients vancomycin should be considered in case the infection is being caused by a resistant staphylococcal strain Ecthyma Ecthyma is a skin infection with loss of the top layers of the skin caused by necrosis The most common cause of ecthyma in children is GAS and typically presents with painful crusts and erosions ( Fig 66.5 ) Ecthyma gangrenosum is a term typically reserved for a pseudomonas infection that presents with a painful purple papule or nodule that quickly ulcerates with expanding redness Pseudomonas ecthyma should not occur in normal hosts so if the diagnosis is made, the patient requires a workup for potential malignancy or other immunosuppression Other bacteria and opportunistic fungi may cause lesions of ecthyma in immunosuppressed children Therefore, culture is vital to establish a diagnosis Therapy should be guided by cultures but empiric broad-spectrum gram-positive and gramnegative coverage should be started immediately for suspected ecthyma gangrenosum in immunosuppressed patients Consideration should also be given to starting an antifungal agent such as amphotericin and doublecovering pseudomonas, depending on the degree of immunosuppression and the patient’s overall clinical appearance FIGURE 66.5 Ecthyma Ecthyma with eroded, red papules with accompanying erosions and crust (Reprinted with permission from Craft N, Fox LP, Goldsmith LA, et al VisualDx: Essential Adult Dermatology Philadelphia, PA: Lippincott Williams & Wilkins; 2010.)