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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 5 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 3 (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.)