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INTRODUCTION

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Intact skin serves as an effective mechanical barrier in the vast majority of healthy infants and children. Constant desquamation continually removes potentially invasive bacteria; however, almost any microorganism can live upon human skin under appropriate conditions.1 It is helpful to view these in the framework of transient, resident, and pathogenic flora. Transient flora are microorganisms deposited on the skin from the environment, typically non-proliferative and easily removed by washing the affected region. Resident flora are a select group of organisms regularly found on the skin of normal individuals in appreciable numbers that form stably reproducing colonies and that are not easily dislodged. The resident flora consists primarily of gram-positive species such as Propionibacterium acnes, aerobic diphtheroids, and Staphylococcus epidermidis. A few gram-negative species such as Escherichia, Enterobacter, Proteus, and Pseudomonas are found uncommonly on normal skin, more likely being found in moist intertriginous regions such as the groin and toe webs.1 Pathogenic organisms are not ordinarily found as part of the resident flora but may persist via continuous replacement from either an internal or external nidus of infection and include a wide range of organisms, most commonly, Staphylococcus aureus and group A β-hemolytic Streptococcus (GABHS).

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STAPHYLOCOCCAL SCALDED SKIN SYNDROME

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BACKGROUND

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Staphylococcal scalded skin syndrome (SSSS), alternatively known as Ritter’s disease or Pemphigus neonatorum, is a toxin-mediated exfoliative dermatitis caused by toxigenic strains of S. aureus, characterized by skin tenderness, flaccid bullae, and eventual skin sloughing. The disease occurs most commonly in children with slight male predominance; 98% being younger than the age of 6 years, 62% under the age of 2 years, and with neonates being especially susceptible.2 SSSS can lead to serious complications such as pneumonia, hypothermia, dehydration, and secondary infections, particularly in newborns and immunocompromised adults in whom these complications can be lethal.2

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PATHOPHYSIOLOGY

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SSSS generally begins with colonization of the conjunctivae, naris, perioral region, perineum, or umbilicus by specific strains of S. aureus capable of producing the exfoliative toxins A (ETA) or B (ETB).1 These usually belong to phage group II, with strains 71 and 55 being the most common. ETA accounts for an estimated 89% of cases.2 Both exfoliative toxins cause intraepidermal splitting at the zona granulosa by destroying the protein desmoglein 1 which is an important component of the desmosome involved in keratinocyte intercellular adhesion and is the same protein targeted in the autoimmune blistering disease Pemphigus foliaceus.2 This leads to fragile, flaccid bullae and eventual detachment of the superficial epidermis. The exfoliative toxins, unlike the toxin involved in staphylococcal toxic shock syndrome, are not known to produce direct hemodynamic compromise.2 Neonates are thought to be particularly vulnerable to SSSS due to their immature immunity and decreased renal excretion of the toxin.

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CLINICAL PRESENTATION

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A local skin infection may ...

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