Staphylococcal scalded skin syndrome

Published on 19/03/2015 by admin

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Staphylococcal scalded skin syndrome

Dimitra Koch and Saleem M. Taibjee

Evidence Levels:  A Double-blind study  B Clinical trial ≥ 20 subjects  C Clinical trial < 20 subjects  D Series ≥ 5 subjects  E Anecdotal case reports

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Staphylococcal scalded skin syndrome (SSSS) is a highly contagious blistering condition triggered by exfoliative toxin-producing Staphylococcus aureus, most commonly affecting neonates and children under the age of 6 years. It rarely presents in adults, usually in association with renal failure or immune compromise, and possibly non-steroidal anti-inflammatory drug (NSAID) use. In healthy infants mortality is uncommon, with reported rates up to 3%, contrasting with up to 50–60% in adults with comorbidity.

SSSS is caused by hematogenous spread of exfoliative toxin (ET), mainly ET-A and/or -B produced by S. aureus, most commonly phage group II (types 3A, 3B, 3C, 55, 71), including both methicillin-sensitive and methicillin-resistant (MRSA) strains. ET, a serine protease, specifically cleaves the desmosomal protein desmoglein-1, leading to disruption of keratinocyte adhesion in the superficial epidermis. Increased susceptibility to SSSS in neonates and adults with renal failure, or immunocompromise, is thought to be due to impaired renal clearance of ET or low titers of ET-specific antibodies, respectively.

Clinical features include a prodrome of malaise, irritability, and fever. Skin manifestations develop within 24 to 48 hours. Tender erythema is followed by superficial, flaccid blistering, most pronounced in flexural and periorificial areas. Nikolsky sign is positive. Mucosal surfaces are not involved. With successful treatment SSSS resolves over 10 to 14 days. Bullae rupture to leave denuded skin, followed by desquamation and re-epithelialization without scarring.

Typically, the causative organism cannot be cultured from affected skin, as this is a toxin-mediated disease. The infection is acquired by skin-to-skin contact or from contact with nasal carriers. The source of infection is mainly via nasal or perianal colonization. It may therefore be possible to culture ET-producing S. aureus from extracutaneous sites, most commonly the nasopharynx, but also the rectum, conjunctivae, urinary tract, umbilicus and blood. Polymerase chain reaction (PCR) or random amplified polymorphic DNA analysis may identify the toxin-encoding genes. Histology of affected skin typically shows a superficial, subcorneal blister, absence of epidermal necrosis, and minimal inflammation. Frozen section of the blister roof is an alternative method of confirming the superficial level of cleavage and may facilitate more rapid diagnosis.

The main differential diagnosis is the Stevens-Johnson syndrome–toxic epidermal necrolysis spectrum, in which targetoid skin lesions, mucosal involvement, and deeper level of blistering with full-thickness epidermal necrosis are distinguishing features.

Management strategy

Treatment includes antibiotic therapy in combination with supportive measures addressing electrolyte and fluid balance, temperature regulation, nutrition, analgesia, and skin care. Bland emollients such as 50 : 50 white soft paraffin/liquid paraffin should be applied regularly to reduce friction and insensible fluid losses. Non-adherent dressings are used to cover denuded areas, with avoidance of adhesive tapes directly to skin. Systemic β-lactamase-resistant antibiotics are necessary to eradicate the causative S. aureus strain. Patients with extensive SSSS require intravenous antibiotics and in-hospital care provided by a multidisciplinary team experienced in delivering optimal skin care, e.g., on a burns unit. In view of the growing emergence of resistant ET-producing S. aureus strains, in particular MRSA and fusidic acid-resistant strains, antibiotic choice should be guided by the local microbiology team.

SSSS outbreaks on maternity and neonatal units are reported. Strict infection control measures are advisable, including patient isolation, barrier nursing, and scrupulous hand-washing. Screening programs may identify S. aureus carriers amongst patient contacts including healthcare workers. Colonized individuals require treatment with topical antiseptics, e.g., chlorhexidine, with nasal carriage eradicated by topical antibiotics such as mupirocin.

The choice of antibiotic therapy should be guided by local incidence of multidrug-resistant S. aureus strains and microbiology advice.

Specific Investigations

First-line therapies

image &#x03B2;-Lactamase resistant penicillins, e.g., flucloxacillin, oxacillin D,E

Second-line therapies

image Glycopeptide antibiotic, e.g., vancomycin E

Third-line therapies

image Quinolones E
image Tetracyclines E
image Cephalosporins E
image Aminoglycosides E
image Pooled human immuneglobulin E
image Fresh-frozen plasma E
image Skin substitute dressings E

Antimicrobial agent of susceptibilities and antiseptic resistance gene distribution among methicillin-resistant Staphylococcal aureus isolates from patients with impetigo and staphylococcal scalded skin syndrome.

Noguchi N, Nakaminami H, Nishijima S, Kurokawa I, So H, Sasatsu M. J Clin Microbiol 2006; 44: 2119–25.

A Japanese study of MRSA including 76 strains isolated from patients with impetigo and SSSS, of which 75 (99%) were community-acquired (C-MRSA). C-MRSA strains frequently demonstrated evolution of multidrug resistance (95% gentamicin- and 80% clarithromycin-resistant), although all remained susceptible to levofloxacin and minocycline. Seventy-one of 76 (93.5%) C-MRSA strains were susceptible to cationic antiseptic agents, contrasting with 112 of 207 (54%) hospital-acquired MRSA.

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