Infections of the Skin

Clinical Findings

Impetigo is one of the most common neonatal skin infections. Bullous impetigo manifests itself as flaccid vesicles/bullae or pustules on an erythematous base, most often seen in the diaper area, periumbilically, or in skin folds ( Fig. 93.1 ). Ruptured lesions leave behind a moist red base with a characteristic collarette of scale. Lesions of bullous impetigo are usually not closely grouped, which distinguishes this infection from herpes simplex virus (HSV) infection. Aggressive cases of S. aureus bullous impetigo may also present as widespread desquamation in a degloving pattern.

In contrast, nonbullous impetigo is characterized by thin-walled vesicles or pustules, often at sites of broken skin on the extremities or face. These lesions rapidly burst and assume their characteristic appearance of variably pruritic, eroded red patches with a superimposed honey-colored crust. In both forms of impetigo, affected areas heal without scarring.

Etiology

S. aureus is the exclusive cause of bullous impetigo and the primary cause of nonbullous impetigo. GAS may also be associated with the nonbullous form. Bullous impetigo is mediated by local production of exfoliative toxin A (ETA) or B (ETB); these toxins cleave the desmosomal protein desmoglein 1 in the superficial layers of the epidermis. This loss of adhesion between keratinocytes results in characteristic flaccid blisters.

Diagnosis

Diagnosis is supported by the presence of gram-positive cocci in clusters on Gram stain of a swab from a pustule, vesicle, or crusted plaque of impetigo. Confirmation is made by bacterial culture taken from blood, skin, and soft tissues.

Clinical Findings

SSSS is most common in full-term infants and young children, although cases of affected premature infants have also been reported. Affected infants demonstrate abrupt onset of temperature instability, lethargy, and irritability, with subsequent generalized skin tenderness and erythema. Initial erythema tends to occur on the face but subsequently becomes more marked in intertriginous areas ( Fig. 93.2 ). Facial swelling, conjunctivitis, and significant periorificial crusting is common; crusting accompanied by radial fissuring about the mouth gives afflicted children a characteristic appearance. Notably, mucosal surfaces are spared in SSSS. Following these initial signs and symptoms, focal or widespread flaccid bullae may develop within hours to days with subsequent desquamation. This is easily elicited by light stroking of intact skin (Nikolsky sign). Following desquamation, affected areas appear as painful shiny denuded patches. At this stage, diffuse skin involvement may cause problems with thermoregulation, fluid and electrolyte balance, and superinfection.

SSSS must be distinguished from toxic epidermal necrolysis (TEN), a life-threatening condition involving full-thickness epidermal necrosis, most commonly secondary to medication administration. A distinguishing feature of these two conditions is the presence of mucosal blistering and hemorrhagic crusting in TEN.

Etiology

The signs and symptoms of SSSS are the result of circulating exfoliative toxins produced from an often subclinical focus of S. aureus infection. Infants are thought to be more at risk of developing SSSS because of immunologic and renal immaturity, which allows excess accumulation of exfoliative toxin within the circulation. Specifically, significantly lower anti-exfoliative toxin antibodies have been noted in patients with SSSS compared with healthy controls. In contrast to bullous impetigo, which is more commonly associated with ETA, SSSS is more frequently caused by ETB. Additionally, while S. aureus is identifiable in the blisters of bullous impetigo, in SSSS, S. aureus is present at a primary distant site such as the nose, mouth, conjunctiva, umbilicus, or circumcision site. Fresh skin lesions are therefore sterile and blister fluid is culture negative.

Diagnosis

If the diagnosis is in question, a skin biopsy sample prepared for frozen section can be examined emergently. The presence of an intraepidermal rather than a full-thickness blister with separation at the dermal-epidermal junction distinguishes SSSS from TEN, allowing rapid initiation of appropriate therapy. If the clinical impression is strong, swabs from potential niduses of infection (nasopharynx, conjunctiva, umbilicus, etc.) may identify the primary focus. Gram staining may be performed emergently, while bacterial culture will confirm the diagnosis. Bullous lesions do not contain organisms. Blood culture specimens should be obtained because sepsis, although uncommon, may occur.

Treatment

Empiric therapy with a cephalosporin- or penicillinase-resistant penicillin, such as oxacillin, is the treatment of choice for SSSS; additional coverage to include methicillin-resistant S. aureus (MRSA) should be considered in areas with higher prevalence of MRSA and patients with severe systemic disease. Clindamycin may also be considered as a first-line agent for treatment of SSSS because of its superior cutaneous penetration, as well as its ability to inhibit bacterial toxin production. However, reports assessing antibiotic resistance in SSSS have shown that there are certain geographic areas in which clindamycin-resistant strains predominate. As such, empiric treatment with both oxacillin and clindamycin may be useful until antibiotic sensitivities return. In cases of widespread disease, fluid and nutritional support and maintenance of normal body temperature may be required. Close monitoring for secondary superinfection (particularly with gram-negative organisms) is also warranted. Approximately 2 to 3 days after initiation of therapy, denuded areas become dry and desquamation ensues. Crusted, flaky areas may be treated with normal saline compresses. Application of a bland ointment emollient may promote skin healing and resolution. Additional treatment of family members may be considered in instances of recurrent staphylococcal skin infections. As in bullous impetigo, the intraepidermal cleavage plane is superficial and therefore does not result in scarring in the absence of secondary infection or other complications.