Staphylococcal and Streptococcal Pyodermas

History

The word “impetigo” is a Middle-English (fourteenth-century) derivation of the Latin word “impetere,” literally meaning “to attack.” It has come to mean a pustular skin condition, usually involving the face, characterized by the formation of scabs and crusts.

Epidemiology

Impetigo (non-bullous impetigo) occurs most frequently in children, with an equal distribution of males and females. It is common in hot, humid climates, which encourage the growth of staphylococci on the skin. Worldwide, the non-bullous form of the disease is now caused predominantly by S. aureus , with a minority of cases caused by S. pyogenes (group A β-hemolytic streptococci), or both.

Bullous impetigo, caused exclusively by strains of S. aureus that secrete a toxin (exfoliatin), occurs most often in children under the age of 2.

Clinical Findings

The early clinical presentation of impetigo is that of grouped, fragile, thin-roofed vesicles that rapidly become cloudy pustules and then rupture. The resulting secondary lesions consist of patches of honey-colored, erythematous and crusted erosions that are most often found on the face, neck, and extremities. In most cases, patients are otherwise well, but regional lymphadenopathy may be present.

In temperate climates bullous impetigo is more common in newborns, but in warm tropical environments it may present as an acute bullous eruption of the axillae, groin, and hands in adults. In the neonatal period, it develops within the first 2 weeks of life with lesions initially developing on the face and hands. Later, lesions may generalize to cover large parts of the body. Bullae are typically large, tense, and cloudy and rupture easily, leaving a shiny, varnish-like crust over the affected area.

Histopathology

A skin biopsy of an intact lesion shows an accumulation of neutrophils below the stratum corneum of the epidermis with a few rounded acantholytic cells. Numerous Gram-positive cocci are seen. In the bullous form, a thin layer of stratum corneum forms the roof of the blister, which is filled with inflammatory cells and bacteria.

Diagnosis and Differential Diagnosis

Primary non-bullous impetigo is generally diagnosed on clinical grounds, although laboratory support is occasionally nec­essary ( Fig. 21-1 ). It is important to remember that impetigo frequently complicates several underlying dermatoses such as scabies, insect bites, atopic dermatitis, or dermatophytosis ( Fig. 21-2 ). Therefore, it is important to accurately diagnose and treat any underlying disorder so as to reduce the risk of relapse ( Table 21-1 ).

In situations where laboratory confirmation is important (epidemics, failure to respond to previous therapy, concern over nephrogenic streptococci), a Gram stain from an intact pustule or the base of the erosion will show Gram-positive cocci in chains (streptococci) or clusters (staphylococci). Culture on selective media with antibiotic sensitivities is necessary when methicillin resistance is suspected or when there is a failure to respond to appropriate therapy.

Treatment

The decision to use topical or oral antibiotics must be made on the basis of extent of disease, age and health status of the patient, presence of constitutional symptoms, and response to previous therapy. Table 21-2 outlines therapeutic options for treating non-bullous impetigo. Limited disease can be treated with frequent washing with hot soapy water followed by twice- or three-times-daily application of a topical antibiotic for a week. For more extensive disease systemic antibiotics are recommended.