Etiology
Impetigo is caused by Staphylococcus aureus (usual causative agent of the bullous type), Group A beta-hemolytic Streptococcus pyogenes (usual causative agent of the nonbullous type), or both.[1] Minor abrasions and skin lesions, associated with a wide variety of skin diseases, allow bacterial introduction into the skin. These bacteria colonize and then infiltrate the superficial layers of the skin, initially creating a small erythematous macule (a flat, discolored area of skin), which soon becomes vesicular.[1] MRSA can be a causative organism and is seen more often in cases of nonbullous impetigo.[15]
Pathophysiology
Bullous impetigo is caused by staphylococci producing exfoliative toxin that contains serine proteases acting on desmoglein 1, a structurally critical peptide bond in a molecule that holds epidermal cells together.[16] This process allows S aureus to spread under the stratum corneum in the space formed by the toxin, causing the epidermis to split just below the stratum granulosum.[17] Large blisters then form in the epidermis with neutrophil and, often, bacterial migration into the bullous cavity. This mechanism of lesion progression may explain how the body is usually able to resist entry beyond the superficial epidermis. In bullous impetigo, the bullae rupture quickly, causing superficial erosion and a yellow crust, while in nonbullous impetigo, Streptococcus typically produces a thick-walled pustule with an erythematous base. Histology of nonbullous established lesions shows a thick surface crust composed of serum and neutrophils in various stages of breakdown with parakeratotic material.[18]
Classification
Clinical classification
Bullous impetigo: bullae are fluid-filled lesions >0.5 cm in diameter.
Nonbullous impetigo: impetigo without bullae.
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