Aetiology
Impetigo is caused by Staphylococcus aureus (usual causative agent of the bullous type), Group A beta-haemolytic Streptococcus pyogenes (usual causative agent of the non-bullous 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 colonise and then infiltrate the superficial layers of the skin, initially creating a small erythematous macule (a flat, discoloured area of skin), which soon becomes vesicular.[1] MRSA can be a causative organism and is seen more often in cases of non-bullous 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 Staphylococcus 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 non-bullous impetigo, Streptococcus typically produces a thick-walled pustule with an erythematous base. Histology of non-bullous 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.
Non-bullous impetigo: impetigo without bullae.
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