An 88-year-old male with flaccid bullae and pustules in the upper arm and axilla, which developed 2 months prior to the consultation and gradually spread over time, was referred to our hospital. Histopathological examination of the bullae showed the formation of fissures in the stratum granulosum. Although pemphigus foliaceus was suspected, direct immunofluorescence was negative. Staphylococcus aureus producing exfoliative toxin A (ETA) was isolated via bacterial culture, and the diagnosis of bullous impetigo was reached. The presence of epidermal intercellular adhesion molecules in the lesion was assessed using immunostaining. The extracellular and intracellular domains of desmoglein (Dsg)1 were undetectable in the stratum granulosum and at the edges of the bullae. Although the expression level of Dsg3 was low, it was detected in the intercellular spaces on the edges of the bullae and directly beneath them. Extracellular domain (EC)1, EC2, and EC3 were undetectable in the intercellular spaces in all epidermal layers at the edges of the bullae. However, a low and punctate expression of the intracellular domain of EC4 was observed in the intercellular space of the stratum spinosum. Moreover, its intracellular domain was almost exclusively localized in the cells, indicating that Dsg1 rapidly disappeared from the intercellular space around the lesion due to shedding caused by ETA. Intercellular dissociation occurred in the stratum granulosum, where low levels of Dsg3 expression presumably contributed to the formation of bullae. By contrast, normal levels of Dsg1 expression were observed in the intercellular space of the non-bullous areas. These findings strongly support the notion that the shedding of the extracellular domain of Dsg1 provoked by ETA contributes to the formation of bullae in bullous impetigo.
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