The predominant mechanism through which bacterial infections develop in flexural dermatitis involves the disruption of the skin barrier. Factors such as moisture, heat, and friction compromise the integrity of the epidermis, facilitating the entry of pathogenic bacteria.
Once introduced to the intertriginous environment, these organisms proliferate, producing virulence factors such as enzymes that degrade host tissues and toxins that promote inflammation. The resulting inflammatory response can cause erythema, edema, and pus formation, leading to considerable discomfort and distress for patients.
In cases where bacterial superinfection occurs in existing dermatitis (including psoriasis), the exacerbated inflammatory response can further obscure the clinical picture, complicating the differential diagnosis.