PATHOGENS

• Inflammatory disease around abnormal and dilated hair follicles with secondary involvement of apocrine glands and surrounding structures, often with superinfection.
• Genetic predisposition is possible; 40% have a family history of hidradenitis supperativa.
• Immune dysregulation in innate and adaptive immune pathways.
• Pathogenesis is believed to start with occlusion and dilation of the pilosebaceous unit → rupture → extrusion of follicular contents into dermis → chemotactic inflammatory response → influx of neutrophils, lymphocytes, histiocytes → abscess formation (thus, it is both an inflammatory disease related to immune dysregulation and infectious disease).
  • Infection appears to result from inflammatory occlusion of ducts rather than the underlying process for hidradenitis suppurativa.
• Microbiology: culture may yield mixed aerobic/anaerobic bacteria with S. epidermidis and S. aureus most commonly isolated.
  
  • Up to 50% of patients are culture-negative.