Pathophysiology
Clinical meaning
Lactational mastitis pathogenesis involves S. aureus biofilm formation within the ductal system. Bacteria adhere to milk fat globule membranes via fibronectin-binding proteins and produce exotoxins including alpha-hemolysin and Panton-Valentine leukocidin (PVL - associated with MRSA strains), which lyse neutrophils and macrophages, enabling tissue invasion. The innate immune response involves toll-like receptor 2 (TLR2) recognition of bacterial lipoteichoic acid, triggering NF-kB-mediated cytokine release (IL-1beta, IL-6, IL-8, TNF-alpha). Complement activation via the alternative pathway enhances opsonization. Milk stasis provides lactose and casein substrates for bacterial metabolism while reducing protective lactoferrin, lysozyme, and secretory IgA concentrations within stagnant ducts. Periductal inflammation causes edema that further obstructs adjacent ducts, creating a positive feedback loop. Abscess formation involves liquefactive necrosis walled off by fibrinous granulation tissue. Non-lactational forms include periductal mastitis (subareolar abscess - associated with smoking, which causes squamous metaplasia of duct epithelium), idiopathic granulomatous mastitis (T-cell mediated granulomatous inflammation of uncertain etiology - associated with Corynebacterium kroppenstedtii), and inflammatory breast cancer (which must be excluded in any non-lactating patient with breast erythema).