Primary Causes & Pathophysiology
Bacteria enter through a break in the epidermis (outer skin barrier). Triggers include cuts, ulcers (open sores), cracks and tinea pedis (athlete foot fungal infection). They spread in dermis (deep skin) and subcutis (under-skin fat). Toxins activate innate immunity (early infection defence). Vessel widening with neutrophil influx (infection-fighting white cells) causes redness, warmth and swelling. Lymph spread causes red streaks and can progress to pus or blood infection.
Adhere to damaged skin then spread through lymph channels and trigger diffuse redness with fever
Colonise skin and wounds then release toxins and enzymes that cause pus-forming inflammation with abscess tendency
Provides an entry point for bacteria into deep skin and under-skin fat
Impairs local defence and lymph drainage (fluid clearing) allowing bacterial growth and recurrence
Reduce white-cell function and wound healing (repair) raising susceptibility and severity
Introduce aggressive organisms directly into tissue causing rapid infection after specific exposures