Pathogenesis

An abscess starts around a bacterial focus. The origin of the infective agent is extremely varied e.g. puncture wounds of the skin, haematogenous spread from a primary infection, perforation of the gastrointestinal tract.

The inflammatory response is initiated. Neutrophils are attracted to the area by chemotactic products. They are overwhelmed by infection, die, and release proteolytic enzyme products. Platelets are activated and these in turn stimulate fibroblasts and blood vessels. Fibrin and collagen are laid down at the periphery and angiogensis occurs; this vascular fibrous layer, rich in cells like polymorphs and monocytes, is termed the pyogenic membrane. The pyogenic membrane physically inhibits bacterial advancement but also hinders the penetration of antibiotics.

Within the abscess cavity, destruction of cells and proteolysis of the products leads to the production of more chemotactic factors. Consequently, more neutrophils and macrophages ingress into the centre of the abscess where liquefactive necrosis is occurring. Once the bacteria have reached a maximal concentration within the pus - dependent on the individual bacterium - they no longer proliferate. This makes them even more insensitive to antibiotics.

If the abscess does not drain by surgical intervention or tracking along tissue planes, macrophages begin to replace neutrophils as the dominant population of cells within the pyogenic membrane. The membrane eventually becomes less vascular and contracts to leave a scarred fibrous sheet that may become calcified. The contents are resorbed by liquefaction and reabsorption of water.

An increasingly large abscess can press on external blood vessels causing thrombosis and necrosis in its path. This process accounts for its ability to track through tissue.