Abstract

There are several resistance mechanisms found in Staphylococcus, the most common being resistance to macrolides, aminoglycosides, beta-lactams and glycopeptides. Directly linked to the hemostasis phase is the inflammation phase, which is characterized by the presence of inflammatory cells in the scar tissue. The localized release of histamine, serotonin and bradykinin causes vasodilation with a consequent increase in blood volume resulting in the clinical manifestations of heat and flushing. The important presence of prostaglandins in the region increases vascular permeability, in addition to favoring plasma exudation. They are responsible for promoting chemotaxis of leukocytes to the wound. Polymorphonuclear leukocytes together with neutrophils that are later replaced by macrophages are responsible for the phagocytic action of this process, helping to destroy bacteria, remove devitalized collagen and fibrin clots. Macrophages also activate fibroblasts and endothelial cells that will be needed in subsequent healing phases. Inflammatory cells undergo apoptosis as the process develops.

Description