Wound Infection: Contributing Factors and Selected Techniques for Prevention

Wound infection is defined as the presence of replicating microorganisms within a wound with subsequent host injury. Infection must be distinguished from wound contamination (microorganisms are not replicating) and wound colonization (replicating microorganisms are present but do not cause host injury). Interestingly, some recent studies of dogs suggest that the organisms that infect a wound may be a subset of those organisms that colonize the wound site. Wound infection is considered a major factor in delayed wound healing, reduced tissue-tensile strength gain, and dehiscence after wound closure. Potential pathogenic bacteria adhere and/or bind to extracellular matrix proteins (e.g., fibronectin and laminin) of exposed tissue, which may have a direct effect on wound healing. By binding fibronectin, this protein is not available for promoting tissue adherence. Additionally, bacteria that produce cytotoxic exotoxins (e.g., Clostridium spp, Strep. pyogenes, and Staph. aureus) cause more tissue damage, creating a microenvironment conducive to their survival. Those with thick capsules (e.g., Strep. pyogenes, Staph. aureus, and Klebsiella pneumoniae) are more resistant to phagocytosis by leukocytes. During the process of bacterial degradation, liberated endotoxins can activate coagulation pathways; this may cause thrombosis of the microvasculature, systemic organ or immune dysfunction, and macrophage activation that releases more inflammatory mediators. Circulatory alterations decrease the efficiency of glucose and oxygen delivery; this creates an environment where the host’s main non-specific defense, the polymorphonuclear leukocyte, is deprived of the materials necessary for optimum bacterial killing. Whether infection develops depends on many factors: (1) The dose of microorganisms (we have the most influence over this); (2) Wound microenvironment/degree of contamination; (3) The virulence and pathogenicity of the microorganism; (4) Functional capacity of the host; and (5) Mechanism of injury. Generally, when bacterial numbers exceed 10 organisms per gram of tissue or per milliliter of exudate in an open wound, the wound becomes infected. A significant increase in failure of delayed wound closure because of infection is seen when the wound bed contains 10 organisms/g tissue. Contaminated wounds with lesser concen-