{'fraction_non_alphanumeric': 0.02266172229089411, 'fraction_numerical': 0.0, 'mean_word_length': 5.763231197771588, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Pathogenic mechanisms in the development of surgical site infections].

INTRODUCTION
Surgical site infections represent a major problem in modern medicine. Bacterial survival and growth in surgical wounds depends on the effectiveness of the host defense mechanisms and on the ability of bacteria to resist these defensive mechanisms. Surgical site contamination causes cellular injury and triggers the inflammatory response.


HOST RESPONSE TO INFECTION
An acute inflammatory response occurs within seconds to minutes of injury or invasion; it is non-specific and self-limiting. Mast cell degranulation, activation of three plasma systems and release of subcellular components from damaged cells occur as a consequence of cellular injury. Inflammation is mediated by a variety of soluble factors, including the complement system, the clotting system and the kinin system. The cell-derived mediators include histamine and serotonin, platelet activating factor, arachidonic acid metabolites (prostaglandins, leukotrienes, lipoxins), nitric oxide, and cytokines (regulators of host responses to infection, inflammation and immune responses). The main role of an inflammatory reaction is to recruit various cells and plasma components to the surgical site. Neutrophils are the first immune cells recruited at the site infection. Intracelhular killing of microbes by neutrophils is accomplished through several mechanisms, including lysosomal enzymes and oxygen-dependent mechanisms. Later, local and blood-borne macrophages also migrate to the surgical site, initiate phagocytosis, and present antigens to T-lymphocytes in a recognizable form. Sepsis is a common systemic complication of infection. Septic shock is associated with severe infection and release of inflammatory mediators into the systemic circulation. The lipopolysaccharide from gram-negative bacteria contributes significantly to the pathogenesis of septic shock. The most common clinical manifestations of sepsis include fever or hypothermia, tachycardia, tachypnea, altered blood pressure, either leukocytosis or leukopenia, and change in mental status.


CONCLUSION
The host response to microbial infection, also known as acute phase response, includes changes of local and systemic functions. ss of local control or an overly activated response results in a systemic response which is clinically identified as a systemic inflammatory response syndrome (SIRS).