Sources of infection

Sources of infection

• The infection of a wound can be defined as the invasion of - organisms into tissues following a breakdown of local and systemic host defences, leading to cellulitis, lymphangitis, abscess formation or bacteraemia. The infection of most surgi - cal wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such abscess after a perforated appendicitis). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens , which is responsible for gas gangrene, releases proteases such as hyalu ronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. 14 The human body harbours approximately 10 organisms. They can be released into tissues before, during or after sur gery , contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular per foration). Any infection that follows surgery may be termed endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of surger y , whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of infection ( Summary box 5.3 Summary box 5.3 Classification of sources of infection /uni25CF /uni25CF Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery . In addition to these mechanical barriers, there are other pro tective mechanisms, which can be divided into: /uni25CF chemical : low gastric pH; /uni25CF humoral : antibodies, complement and opsonins; /uni25CF cellular : phagocytic cells, macrophages, polymorphonu clear cells and killer lymphocytes. All of these natural mechanisms may be compromised by surgical intervention and treatment. The chance of developing an SSI after surgery is also determined by the pathogenicity of the organisms pr esent and by the size of the bacterial inoculum. The more virulent the organism or the larger the extent of bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired ( Summary box 5.4 ). Devital ised tissue, excessive dead space or haematoma, which are all the results of poor surgical technique, increase the chances of infection. The same applies to foreign materials of any kind, including sutures and drains . These principles are important to an understanding of how best to prevent infection in surgical practice ( Summary box 5.5 ). Factors that determine whether a wound will become infected /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - - Summary box 5.5 Risk factors for increased risk of wound infection /uni25CF /uni25CF /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF

Endogenous : present in or on the host, e.g. SSSI following contamination of the wound from a perforated appendix Exogenous : acquired from a source outside the body, such as the operating theatre (inadequate air /f_i ltration, poor antisepsis) or the ward (e.g. poor handwashing compliance). The cause of hospital-acquired infection (HAI) Host response Virulence and inoculum of infective agent Vascularity and health of tissue being invaded (including local ischaemia as well as systemic shock) Presence of dead or foreign tissue Presence of antibiotics during the ‘decisive period’ Malnutrition (obesity, weight loss) Metabolic disease (diabetes, uraemia, jaundice) Immunosuppression (cancer, acquired immunode /f_i ciency syndrome [AIDS], steroids, chemotherapy and radiotherapy) Colonisation and translocation in the gastrointestinal tract Poor perfusion (systemic shock or local ischaemia) Foreign body material Poor surgical technique (devitalised tissue, dead space, haematoma)

Sources of infection

• The infection of a wound can be defined as the invasion of - organisms into tissues following a breakdown of local and systemic host defences, leading to cellulitis, lymphangitis, abscess formation or bacteraemia. The infection of most surgi - cal wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such abscess after a perforated appendicitis). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens , which is responsible for gas gangrene, releases proteases such as hyalu ronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. 14 The human body harbours approximately 10 organisms. They can be released into tissues before, during or after sur gery , contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular per foration). Any infection that follows surgery may be termed endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of surger y , whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of infection ( Summary box 5.3 Summary box 5.3 Classification of sources of infection /uni25CF /uni25CF Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery . In addition to these mechanical barriers, there are other pro tective mechanisms, which can be divided into: /uni25CF chemical : low gastric pH; /uni25CF humoral : antibodies, complement and opsonins; /uni25CF cellular : phagocytic cells, macrophages, polymorphonu clear cells and killer lymphocytes. All of these natural mechanisms may be compromised by surgical intervention and treatment. The chance of developing an SSI after surgery is also determined by the pathogenicity of the organisms pr esent and by the size of the bacterial inoculum. The more virulent the organism or the larger the extent of bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired ( Summary box 5.4 ). Devital ised tissue, excessive dead space or haematoma, which are all the results of poor surgical technique, increase the chances of infection. The same applies to foreign materials of any kind, including sutures and drains . These principles are important to an understanding of how best to prevent infection in surgical practice ( Summary box 5.5 ). Factors that determine whether a wound will become infected /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - - Summary box 5.5 Risk factors for increased risk of wound infection /uni25CF /uni25CF /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF

Endogenous : present in or on the host, e.g. SSSI following contamination of the wound from a perforated appendix Exogenous : acquired from a source outside the body, such as the operating theatre (inadequate air /f_i ltration, poor antisepsis) or the ward (e.g. poor handwashing compliance). The cause of hospital-acquired infection (HAI) Host response Virulence and inoculum of infective agent Vascularity and health of tissue being invaded (including local ischaemia as well as systemic shock) Presence of dead or foreign tissue Presence of antibiotics during the ‘decisive period’ Malnutrition (obesity, weight loss) Metabolic disease (diabetes, uraemia, jaundice) Immunosuppression (cancer, acquired immunode /f_i ciency syndrome [AIDS], steroids, chemotherapy and radiotherapy) Colonisation and translocation in the gastrointestinal tract Poor perfusion (systemic shock or local ischaemia) Foreign body material Poor surgical technique (devitalised tissue, dead space, haematoma)

Sources of infection

• The infection of a wound can be defined as the invasion of - organisms into tissues following a breakdown of local and systemic host defences, leading to cellulitis, lymphangitis, abscess formation or bacteraemia. The infection of most surgi - cal wounds is referred to as superficial surgical site infection (SSSI). The other categories include deep SSI (infection in the deeper musculofascial layers) and organ space infection (such abscess after a perforated appendicitis). Pathogens resist host defences by releasing toxins, which favour their spread, and this is enhanced in anaerobic or frankly necrotic wound tissue. Clostridium perfringens , which is responsible for gas gangrene, releases proteases such as hyalu ronidase, lecithinase and haemolysin, which allow it to spread through the tissues. Resistance to antibiotics can be acquired by previously sensitive bacteria by transfer through plasmids. 14 The human body harbours approximately 10 organisms. They can be released into tissues before, during or after sur gery , contamination being most severe when a hollow viscus perforates (e.g. faecal peritonitis following a diverticular per foration). Any infection that follows surgery may be termed endogenous or exogenous, depending on the source of the bacterial contamination. Endogenous organisms are present on or in the patient at the time of surger y , whereas exogenous organisms come from outside the patient. In modern hospital practice, endogenous organisms colonising the patient are by far the most common source of infection ( Summary box 5.3 Summary box 5.3 Classification of sources of infection /uni25CF /uni25CF Microorganisms are normally prevented from causing infection in tissues by intact epithelial surfaces, most notably the skin. These surfaces are broken down by trauma or surgery . In addition to these mechanical barriers, there are other pro tective mechanisms, which can be divided into: /uni25CF chemical : low gastric pH; /uni25CF humoral : antibodies, complement and opsonins; /uni25CF cellular : phagocytic cells, macrophages, polymorphonu clear cells and killer lymphocytes. All of these natural mechanisms may be compromised by surgical intervention and treatment. The chance of developing an SSI after surgery is also determined by the pathogenicity of the organisms pr esent and by the size of the bacterial inoculum. The more virulent the organism or the larger the extent of bacterial contamination, the more likely is wound infection to occur. Host factors are also important, so a less virulent organism or a lower level of wound contamination may still result in a wound infection if the host response is impaired ( Summary box 5.4 ). Devital ised tissue, excessive dead space or haematoma, which are all the results of poor surgical technique, increase the chances of infection. The same applies to foreign materials of any kind, including sutures and drains . These principles are important to an understanding of how best to prevent infection in surgical practice ( Summary box 5.5 ). Factors that determine whether a wound will become infected /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - - Summary box 5.5 Risk factors for increased risk of wound infection /uni25CF /uni25CF /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF

Endogenous : present in or on the host, e.g. SSSI following contamination of the wound from a perforated appendix Exogenous : acquired from a source outside the body, such as the operating theatre (inadequate air /f_i ltration, poor antisepsis) or the ward (e.g. poor handwashing compliance). The cause of hospital-acquired infection (HAI) Host response Virulence and inoculum of infective agent Vascularity and health of tissue being invaded (including local ischaemia as well as systemic shock) Presence of dead or foreign tissue Presence of antibiotics during the ‘decisive period’ Malnutrition (obesity, weight loss) Metabolic disease (diabetes, uraemia, jaundice) Immunosuppression (cancer, acquired immunode /f_i ciency syndrome [AIDS], steroids, chemotherapy and radiotherapy) Colonisation and translocation in the gastrointestinal tract Poor perfusion (systemic shock or local ischaemia) Foreign body material Poor surgical technique (devitalised tissue, dead space, haematoma)