IV. Pathogenesis of Staphylococcus aureus
A. Mode of Pathogenicity
Staphylococcus aureus is both a commensal bacterium and a versatile pathogen. It is commensal because it can harmlessly colonize in the nares, axillae, vagina, pharynx, or damaged skin surfaces (Jenkins et al. 2015). Commensal bacteria supports the superficial layer of our body from pathogenic bacteria. For instances, S. aureus produces bacteriocins (toxins created by bacteria) that impedes pathogenic staphylococcal organism from developing. Therefore, it is important to preserve commensal bacteria to continue protect us, directly or indirectly from several other microorganisms (Chiller et al. 2001).
A versatile pathogenic bacteria is formed when an organism successful …show more content…
aureus is found primarily in the nares, and nearly 20% of the population are considered to be carriers for this pathogen, which increases risk of contracting an infection (Naber 2009). Cells are capable of binding to host cells and to extracellular-matrix elements with the support of microbial-surface-components recognizing adhesive-matrix molecules, mostly known as MSCRAMM, which contain a collection of adhesive molecules (Clarke and Foster 2006). MSCRAMM adheres to fibrinogen (protein that assists with the formation of blood clots), via different binding sites (Cognasse et al. 2015). Consequently, MSCRAMM perform in initiation of systemic infections. Due to the broad range of MSCRAMM types, a variety of S. aureus strains may initiate an array of diseases (Bien et al. 2011). For instance, coagulase is a type of adhesive molecules in the MSCRAMM which links to prothrombin to produce staphylothrombin (Cognasse et al. 2015). The presence of staphylothrombin converts fibrinogen into fibrin, leading to the activation of platelet aggregation and consequently, allowing the combination of S. aureus and platelets to occur (Vanassche et al. 2012). Decreasing staphylothrombin will impact the Staphylococcus aureus, which ultimately, inhibits the amount of platelets being activated (Vanassche et al. 2012). Fibrin clots protect cells from phagocytosis, and as a result, they will persist and cause staph infections (Cheng et al. 2010). All clinical isolates of S. aureus are known to be …show more content…
2012). In humans, platelets, erythrocytes, and monocytes show sensitivity to alpha-toxin (Berube and Wardenburg 2013). It is considered to form necrosis in the skin and toxicity in the nervous system (Los et al. 2013). The toxin is secreted by S. aureus in a monomeric form that binds to the eukaryotic cell membranes. On target membranes, the subunits oligomerize to create heptameric rings with a central pore, leading to cell death (Berube and Wardenburg 2013). The central pore formed on the target membrane can now permit the exchange of simple ions, like Ca2+, that would result in apoptosis. (Berube and Wardenburg 2013). All of these factors can lead to bacterial spread and modification of the
A. Mode of Pathogenicity
Staphylococcus aureus is both a commensal bacterium and a versatile pathogen. It is commensal because it can harmlessly colonize in the nares, axillae, vagina, pharynx, or damaged skin surfaces (Jenkins et al. 2015). Commensal bacteria supports the superficial layer of our body from pathogenic bacteria. For instances, S. aureus produces bacteriocins (toxins created by bacteria) that impedes pathogenic staphylococcal organism from developing. Therefore, it is important to preserve commensal bacteria to continue protect us, directly or indirectly from several other microorganisms (Chiller et al. 2001).
A versatile pathogenic bacteria is formed when an organism successful …show more content…
aureus is found primarily in the nares, and nearly 20% of the population are considered to be carriers for this pathogen, which increases risk of contracting an infection (Naber 2009). Cells are capable of binding to host cells and to extracellular-matrix elements with the support of microbial-surface-components recognizing adhesive-matrix molecules, mostly known as MSCRAMM, which contain a collection of adhesive molecules (Clarke and Foster 2006). MSCRAMM adheres to fibrinogen (protein that assists with the formation of blood clots), via different binding sites (Cognasse et al. 2015). Consequently, MSCRAMM perform in initiation of systemic infections. Due to the broad range of MSCRAMM types, a variety of S. aureus strains may initiate an array of diseases (Bien et al. 2011). For instance, coagulase is a type of adhesive molecules in the MSCRAMM which links to prothrombin to produce staphylothrombin (Cognasse et al. 2015). The presence of staphylothrombin converts fibrinogen into fibrin, leading to the activation of platelet aggregation and consequently, allowing the combination of S. aureus and platelets to occur (Vanassche et al. 2012). Decreasing staphylothrombin will impact the Staphylococcus aureus, which ultimately, inhibits the amount of platelets being activated (Vanassche et al. 2012). Fibrin clots protect cells from phagocytosis, and as a result, they will persist and cause staph infections (Cheng et al. 2010). All clinical isolates of S. aureus are known to be …show more content…
2012). In humans, platelets, erythrocytes, and monocytes show sensitivity to alpha-toxin (Berube and Wardenburg 2013). It is considered to form necrosis in the skin and toxicity in the nervous system (Los et al. 2013). The toxin is secreted by S. aureus in a monomeric form that binds to the eukaryotic cell membranes. On target membranes, the subunits oligomerize to create heptameric rings with a central pore, leading to cell death (Berube and Wardenburg 2013). The central pore formed on the target membrane can now permit the exchange of simple ions, like Ca2+, that would result in apoptosis. (Berube and Wardenburg 2013). All of these factors can lead to bacterial spread and modification of the