tailieunhanh - Chapter 129. Staphylococcal Infections (Part 4)

Evasion of Host Defense Mechanisms Evasion of host defense mechanisms is critical to invasion. Staphylococci possess an antiphagocytic polysaccharide microcapsule. Most human S. aureus infections are due to capsular types 5 and 8. The S. aureus capsule also plays a role in the induction of abscess formation. The capsular polysaccharides are characterized by a zwitterionic charge pattern (the presence of both negatively and positively charged molecules) that is critical to abscess formation. Protein A, an MSCRAMM unique to S. aureus, acts as an Fc receptor. It binds the Fc portion of IgG subclasses 1, 2, and 4, preventing opsonophagocytosis by. | Chapter 129. Staphylococcal Infections Part 4 Evasion of Host Defense Mechanisms Evasion of host defense mechanisms is critical to invasion. Staphylococci possess an antiphagocytic polysaccharide microcapsule. Most human S. aureus infections are due to capsular types 5 and 8. The S. aureus capsule also plays a role in the induction of abscess formation. The capsular polysaccharides are characterized by a zwitterionic charge pattern the presence of both negatively and positively charged molecules that is critical to abscess formation. Protein A an MSCRAMM unique to S. aureus acts as an Fc receptor. It binds the Fc portion of IgG subclasses 1 2 and 4 preventing opsonophagocytosis by PMNs. Both chemotaxis inhibitory protein of staphylococci CHIPS a secreted protein and extracellular adherence protein EAP a surface protein interfere with PMN migration to infection sites. The arginine catabolic mobile element ACME a cluster of genes unique to the USA300 clone also may facilitate evasion. An additional mechanism of S. aureus evasion is its capacity for intracellular survival. Both professional and nonprofessional phagocytes internalize staphylococci. Internalization by endothelial cells may provide a sanctuary that protects bacteria against the host s defenses. It also results in cellular changes such as the expression of integrins and Fc receptors that may contribute to systemic manifestations of disease including sepsis and vasculitis. The intracellular environment favors the phenotypic expression of S. aureus small-colony variants. These menadione and hemin auxotrophic mutants are generally deficient in a toxin and can persist within endothelial cells. Smallcolony variants are often selected after aminoglycoside therapy and are more commonly found in sites of persistent infections . chronic bone infections and in respiratory secretions from patients with cystic fibrosis. These variants represent another mechanism for prolonged staphylococcal survival that may .