tailieunhanh - Chapter 114. Molecular Mechanisms of Microbial Pathogenesis (Part 10)

Invasion Many diseases are caused primarily by pathogens growing in tissue sites that are normally sterile. Pneumococcal pneumonia is mostly attributable to the growth of S. pneumoniae in the lung and the attendant host inflammatory response, although specific factors that enhance this process (., pneumolysin) may be responsible for some of the pathogenic potential of the pneumococcus. Disease that follows bacteremia and invasion of the meninges by meningitisproducing bacteria such as N. meningitidis, H. influenzae, E. coli K1, and group B streptococci appears to be due solely to the ability of these organisms to gain access to these tissues, multiply. | Chapter 114. Molecular Mechanisms of Microbial Pathogenesis Part 10 Invasion Many diseases are caused primarily by pathogens growing in tissue sites that are normally sterile. Pneumococcal pneumonia is mostly attributable to the growth of S. pneumoniae in the lung and the attendant host inflammatory response although specific factors that enhance this process . pneumolysin may be responsible for some of the pathogenic potential of the pneumococcus. Disease that follows bacteremia and invasion of the meninges by meningitisproducing bacteria such as N. meningitidis H. influenzae E. coli K1 and group B streptococci appears to be due solely to the ability of these organisms to gain access to these tissues multiply in them and provoke cytokine production leading to tissue-damaging host inflammation. Specific molecular mechanisms accounting for tissue invasion by fungal and protozoal pathogens are less well described. Except for studies pointing to factors like capsule and melanin production by C. neoformans and possibly levels of cell wall glucans in some pathogenic fungi the molecular basis for fungal invasiveness is not well defined. Melanism has been shown to protect the fungal cell against death caused by phagocyte factors such as nitric oxide superoxide and hypochlorite. Morphogenic variation and production of proteases . the Candida aspartyl proteinase have been implicated in fungal invasion of host tissues. If pathogens are effectively to invade host tissues particularly the blood they must avoid the major host defenses represented by complement and phagocytic cells. Bacteria most often avoid these defenses through their cell surface polysaccharides either capsular polysaccharides or long O-side-chain antigens characteristic of the smooth LPS of gram-negative bacteria. These molecules can prevent the activation and or deposition of complement opsonins or limit the access of phagocytic cells with receptors for complement opsonins to these molecules when they