The Pathogenesis of Bacterial Infections
Published on 1. May 1985
Book
Hardback
XVI, 432 pages
978-3-540-15304-7 (ISBN)
Description
G. G. Jackson The pathogenesis of bacterial infection defines the dynamics at an interface of ecologic association of bacteria and host. First, it occurs at the portal of initial contact with a per missive target cell. The infected cell provides either a passive or a specific receptor for the bacterium or its products, to gether with ligands and an environment of helper and inhibiting factors. The result is bacterial replication to produce an im balance of a potentially commensal relation which, under other defined conditions, would be optimal for the survival of both the host and bacterial cells. Virulence and pathogenesis are both absolute and relative terms. They must be interpreted strictly according to the circumstances of site-specific inter actions of bacterial and host cells, membrane composition, structure, characteristics, and environmental substances. The bacteria themselves may have, acquire, or switch on or off under certain conditions, the products or properties that produce cellular damage that we recognize as virulence. Another result of bacterial infection may be to stimulate a normal host cell function to perform at a pathophysiologic level, causing illness that we recognize as virulence. A third marker of virulence may be the ability to invade a cell or tissue barrier and produce a pathologic effect at a site that is remote from the portal of commensal association or pathologic entry.
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George G. Jackson | Herbert Thomas
The Pathogenesis of Bacterial Infections
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03/2013
Springer
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George G. Jackson | Herbert Thomas
The Pathogenesis of Bacterial Infections
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Content
Welcome.- Session 1: Infection of Mucosal Surfaces.- Molecular Mechanisms by Which Pathogenic Bacteria Interact with Host Mucosal Cells.- Antigen Expression Influencing Tissue Invasion of Hemophilus influenzae Type B.- Surface Factors and Nasopharyngeal Colonization by Hemophilus influenzae B.- Discussion (pp. 8-38).- The Molecular Organization of Gonococcal Pili.- Functions of the Outer Membrane Proteins of Neisseria gonorrhoeae.- Discussion (pp. 41-66).- Regulation of Lipopolysaccharide Biologic Activity by Polysaccharide.- Mucosal Immunoregulation: IgA Inductive Sites, Isotype-Specific Helper T Cells, Gut LPS Influence, and Subclass Distribution of IgA Antibodies.- Discussion (pp. 68-98).- Session 2: Extension of Infection Beyond the Surface Cells - Circumvention of the Host Defense System.- Molecular Interactions Between the Third Complement Protein and Bacterial Cell-Surface Macromolecules.- Discussion (pp. 102-120).- Mechanisms of Bacterial Resistance to Complement-Mediated Killing.- Discussion (pp. 122-136).- Gram-Negative Septicemia: Antibody Deficiency and Specific Protection.- Discussion (pp. 138-145).- Mechanisms for Evasion and Survival of Bacteria by Perturbation of Phagocytes.- Discussion (pp. 147-156).- Interacting T Cell Functions Elicited by Facultative Intracellular Bacteria.- Discussion (pp. 158-165).- Session 3: Features of Bacterial Virulence.- Iron Supply as a Virulence Factor.- The Relationship Between Iron Utilization and Virulence of the Pathogenic Neisseria.- Discussion (pp. 168-191).- Binding of Microbial Pathogens to Connective Tissue Fibronectin: An Early Step in Localized and Invasive Infections.- Protective Immunogenicity of Chemically Synthesized Peptide Fragments of Group A Streptococcal M Proteins.- Discussion (pp. 193-218).- Molecular Analysis of Virulence Determinants of Neisseria gonorrhoeae.- Clonal Polymorphism of Surface Antigens in a Relapsing Fever of Borrelia Species.- Discussion (pp. 221-245).- The Role of the Cell Surface Components of Pseudomonas aeruginosa in Virulence.- Extracellular Factors in the Virulence of Pseudomonas aeruginosa.- Discussion (pp. 247-266).- Damage to the Host by Channel-Forming Bacterial Toxins.- Discussion (pp. 268-279).- Virulence Promotion by Mixed Bacterial Infections.- Discussion (pp. 281-291).- Session 4: Tissue Invasion, Inflammation, and Immunopathologic Disease.- Vascular Endothelium: The Interface Between the Site of of Antigen and Cellular Immunity.- Augmenting Interactions of the Clotting System and Immune Responses in Inflammatory Tissue Injury.- Discussion (pp. 294-319).- Fever, Interleukin-1, and the Defense Against Bacterial Pathogens.- Discussion (pp. 322-333).- The Immunological Significance of Antibody Affinity.- Discussion (pp. 336-348).- Trigger Mechanisms for the Release of Tissue Active Products of Phagocytic Cells.- Discussion (pp. 351-363).- Concluding Remarks to Sessions.- Session 1: Closing Remarks of the Schloss Gracht Conference.- Session 2: Statement.- Session 3: Perspectives.- Session 4: Symposium Summary. Current Status, Forefront, and Future: Immunologic Determinants.- Session 5: Research Perspectives.- Methods for Research on Bacterial Pathogenesis.- New Approaches to Evaluate Microbial Macromolecules as Potential Vaccines: Studies of the Surface of Neisseria gonorrhoeae Using Antibody-Gold Sphere Immunological Probes.- Activity of Macrophage Processed Endotoxin.- Laboratory Characterization of Lipopolysaccharides (LPS).- Bacterial Growth on Biomaterials.- Specific Microbial Adaptation in Pathogenesis.- Iron Utilization and Invasiveness of Hemophilus influenzae.- Complement Resistance and the tra-T Gene.- Antibiotic Alteration of Bacterial Membranes.- Host Tissue and Parasite Interactions in Bacterial Pathogenesis.- Persistent Bacterial Meningitis: Lyme Disease.- Antiadhesive Properties of Monoclonal Antibody Against Type 1 Fimbriae of E. coli.- Molecular Basis of Host-Tissue-Specific Pathogenesis of Enterobacteriaceae.- Immunologic Protection Against Host Disease.- Enhanced Antibody Responses to the Capsular Antigen of Hemophilus influenzae Type B in Infants Vaccinated with Oligosaccharides Coupled to a Protein Carrier.- Monoclonal Antibody Protection Against Pseudomonas aeruginosa.- Antibody Responses in Patients with Cystic Fibrosis.- Cell Mediated Immunity Against Bacterial Abscess Formation.- Induction of the Common Mucosal Immune System.