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Bacteria & Host Interactions


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Persistence
of bacteria to colonize host depends upon tissue tropism, attachment/adherence (fimbriae, ahesins) and competition (with normal flora or pathogens)
Colonisation and adherence
may be either non-specific reversible attachment or "docking" (eg. capsule) or specific, permanent attachment or "anchoring" (eg. fimbriae, adhesins)
Motility and chemotaxis
permits movement towards mucosal membrane, through mucin layer and/or through cells along actin filaments
Tissue invasion
is mediated by specific enzymes (eg. collagenase, hemolysins) preventing host cell interactions or pathogen specific mechanisms (eg. strep/staphylokinase activating plasminogen)
Intracellular residence
of non-phagocytic cells as invasins induce cytoskeletal changes (eg. polymerising actin) or pseudopod formation (from cell membrane) to facilitate bacterial entry
Extracellular enzymes
are secreted to inhibit immune response (eg. sIgA) and digest host structures releasing nutrients (eg. proteases, lipases, nucleases)
Avoid contact with phagocytes
by inhibiting chemotaxis, inducing minimal/no inflam., tissue tropism (eg. skin), hiding antigen surface (eg. cell-bound coagulase clots fibrin on S. aureus), altering surface antigens
Inhibit phagocytic engulfment
by mimicking host proteins, using -vely charged capsules (eg. S. pneumoniae), surface slime (eg. P. aeruginosa), Protein A binds human Igs making them inactive (eg. S. aureus)
Survival inside phagocytes
by inhibition of lysosome fusion with phagosome (eg. M. tuberculosis), resisting lysosomal enzymes to survive inside phagolysosome (eg. B. anthracis), escape back to cytoplasm (eg. Rickettsias)
Kill phagocytes
before ingestion by hemolysins, leukocidins, streptolysins or exotoxin A or after ingestion by release of toxin from within
Exotoxins
are heat labile, soluble proteins that disrupt plasma membranes (=leakage) and synaptic transmission, inhibit protein synth. and enhance bacterial evasiveness
Endotoxins
are heat stable bacterial components released on lysis causing pyrexia (by acting on hypothalamus), inflam., thrombolysis and fluid leakage.
Superantigens
bind non-specifically on Tcell receptors thus activating up to 25% of Tcells and inducing a major, host damaging immune response