Summary Reader Microbial Disease Mechanisms

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Summary - Reader Microbial Disease Mechanisms

  • 1.1 Types of symbiotic associations

  • Mutualism
    Both benefit
  • Commensalism
    No appparent benefit or harm to both, but usually one side is helped
  • Parasitism
    One side benefits
  • 1.2 Bacterial Pathogenesis

  • Pathogenicity
    The ability to cause disease in another organism
  • Opportunistic pathogen
    Usually commensal, but may cause disease in case of decreased immune system
  • Obligate pathogen
    Only association with host in case of disease
  • Infection
    When a mo reaches sterile surfaces such as blood and internal tissues
  • Virulence
    The degree of pathogenicity
  • Virulence determinants
    Sum of characteristics that make a bacterium disease-causing
  • Toxigenesis
    Ability to produce toxins
  • Invasiveness
    Ability to invade tissues
  • What 3 factors encompass invasiveness?
    1. Colonization mechanisms
    2. Invasin production that promote tissue invasion
    3. Ability to bypass or overcome host defence mechanisms
  • 2.1 Introduction

  • Five essential structural compounds of prokaryotes
    1. Nucleoid
    2. Ribosomes
    3. Cell wall
    4. Cell membrane
    5. Surface layer
  • 3 architectural regions
    1. Appendages
    2. Envelope
    3. Cytoplasmic region
  • 2.2 Appendages: flagella, fimbriae and pili

  • Flagella
    Filamentous protein structures attached to the cell surface for swimming
  • Polar flagella
    Only at one or both poles
  • Peritrichous
    Flagella that are spread over the whole bacterium
  • 3 ways to spot bacterial movement
    1. Staining technique
    2. Swim medium
    3. Direct observation in wet mount
  • Fimbriae/pilli
    Hairlike structures for adherence to surfaces
    - Gram-negative vooral
  • F pillus / Sex pilus
    Stabilize mating during conjugation
  • Pili are major determinants in virulence because:
    - allow attachment
    - prevent phagocytic attacks
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7 stages of endospore formation
1. Axial filament of nuclear material
2. Inward fold of cell membrande to enclose DNA
3. Membrane engulfs immature endospore in second membrane
4. Cortex laid down between the 2 membranes
5. Protein coats formed around cortex
6. Maturation of endospore
7. Sporangium destroyed by lytic enzymes --> spore released.
Periplasm gramnegatives
Space between the plasma membrane and the outer membrane of G- bacteria. Here, the peptidoglycan sheet is located.
Gramnegative Cell wall
- Turns pink by staining
- Single peptidoglycan  layer with outer membrane
- LPS as unique component
G+ Cellwall
- retain purple after staining
- Several layers of peptidoglycan + perpendicular teichoic acids
B-cell mitogen
Another characteristic of LPS: inducing the polyclonal differentiation and multiplication of B-cells and the secretion of immunoglobulins, espially IgG and IgM
3. Activation of the coagulation cascade composes (4)
A. Coagulation
B. Alterative complement activation
C. Plasmin actication 
D. Kinin activation
2. Activation of the complement cascade
C3a and C5a cause histamine release and affect neutrophil chemotaxis and accumulation --> results in inflammation
1. Production of cytokines
- IL1, 6, 8 and TNF-alpha, stimulating the production of mediators of inflammation and septic shock.
- LPS activates macrophages to enhanced phagocytosis and cytotoxicity.
What 3 events are triggered in monocytes and macrophages when interact with LPS?
1. Cytokine production
2. Complement cascade activation
3. Coagulation cascade activation
Endotoxic shock
A compex process. 
- LPS binds to a lipid binding protein (LBP) in the serum which transfers it to CD14 on the cell membrane.
- This associates with MD2 and this associates with TLR4
- THis triggers the signalling cascade for the release of cytokine by macrophage/endothelial cells ----> endotoxic shock