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    Host Defense & Pathogenicity of Microbes: Bacterial Structure

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    Luqman Al-Bashir Fauzi
    This document discusses host defense mechanisms against bacterial infection, including both innate and adaptive immunity. It outlines the structures of different bacterial cell walls and how they relate to susceptibility to immune mechanisms. The first line of defense includes barrier functions and chemicals, while the second line recognizes common bacterial components and activates the complement system. Adaptive immunity produces antibodies that can opsonize bacteria, block toxins and transport mechanisms, or prevent attachment. Certain bacteria can induce strong cytokine release through superantigens, potentially causing shock syndromes. Overall, most bacteria are ultimately killed by phagocytosis.

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    Host Defense & Pathogenicity of Microbes: Bacterial Structure

    Uploaded by

    Luqman Al-Bashir Fauzi
    54 views4 pages
    This document discusses host defense mechanisms against bacterial infection, including both innate and adaptive immunity. It outlines the structures of different bacterial cell walls and how they relate to susceptibility to immune mechanisms. The first line of defense includes barrier functions and chemicals, while the second line recognizes common bacterial components and activates the complement system. Adaptive immunity produces antibodies that can opsonize bacteria, block toxins and transport mechanisms, or prevent attachment. Certain bacteria can induce strong cytokine release through superantigens, potentially causing shock syndromes. Overall, most bacteria are ultimately killed by phagocytosis.

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    HD&PoM

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    This document discusses host defense mechanisms against bacterial infection, including both innate and adaptive immunity. It outlines the structures of different bacterial cell walls and how they relate to susceptibility to immune mechanisms. The first line of defense includes barrier functions and chemicals, while the second line recognizes common bacterial components and activates the complement system. Adaptive immunity produces antibodies that can opsonize bacteria, block toxins and transport mechanisms, or prevent attachment. Certain bacteria can induce strong cytokine release through superantigens, potentially causing shock syndromes. Overall, most bacteria are ultimately killed by phagocytosis.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    54 views4 pages

    Host Defense & Pathogenicity of Microbes: Bacterial Structure

    Uploaded by

    Luqman Al-Bashir Fauzi
    This document discusses host defense mechanisms against bacterial infection, including both innate and adaptive immunity. It outlines the structures of different bacterial cell walls and how they relate to susceptibility to immune mechanisms. The first line of defense includes barrier functions and chemicals, while the second line recognizes common bacterial components and activates the complement system. Adaptive immunity produces antibodies that can opsonize bacteria, block toxins and transport mechanisms, or prevent attachment. Certain bacteria can induce strong cytokine release through superantigens, potentially causing shock syndromes. Overall, most bacteria are ultimately killed by phagocytosis.

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    HOST DEFENSE & PATHOGENICITY OF MICROBES (With special reference to

    bacterial infection)

    Host defense mechanisms related to:-

    1. Bacterial Structure
    2. Mechanisms of pathogenicity

    (Hence related to susceptibility of bacteria to appropriate to appropriate immunological


    mechanisms)

    Bacterial Structure

    4 main types of cell walls

    1. Gram positive
    2. Gram negative
    3. Mycobacterium
    4. Spirochaetes

    1. Capsule*/Microcapsule*/Envelope* +/- +/- +/- +/-


    2. Fimbriae*/Flagella* +/- +/- - +/-
    3. Outer membrane# - + + +
    a. LPS* - + - -
    b. Glycolipid & Mycolic Acid* - - + -
    c. Arabinogalactan - - + -
    d. Lipoprotein - + - +
    4. Peptidoglycan (Murein/Mucopeptide) + + + +
    5. Cytoplasmic membrane + + + +
    a. Lipoteichoic Acid + - - -
    b. Lipoarabino Mannan - - + -
    * Structures with adjuvant properties (lead to immune response)

    # Susceptible to lysis (complement and cytotoxic cells)

    IMMUNITY TO BACTERIAL INFECTIONS

    1. First line of defense


    - Antibacterial mechanisms that do not depend on antigen recognition.
    - INNATE IMMUNITY
    a. Barrier / Prevention of entry
    b. Chemicals
    2. Second line of defense
    - Mediated via recognition of common bacterial components
    - Innate Immunity

    The following cause the attraction of the complement system:

    - Lipoproteins
    - Lipoteichoic acids
    - Lipoarabinomanna
    - LPS
    - Formyl peptides
    - Muramyl peptides
    - Peptidoglycan
    - CKP
    - Mannose binding lectin

    Consequences

    1. Complement activation through Alternative / Lectin pathway


    - Lysis
    - Mast cell degranulation
    - Vasoactive amine release leads to:
    a. Increased vascular permeability
    b. Smooth muscle contraction
    = Anaphylaxis

    2. Release of cytokines from macrophage


    - IL-1
    - TNF
    = These 2 cytokines lead to activation of phagocytes and increase adhesion to
    endothelium

    3. Release of cytokines from NK Cells


    - IFN (especially IFN-γ)
     MHC Expression 
     Activates monocytes
    = Delayed Type HS effect

    4. Adjuvant Effect (Adjuvant = to help)


     Stronger B & T cell response

     Outer membrane of Gram negative bacteria

    = Susceptivle to lysis by complement components and cytotoxic cells

     Other bacteria = Mainly gotten rid of by phagocytosis

    - Fimbriae, flagella & capsule on outer surface of bacteria protects bacteria from
    phagocytosis and complement activities…but they are TARGETS from Antibody response (i.e,
    they are IMMUNOGENIC!)

    HOST IMMUNITY RELATED TO PATHOGENICITY

    2 Extremes of bacterial pathogenicity


    i. Toxicity without invasion (e.g, Corynebacterium Diptheriae, Vibrio Cholerae, Clostridium
    Tetani)
    ii. Invasion without toxicity (e.g, Mycobacterium Tuberculosis, Mycobacterium Leprae)

    But MOST bacteria are in between (eg, Staphylococcus Aureus)

    Ultimately most bacteria are killed by phagocytosis

    Bacterium that induce HS Type IV:

    - Listeria monocytogenes
    - Mycobacterium Tuberculosis
    - Mycobacterium Leprae
    - Salmonella Spp.

    SHOCK SYNDROME

    (Antigen non-specific immune mechanisms)

    If cytokine release is sudden & massive -> Severe and acute tissue damage -> Shock syndromes
    which are potentially fatal

    ANTIGEN SPECIFIC IMMUNITY

    Depends on mechanism of pathogenicity


    Bacterial toxin ---leads to---> Specific anti-toxin that neutralizes the toxin

    e.g, Diptheria toxin neutralized by blocking attachment of binding portion to target cell

    Mucosal sIgA prevents attachments of specific bacteria to epithelium

    E.g, Anti-M protein of S. Pyogenes

    Role of specific antibodies in pathogenesis of bacterial infection

    a. Attachment to:
    - Fimbriae
    - Lipoteichoic Acid
    - Capsules
    b. Triggers complement mediated lysis of Gram negative outer membrane
    c. Block transport mechanism and receptors
    - Fe chelating compounds
    d. Avoidance of phagocytosis
    - Anti M and anti capsule -> Opsonization -> Phagocytosis

    Superantigens

    Bacterial components

    - Bind directly (unprocessed) to TCR (Vβ)


    - Cross-link to MHC
    - Activate all T-cells bearing Vβ gene products
    E.g; S. Aureus& Epidermolytic toxins A&B, Streptococci, Mycoplasma
    - Massive cytokine/lymphokine release
    E.g; S. Aureus and toxic shock syndrome

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