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c 

c      (With special reference to


bacterial infection)

Host defense mechanisms related to:-

1. acterial Structure
2. Mechanisms of pathogenicity

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


mechanisms)



G main types of cell walls

1. ›ram positive
2. ›ram negative
3. Mycobacterium
G. Spirochaetes

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


2. Fimbriae*/Flagella* +/- +/- - +/-
3. Outer membrane# - + + +
a. LPS* - + - -
b. ›lycolipid & Mycolic Acid* - - + -
c. Arabinogalactan - - + -
d. Lipoprotein - + - +
G. 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)

  

   

1. First line of defense


- Antibacterial mechanisms that =   depend on antigen recognition.
- à ATE àMMU àTY
a. arrier / Prevention of entry
b. Chemicals
2. Second line of defense
- Mediated via recognition of common bacterial components
- ànnate àmmunity

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. àncreased vascular permeability
b. Smooth muscle contraction
= Anaphylaxis

2. Release of cytokines from macrophage


- àL-1
- T F
= These 2 cytokines lead to activation of phagocytes and increase adhesion to
endothelium

3. Release of cytokines from K Cells


- àF (especially àF -ɶ)
 MHC Expression AA
 Activates monocytes
= Delayed Type HS effect

G. Adjuvant Effect (Adjuvant = to help)


 Stronger  & T cell response

0 Outer membrane of ›ram negative bacteria

= Susceptivle to lysis by complement components and cytotoxic cells

0 Other bacteria = Mainly gotten rid of by phagocytosis

- Fimbriae, flagella & capsule on outer surface of bacteria protects bacteria from
phagocytosis and complement activities͙but they are TAR›ETS from Antibody response (i.e,
they are àMMU O›E àC!)

c   


 
c  

2 Extremes of bacterial pathogenicity


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

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

Ultimately most bacteria are killed by phagocytosis

acterium that induce HS Type àV:

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

c  

(Antigen non-specific immune mechanisms)

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

      

Depends on mechanism of pathogenicity


acterial 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 sàgA 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 ›ram negative outer membrane
c. lock transport mechanism and receptors
- Fe chelating compounds
d. Avoidance of phagocytosis
- Anti M and anti capsule -> Opsonization -> Phagocytosis

 

acterial components

- ind directly (unprocessed) to TCR (Vɴ)


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