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2052 DYLAN > bacterial pathogenesis > Flashcards

bacterial pathogenesis Flashcards

1
Q

Local infection

A
  • Entry of pathogen + multiplication at site
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2
Q

Disseminated infection

A
  • Entry of pathogen + multiplication + spread
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3
Q

NM as opportunistic pathogens

A
  • Change in circumstance / niche
    ○ Breach/injury at body surface, increase in numbers, altered immune status of host
    • Nosocomial infection
      ○ NM transferred to or between compromised individuals
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4
Q

functions of virulence factors

A
  • Enter host and colonise
    • Adhesion via adhesins that are ligands for host cell receptor
    • Invade and multiply host niches
    • Cause cell damage
    • Evade immune system - avoid phagocytosis (e.g. capsules), inflammatory response
    • Cause damage via toxins and cytotoxic proteins, degradative enzymes
      Resist antibiotics
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5
Q

Genes for VF’s means of transfer

A
  • Mostly on plasmids and bacteriophages
    • Horizontal gene transfer
      ○ Plasmids
      ○ Bacteriophages
      ○ Transposons
      Vf genes can be expressed together called pathogenicity islands
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6
Q

HGT via plasmids

A
  • Ds circular DNA
    • Self replicating
    • Encode for toxins, adhesins, invasion, drug resistance
    • Transmitted via conjugation
      If VFs absent on plasmids = no disease
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7
Q

HGT via bacteriophages

A
  • Virus infects bacteria
    • Encode for toxins
      Lysogenic phage integrates into the bacterial genome
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8
Q

HGT via Transposons

A
  • Jumping genes
    • Sections of DNA that can mover around in and out of the genome and between plasmids and bacteriophages
    • Well known for transferring
      ○ Antibiotic resistance
      ○ Toxins
      Pili
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9
Q

Pathogenicity islands

A
  • Large areas of chromosomal DNA that contain clusters of genes encoding VFs
    Permanently integrated and dedicated to virulence
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10
Q

how does virulence gene expression regulate

A
  • To conserve energy
    • Lack of nutrients, oxygen concentration, osmolarity, bile salts, temperature, antimicrobial compounds, oxidative stress
    • Switch on and off
      Regulated in response to population density = quorum sensing
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11
Q

Updated Koch’s postulate

A
  1. The ‘virulence’ gene is always found in strains with a particular virulence phenotype
    1. The gene should be expressed in the host
    2. Mutation (inactivation) of that particular gene abolishes (reduces) the virulence phenotype
  2. Reintroduction of the gene reconstitutes the virulence phenotype
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12
Q

portals of entry

A 
○ Epithelial and mucosal membranes
		○ Skin
		○ Respiratory tract
		○ Gastrointestinal tract
		○ Urogenital tract
Eye
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13
Q

innate immunity

A 
○ Physical barriers
			§ shedding
		○ Chemical and biochemical barriers
			§ Secretions
			§ Reflex response (sneeze, cough)
pH
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14
Q

colonisation

A
  • Outcompete NM - biofilms
    • Multiply
    • Remain at site = localised
    • May invade further
      H. Pylori
    • Urease
      ○ Cleaves urea in stomach to produce ammonia which neutralise acid
    • Flagella
      Creates motility driven by chemotaxis according to pH gradient
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15
Q

adhesion

A

○ Contact with host cell - docking
○ Binding - specific - surface interactions
○ Mediated via adhesins - ligands that bind to complementary surfaces receptors on host cells

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16
Q

what are the 3 types of adhesions

A

pili/fimbriae
afimbrial adhesions
bacterial capsules

17
Q

pili/fimbriae

A

□ Attachment to surface, motility DNA transfer
□ Long filamentous hair like
□ Pili - thick tubular structure
□ Fimbriae - thin and shorter than pili
□ Adhesion via tip of pilus
□ Composed of protein subunits (pilin)
□ Host receptors - glycoprotein

18
Q

afimbrial adhesions

A

□ Short monomeric or trimeric structures - not ordered structure like pili/fimbriae
□ Widely spread
□ Establish close and strong adhesion
□ Cell attachment to host cells via glycoprotein, integrin

19
Q

what are bacterial capsules. what are there functions

A 
□ Polymeric structure surrounds the bacterial cell membrane
			□ Protection
			□ Sticky adhesion
				□ To each other (biofilm)
				□ To surfaces (plaque on teeth
20
Q

what is the function of invasins

A

○ Enter into and through epithelial/mucosal layer, through basement membrane through BV into blood
○ Invade through cells - transcytosis
○ Allows entry to non-phagocytic cells

21
Q

Zipper mechanism

A

○ Cell surface receptor/ligand interactions
○ Binding of invasins to integrins activates receptor which signal to initiate polymerisation to form pseudopods and surround pathogen
Mediated from outside cell

22
Q

Trigger mechanism

A

○ Syringe-like structure that injects bacterial proteins into host cell
○ Initiation of actin polymerisation to form pseudopods and surround pathogen
Interaction from inside host cell

23
Q

mechanisms to avoid immune response

A 
Avoid recognition by complement proteins, Ab and phagocytes
	- Hide intracellularly
	- Mask surface antigens - capsules
	- Antigen variation/phase variation
	- Use mimicry
	- Inhibit/destroy Ab - bind Fc of antibody, IgA protease
Avoid phagocytosis
Modify inflammation e.g. toxins
24
Q

what is Phagocytosis

what is the process

A
  • Microbe destruction by phagocytes of innate immune system
    • Pathogen has PAMPS e.g. LPS - if detected, may be coated with C3b and or Ab
    • Phagocyte recognises
      ○ Pattern recognition receptors
      ○ C3b receptor
      ○ Fc receptor
      1. Engulf pathogen in a phagosome
      2. Phagosome fuses with lysosome to form phagolysosome
      1. Degradation of pathogen by microbiocidal agents
25
Q

complement

A

Set of serum proteins important in innate immune system

26
Q

avoiding phagocytosis prior and during

A
  • Prior
    ○ Form biofilms - difficult for phagocytes to recognise individual cells and induce apoptosis
    • During
      ○ Inhibit internal phagocytic pathway to survive
      ○ Block assembly of NADPH oxidase
      Block fusion of lysosome
27
Q

how do capsules avoid immune response

A
  • Hide PAMPS (LPS) - prevent phagocytosis
    • Prevent complement binding
      Avoid ab
28
Q

Specific enzymes used to avoid an immune response

A
  • C5a peptidase
    ○ Degrade C5a - reduce leucocyte recruitment
    IgA proteases - cleaves IgA
29
Q

Fc receptor capture of Ab

A
  • Blocks complement binding

Avoid detection of antibodies

30
Q

Host mimicry

A
  • Copy structures to minimise eliciting Ab detection

Capsules with sugars that mimic host surface glycoproteins

31
Q

Antigenic variation /phase variation

A
  • Change surface components

Phase variation - switch on and off expression of genes

32
Q

Fe acquisition

A
  • Secretion of Siderophores - high affinity iron-chelators
    • Express receptors for iron capture
    • Express high-affinity iron-binding receptor for haemoglobin
      Express toxins to release host Fe
33
Q

Damage to host

A
  • Multiplication = damage
    • Extracellular enzymes
      Exaggerate inflammatory response
34
Q

Toxins

A 
- Direct effect
		○ Damage at site of infection
		○ Secreted
	- Indirect effect
Exaggerated immune response via toxin
35
Q

Exotoxins

A
  • Secreted out of bacteria or released by bacterial lysis
    • Heat-liable toxins (proteins)
      ○ Type I - active immune response
      ○ Type II membrane disrupting toxins
      ○ Type III A-B toxins - active inside cells
    • Heat-stable toxins (non-protein)
      E.g. glycopeptides, polyketides
36
Q

Type I Exotoxin - superantigens

A
  • Very potent
    • Form superantigen - MHC class II complex in APC’s, activates CD4 T cells without antigen
    • T-cell activation without antigen, triggers intense immune response and toxicity
      Polyclonal activation of pro-inflammatory cytokines leading to cytokine storm
37
Q

Type II - membrane disrupting exotoxins

A
  • Damage by cell membrane lysis = haemolysin
    ○ Phospholipases
    § Hydrolyses phosphatidylcholine in host cell membrane causing lysis
    ○ Pore-forming toxins
    Insertion of pores in cell membrane causing cell rupture via osmosis
38
Q

Type III - A-B toxins

A
  • Binary toxin = A subunit + B subunit
    • A = catalytic activity
    • B = binds to host cell receptor
      1. B binds to host cell receptor -
      2. toxin endocytosed
      3. Inside vacuole A separates from B
      4. A component gains access to cytoplasm, exerts effect
    • Diphtheria toxin (DT) - B targets respiratory cells - A blocks protein synthesis = cell death
    • Cholera toxin (CT) - B targets intestinal cell - A causes ion efflux = fluid loss - diarrhoea
  • Botulinum toxin (BoNT) - A endopeptidase, blocks acetylcholine release - inhibits muscle contraction
39
Q

Endotoxins

A
  • Within bacteria, usually cell wall components, release when cell wall breaks or cell death
    • Gram -ve - LPS, LOS
    • Gram +ve - LTA,
    • LPS induces exaggerated immune response - increased inflammatory cytokines - variable O-antigen
      LOS indices sepsis and inflammation - no O-antigen

2052 DYLAN (12 decks)

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