CMB1003/L09 Host-Pathogen Interactions Flashcards

1
Q

What is pathogenicity, or virulence factors?

A

Structures, molecules or regulatory systems that enable the disease process

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2
Q

What drives pathogenicity?

A

Adhesion to epithelial surface or invasion of underlying tissue

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3
Q

What must bacteria to do to become a pathogen?

A

Get into a place where they shouldn’t be

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4
Q

Approximately how many pathogens make up the microbiome?

A

10^13

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5
Q

How can pathogens adhere to mucosal surfaces? (2)

A

Subvert host cell function (extracellular)
Invade underlying tissue (invasive)

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6
Q

What is the role of polysaccharide capsules on pathogens? (3)

A

Physical barriers to desiccation
Immune masks
Aid adherence

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7
Q

What is the role of the bacterial capsule?

A

Encases bacterial cell
Provided resistance against immune recognition, phagocytosis & complement killing
Precursor to biofilm formation

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8
Q

Cell surface appendages promote initial interactions with which surfaces?

A

Host tissues
Medical devices e.g., catheters
Abiotic surfaces in industry

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9
Q

What do structures offer to pathogens? (4)

A

Physical defence
Nutrition
Intercellular communication
Exchange of genetic material

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10
Q

Describe the 4 stages of biofilm formation.

A

Adsorption
Irreversible attachment
Growth and division
Mature macrocolony

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11
Q

What is the likely default mode of growth for bacteria in nature?

A

Biofilms

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12
Q

What are fimbriae capped by?

A

Sugar-binding, lectin-like proteins

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13
Q

Describe type 1 fimbriae. (2)

A

CUP type adhesin
Found widely in Gram -ves

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14
Q

What does FimH have a specific affinity for?

A

Mannose

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15
Q

How are pili different from fimbriae? (3)

A

Pili are longer, less abundant and involved in genetic exchange

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16
Q

Describe the fimbrial catch-bond theory. (3)

A

Mechanistic benefit in natural environments subject to fluid shear stress
Strength of binding dictated by an allosteric switch in the FimH-sugar interaction
Can be chemically inhibited

17
Q

What are the two general pathways of transport across the IM?

A

SEC - unfolded, common
TAT - folded, elusive substances

18
Q

What does the SEC pathway of transport across the IM facilitate?

A

Insertion of proteins into the IM

19
Q

What do 2 step systems in Gram -ves generally follow?

A

SEC translocation to periplasm followed by specific system for OM transport

20
Q

Describe a type 3 secretion system (T3SS). (2)

A

Required for epithelial attachment (EHEC)
In some cases invasion

21
Q

Describe a type 6 secretion system (T6SS). (2)

A

Used for inter-bacterial warfare and host-cell subversion

22
Q

Describe a type 4 secretion system (T4SS).

A

Primarily involved in genetic exchange (conjugation)

23
Q

Where is the damage usually located by bacterial toxins?

A

Distal to site of infection

24
Q

What advantages do toxins offer to bacteria?

A

Access to tissue and nutrients
Facilitating transmission
Enhancing other virulence processes

25
What 3 mechanisms of action do exotoxins facilitate?
Cytolytic Disruptive Stimulatory
26
Give an example of a cytolytic exotoxin.
Hemolysin Alpha-toxin
27
Give an example of a disruptive exotoxin.
AB toxins
28
Give an example of a stimulatory toxin.
Superantigens
29
Describe the repressive effect of Stx-phage. (2)
On T3SS Stimulates cell receptor expression in host
30
What are endotoxins?
Cell-bound lipopolysaccharides of Gram -ve bacteria
31
When are endotoxins released?
When cells lyse
32
What can endotoxin release induce? (2)
Fever, tissue inflammation, diarrhoea
33
How does the toxicity of endotoxins compare to exotoxins?
Endotoxins far less toxic
34
What are pathogenicity islands?
Portions of DNA that encode toxins and secretion systems