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cmb1003-microbiology & immunology > CMB1003/L09 Host-Pathogen Interactions > Flashcards

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
Q

What 3 mechanisms of action do exotoxins facilitate?

A

Cytolytic
Disruptive
Stimulatory

26
Q

Give an example of a cytolytic exotoxin.

A

Hemolysin
Alpha-toxin

27
Q

Give an example of a disruptive exotoxin.

A

AB toxins

28
Q

Give an example of a stimulatory toxin.

A

Superantigens

29
Q

Describe the repressive effect of Stx-phage. (2)

A

On T3SS
Stimulates cell receptor expression in host

30
Q

What are endotoxins?

A

Cell-bound lipopolysaccharides of Gram -ve bacteria

31
Q

When are endotoxins released?

A

When cells lyse

32
Q

What can endotoxin release induce? (2)

A

Fever, tissue inflammation, diarrhoea

33
Q

How does the toxicity of endotoxins compare to exotoxins?

A

Endotoxins far less toxic

34
Q

What are pathogenicity islands?

A

Portions of DNA that encode toxins and secretion systems

cmb1003-microbiology & immunology (26 decks)

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