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CMB2004 > CMB2004/L08 Immunity Against Infection I > Flashcards

CMB2004/L08 Immunity Against Infection I Flashcards

1
Q

What bacteria causes food-poisoning?

A

Salmonella

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2
Q

Which bacteria causes tonsillitis?

A

Streptococci

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3
Q

Give the 4 host defence mechanisms in order of action/

A

Anatomic barriers
Complement/antimicrobial proteins
Innate immune cells
Adaptive immunity

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4
Q

Give 3 cells involved in the innate defence mechanism.

A

Complement
Phagocytes
NK cells
Antimicrobial peptides

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5
Q

What is the role of T(H)1 cells?

A

Active against intracellular pathogens
Activate macrophages and stimulate cytotoxic T cells (CD8+ cell)

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6
Q

What is the role of T(H)2 cells?

A

Active against extracellular pathogens
Support antibody production, particularly to IgE
Activate eosinophils, basophils and mast cells

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7
Q

What is the role of T(H)17 cells?

A

Active against extracellular bacteria and fungi
Attract inflammatory cells e.g., neutrophils

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8
Q

Give an example of a Gram positive bacteria.

A

Staphylococcus aureaus
Streptococcus spp.

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9
Q

Give an example of a Gram negative bacteria.

A

Campylobacter
Salmonella
Shigella
Haemophilus
Neisseria

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10
Q

Describe the cell wall of Gram positive bacteria.

A

Lipid bilayer plasma membrane with integral proteins
Lipoteichoic acids traversing wall and anchored in membrane

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11
Q

Describe the cell wall of Gram negative bacteria.

A

Lipid bilayer plasma membrane with integral proteins

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12
Q

How can components of bacterial cell walls induce innate responses?

A

Binding to Toll-like receptors (TLR) on macrophages

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13
Q

Where are distinct molecular patterns that are recognised by receptors on pathogens?

A

Plasma membrane
Endocytic vesicles

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14
Q

Where are NOD-like receptors found?

A

Cytoplasm

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15
Q

What do Toll-like receptors bind?

A

Pathogen-associated molecular patterns (PAMPs)

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16
Q

What does binding of PAMPs to TLRs trigger? (2)

A

Inflammation
Dendritic cell maturation
Influence differentiation of T cells
Activate B cells

17
Q

What do TLRs on the endosome membrane recognise?

A

Microbial components exposed after microbe has been broken down

18
Q

How can the bacterial capsule be overcome by the body’s defences?

A

Opsonisation by antibody/complement

19
Q

Give 3 roles of antibodies in bacterial infection.

A

Opsonisation
Complement activation
Bind to and neutralise toxins
Bind to surface structures to prevent mucosal adherence

20
Q

How can Gram negative bacteria be killed?

A

By complement lysis

21
Q

Which cells are central to the T(H)1 response?

A

Macrophages

22
Q

Give an example of a bacterium which can survive within phagocytes.

A

Mycobacterium tuberculosis
Inhibit lysosome/phagosome fusion

23
Q

Describe the body’s response to:
a) tuberculoid leprosy
b) lepromatous leprosy.

A

a) Strong T(H)1 response, few live bacteria, slow progression, granuloma formation
b) Strong T(H)2 and antibody response, lots bacteria in macrophages, disseminated infection, fatal

24
Q

Describe how a granuloma is formed.

A

Macrophages engulf foreign material but cannot eliminate it
Become activated
Become giant cells and fuse together
More inflammation with lymphocytes

25
Q

Describe tuberculoid leprosy.

A

Low levels of bacteria
Low infectivity
Granulomas and local inflammation
Peripheral nerve damage
Normal serum immunoglobulin levels
Normal T cell responsiveness

26
Q

Describe lepromatous leprosy.

A

Florid growth in macrophages
High infectivity
Disseminated infection
Bone, cartilage, and diffuse nerve damage
Hypergammaglobulinemia
Low or absent T cell responsiveness

27
Q

In which form of leprosy are monokines produced?

A

Granulomatous

28
Q

What factors do the different effector mechanisms needed to fight infection dependent on? (3)

A

Type of pathogen
Localisation
Challenge
Stage of infection

CMB2004 (12 decks)

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