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

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

A

Type of pathogen
Localisation
Challenge
Stage of infection

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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)

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
Describe how a granuloma is formed.
Macrophages engulf foreign material but cannot eliminate it Become activated Become giant cells and fuse together More inflammation with lymphocytes
25
Describe tuberculoid leprosy.
Low levels of bacteria Low infectivity Granulomas and local inflammation Peripheral nerve damage Normal serum immunoglobulin levels Normal T cell responsiveness
26
Describe lepromatous leprosy.
Florid growth in macrophages High infectivity Disseminated infection Bone, cartilage, and diffuse nerve damage Hypergammaglobulinemia Low or absent T cell responsiveness
27
In which form of leprosy are monokines produced?
Granulomatous