Immunity Against Infection I Flashcards

(37 cards)

1
Q

Give an example of a bacteria which is ec and depends on epithelial cell binding

A

Streptococcus

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2
Q

Which epithelial surface bacteria causes gonorrhoea and meningitis

A

Neisseria

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3
Q

Which fungi causes oral candidiasis

A

Candida albicans (oral thrush)

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4
Q

Name a few parasites

A

Trypanosoma

Worms

Protozoa

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5
Q

What does different effector response depend on

A

Localisation of pathogen (EC or ic)

Stage of infection

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6
Q

Which 2 areas can viruses be seen

A

EC in fluid like blood - at early stage of infection

Or

Cytoplasmic intracellular

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7
Q

Give 2 examples of intracellular pathogens that live vesicular eg in macrophages

A

Leishmania and mycobacterium

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8
Q

Can Protozoa be ic and EC

A

Yes

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9
Q

Which responses are important for extracellular pathogens like candida,streptococcus, viruses in early stages

A

Antibodies , complement, phagocytosis, epithelial adhesion block by iga, amps

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10
Q

Where are amps made for extracellular protection

A

Epithelial cells

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11
Q

What responses are for ic cytoplasmic pathogens (viruses or Protozoa)

A

CD8 cells, NK cells

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12
Q

Which responses needed for vesicular intracellular pathogens like leishmania and mycobacterium

A

T cell/NK cell macrophage activation

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13
Q

are NK cells part of innate along with barriers , amps and complement

A

Yes

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14
Q

What type of pathogen needs th1 response and why

A

Vesicular pathogens - for macrophage activation

Cytoplasmic - for NK and CD8 activation

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15
Q

What type of pathogen is th2 for

A

Extracellular, stimulates eosinophils granule release, mast cells histamine, antibody igE switching

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16
Q

Why are th17 for extracellular pathogens/fungi like candida

A

Il17 causes chemotaxis of important cells like neutrophils and other inflammatory cells

17
Q

Which types of bacteria have thick peptidoglycan wall

A

Gram positive like streptococcus and staphylococcus

18
Q

How many types of TLR are there which stimulate innate response

19
Q

Which prr are intracellular

A

Nod like receptors

20
Q

Where are tlr located

A

On vesicles inside cells (for ic killing) or on cell surface (EC killing)

21
Q

What do Tlr do

A

Induce inflammation
Mature dendrites via danger signal (upregulate B7 and MHC)
Induce differentiation of T cells by determining cytokine release of apc

B cell ti 1 activation

22
Q

Can bacteria be ic and EC

A

Yes.

Mycobacterium are vesicular ic

Strep and neisseria on cell surface

23
Q

What protects bacteria from phagocytosis

24
Q

What does streptococcus EC bacteria cause

A

Pneumonia and meningitis

25
What does vaccine for strep include
23 diff polysaccharides strep has to produce diff antibodies specific for them
26
Which vaccine for strep helps a TD response by B cells
Conjugate vaccines (for children under 2 don’t recognise the ti2 ag on strep)
27
Which bacteria are killed by Mac in complement which is activated by antibodies igm and igG
Gram -ve like neisseria
28
What is importance of antibodies in EC bacteria protection eg strep or neisseria
Opsonisation via fc receptors Activation of complement and c3b opsonisation Neutralise toxins eg tetanus Prevent epithelial adhesion via iga
29
What are you susceptible to without complement / if you have genetic defect in eg c3b or Mac
Neisseria gonorrhoea (EC cell surface, killed by Mac because gram -ve)
30
When are bacteria most vulnerable to complement lysis
When dividing
31
How do mycobacterium tb survive phagocytosis
Survive in macrophages (ic bacteria) Prevent phagosome fusion with lysosome
32
Although th1 are mostly important in ic pathogens. How are they important for EC too
Activate macrophages via ifny and cd40L signal | Better at antigen presenting eg to stimulate th2 response and also release cytokines
33
What does mycobacterium leprae cause (IC)
Tuberculoid leprosy and lepromatous leprosy
34
Why is tuberculoid leprosy slower in progression and low infect ivory
Th1 response Allows activation of macrophages, NK and CD8 cells to kill mycobacterium intracellular
35
why is lepromatous leprosy not effective in response
Th2 response. More ab and not effective for ic pathogens like mycobacterium Low T cell responses
36
What forms when th1 macrophages aren’t killing mycobacterium fast enough and they aggregate
Granulomas - necrotic area where infection isn’t cleared fast enough
37
Do mycobacterium leprae stay alive in macrophages in lepromatous leprocy
Yes. They are not being killed by antibodies because they aren’t effective for ic pathogens