Immunity Against Infection I Flashcards

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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

A

10

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

A

Capsule

24
Q

What does streptococcus EC bacteria cause

A

Pneumonia and meningitis

25
Q

What does vaccine for strep include

A

23 diff polysaccharides strep has to produce diff antibodies specific for them

26
Q

Which vaccine for strep helps a TD response by B cells

A

Conjugate vaccines (for children under 2 don’t recognise the ti2 ag on strep)

27
Q

Which bacteria are killed by Mac in complement which is activated by antibodies igm and igG

A

Gram -ve like neisseria

28
Q

What is importance of antibodies in EC bacteria protection eg strep or neisseria

A

Opsonisation via fc receptors
Activation of complement and c3b opsonisation
Neutralise toxins eg tetanus
Prevent epithelial adhesion via iga

29
Q

What are you susceptible to without complement / if you have genetic defect in eg c3b or Mac

A

Neisseria gonorrhoea (EC cell surface, killed by Mac because gram -ve)

30
Q

When are bacteria most vulnerable to complement lysis

A

When dividing

31
Q

How do mycobacterium tb survive phagocytosis

A

Survive in macrophages (ic bacteria)

Prevent phagosome fusion with lysosome

32
Q

Although th1 are mostly important in ic pathogens. How are they important for EC too

A

Activate macrophages via ifny and cd40L signal

Better at antigen presenting eg to stimulate th2 response and also release cytokines

33
Q

What does mycobacterium leprae cause (IC)

A

Tuberculoid leprosy and lepromatous leprosy

34
Q

Why is tuberculoid leprosy slower in progression and low infect ivory

A

Th1 response

Allows activation of macrophages, NK and CD8 cells to kill mycobacterium intracellular

35
Q

why is lepromatous leprosy not effective in response

A

Th2 response. More ab and not effective for ic pathogens like mycobacterium

Low T cell responses

36
Q

What forms when th1 macrophages aren’t killing mycobacterium fast enough and they aggregate

A

Granulomas - necrotic area where infection isn’t cleared fast enough

37
Q

Do mycobacterium leprae stay alive in macrophages in lepromatous leprocy

A

Yes. They are not being killed by antibodies because they aren’t effective for ic pathogens