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Infection and Immunity > 22 Fungal Pathogens > Flashcards

22 Fungal Pathogens Flashcards

1
Q

where are superficial fungal infections

A

skin and mucosa

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2
Q

who is at risk to getting fungal infections

A

Appears in apparently healthy individuals (so all can be at risk e.g. athlete’s foot)
- Genetic predisposition assumed

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3
Q

what causes thrush

A

Candida albicans

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4
Q

what is Candida albicans like

A

commensal – living inside the body participating in the food that you take up but does not cause disease – however

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5
Q

what are superficial fungal infections like

A

not life threatening

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6
Q

what are invasive fungal infections like

A

life threatening
will penetrate into the tissues and may disseminate within the body and affect different organs
(require predisposition)

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7
Q

examples of those that are more vunerable to infection

A
  • HIV infection - AIDS
  • Surgery
  • Open wounds (burn wounds)
  • Immunodeficiency disorders
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8
Q

what is the major risk factors for acquisition of invasive fungal infections

A

Defects in innate immune response are

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9
Q

what is important with fungal infection treatment

A

progression of disease is very fast – requires early diagnosis and early start of therapy

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10
Q

why are antibodies not effective in fungal infections

A

AB formation takes a long time (too late for fungal infection)

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11
Q

what are the key cells involved in innate immunity in invasive fungal infections

A
  • Macrophages/Monocytes
  • Neutrophils
  • Dendritic cells
  • T-cells
  • Complement
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12
Q

what is the role of neutrophils in innate immunity

A

very effective, but will cause tissue damage if always recruited (need to be recruited to the site of infection – they’re made in bone marrow and circulate in the blood)

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13
Q

what is the role of dendritic cells in innate immunity

A

professional phagocytic cells, main cells that migrate to draining lymph nodes and present antigens to T cells

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14
Q

what is the role of T cells in innate immunity

A

orchestrate the immune response by stimulating further immune response or by tuning down the immune response

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15
Q

what is the role of complement in innate immunity

A

(opsonisation) fungal pathogens to be recognised by immune cells and taken up

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16
Q

what do receptors recognise

A

fungal cell wall components

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17
Q

what is the cell wall mainly made of

A

sugar polymers

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18
Q

how are closed form glucose molecules made

A

OH important in the polymer formation, by connecting to another glucose unit
Closure of the glucose ring can lead to alpha (point down) or beta (point up) glucose
OH on 1 attaches to glucose on 6

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19
Q

what is in the standard core components of fungal the cell wall

A

top layer as protein rich in mannose sugar
glucans (beta1,3 glucan is the dominating) – formed by beta 1,3 glucan synthase
inner layer above cell membrane – chitin layer (polymer)

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20
Q

what is used in species-dependent presentation of other components

A

PAMPS

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21
Q

which PRRs are used when

A

many different receptors that are able to identify specific PAMPS

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22
Q

what is CLR

A

C-type lectin receptors

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23
Q

what is NLRs

A

NOD-like receptors

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24
Q

what is TLRs

A

toll like receptors

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25
Q

what cells can interact with the different fungal elements

A

macrophage, neutrophil, dendritic cells, NK cells

26
Q

macrophage interaction with immune cells

A

Macrophages can feed info to T cells as they can present antigens and are stimulated in response

27
Q

what do the receptors on macrophage, neutrophil, dendritic cells, NK cells cause

A

Number of different receptors on these cells (not as many on NK) elicit a specific response

28
Q

what are Macrophages and Monocytes

A

Professional phagocytes

29
Q

what do macrophages and monocytes recognise

A

fungi using PRR

30
Q

what do macrophages and monocytes make

A

acidic phagolysosomes

31
Q

what do macrophages and monocytes cause

A

Orchestrate immune response by cytokines

32
Q

what does RAB in monocytes and macrophages cause

A

GTPases for fusion with lysosomes

33
Q

what happens in macrophage escape

A
  • Intracellular proliferation

- Elongating hyphae

34
Q

what is the specific macrophages in the lungs

A

alveolar macrophages

35
Q

what do the alveolar macrophages do

A

policed to recognise anything foreign entering the lungs (may or may not be pathogenic) if high concentration of pathogens recruit other cells to aid clearing

36
Q

what do dendritic cells with anti-fungal PRRs recognise and effect

A

Th1/17 (INF/IL17)

adaptive immune response with activation of innate effector cells

37
Q

where are neutrophils

A

Recruited from blood to site of infection

38
Q

what do neutrophils do

A
  • Phagocytose bacteria and fungi

- Release toxic metabolites and peptides

39
Q

what do neutrophils produce

A
  • Produce reactive oxygen species

- Produce extracellular traps

40
Q

what is NET

A

Neutrophil Extracellular Trap

41
Q

when is a NET made

A

when neutrophil dies

42
Q

what occurs in NET formation

A

Leads to modification of macrophage to cause chromatin condensation
DNA strongly packed in nucleus – starts to unpack (gets larger) histones (sticky molecules) stay on the membrane
Will have granules with toxic metabolites

43
Q

what can neutrophils attack

A

large structures

44
Q

how do fungi avoid phagocytosis

A

increase in size

45
Q

what is the importance of T cells

A

Main contributors in fungal infections: Regulatory T-cells, cytotoxic T-cells

46
Q

what are the main sub-types of T cells

A 
- CD4+CD8- T cells
> Th1
> Th2
> Th17
- CD4-CD8+ killer T cells
47
Q

what is the Th1 response

A

Stimulation of macrophages

48
Q

what is the Th2 response

A

B cells, Eosinophils, Basophils –> Chronic disease

49
Q

what is the Th17 response

A

Recruitment and activation of neutrophils

50
Q

what is important in complement pathway

A

C3-dependent alternative pathway

rely on opsonisation to increase recognition by phagocytes

51
Q

what is the problem with antifungal treatment options

A
  • Fungi and human host are both eukaryotes (want to taret the fungal eukaryotes not the human eukaryotes – so only target fungus pathogen, need to find differences)
  • Antifungal drug should specifically target the fungal pathogen
  • Targets need to consist of molecules essential for fungal survival
52
Q

what are the three major classes of antifungals

A
  • Polyene macrolides
  • Echinocandins
  • Azoles
53
Q

what are examples of major targets of antifungals

A

beta-1,3 glucan
beta-1,3 glucan synthase
ergosterol
ergosterol synthesis pathway

54
Q

what is the difference in cholesterol and ergosterol

A

Cholesterol in humans

Ergosterol in fungi

55
Q

what does cholesterol and ergosterol do

A
  • Regulate the fluidity of membranes

- Essential molecule in eukaryotic cell membranes

56
Q

what is the action of polyene macrolides

A
  • Bind to ergosterol in the cell membrane

- Higher affinity to ergosterol than cholesterol

57
Q

what is the mechanism of polyene macrolides

A

mechanism 1 - Binding Pore formation Permeabilisation

mechanism 2 - Forms ion leakage channels (K+, Na+, Ca2+)

58
Q

what is the action of azoles

A
  • bind to inhibit demethylation

- Block ergosterol biosynthesis

59
Q

what is the affect of azoles

A

> Accumulation of (toxic) intermediates

> Alteration of membrane fluidity

60
Q

what is the action of echinocandins

A
  • cell wall depleted with beta 1,3 glucan due to inhibition of β-1,3-glucan synthase
  • weakening of fungal cell wall (loserigidity of cell wall)

Infection and Immunity (29 decks)

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