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MCD Microbiology > Fungal Immunity > Flashcards

Fungal Immunity Flashcards

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Biology 101 flashcards
1
Q

what are the four groups of fungi?

A

Zygomycota
Ascomycota
Basidiomycota
Deuteromycota

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2
Q

what are fungi opsonised by to enable phagocytosis?

A

pentraxin-3 and mannose-binding lectin (MBL)

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3
Q

what cells are involved in the immune response to fungi?

A 
o Phagocytes 
– first line of defence.
o NK cells 
– provide early IFN-gamma. 
nb immune cells produce type 2 IFNs
o Dendritic cells
 – influence T-cell differentiation.
o Th1 and Th17 cells.
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4
Q

what enables the virulence of candida?

A

dimorphism allows tissue invasion

candida albicans causes mucosal infections

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5
Q

what enables the virulence of cryptococcus?

A

capsule evades phagocytosis

causes meningitis in HIV patients

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6
Q

what enables the virulence of aspergillus?

A

inhaled as conidia, invade as hyphae

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7
Q

deficiencies and polymorphisms in which proteins can lead to fungal infections?

A
  • dectin 1 (PRR-impaired macrophage IL-6 production)
  • CARD9 (an adaptor molecule needed for TNF-alpha production and Th17 differentiation. Both needed to surmount macrophages action.)
  • TLR4
  • SNPs
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8
Q

how does Dectin 1 def lead to fungal infection?

A
  • dectin 1 is a fungal PRR
  • def. leads to impaired macrophage IL-6 production and binding in response to infection
  • leads to mucocutaneous fungal infections – e.g. vulvovaginitis & onychomycosis
  • increased susceptibility to invasive aspergillosis in stem cell transplants
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9
Q

how does CARD9 deficiency lead to fungal infection?

A
  • CARD-9 is a downstream to dectin 1, an adapter protein required for
    TNFa production in response to beta-glucan stimulation.
  • enables T-cell Th17 differentiation
  • leads to chronic mucocutaneous candidiasis
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10
Q

what is the associated increased risk with TLR4 polymorphisms?

A

increased risk of Invasive Aspergillosis (IA) in transplantation (i.e. haematopoietic stem cell transplants).

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11
Q

what is the associated increased risk with SNPs?

A

increased susceptibility to invasive fungal infections and disease
examples of SNPS: CXCL10, IL1-R, IL-23R, TLR-2/4/6/9.

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12
Q

what mutations confer increased susceptibility to fungal disease?

A

Dectin-1, TLR4 and plasminogen

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13
Q

what is the important immune cell in fungal defence?

A

neutrophils
macrophages
monocytes

neutrophils particularly for aspergillius

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14
Q

how do neutrophils neutralise pathogens?

A
  • neutrophils throw out chromatin “nets” to capture pathogens.
  • chromatin molecules outside the nucleus act as “danger signals” and recruit’s effector cells to the area as well.
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15
Q

how does fungal morphogenesis impact the dendrite cell response?

A
  • fungi can transition between yeast, candida and hyphae forms (unicellular to multicellular)
  • this can drive a modulation of Dendritic cell response
  • this can be bad for the immune response (as it gets confused)
  • mucosal immunity governs fungal tolerance and resistance
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16
Q

how can fungal infections be treated?

A

o Adoptive (T-cell) immunotherapy
o Gene therapy
- IFN gamma

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17
Q

what is adoptive immunotherapy?

A

generate lots of antifungal T-cells in a sample and then give these to the patients that need to fight a fungal infection.

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18
Q

what is gene therapy?

A

e.g. restore gp91 function (make reactive oxidative species to fight fungal spores) to treat chronic granulomatous disorder.
E.g. restore neutrophil NET formation.

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19
Q

what cells modulate adaptive immune responses?

A

dendritic cells

Adaptive T-cell INF-gamma responses augment host immunity to fungi.

error in dendritic cell response leads to ABPA

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20
Q

what is a primary driver of fungal allergy?

A

o Aspergilli
– Aspergillus niger, Aspergillus fumigatus –> lung irritation
o Other supporting fungi
– Alternaria, Cladosporium, Penicillum

21
Q

what hypersensitivity reactions are involved in fungal reactions?

A

1,3,4

22
Q

type 1 hypersensitivity reaction

A

IgE-driven, involves histamine and leukotrienes, in minutes

23
Q

type 2 hypersensitivity reaction

A

IgG-, IgM-driven, involves complement, in 1-24 hours

24
Q

type 3 hypersensitivity reaction

A

IgG-, IgM-driven, involves immune complexes, in 1-24 hours

  • deposit in endothelium
  • cause compliment activation
25
Q

type 4 hypersensitivity reaction

A

T-cell-driven, involves lymphokines, in 2-3 days.

26
Q

what is the criteria for diagnosis of Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

o Predisposing condition –
asthma or cystic fibrosis.

o Obligatory criteria –

  • high baseline serum IgE
  • +ve T1 hypersensitivity (immediate response) skin test
  • Aspergillus-specific IgE

o Supportive criteria (more than 2) –

  • eosinophilia
  • IgG AB to Aspergillus fumigatus
  • consistent radiologic abnormalities.
27
Q

what are the radiological abnormalities seen in ABPA?

A
  • Dilated bronchi, thick walls.
  • Upper/central predilection.
  • Lobar collapse.
  • Ring or linear opacities
  • Proximal bronchiectasis.
  • Fibrotic scarring.
28
Q

what is the damage response framework?

A

outcome dependent on host-microbe interaction:
an integrated theory of microbial pathogenesis that puts forth the view that microbial pathogenesis reflects the outcome of an interaction between a host and a microbe, with each entity contributing to the nature of the outcome, which in turn depends on the amount of host damage that results from the host-microbe interaction.

29
Q

what leads to ABPA?

A

abnormality in dendritic cell response

30
Q

how is ABPA managed?

A

o Corticosteroids.

o Itraconazole (steroid-sparing agent)

  • Indicated if not responding to steroids or if steroid-dependency.

o Omalizumab
– recombinant IgE monoclonal ABs

31
Q

which are the important fungi causing infection?

A
  • candida
  • aspergillus
  • crytococcus
32
Q

who are the most vulnerable to fungal infection?

A
  • immune compromised
    e. g. cancer patients
  • AIDS patients
  • transplant recipients
33
Q

which fungal infection is associated with AIDS?

A

pneumocystis pneumonia (pneumocystis jirovecii)

34
Q

why are haematological cancer patients vulnerable to fungal infection?

A

prolonged and profound neutropenia (low neutrophil count)

after treatment with highly cytotoxic chemotherapy for haematological malignancies and recipients of haematopoietic stem cell transplantation (HSCT)

puts them at risk

35
Q

why does the fungal morphotype determine the host response?

A

yeasts and spores are often effectively phagocytosed

the larger size of hyphae precludes effective ingestion.

36
Q

which are the fundamental antigen fungal effector cells?

A

Neutrophils, macrophages and monocytes

37
Q

what are some fungal ligands that can be recognised by immune cells?

A

1,3 β-glucans
mannans
chitin

38
Q

what effect do fungi have on complement?

A
  • Fungi are potent activators of the complement system, resulting in opsonisation due to deposition of C3b on the fungal surface and recruitment of inflammatory cells
  • C3a and C5a are generated
  • fungi are resistant to complement-mediated lysis, presumably due to their thick cell wall
  • Fungi can activate the classical, alternative, and lectin complement pathways
39
Q

which receptor is important in mediating the immune response to fungal infection?

A

Toll-like receptor

40
Q

which rare genetic disease leaves people vulnerable to fungal infection?

A

Chronic granulomatous disease (CGD)

  • have defects in the enzyme NADPH oxidase
  • therefore their neutrophils are unable to kill ingested pathogens
  • vulnerable to aspergillus species

neutrophils are important

41
Q

who are the highest risk of infection?

A

those with prolonged, profound neutropenia after treatment with highly cytotoxic chemotherapy for haematological malignancies

recipients of haematopoietic stem cell transplantations

42
Q

how does hyphae size affect phagocytosis ?

A

the larger the harder

43
Q

how are fungal cell wall detected by innate immunity ?

A

pattern recognition receptors
e.g. dectin-1 , CD5, mannose receptor

the fungal cell wall is the main target for treatment therapies

44
Q

what are some fungal PAMPs/ligands?

A

1,3 beta glucans
mannans
chitin

45
Q

why are fungi resistant to complement mediated lysis despite triggering the complement system?

A

thick cell wall

they activate the classical, alternative and lectin complement pathways

46
Q

when is the lectin complement pathway activated by fungi?

A

recognition of exposed mannans by mannose-binding lectin (MBL)

triggers MBL-associated serine proteases

47
Q

what genetic defect is seen in chronic granulomatous disease?

A
  • defect in NAPDH oxidase

- neutrophil underable to kill ingested pathogens

48
Q

what Fingal infection are people with chronic granulomatous disease most susceptible to?

A

aspergillus species (explained by low neutrophil count)

49
Q

what T cells are predominate in the protective response to fungal infections?

A

Th1 Cd4+

MCD Microbiology (6 decks)

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