Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Infection and Immunity > 23 Pathogenicity-fungi immune evasion > Flashcards

23 Pathogenicity-fungi immune evasion Flashcards

1
Q

what is the most common type of superficial fungal infections

A

Dermatophytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where does dermatophytosis infect

A
  • Stratum corneum (upper skin surface)
  • Nails
  • Hair (scalp)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does dermatophytes infect

A

humans
animals
saprophyte in soil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is anthropophilic

A

infects humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is zoophilic

A

infects animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is geophilic

A

generally saprophyte in soil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the Stratum corneum

A
  • Epidermal layer of dead cells
  • Rich in keratin
  • Protects underlying tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what increases risk of zoonotic infections

A

Direct contact with these infected animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what do antropophilic fungi cause

A

generally chronic infections with low inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what do zoonotic infections usually come with

A

accompanied by inflammatory host response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do dermatophytic fungi require

A

ability to degrade keratin staining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does keratin form

A

alpha helical structure and builds filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is keratin

A

protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how flexible is keratin

A

Amount of cysteine residues determine the rigidity of keratin fibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is cystine

A

Disulfide bond from two cysteines = cystine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are dermatophytes rich in

A

proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do dermatophytes make from cysteine degradation

A

sulfite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what happens when sulfite is secreted

A

reduces cysteine bridges (cystines)

= Proteins become accessible for degradation by proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how are fungal infections diagnosed

A

Cultivation of fungi
Staining and visualisation of hyphae in infected tissues
Diagnostic PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how are fungal infections treated - superficial skin

A

topical application of azoles or terbinafine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how are fungal infections treated - scalp infections

A

azoles, sometimes systemic application

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how are fungal infections treated - nail infection

A

Topical + systemic treatment and nail removal to be considered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how long does therapy last for fungal infection

A

takes between 2 and 48 weeks of treatment, depending where it is located

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are major risk factors in fungal infection

A
  • Immunosuppressive regimen (graft versus host disease, leukaemia)
  • Chronic granulomatous disease (CGD)
  • Other inborne immunodeficiency
  • AIDS (HIV infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is Histoplasma capsulatum

A

Environmental dimorphic fungus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

where is Histoplasma capsulatum found

A

Strongly enriched in droppings of birds and bats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does Histoplasma capsulatum infect

A

immunocompromised and healthy individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how does Histoplasma capsulatum avoid immune mechanisms

A
  • Immune cells generally detect β-glucans in the fungal cell wall via Dectin-1
  • Dectin-1-mediated phagocytosis elicits an inflammatory immune response
  • α-glucan is not immune stimulatory
  • α-glucan overlays the β-glucan layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what does Histoplasma capsulatum acquire

A

essential nutrients from the host and replicates within macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Histoplasma capsulatum and antimicrobial defense molecules

A

Detoxifies antimicrobial defense molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how does condida get into body

A

uptake by inhalation (lung alveoli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what happens once entered cell

A

Adherence to macrophage β-integrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are CD18

A

complement receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what blocks phagocytosis

A

Antibodies against HSP60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

when are the first symptoms of Histoplasmosis

A

about two weeks after conidia inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the symptoms at start

A

Silent manifestation (no symptoms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what happens in the acute phase of Histoplasmosis

A

non-specific respiratory symptoms (cough or flu-like)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what happens in the chronic phase of histoplasmosis

A

similar symptoms as tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what can Histoplasmosis

lead to in immunocompromised patients

A

especially AIDS = reduced T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the problem with HIV and macrophage function

A

HIV reduces number of CD4+ cells that activate CD8+ killer cells
CD8+ killer cells are essential to recognise and kill infected macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the therapy for Histoplasmosis

A

Primary therapy with amphotericin B

Secondary therapy with azoles (may need one year for clearance of infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is PCP

A

Pneumocystis pneumonia

43
Q

what is throphozoit

A

Pneumocystis trophic form

44
Q

what is cyst

A

Pneumocystis cyst form

45
Q

what is special about Pneumocystis

A

species are specialised towards their host

46
Q

what is the pneumocystis life cycle

A 
Trophic form (asexual) multiplies by binary fission
Cysts result from sexual crossing, meiosis and mitosis
47
Q

what are the cysts cell walls like

A

thick cell wall mainly made of β-glucans, chitin, mannoproteins

48
Q

what do β(1,3/1,6)-glucans cause in cysts cell wall

A

severe inflammatory response by immune recognition

49
Q

what us the trophic cell wall like

A

without β-glucans and very thin cell wall

50
Q

what is the flexibility of trophic cell wall

A

Flexible in the cell wall (as no beta glucan)

51
Q

what does trophic express

A

integrin like molecule PcInt1

52
Q

what does integrin interact with

A

extracellular matrix of epithelial cells (fibronectin and vitronectin)

53
Q

what is reduced in trophic cell wall

A

Expression of surfactant phospholipids by epithelial cells reduced

54
Q

why is AIDS cause a major problem to Pneumocystic infection

A

Implies major role of CD4+ cells in clearance, but mainly through cytokine response
CD8 T cell depletion does not increase risk for infection
Adaptive B-cell response important for clearance
Macrophages and neutrophils phagocytose and inactivate cysts and trophozoits

55
Q

what causes major disease transmission in Pneumocystis

A

cysts

56
Q

what does Pneumocystis not produce (unlike other fungi)

A

ergosterol

57
Q

what are the problems with treating Pneumocystis

A
  • Natural resistance against azoles
  • Low sensitivity against amphotericin B
  • don’t have beta glucan = no trophozoits
58
Q

what is important for transmission control in Pneumocystis

A

Echinocandins active against cysts, but need co-application of sterols

59
Q

what is Cryptococcus neoformans divided into

A

four serotypes A, B, C, D

60
Q

who are the individuals at risk to Cryptococcus neoformans

A

mainly infects immunocompromised individuals

  • Highest risk for HIV infected patients with AIDS
  • Transplant recipients identified as emerging group at risk
61
Q

what does Asexual Cryptococcus form

A

yeast cells

62
Q

how do Asexual Cryptococcus infect

A

by inhalation of

  • Blastoconidia
  • Desiccated spores
63
Q

what causes Cryptococcosis

A

released from bird droppings

64
Q

why does cryptococcosis not infect birds

A

birds don’t get infected as their body temperature is too high – cannot proliferate in the tissues, but can survive and proliferate in intestine – in bird droppings

65
Q

what is the major virulence factors of cryptococcus

A

Polysaccharide capsule

66
Q

what is the polysaccharide capsule made of

A

galactoxylomannan (GXM)

67
Q

what does the polysaccharide capsule do

A

Protects from cell-wall recognition and immune activation

68
Q

what is melanisation in crypotococcus

A

Activation of host diphenolic compounds

69
Q

what does melanisation stabilise

A

fungal cell wall

70
Q

what does melanisation reduce

A

susceptibility to antifungal agents

71
Q

what can melanin scavenge

A

reactive oxygen species

72
Q

what can some cryptococcus cells form

A

titan/giant cells

73
Q

when are titan cells made

A

formation is stimulated when both mating partners cause infection

74
Q

what cant occur to titan cells

A

cannot be phagocytosed – surrounded by large capsule (cannot be opsonised)
Promotes survival within the host

75
Q

what is the the main disease from cryptococcus

A

acute meningitis

76
Q

what can occur in cryptococcus infections

A

Latent infection frequent (no complete clearance) = Reactivation possible

77
Q

dendritic cell role in cryptococcus clearance

A

phagocytose Cryptococcus and present antigens to T-cells

78
Q

adaptive T cell role in cryptococcus clearance

A

Adaptive T-cell response from CD4+ and CD8 cells play major role in clearance
- Low CD4+ counts in HIV patients major risk factor

79
Q

what is the therapy for acute meningitis

A

Initial therapy with combination of two
Maintenance therapy with another
Echinocandins are not effective

80
Q

what are Aspergillus species

A

environmental saprophytes

81
Q

where are Aspergillus species

A

common in soil and on decaying organic matter

82
Q

where is Aspergillus terreus

A

Common in soil and on decaying organic matter

83
Q

what is Aspergillus terreus problem

A

Natural Amphotericin B resistance

84
Q

what is frequent in Aspergillus terreus

A

dissemination

85
Q

what is the thermotolerance of Aspergillus terreus

A

Moderately thermotolerant (42°C)

86
Q

where is Aspergillus fumigatus

A

Common in soil and on decaying organic matter

87
Q

what is the thermotolerance of Aspergillus fumigatus

A

Highly thermotolerant (55°C)

88
Q

what is dissemination of A. terreus interaction with DC

A

Activation of DCs leads to transmigration to lymph nodes
Present antigens mainly to T-cells (and B-cells)
Mediators between innate and the adaptive immune response

89
Q

Phagocytosis of A. fumigatus and A. terreus by DCs

A

DCs phagocytose A. fumigatus faster than A. terreus
A. fumigatus escapes from DCs
A. terreus mainly persists

90
Q

what is the germination of A. fumigatus like

A

a very low nutrient threshold

91
Q

what is the germination of A. terreus like

A

speed is dependent on nutrient availability

92
Q

what is the survival of A. fumigatus conidia after DC phagocytosis

A

inactivated

93
Q

what is the survival of A. terreus conidia after DC phagocytosis

A

remain viable

94
Q

what is the survival in presence of antimycotics and DCs - A. fumigatus conidia

A

not protected from antifungals

95
Q

what is the Survival in presence of antimycotics and DCs - A. terreus conidia

A

Persistent A. terreus conidia are protected

96
Q

does A. fumingatus cause DC activation

A

Viable A. fumigatus candida trigger DC activation and transmigration

97
Q

does A. terreus cause DC activation

A

do not elicit DC activation

98
Q

does A. fumingatus cause cytokine production by DC

A

trigger an inflammatory immune response

99
Q

does A. terreus cause cytokine production by DC

A

no

100
Q

where can A. terreus conidia persist

A

macrophages and DCs and TNF-α stimulated DCs

101
Q

what does TNF-alpha stimulate

A

transmigration of A. terreus infected DCs

102
Q

what is a suitable vehicle for A. terreus

A

DCs

103
Q

A. fumigatus infections strategies

A

rapid acute pulmonary disease

  • A. fumigatus follows a “germinate and escape” strategy
  • Rapid progression is life-threatening
104
Q

A. terreus infections strategy

A

“sit and wait” strategy

  • A. terreus conidia can hitchhike innate immune cells for dissemination
  • Disseminated infection has mortality rates > 90%

Infection and Immunity (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions