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Microbiology > Fungal infections > Flashcards

Fungal infections Flashcards

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Biology 101 flashcards
1
Q

Opportunistic fungi

A

Live in GI tract/on skin of host. Suppression of immune system > dissemination.
Nosocomial infections.
Eg Candida.

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2
Q

Dangers of fungal pathogens?

A

Some obligate pathogens, but infections are rare in temperate climate zones. Predisposing factors: breaking of physical barriers, immunosuppresion.

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3
Q

Immune response to fungi

A

Mainly mediated through Th17, IL17 response.

Some TLRs involved in innate mucosal immunity.

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4
Q

Fungi characterists

A

Discrete eukaryotic phylum.

Non-motile, unicellular or multicellular, aerobic. Heterotroph, first digestion then uptake (exoenzymes).

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5
Q

Fungi structure

A

Large vacuole. Cell wall consisting of chitin, glucan and mannan polymers. Storage of glycogen (like animals) not starch (like plants). Membranes contain ergosterol (not cholesterol, like animals).

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6
Q

Fungi reproduction

A

Reproduction by spores (often dispersed by wind).

Sexual (meiotic) and asexual (mitotic) spores.

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7
Q

Basidiomycota

A

fungus lives undergorund and forms mycelium. over ground: mushroom (reproductive organ)
cells have limited life span

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8
Q

Cryptococcus neoformans

A

Can cross BBB and cause brain infections.

Often in immunocompromised patients

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9
Q

Ascomycota

A

Filamentous fungi. Ascus for sexual reproduction

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10
Q

Yeast

A

S. cerevisae>

sexual reproduction: alpha cell, a cell

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11
Q

Clinical manifestations (4 examples)

A 
Tenia versicolor (Malasseizia furfur)
Skin lesions (Cryptococcus neoformans)
Oral thrush (Candida labicans)
Lung infection (Aspergillus fumigatus)
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12
Q

How can fungi cause disease in humans (3 ways)?

A

Disease in humans due to allergies, poisoning, infection.

Infection can be severe but very rare.

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13
Q

Why are fungal infections rare?

A

Most fungi are not able to grow in humans as host. Usually grow on dead matter under environmental conditions. Rare: feed on live matter such as humans with full immune system under non-environmental conditions.

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14
Q

Parasitic lifestyles within hosts (plants/animals)

A

Plants: biotrophic (long time) or necrotrophic (actively kill)

Animals: commensalism (long-term), few obligate pathogens
opportunism: commensals infect host bc of defense system failure

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15
Q

Defense mechanisms against fungi

A
  1. Physical barriers (skin/mucosal surfaces, temperature)

2. Immune systems (fungal PAMPs recognized by TLRs, IL-17/Th17 response: dectin-1/2 recognize fungal glucan)

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16
Q

Predisposing factors for fungal infections

A

Immunodeficiency,
Breaking of physical barriers

(mainly Candida, Aspergillus)

17
Q

Candida risk groups

A
  • systemic candidosis dangerous for early born infants
  • women: vaginal candidosis
  • HIV patients: oral Candida
18
Q

Classes of antifungal drugs

A

Polyenes,
azoles/morpholines.
echinocandins

19
Q

Candida infections (sequence)

A

Mainly C. albicans.
Colonization(adhesions) > superficial infection (tissue destriction, invasive growth) > invasive infection (immune escape) > systemic infection (hyphae > yeast transition, spread through blood stream)

20
Q

C. albicans

A

Polymorphic yeast: yeast form and hyphal (mycelial) form.
Lives as commensal in GI-tract. Reproduces mainly clonal.
Porduces: SAPs, secretory lipases, phospholipases, peptide importers.

21
Q

Tissue destruction by Candida

A

Hyphae allow tissue penetration.
Contact sensing (thigmotropism).
Growing hyphae secrete molecules that destroy host cell (stage-specific enzymes).

22
Q

Fungal cell wall - functions

A

Prevents lysis. Provides matrix for protein attachment. Additional compartment for nutrient acquisistion/digestions.
Site of host-pathogen interaction!

23
Q

Fungal cell wall - defense (components)

A
  • carbohydrate layer (prevents lysis, manual damage)
  • dual composition: glucan/chitin (compensation if either is defective)
  • mannoprotein coat (protection, masking)
  • enzymes that negate host defense
24
Q

Fungal cell wall adhesion components

A
  • neg mannan (adherence to pos. plastic)
  • specific adhesion molecules
  • biofilm formation
    (> dissemination into blood stream > fungal sepsis)
25
Q

Histoplasma capsulatum infection

A 
Environmental form (mold/conidia) and disease causing form (yeast).
Histoplasmosis: mostly asymptomatic, unless immunocompromised. (Healthy: encapsulation/calcification of fungal cells.)

Iron-aquisition: surface receptor captures hemin, secretion of siderophores (chelate iron), ferric reduction

26
Q

Aspergillus fumigatus infection

A

Grows on compost > inhalation of conidia > germination in immunocompromised > localised infection.
Response: Phagocytosis (but: fungi produce ROS-scavenging melanin pigments).

27
Q

MICx

A

MICx: minimal inhibitory concentration (conc at which growth is inhibited by at least x%)

28
Q

Measuring antimicrobial drug susceptibility

A 
Epsilometer-test (test strip with gradient),
broth microdilution (ELISA)
29
Q

Approaches to fight fungal infections

A

1) improve host immune status
2) inhibit pathogen growth (fungistatic)
3) kill pathogen (fungicidal)

(immunization not possible)

30
Q

Polyenes (Amphotericin B)

A

Bipolar. Forms pores in membrane by complexing ergosterol > proton gradient disturbed > cell death/growth-stop

31
Q

Azoles

A

Target ergosterole biosysnthesis:
Ergosterol depletion >membrane becomes stiff, protein compounds cannot interact.

Enzme inhibition by toxic byproduct:
inhibit ERG11/CYP51 > membrane alteration, formation of growth-inhibiting byproduct

32
Q

Echinocandinds

A

Target glucan synthesis. Enzyme inhibition.

33
Q

Reasons for fungal therapy failure

A

Species shift due to intrinsic resistance: new drug > depletion of susceptible species > rise of resistance species

34
Q

Resistance transmission

A

No resistance plasmids. No horizontal gene transfer. No spread of resistant strains between patients.

35
Q

Transient resistance.

A

Generated via upregulation of compensatory mechanisms.

Eg cell wall strengthening, increased drug efflux etc

36
Q

Resistance mutations

A

Amphotericin B resistance: ERG3 mutation > loss of ergosterol, no toxic byproduct
Azole resistance: ER11/CYP51 mutation > > reduced durg affinity, increased efflux
Echinocardins : (glucan synthase)

37
Q

Phylogenetic classification of fungi

A

By 18S sequencing of ribosomal RNA.

On basis of sexual reproduction

38
Q

Why is it difficult to find drug targets in fungi?

A

Are eukaryotes > similar to us, selectivity problematic

Microbiology (10 decks)

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