Pathogens > Week 4 Core > Flashcards

Week 4 Core Flashcards

(52 cards)

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1
Q

What are the four major classes of antifungals?

A
  • Azoles
  • Echinocandins
  • Polyenes
  • Flucytosine (5-FC)

These classes represent the main types of antifungal medications available.

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2
Q

Why do we have fewer antifungals than antibacterials? (1)

A

Fungi are eukaryotic, so they share many pathways with humans → fewer selective drug targets.

This similarity complicates the development of antifungal drugs.

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3
Q

Why do we have fewer antifungals than antibacterials? (2)

A

Limited pharmaceutical investment / low market value.

The economic incentive for developing antifungals is lower compared to antibacterials.

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4
Q

Why do we have fewer antifungals than antibacterials? (3)

A

Fungal pathogenicity and biology are less well characterised.

This lack of understanding hinders drug development.

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5
Q

Why do we have fewer antifungals than antibacterials? (4)

A

Higher risk of toxicity because host cells resemble fungal cells.

This similarity increases the potential for adverse effects.

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6
Q

What is a fungistatic drug?

A

Inhibits fungal growth but does not kill the fungus; infection may relapse after stopping therapy.

Fungistatic drugs are used to control infections rather than eliminate them.

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7
Q

What is a fungicidal drug?

A

Kills fungal cells; preferred for severe systemic infections.

These drugs are crucial for treating life-threatening fungal infections.

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8
Q

Which antifungal classes are fungicidal?

A
  • Echinocandins (vs Candida)
  • Polyenes

These classes are effective in killing fungi rather than just inhibiting their growth.

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9
Q

Which antifungal classes are fungistatic?

A
  • Azoles
  • Flucytosine

These classes inhibit fungal growth without directly killing the cells.

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10
Q

What is the target of azole antifungals?

A

Lanosterol 14-α-demethylase (CYP51).

This enzyme is crucial for ergosterol synthesis in fungi.

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11
Q

What is the mechanism of action of azoles?

A

Inhibit ergosterol synthesis → toxic sterol buildup → membrane dysfunction.

This disruption affects the integrity of the fungal cell membrane.

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12
Q

Imidazoles vs triazoles — what’s the difference?

A

Imidazoles = 2 nitrogen atoms (mainly topical).
Triazoles = 3 nitrogen atoms (systemic use).

This structural difference influences their applications and effectiveness.

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13
Q

Examples of triazoles

A
  • Fluconazole
  • Itraconazole
  • Voriconazole
  • Posaconazole
  • Isavuconazole

These are commonly used triazole antifungals.

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14
Q

Main clinical uses of azoles

A
  • Candida infections
  • Aspergillus
  • Cryptococcus (fluconazole)
  • Endemic fungi

Azoles are versatile antifungals used for various fungal infections.

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15
Q

Why do azoles have many drug interactions?

A

They inhibit human cytochrome P450 enzymes.

This inhibition can affect the metabolism of other medications.

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16
Q

Three major mechanisms of azole resistance

A
  • ERG11 mutations
  • Efflux pumps
  • Altered sterol pathways

These mechanisms reduce the effectiveness of azole antifungals.

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17
Q

What is ERG11?

A

Gene encoding lanosterol demethylase; mutations reduce azole binding.

Changes in this gene can lead to azole resistance.

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18
Q

How do efflux pumps cause azole resistance?

A

Increase drug export → lower intracellular azole levels.

This mechanism helps fungi survive despite the presence of azole drugs.

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19
Q

Which efflux pumps are involved in resistance?

A
  • CDR1
  • CDR2 (ABC transporters)
  • MDR1

These pumps actively transport azoles out of fungal cells.

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20
Q

How does agriculture drive azole resistance?

A

Environmental use selects resistant A. fumigatus (e.g., TR34/L98H mutation).

Agricultural practices can contribute to the development of resistant fungal strains.

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21
Q

Why are biofilms resistant to azoles?

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A

Poor penetration + high efflux pump activity + metabolic dormancy.

Biofilms create a protective environment for fungi, making treatment more difficult.

22
Q

What is the target of echinocandins?

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A

β-1,3-glucan synthase.

This enzyme is essential for fungal cell wall synthesis.

23
Q

Mechanism of action of echinocandins

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A

Inhibit β-1,3-glucan synthesis → weakened cell wall → osmotic lysis.

This action leads to the death of fungal cells.

24
Q

Examples of echinocandins

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A
  • Caspofungin
  • Micafungin
  • Anidulafungin

These are key echinocandin antifungals used in clinical settings.

25
Spectrum of **echinocandins**
* Fungicidal vs Candida * Fungistatic vs Aspergillus ## Footnote Echinocandins have different effects depending on the fungal species.
26
Why are **echinocandins** well tolerated?
Humans lack β-glucan → high selectivity. ## Footnote This selectivity reduces the risk of toxicity in human cells.
27
Main mechanism of **echinocandin resistance**
FKS1 and FKS2 mutations in glucan synthase. ## Footnote These mutations can lead to treatment failure.
28
What compensatory change helps **echinocandin resistance**?
Increased chitin synthesis in the cell wall. ## Footnote This adaptation can help fungi survive despite the presence of echinocandins.
29
What is the paradoxical **“Eagle effect”**?
Decreased activity at high echinocandin concentrations. ## Footnote This phenomenon complicates treatment strategies.
30
What is the mechanism of action of **polyenes**?
Bind ergosterol → form membrane pores → ion leakage → cell death. ## Footnote This action disrupts the integrity of the fungal cell membrane.
31
Why are **polyenes** toxic?
They also bind human cholesterol (lower affinity than ergosterol). ## Footnote This binding can lead to side effects in humans.
32
What is **AmBisome**?
Liposomal amphotericin B: reduces renal toxicity and improves delivery. ## Footnote This formulation enhances the safety profile of amphotericin B.
33
When are **polyenes** used?
* Severe systemic infections * Cryptococcosis * Mucormycosis * Invasive Candida ## Footnote Polyenes are critical for treating serious fungal infections.
34
Why is **nystatin** not used systemically?
High systemic toxicity → used only topically. ## Footnote Nystatin is effective for localized infections but not safe for systemic use.
35
Major mechanism of **polyene resistance**
Reduced or altered ergosterol in fungal membranes. ## Footnote Changes in ergosterol content can lead to treatment failure.
36
How does **5-FC** enter fungal cells?
Via cytosine permease. ## Footnote This transport mechanism is crucial for its antifungal activity.
37
What happens to **5-FC** inside the cell?
Converted by cytosine deaminase into 5-fluorouracil (5-FU). ## Footnote This conversion is necessary for its antifungal effect.
38
How does **5-FU** inhibit fungi?
Inhibits DNA and RNA synthesis. ## Footnote This action disrupts fungal cell replication and function.
39
Why is **5-FC** selectively toxic?
Humans lack cytosine deaminase → do not convert drug to active form. ## Footnote This selectivity minimizes toxicity to human cells.
40
When is **5-FC** used clinically?
* Cryptococcal meningitis (with Amphotericin B) * Severe Candida infections ## Footnote 5-FC is often used in combination therapy for serious infections.
41
Why is **5-FC** never used alone?
Resistance develops rapidly when used as monotherapy. ## Footnote This limitation necessitates combination therapy.
42
What is the main component targeted in **fungal cell walls**?
β-1,3-glucan. ## Footnote Targeting this component is crucial for antifungal drug action.
43
Why does **cell wall variation** cause drug issues?
Different fungi have different wall compositions → variable sensitivity. ## Footnote This variability complicates treatment strategies.
44
Which pathogen has a **capsule** instead of exposed glucan?
Cryptococcus neoformans. ## Footnote This unique feature affects its susceptibility to antifungal treatments.
45
Why are **Mucorales** resistant to echinocandins?
Low β-glucan content in their cell wall. ## Footnote This characteristic limits the effectiveness of echinocandins.
46
Why is **antifungal resistance** a global crisis?
Only 3–4 drug classes + growing resistance + high mortality rates. ## Footnote This situation poses significant challenges in treating fungal infections.
47
Which fungi are commonly **drug-resistant**?
* C. auris * Candida glabrata * A. fumigatus * Mucorales ## Footnote These species are notable for their resistance to multiple antifungal agents.
48
How do **biofilms** contribute to resistance?
Increase tolerance to azoles and other antifungals. ## Footnote Biofilms create a protective environment that enhances fungal survival.
49
Why are **new antifungals** slow to develop?
Eukaryotic complexity + toxicity issues + low financial incentive. ## Footnote These factors hinder the research and development of new antifungal drugs.
50
Why is **Candida auris** a major threat?
Multidrug-resistant, survives on surfaces, spreads in hospitals, high mortality. ## Footnote Its resilience and transmission in healthcare settings make it particularly concerning.
51
What percent of **C. auris** is multidrug-resistant?
≈30–35%; some isolates pan-resistant. ## Footnote This level of resistance complicates treatment options.
52
Why is **C. auris** hard to diagnose?
Often misidentified by standard laboratory systems. ## Footnote This misidentification can delay appropriate treatment.
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