Brainscape's Knowledge GenomeTM

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


See full index

a path 3 > MICRO: Fungal infections > Flashcards

MICRO: Fungal infections Flashcards

1
Q

What are fungi?

A

Eukaryotic cells - chitinous cell walls, membrane containing ergosterol, 80S ribosomes

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

What are the main 2 types of fungi?

A
  • Dimorphic = change between yeasts and moulds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the commonest fungal infection?

A

Candida spp - this is a yeast

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

Where can candida be grown in the lab?

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

Where can you grow candida to distinguish between different species?

A

Chromogenic agar

  • Aetiological agents:
    • Candida albicans (MOST COMMON)
    • Candida glabrata
    • Candida krusei
    • Candida tropicalis
    • Candida auris (newly discovered and very dangerous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the types of superficial candida infections?

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

How do you treat superficial candida infections?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which one is yeast?

A
  • Form individual cells (a bit like bacteria but much bigger)
  • Replicate by budding
  • Grow in colonies (a bit like bacteria)
  • Distributed world-wide
  • Periodic Acid-Schiff (PAS) stain

Stain gram positive on the gram stain.

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

What are the risk factors for candidaemia?

A
  • malignancy esp haem
  • burns
  • complicated post-op courses
  • long lines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the management of candidaemia?

A

Candida is very sticky so can stick to many different organs hence the many investigations.

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

What is the first line antifungal when you are told that there is a yeast infection in the blood?

A

Echinocandin e.g. anidulafungin

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

Give examples of invasive candida infections.

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

What are the main types of cryptococcis?

A

Characterised by having a large capsule

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

Which animal is cryptococcus associated with?

A

Pigeons

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

What is the lifecycle of cryptococcus?

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

What are the risk factors for cryptococcosis?

A

Impaired T cell immunity e.g. in reduced CD4 helper T cells <200/ml

Taking T cell immunosuppressants for organ transplant - 6% lifetime risk

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

What is the difference between cryptococcus neoformans and gatti?

A
  • Cryptococcus neoformans Immunodeficient
    • Greatly increased in patients with impaired T-cell immunity (AIDS with very low CD4+ counts)
    • Second most common cause of death in AIDS
    • Patients taking immunosuppressants for solid organ transplant (6% lifetime risk)
  • Cryptococcus (neoformans var) gattii Immunocompetent
    • Affects immunocompetent individuals in tropics (especially SE Asia and Australia)
    • High incidence of SOLs in the lung and brain
    • Increased resistance to amphotericin B
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which stain is used to identify cryptococcus? What other diagnostic tools are used?

A
  • India ink stain of CSF (seen below with large capsule)
  • Imaging
  • Lateral flow for cryptococcal antigen
  • Culture from body fluids/blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the management of cryptococcosis?

A
20
Q

What are the spectrum of diseases caused by aspergillus?

A
21
Q

What does aspergillus look like on culture?

A
22
Q

What is seen here?

A

TB has left a cavity which has then been invaded by aspergillus

23
Q

How do you diagnose aspergillus?

A
  • Imaging
  • Sputum/BAL
  • Aspergillus Abs (precipitans)
  • Galactomannan - bronchial sample or circulating in blood
    *
24
Q

What is the management of aspergillosis?

A
  • Voriconazole
  • Ambisome
  • Duration based on host/radiological/mycological factors - at least 6 weeks
25
Q

How is pneumocystis jiroveci acquired? What is the cell wall like?

A
26
Q

What is this infection?

A

Pneumocystic jirovecii

Diffuse bilateral infiltrates affecting all lobes of lung

Exertion after minimal activity

27
Q

What is the diagnosis and mangement of pneumocystic jirovecii?

A
28
Q

Which groups are affected by mucormycosis? What are the aetiological agents?

A

Diabetics and immunosuppressed

  • Aetiological Agents
    • Rhizopum spp.
    • Rhizomucor spp.
    • Mucor spp.
29
Q

What are the clinical features of mucormycosis?

A
30
Q

What is the management of mucormycoses?

A
31
Q

What are the features of dermatophyte infection?

A
32
Q

What causes pytyriasis vesicolor?

A

FUNGAL infection -

33
Q

How are dermatophytes diagnosed?

A
  • Diagnosis of the above organisms:
    • These are diagnosed by taking skin scrapings
    • The organisms are then cultured (can take up to 4 weeks to grow)
    • Microscopy is used to identify the organisms
34
Q

Azole SE

A

Most common: LFT abnormal

35
Q

Echinocandins SE

A

Common: relatively innocuous

36
Q

Pyrymydine analogues SE

A

Blood disorders

37
Q

Polyene SE

A

Neohrotoxocity most common

38
Q

What are the targets of antifungals?

A
39
Q

What do echinocandins not treat?

A

Do not get into urine

Do not treat cryptococcus

40
Q

What is the MOA of echinocandins? What are they active against?

A
  • Mechanism of action = cyclic lipopeptide antibiotic:
    • Inhibit Beta-(1,3) D-glucan synthase
    • Inhibits production of Beta-D glucan (a component of the fungal cell wall) à osmotic fragility
  • Active Against:
    • Candida species (including non-albicans isolates that are resistant to fluconazole)
    • Aspergillus species (but NOT other moulds e.g. Fusarium, Zygomycosis)
41
Q

What is the MOA of flucytosine/pyrimidine analogues? What is it indicated for? What is resistant to it? SE?

A
  • Mechanism of action = inhibits DNA in the fungal cells
    • Monotherapy now limited
    • Resistance is due to:
      • Decreased uptake (permease activity)
      • Altered 5-FC metabolism (cytosine deaminase or UMP pyrophosphorylase activity)
  • Indications:
    • Candidiasis
    • Cryptococcosis (in combination with amphotericin B or fluconazole)
  • Side Effects:
    • Infrequent (D&V, changes in LFTs, blood disorders)
    • Blood concentrations need monitoring when used in conjunction with amphotericin B
42
Q

What is ambisome composed of?

A

Amphotericin B + phospholipid bilayer = more lipophilic so can enter CNS and less SE

NB: Amphotericin B is a fermentation product of Streptomyces nodusus

43
Q

What is the MOA of polyene antifungals? What is it active against and what are the SE?

A
  • Mechanism of action:
    • Binds ergosterol à creates transmembrane channels à electrolyte leakage à cell death
  • Active against MOST FUNGI except:
    • Aspergillus terreus
    • Scedosporium spp.
  • The original formulation of amphotericin B is amphotericin B deoxycholate (Fungizone) which had serious toxic side-effects (e.g. nephrotoxicity) à partially ameliorated with a lipid carrier:
    • Liposomal amphotericin B
    • Amphotericin B colloidal dispersion
    • Amphotericin B lipid complex
  • Nephrotoxicity:
    • Most significant delayed toxicity
44
Q

What is the mechanism of the nephrotoxicity caused by polyene antifungals? How can it be prevented?

A

Renovascular and tubular mechanisms:

  • Vascular – decrease in renal blood flow leading to a drop in GFR (azotaemia)
  • Tubular – distal tubular ischaemia, wasting of sodium, potassium and magnesium
  • Enhanced in patients who are volume-depleted or who are on concomitant nephrotoxic agents

Nephrotoxicity partially ameliorated with a lipid carrier:

  • Liposomal amphotericin B
  • Amphotericin B colloidal dispersion
  • Amphotericin B lipid complex
45
Q

What is the MOA of azoles? What are the types?

A

Mechanism of action –> inhibit ergosterol production (lanosterol –> ergosterol) –> toxic steroids + cell death

  • Inhibit CYP450 enzyme lanosterol 14-a demethylase
  • N.B. may inhibit other CYP450 enzymes –> drug interactions and impairment of steroidogenesis
    • Hence, why ketoconazole and itraconazole are used to reduce steroidogenesis
  • Types of Azoles:
    • Water-Soluble Triazoles
      • Fluconazole (good against Candida and Cryptococcus)
      • Voriconazole (similar to fluconazole but has improved activity against Aspergillus)
    • Lipophilic Triazoles
      • Itraconazole (useful against dermatophytes)
      • Posaconazole (has activity against Mucor)
46
Q

Give examples of each antifungal type.

A

a path 3 (89 decks)

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