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Fungal infections Flashcards

1
Q
  1. List three examples of:
    a. Yeast

b. Moulds

A 
a.	Yeast
Candida
Cryptococcus
Histoplasma (dimorphic)
b.	Moulds
Aspergillus
Dermatophytes
Agents of mucormycosis
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2
Q
  1. Describe the appearance of Candida under the microscope.
A

Single-celled organisms that replicated by budding

They are much bigger than bacteria

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3
Q
  1. Which systemic infections can be caused by Candida?
A

Septicaemia, endocarditis, meningitis

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4
Q
  1. List some patient groups that are at risk of invasive Candida infection.
A

VLBW infants
Immunocompromised
Patients on ITU (especially if they have lines in)
Patients receiving TPN (Toal parental nutrition)
Immunocompetent patients who have had antibiotic treatment

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5
Q
  1. List some agents that can cause candidiasis.
A

Candida albicans (MOST COMMON)
Candida glabrata
Candida krusei
Candida tropicalis

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6
Q
  1. Describe a screening test for candidiasis.
A

Candida albicans forms a germ tube

Can be identified by microscopy

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7
Q
  1. What is the acute treatment for candida?
A

Fluconazole – empirical for Candida albicans, topical nystatin (oral thrush) and clotrimazole (vulvovaginitis)

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8
Q
  1. Outline diagnostic tests used for candidemia.
A 
Swabs 
Blood cultures 
Beta-D glucan assay (serology)
Imaging 
Fundoscopy – for endopthalmitis
ECHO – endocarditis
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9
Q
  1. What type of agar is needed for culturing Candida?
A

Sabouraud agar – impregnated with antibiotics to prevent bacteria from outcompeting the fungi

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10
Q
  1. Outline the management of candidemia.
A

At least 2 weeks of antifungals after the last negative culture
Echinocandins – empirical for non-albicans infections
Take out any lines and repeat blood cultures every 48 hours

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11
Q
  1. What are the serotypes of cryptococcus and who do they affect?
A

Serotypes A and D – immunodeficient – C neoformans

Serotypes B and C – immunocompetent – C gattii

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12
Q
  1. What types of disease does Cryptococcus tend to cause?
A

Pulmonary, systemic and meningitic disease

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13
Q
  1. Which group of antifungals is Cryptococcus inherently resistant to?
A

Echinocandins

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14
Q
  1. What is the treatment of choice for Cryptococcus infection?
A

Ambisome (amphotericin B)

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15
Q
  1. Which patients are particularly at risk of cryptococcosis?
A

Impaired T cell immunity (AIDS)

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16
Q
  1. What does Cryptococcus gatii cause?
A

Causes meningitis in immunocompetent individuals in tropical countries
High incidence of space-occupying lesions in the lung and brain
Increasing resistance to amphotericin B

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17
Q
  1. Describe the appearance of Cryptococcus under the microscope.
A

Distinct capsule around the yeast
India ink can be used to stain
NOTE: the capsule is not always present

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18
Q
  1. Outline the treatment options for Cryptococcus infection.
A

3 weeks amphotericin B (ambisome) +/- flucytosine
Repeat LP for pressure measurement
Secondary suppression – fluconazole

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19
Q
  1. List the diseases that can be caused by Aspergillus.
A

Mycotoxicosis
Allergic bronchopulmonary aspergillosis
Aspergilloma
Invasive/disseminated disease

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20
Q
  1. List the aetiological agents that can cause Aspergillus infection.
A 
Aspergillus fumigatus 
Aspergillus flavus
Aspergillus niger
Aspergillus niduland
Aspergillus terreus
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21
Q
  1. List some investigations used in the diagnosis of Aspergillus infection.
A 
Blood test 
Serology (check IgE for allergic response (e.g. ABPA))
•	Antigen detection (galactomannan) 
•	Also detected in BAL 
PCR 
Histology 
Culture
22
Q
  1. What is the mainstay of diagnosis of Aspergillus infection?
A

Microscopy – looking at fungal spores

23
Q
  1. What is the mainstay of treatment for aspergillosis?
A

Amphotericin for at least 6 weeks

Other options: voriconazole, caspofungin, itraconazole

24
Q
  1. What is used to treat pneumocystic pneumonia?
A

High dose Co- trimoxazole (as it lacks ergosterol in its cell wall, therefore targeting the cell membrane will not work)

25
Q
  1. List some examples of dermatophyte infections.
A

Ringworm
Tinea
Nail infections

26
Q
  1. What is tinea pedis caused by?
A

Tricophyton rubrum
Tricophyton interdigitale
Epidermophyton floccosum

27
Q
  1. What is tinea cruris caused by?
A

Tricophyton rubrum

Epidermophyton floccosum

28
Q
  1. What is tinea corporis caused by?
A

Tricophyton rubrum

Tricophyton tonsurans

29
Q
  1. What is onychomycosis caused by?
A

Tricophyton spp.
Epidermophyton spp.
Microsporum spp.

30
Q
  1. How is onychomycosis treated?
A

Nail lacquers
If unsuccessful, systemic treatment with terbinafine
Itraconazole is also an option

31
Q
  1. What is pityriasis versicolor caused by?
A

Malassezia furfur

32
Q
  1. What is mucormycosis?
A

Group of moulds that cause very severe and invasive disease

33
Q
  1. What is the characteristic clinical manifestation of mucormycosis?
A

Cellulitis of the orbit and face which progresses with discharge and black pus from the palate and nose
NOTE: black eschars may be seen as the fungus destroys tissues

34
Q
  1. What can retro-orbital extension of mucormycosis lead to?
A

Proptosis, ophthalmoplegia and blindness

35
Q
  1. List three aetiological agents that can cause mucormycosis.
A

Rhizopum spp.
Rhizomucor spp.
Mucor spp.

36
Q
  1. How is mucormycosis managed?
A

SURGICAL EMERGENCY
Refer to ENT for debridement
May need high-dose amphotericin

37
Q
  1. What are the three targets of antifungals?
A

Cell membrane
DNA/RNA synthesis
Cell wall

38
Q
  1. List antifungals that target:
    a. Cell membrane

b. DNA/RNA synthesis
c. Cell wall

A 
a.	Cell membrane 
Polyene – amphotericin B, nystatin
Azole – ketoconazole, itraconazole, fluconazole, clotrimazole
b.	DNA/RNA synthesis
Flucytosine (pyrimidine analogue)
c.	Cell wall
Echinocandins – caspofungin acetate
39
Q
  1. What is the mechanism of action of azoles?
A

Inhibit ergosterol production by inhibiting CYP450 enzyme lanosterol 14 alpha-demethylase
This inhibition leads to the accumulation of toxic steroids in the cell membrane which cause cell death

40
Q
  1. What are the consequences of cross-reaction of azoles with other CYP450 enzymes?
A

Drug interactions

Impairment of steroidogenesis

41
Q

Which fungi are polyenes effective against?

A

all fungi except Aspergillus terreus and scedosporium

42
Q

What is a side effect of polyenes

A

nephrotoxicity

Renovascular – decrease in renal blood flow leads to reduced GFR (azotaemia)
Tubular – distal tubular ischaemia, wasting of sodium, potassium and magnesium

43
Q
  1. What is the mechanism of action of echinocandins?
A

cyclic lipopeptide antibiotic that inhibits beta-(1,3) D-glucan synthase
This enzyme is responsible for the production of beta D-glucan which is a component of the fungal cell wall
This inhibition results in osmotic fragility of the cell

44
Q
  1. Which fungi are echinocandins active against e.g. Caspofungin?
A 
Candida species
Aspergillus species (NOT other moulds)
45
Q
  1. What is the main polyene antifungal?
A

Amphotericin B

46
Q
  1. How is amphotericin packaged in most formulations?
A

Put in liposomes to try and reduce toxicity and improve penetration

e.g. ambisome - amphotericin within a phospholipid bilayer

47
Q
  1. Describe the mechanism of action of amphotericin B.
A

Binds to ergosterol in the fungal cell membrane and creates transmembrane channels leading to electrolyte leakage
This leads to fungal cell death

48
Q

What are the sifde effect of azoles?

A

impaired LFT

49
Q
  1. Describe the mechanism of action of flucytosine.

Mechanisms of resistance?

A

Inhibits DNA synthesis (pyrimidine analogue)

Decreased uptake (permease activity)
Altered 5-FC metabolism
50
Q
  1. Which fungi are flucytosine active against?
A

Candidiasis

Cryptococcosis

micropath (10 decks)

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