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PathY5 > Fungal Infections > Flashcards

Fungal Infections Flashcards

1
Q

What are fungi?

A

Eukaryotic organisms with chitinous cell walls and ergosterol containing plasma membranes and 80s RNA

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2
Q

What is the difference between a yeast and a mould?

A

Yeasts – single celled, reproduce by budding

Moulds – multicellular hyphae, grow by branching and extension

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3
Q

Give some examples of yeasts

A

– Candida
– Cryptococcus
– Histoplasma (dimorphic- mould at low temp and yeast at high temp)

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4
Q

Give some examples of moulds

A

– Dermatophytes
– Aspergillus
– Agents of mucormycoses

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5
Q

What is the most common fungal infections in humans?

A

Candida spp

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6
Q

How many Candida species are there?

A

> 150 Candida spp., but < 10 are human pathogens

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7
Q

What are the clinical manifestations of candida?

A

– Acute, subacute, chronic, episodic

– Superficial or systemic/invasive

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8
Q

What are the superficial candida infections?

A 
• Oral thrush
• Candida oesophagitis
• Vulvovaginitis
• Cutaneous
– Localised or generalised
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9
Q

What is the treatment of Oral thrush?

A

Topical nystatin

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10
Q

What is the treatment of vulvovaginitis?

A

Topical clotrimazole or oral fluconazole

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11
Q

What is the treatment of local cutaneous candida?

A

Topical clotrimazole

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12
Q

What is the treatment of oesophagitis?

A

Oral fluconazole

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13
Q

What are the risk factors for candidaemia?

A

– Malignancies, esp haematological
– Burns patients
– Complicated post-op courses (eg Tx or GIT Sx)
– Long lines

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14
Q

What is the management of candidaemia?

A

Source Control: Look for source and signs of dissemination: Imaging, Serology for beta-D-glucan, ECHO, Fundoscopy. REMOVE LINES AND PROSTHETICS

Systemic intervention: Antifungals for at least 2/52 (from date of first –ve BC) – Echinocandin eg anidulafungin (whilst a/w identification and susceptibilities)

•Blood Culture every 48 hours

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15
Q

How do you treat invasive CNS candida?

A

Ambisome/ voriconazole

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16
Q

How do you treat candida endocarditis (from valve issues/ long lines/ IVDU) and candida bone and joint infection?

A

Ambisome/ voriconazole and symptomatic treatment

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17
Q

How do you treat UTI with candida (vulvovaginitis/ catheter associated)?

A

Fluconazole

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18
Q

How do you treat intra abdominal candida?

A

Echinocandin/ Fluconazole

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19
Q

What is cryptococcus?

A

Encapsulated yeast
Serotypes A&D = neoformans
Serotypes B&C = gattis

Aerosol transmission

Chronic, subacute to acute pulmonary, meningitic or systemic disease

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20
Q

Which animal is cryptococcus associated with?

A

Pigeons

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21
Q

What are the risk factors for cryptococcosis?

A

• Impaired T-cell immunity
– E.g patients with HIV, who have reduced CD4 helper T-cell numbers (typically less than 200/ml)

• Patients taking T-cell immunosuppressants for solid organ transplant also have a 6%
lifetime risk

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22
Q

When does C gatti happen?

A
  • Causes a meningitis in apparently immunocompetent individuals in tropical latitudes, esp. SE Asia and Australia
  • Outbreak in Vancouver Island 2004
  • High incidence of space-occupying lesions in brain and lung
  • Increased resistance to amphotericin B clinically
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23
Q

What type of ink is used for a cryptococcal stain?

A

India ink

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24
Q

How do you diagnose cryptococcal disease?

A
  • Typical clinical history/features – Immunosuppressed host
  • Imaging
  • India ink staining of CSF
  • Serum/CSF cryptococcal Ag (CRAG)
  • Can culture from blood/body fluids
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25
Q

How do you manage cryptococcal disease?

A
  • Induction: Amphotericin B + flucytosine (at least 2/52)
  • Consolidation: High dose fluconazole (at least 8/52)
  • Maintenance: Low dose fluconazole (at least 1 year). Repeat LP for pressure management.
  • Pulmonary disease: If mild, fluconazole alone
26
Q

What is aspergillosis?

A

A mould with worldwide distribution

27
Q

What diseases can aspergillus cause?

A

– Mycotoxicosis - ingestion of contaminated foods
– Allergy and sequelae - presence of conidia/transient growth of the organism in body orifices
– Colonization - in preformed cavities and debilitated tissues
– invasive, inflammatory, granulomatous, necrotizing disease of lungs, and other organs
– systemic and fatal disseminated disease

28
Q

How do you diagnose an aspergilloma/ aspergillus disease in the lung?

A
  • Imaging
  • Sputum/BAL – MC&S, Ag testing
  • Aspergillus Abs (precipitans)
  • Galactomannan
  • Bx – histology, MC&S
29
Q

What is the management of aspergillus?

A 
• Voriconazole
• Ambisome
• Duration based on host/radiological/mycological factors
– At least 6/52
• Sx
30
Q

What is pneumocystis jiroveci?

Why is it different to other fungi?

A

• Ubiquitous fungus in the environment and distributed worldwide

• Acquisition by airborne route
– Pneumonia
– Extrapulmonary disease = rare

• Lacks ergosterol in it’s cell wall

31
Q

What are the risk factors for P jiroveci?

A

– Immunodeficiency
– Immunosuppressive drugs
– Debilitated infants
– Severe protein malnutrition

32
Q

How do you diagnose P. jiroveci?

A

– Microscopy
– PCR
– Beta-D-glucan

33
Q

What is the management of P. jiroveci?

A

– High dose cotrimoxazole 2-3/52
– Alternatives: atovaquone, clindamycin + primaquine
– Steroids if hypoxia present

34
Q

Why might antifungals targeting the cell membrane not work in PCP (P jiroveci)?

A

It lacks ergosterol in it’s cell wall

35
Q

What is mucormycoses?

A
  • Clinical syndrome caused by a number of fungal species belonging to the order Mucorales eg Rhizopus, Rhizomucor, Mucor
  • Inoculation via inhalation of spores or primary cutaneous inoculation
  • Favours immunosuppressed/diabetic patients
36
Q

What are the clinical features of mucormycoses?

A

• Rhinocerebral => CNS
– Cellulitis of the orbit and face + black pus from the palate and nose.
– Eyes: proptosis, chemosis, ophthalmoplegias and blindness.
– Decreasing levels of consciousness.

  • Pulmonary
  • Cutaneous
37
Q

How do you diagnose mucormycoses?

A

– Isolation from tissue Bx

38
Q

What is the management of mucormycoses?

A

– Ambisome/Posaconazole
– Sx
– Rx guided by response

39
Q

What are dermatophytes?

A
  • A group of fungi capable of invading dead keratin of skin, hair and nails
  • Classified by site infected e.g tinea capitis
  • Spread via contact with desquamated skin scales
40
Q

What are the risk factors for dermatophytes?

A

– Moisture
– Deficiencies in cell mediated immunity
– Genetic predisposition

41
Q 
Where do:
Tinea cruris
Tinea corporis
Tinea pedis
Tinea capitis
Target?
A

Groin
Abdomen
Foot
Scalp

42
Q

What is the diagnosis of dermatophytes?

A

– Skin scrapings, nail specimens and plucked hairs

• MC&S

43
Q

What is the management of dermatophytes?

A

– Topical eg clotrimazole, ketoconazole

– Oral eg griseofulvin, terbinafine, itraconazole

44
Q 
What is the most associated side effect of:
Azoles
Polyenes
Echinocandins
Pyrimidine analogues
A

Abnormal LFTs
Nephrotoxicity
Relatively innocuous
Blood disorders

45
Q

What are the targets for antifungal therapy?

A

Cell wall -Echinocandins (e.g. caspfungins)

Cell membrane - Polyene Abx, Azole antifungals

DNA synthesis - Pyramidine analogues (flucytosine)

46
Q

What is in the fungal cell membrane?

A

Ergosterol rather than cholesterol

47
Q

How may DNA synthesis be targeted by antifungal therapy?

A

Selective activation in fungi

48
Q

How can the cell wall in fungi be targeted?

A

Mammalian cells do not have a cell wall

49
Q

What do azoles do?

A

• In fungi, the cytochrome P450-enzyme lanosterol 14-a demethylase is responsible for
the conversion of lanosterol to ergosterol

• Azoles bind to lanosterol 14a-demethylase inhibiting the production of ergosterol

50
Q

What is a caution with azoles?

A

Some cross-reactivity is seen with mammalian cytochrome p450 enzymes
• Drug Interactions
• Impairment of steroidneogenesis (ketoconazole, itraconazole)

51
Q

What are polyenes?

A

Abx e.g. Amphotericin B

  • Fermentation product of Streptomyces nodusus
  • Binds sterols in fungal cell membrane
  • Creates transmembrane channel and electrolyte leakage
  • Active against most fungi except Aspergillus terreus, Scedosporium spp.
52
Q

How do polyenes cause nephrotoxicity?

A

Delayed toxicity-

  1. Vascular-decrease in renal blood flow leading to drop in GFR, azotemia
  2. Tubular-distal tubular ischemia, wasting of potassium, sodium, and magnesium

WORSE IN PTS WHO ARE VOLUME DEPLETED/ OTHER NEPHROTOXIC DRUGS

53
Q

Why is amphotericin B bad?

A

Classic amphotericin B deoxycholate (Fungizone™) formulation: serious toxic side effects

54
Q

What are the less toxic formulations of amphotericin B?

A

1) Liposomal amphotericin B
2) Amphotericin B colloidal dispersion
3) Amphotericin B lipid complex

55
Q

What are echinocandins?

A

• Cyclic lipopeptide antibiotics that interfere with fungal cell wall synthesis by
inhibition of ß-(1,3) D-glucan synthase
• Loss of cell wall glucan results in osmotic fragility

56
Q

What is the spectrum of coverage for echinocandins?

A

• Spectrum:
– Candida species including non-albicans isolates resistant to fluconazole
– Aspergillus spp. but not activity against other moulds (Fusarium, Zygomycosis)
– No coverage of Cryptococcus neoformans

57
Q

Why is flucytosine bad?

A

Restricted spectrum of activity

Resistance (rapid/ in monotherapy)

58
Q

How does resistance occur to flucytosine?

A

– Decreased uptake (permease activity)

– Altered 5-FC metabolism (cytosine deaminase or UMP pyrophosphorylase activity)

59
Q

What use is flucytosine?

A

Candida

Cryptococcus (with Ambisome/ fluconazole)

60
Q

What are the side effects of flucytosine?

A

Infrequent – include D&V, alterations in liver function tests and blood disorders.

61
Q

How do you monitor flucytosine?

A

Blood concentrations need monitoring when used in conjunction with Amphotericin B

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