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Year 5 Path Charis > Micro 8 - Fungal infections > Flashcards

Micro 8 - Fungal infections Flashcards

1
Q

Fungal cell walls
Plasma membranes
Ribosomes

A

cell walls contain chitin

plasma membranes contain ergosterol (except Pneumocystis jiroveci)

ribosomes are 80s RNA

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2
Q

yeast vs mould

A

o Candida – most common yeast + commonest cause of fungal infections in humans
o Cryptococcus
o Histoplasma (dimorphic)
 Dimorphic – change between yeasts and moulds
 Low temperature – mould, high temperature – yeast
 Yest during infection, mould in nature

• Moulds – multicellular hyphae, grow by branching and extension of hyphae
o Aspergillus
o Dermatophytes
o Agents of mucormycosis

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3
Q

Aspergillus buzzwords

presentation
mainstay of dx
how to determine type
stain
antigen
A 
pneumonia in immunocompromised
Aspergilloma formation (haemoptysis) in patients w PMH of TB

Microscopy - mainstay of dx

Spores - type of Aspergilllus

Stain - methamine silver

Antigen - Galactomannan

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4
Q

Cryptococcus buzzwords

animal
presentation
MRI
ix

A

birds, pigeons

AIDs defining illness
meningitis, pneumonia in HIV/ immunosuppressed

MRI - multiple cryptococcomas in the brain

india ink stain
CSF/serum cryptococcal antigen
very high opening pressures on LP
massive capsule around the yeast on microscopy which doesnt stain with india ink

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5
Q

Which agar, which stain and which assay can be used for candida?

A

Sabouraud agar

Periodic Acid Schiff stain (PAS)

Beta-D Glucan assay

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6
Q

Candida mx

– Oral thrush
– Vulvovaginitis
– Localised cutaneous
– Oesophagitis

A

Topical
– Oral thrush: nystatin
– Vulvovaginitis: cotrimazole
– Localised cutaneous: cotrimazole

Oral
– Vulvovaginitis: fluconazole
– Oesophagitis: fluconazole

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7
Q

Candidemia mx

A

2/52 antifungals from date of first -ve BC

echinocandin e.g. anidulafungin

BC every 48h until they have 2 persistently negative ones

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8
Q

mx of candidemia in

CNS
endocarditis
bones and joints
UTI

A

Mx - ambisome/ voriconazole
CNS
endocarditis
bone and joints

UTI
Fluconazole

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9
Q

Cryptococcus mx

A

o Induction – amphotericin B + flucytosine (at least 2/52)
o Consolidation – high dose fluconazole (at least 8/52)
o Maintenance – low dose fluconazole (at least 1 year)

o Repeat LP (pressure management from chance of hydrocephalus)
o Pulmonary disease – if mild, fluconazole alone

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10
Q

• You are the FY1 on a respiratory ward. Your consultant has referred a patient from
clinic who is experiencing heamoptysis and weight loss. PMHx includes treated
pulmonary TB.

A

• PMHx of TB – left a cavity – aspergillus grew in the cavity and formed an aspergilloma  invades into surrounding tissues and pulmonary vessels  causes massive haemoptysis

(aspergillus colonises without extension in preformed cavities and debilitated tissues – can cause aspergilloma )

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11
Q

Aspergillus mx

A

amphotericin B + voriconazole

at least 6/52

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12
Q

Pneumocystis jiroveci typical presentation + typical XR

A

Desaturation on walking

Bilateral infiltrates
Fine reticular appearance

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13
Q

Pneumocystis jiroveci stain

A

Methamine silver

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14
Q

Pneumocystis jiroveci mx

A

High-dose cotrimoxazole 2-3/52

Steroids if hypoxia

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15
Q

• Why might antifungals targeting cell membrane not work in PCP?

A

o It lacks ergosterol in its cell wall

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16
Q

How do mucormycoses present and which patients do they target?

A

target diabetic patients

 Cellulitis of the orbit + face which progresses, extends into the brain
 Discharge of black pus from palate and nose
 Black eschars may be seen as the fungus invades and destroys the tissues
 Retro-orbital extension  proptosis, chemosis, ophthalmoplegias, blindness
 Decreasing level of consciousness (invasion of brain = rhinocerebral mucormycosis)

 Think about it when Severe orbital sinus disease esp. in diabetic patients

17
Q

mucormycoses mx

A

Surgical ENT emergency- debridement of all dead tissue

high dose amphotericin B or posaconazole

18
Q

Dx of

Candida 
Crypotococcus
Aspergillosis
PCP 
Mucormycoses 
Dermatophytes
A

Candida - swabs, blood cultures, beta d glucan assay, imaging

Crypotococcus - CSF stain, serum/CSF cryptococcal ag, culture, microscopy

Aspergillosis - imaging, sputum MCS + Ag testing, biopsy

PCP microscopy, pcr, beta d glucan

Mucormycoses - tissue biopsy

Dermatophytes - MCS skin scrappings/ nail specimens/ plucked hairs

19
Q

Pityriasis versicolor causative agent (dermatophyte)

A

Pityriasis versicolor – Malassezia furfur

20
Q

causative dermatophytes

tinea pedis 
tinea capitis
 tinea cruris 
tinea corporis
Nails
A

o Foot (athlete’s foot) – tinea pedis – Trichophyton rubrum, Trichophyton interdigitale, Epidermophyton flocosum (less common)

o Scalp – tinea capitis – T rubrum or T Tonsurans

o Groin – tinea cruris – T rubrum or Epidermophyton floccosum

o Abdomen – tinea corporis – several causes, ringworm

o Nails – onychomycosis – Trichophyton spp, Epidermophyton spp, Microsporum spp

21
Q

Dermatophytes mx

A

o Topical – clotrimazole, ketoconazole

o Oral – griseofluvin, terbinafine, itraconazole

22
Q

• Side effects associated with antifungals

o Echinocandins
o Azoles
o Polyenes
o Pyrimidine analogues

A

o Echinocandins – relatively innocuous

o Azoles – abnormal LFTs

o Polyenes – Nephrotoxicity

o Pyrimidine analogues – blood disorders

23
Q

How do azole antifungals work?

A

target cell membrane

o Lanosterol  ergosterol by Lanosterol 14-a demethylase (CYP450 enzyme)
o Azole binds to lanosterol 14-a demethylase inhibiting production of ergosterol

24
Q

Where are the following azoles used?

o Water-Soluble Triazoles
 Fluconazole
 Voriconazole

o Lipophilic Triazoles
 Itraconazole
 Posaconazole

A

o Water-Soluble Triazoles
 Fluconazole (against Candida and Cryptococcus)
 Voriconazole (similar to fluconazole but has improved activity against Aspergillus)

o Lipophilic Triazoles
 Itraconazole (against dermatophytes)
 Posaconazole (against Mucor)

25
Q

Polyene antifungals

examples
MOA

A

Amphotericin B, Nystatin

o Binds sterols in fungal membrane
o Creates transmembrane channel and electrolyte leakage + also causes cells to lyse  cell death

26
Q

How do polyene antifungals cause nephrotoxicity

A

Vascular-decrease in renal blood flow leading to drop in GFR, azotemia

Tubular-distal tubular ischemia
Wasting of potassium, sodium, and magnesium

27
Q

Where and how do echinocandins work?

A
  • Target fungal cell wall synthesis by inhibition of β(1,3) D-glucan synthase
  • Loss of cell wall glucan  osmotic fragility

 Candida aspergillus
Important: Cryptococcus in inherently resistant to echinocandins

28
Q

Give an example of a pyrimidine analogue, its MOA and why resistance has been developed

A

Flucytosine

candida crptococcus

Inhibits fungal DNA synthesis

 Permease activity  Decreased uptake
 Cytosine deaminase or UMP pyrophosphorylase activity  Altered 5-FC metabolism

29
Q

look at tables on p67

A

good summary of drugs

30
Q

risk factors for fungal disease

A

– Immunodefficiency, immunosuppresive meds
– Inhaled steroids
– Malignancy, burns, complicated post op, long lines – invasive candida
– Diabetes – mucormycosis
– Moisture, genetics, CMI - dermatophyte

Year 5 Path Charis (44 decks)

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