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Micro 5: Fungal infections Flashcards

1
Q

What are examples of yeast?

A

Candida, Cryptococcus, and Histoplasma (dimorphic)

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2
Q

What are examples of moulds?

A

Aspergillus, Dermatophytes, agents of mucormycosis

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3
Q

What is a dimorphic fungi?

A

Some fungi are dimorphic and can change between being yeast and moulds

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4
Q

What is the most common yeast?

A

Candida

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5
Q

How does Candida look and how does it replicate?

A

They form individual cells (a bit like bacteria but much bigger). They replicate by budding. Candida grow in colonies (a bit like bacteria).

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6
Q

What is Candidiasis and what can it affect?

A

It is a primary or secondary mycotic infection caused by members of the genus Candida. It can affect the mouth, perineum, scalp, skin, vagina, nails, lungs and GI tract.

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7
Q

How can Candidiasis become systemic?

A

It can become systemic as in septicaemia, endocarditis and meningitis.

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8
Q

Who is more likely to get systemic candida infections?

A

VLBW infants are more likely to get systemic candida infections

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9
Q

What treatment may infants with systemic candida infection require?

A

They may require fluconazole and nystatin prophylaxis.

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10
Q

Who is more likely to get invasive candidiasis?

A
  1. Immunocompromised patients are more likely to get invasive candidiasis.
  2. Patients on ITU with lots of lines in (e.g. central lines) are also at risk because Candida is very good at forming biofilms and colonising prosthetic material.
  3. More common in people receiving TPN.
  4. Immunocompetent people can get candidiasis receiving antibiotic therapy because the antibiotics will kill the commensals
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11
Q

Where is candidiasis found?

A

This disease is found world-wide

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12
Q

What aetiological agents cause candidiasis?

A

Candida albicans (MOST COMMON), Candida glabrata, Candida krusei, Candida tropicalis, and many others. All of them are ubiquitous and occur naturally in humans.

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13
Q

Are the yeast causing candidiasis sensitive to antifungals?

A

Candida albicans is sensitive to all the first line antifungals. On the other hand, C. glabrata and C. krusei are resistant to a lot of first-line drugs.

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14
Q

Why aren’t cultures ideal to screen for candidiasis/fungal infections?

A

Early identification of the fungal guides treatment. Candida albicans forms a germ tube whereas the other types will not. Yeasts take a lot longer than bacteria to grow colonies so doing cultures will take much more time. This is why an alternative identification system is needed.

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15
Q

What organs does systemic candidiasis involve?

A

Can involve the liver and the spleen. Candida can also affect the eyes causing endophthalmitis.

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16
Q

How does generalised candidiasis present in babies?

A

This is often secondary to seborrhoeic dermatitis. It can often affect the folds of the skin - called intertrigo. (In immunocompromised patients candida can also invade tissues).

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17
Q

How is candida diagnosed?

A

Swabs, blood cultures for candidaemia using a selective agar plate (Sabourard agar), Beta-D Glucan assay and imaging

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18
Q

Why must you use a selective agar plate for Candida?

A

Candida is often outcompeted in cultures because bacteria grow more quickly. So, a selective agar plate that is impregnated with antibiotics is usually used (Sabouraud agar). Therefore, if you are suspicious that someone has a Candida infection then you should say so when you send the sample. Grows in about 48 hours.

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19
Q

What is the management for candidiasis?

A

Treat for at least 2 weeks of antifungals from the first negative blood cultures. Echo and fundoscopy (look for endocarditis and endophthalmitis). Echinicandins are used empirically and for non-Candida infections. Fluconazole is still effective for Candida albicans. May need to use a certain type of antifungal because of its pharmacokinetics/pharmacodynamics

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20
Q

Echinicandins don’t penetrate well into the CNS, what can you use instead?

A

Ambisome

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21
Q

What is cryptococcus?

A

A chronic, subacute to acute pulmonary, systemic or meningitic disease, initiated by the inhalation of a fungus. Primary pulmonary infections are usually subclinical.

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22
Q

What does cryptococcus show a predilection for?

A

On dissemination, the fungus usually shows a predilection for the CNS

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23
Q

What treatments can be used for cryptococcus, and what is it resistant to?

A

It looks like a yeast and will stain similarly but it is inherently resistant to echinicandins. It is susceptible to fluconazole and amphotericin. Treatment of choice: ambisome

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24
Q

What is the aetiological agent for cryptococcus?

A

Cryptococcus neoformans

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25
Who is susceptible to cryptococcosis?
Patients with impaired T cell immunity; AIDS patients with very low CD4+ counts (typically <200 m/L) - second most common cause of death in AIDS; patients taking immunosuppressants for solid organ transplant also have 6% lifetime risk.
26
What happens in Cryptococcus neoformans var. gatii and who gets it?
It causes meningitis in apparently immunocompetent individuals in tropical latitudes (especially SE Asia and Australia). There is a high incidence of space-occupying lesions in the lung and brain. Recent outbreak in Vancouver Island.
27
What does Cryptococcus neoformans var. gatii have an increased resistance to?
Increased resistance to amphotericin B.
28
What is the life cycle of Cryptococcus?
The spores are ubiquitous. (Originating from eucalyptus tree and bird excreta?) It will be inhaled and then, in immunocompromised patients, it will disseminate. There is a predilection for the central nervous system.
29
What is used to stain cryptococcus and how does it look like under microscopy?
Cryptococcus has a very distinct capsule around the yeast. India ink is used to stain for Cryptococcus. The ink will stain everything black except for the capsule around the yeast. The capsule is NOT always present (if the organism is not under any form of stress it will not need the capsule (e.g. in blood cultures)). India ink is not used very frequently anymore.
30
What has replaced ink staining to detect cryptococcus?
Instead, an enzyme immunoassay (EIA) to look for components of the capsule are used now. (Cryptococcus can grow in culture but the antigen test is much quicker).
31
How is cryptococcus diagnosed?
- Mainly relies on the antigen test. - Typical clinical features (pulmonary infection or meningitis) - Immunocompromised host. - Often culturable from blood and bodily fluids - IMPORTANT: Cryptococcal meningitis can cause hydrocephalus which prevents the circulation of CSF so that the sample you take from an LP is not mixing with the CSF in the brain
32
How is cryptococcus managed?
1. 3 weeks of amphotericin B with or without flucytosine 2. Repeat LP for pressure management 3. Secondary suppression with fluconazole 4. High dose fluconazole may be effective 5. KEY POINT: echinicandins are used as empirical therapy for Candida infections, however, Cryptococcus is resistant to echinicandins
33
What is aspergillosis caused by?
Aspergillosis is a spectrum of diseases of humans and animals caused by members of the genus Aspergillus
34
In aspergillosis, what diseases are included?
Mycotoxicosis due to ingestion of contaminated foods. Allergy (e.g. wheeze). Colonisation without extension in preformed cavities (e.g. Aspergillus can colonise a cavity that was produced by TB). Invasive disease. Systemic and fatal disseminated disease..
35
What are the aetiological agents in aspergillosis?
Aspergillus fumigatus, Aspergillus favus, Aspergillus niger, Aspergillus niduland, Aspergillus terreus.
36
How is aspergillosis diagnosed?
Diagnosis: blood test, serology (look for IgE, antigen detection (galactomannan), can be detected in BAL fluid), PCR, histology, culture. Microscopy is still the mainstay of diagnosis - by looking at the type of spores that the Aspergillus is producing you can determine the type of Aspergillus. Aspergillus is a mould and it takes a reasonably long time to grow (1 week). You cannot identify the species based on the hyphae, however, you can by looking at the spores.
37
Who do fungus balls form in?
In TB patients in previous TB regions. Normal tissues is usually quite resistant to invasion by Aspergillus. Invasive Aspergillus infection is more common in immunocompromised patients (especially haematology patients e.g. leukaemia).
38
How is aspergillosis managed?
NOTE: fluconazole has POOR activity against moulds. Voriconazole; ambisome; caspofungin/itraconazole is less good; amphotericin is the mainstay of treatment (broad-spectrum with good activity against Aspergillus). At least 6 weeks of therapy. Duration is based on host/radiological/mycological factors.
39
What are examples of dermatophyte infections?
These are very common. Examples include: ringworm, tinea and nail infections.
40
What are aetiological agents in tinea pedis (Athlete's foot)?
Trichophyton rubrum, Trichophyton interdigitale, and Epidermophyton floccosum (LESS COMMON).
41
What are the aetiological agents in tinea cruris (in the groin area)?
Trichophyton rubrum, Epidermophyton floccosum
42
What does tinea corporis look like (on the body)?
Caused by ringworm. Annular lesion.
43
What are the aetiological agents in tinea capitis?
Trichophyton rubrum, Trichophyton tonsurans.
44
What are the aetiological agents in onchomycosis (thickened nails)?
Trichophyton spp., Epidermophyton spp., Microsporum spp.
45
How is onchomycosis diagnosed?
Skin scraping. The organisms are then cultured (can take up to 4 weeks to grow). Microscopy is used to identify organisms.
46
How is onchomycosis treated?
May require long course of treatment. Usually treated with nail lacquers. If this does not work, systemic treatment with turbinafine. Itraconazole may be used.
47
What causes pityriasis versicolor?
Caused by Malassezia furfur
48
Who does mucormycosis affect?
This is a group of moulds that can cause very severe and invasive disease. Affects: immunocompromised patients and poorly controlled diabetics.
49
How is mucormycosis characterised? What are the effects?
Characterised by cellulitis of the orbit and face which progresses with discharge and black pus from the palate and nose. Black eschars may be seen as the fungus invades and destroys the tissues. Retro-orbital extension produces proptosis, chemosis, ophthalmoplegias and blindness. As the brain is involved, it can cause decreasing levels of consciousness. Invasion of the brain is called rhinocerebral mucormycosis.
50
What are the aetiological agents in mucormycosis?
Rhizopum spp., Rhizomucor spp., Mucor spp.
51
What is the management for mucormycosis?
IMPORTANT: this is mainly a SURGICAL EMERGENCY because all the dead and necrotic tissue needs to be debrided. It requires early referral to ENT. Antifungal agents may be used: amphotericin (HIGH DOSE), posaconazole.
52
What do antifungals target?
Cell membrane (fungi use principally ergosterol instead of cholesterol), DNA synthesis (some compounds may be activated by fungi, arresting DNA synthesis), cell wall (unlike mammalian cells, fungi have a cell wall).
53
What are examples of cell membrane antifungals?
Polyene ABx (e.g. amphotericin B, lipid formulations, nystatin - topical); azole antifungals (ketoconazole, itraconazole, fluconazole, voriconazole, and miconazole and clotrimazole - and other topicals).
54
What are examples of DNA/RNA synthesis antifungals?
Pyrimidine analogues (flucytosine)
55
What are examples of cell wall antifungals?
Echinocandins e.g. caspofungin acetate
56
What is the mechanism of action of azoles?
1. Inhibit ergosterol production. 2. They do this by inhibiting cytochrome P450 enzyme lanosterol 14-alpha demethylase which converts lanosterol to ergosterol 3. There is some cross-reactivity with mammalian CYP450 enzymes 4. This can lead to drug interactions and impairment of steroidogenesis (ketoconazole, itraconazole) 5. By inhibiting the ergosterol pathway, you will get an accumulation of toxic steroids in the cell membrane which will result in cell death.
57
What are the different types of azoles?
Water-soluble triazoles e.g. fluconazole, voriconazole. Lipophilic triazoles e.g. itraconazole and posaconazole.
58
What is fluconazole good against?
Water-soluble triazole, good against Candida and Cryptococcus.
59
What is voriconazole good against?
Water-soluble triazole, similar to fluconazole but has improved activity against Aspergillus.
60
What is itraconazole useful against?
Lipophilic triazole, useful against dermatophytes
61
What is posaconazole good against?
Lipophilic triazole, has activity against mucor.
62
What are examples of echinocandin antifungals?
Caspofungin, micafungin and anidulafungin.
63
What is resistant to echinicandins?
Cryptococcus is inherently RESISTANT to echinicandins
64
What is the mechanism of action of echinicandins?
Cyclic lipopeptide antibiotic. It inhibits Beta-(1,3) D-glucan synthase. This inhibits production of Beta-D glucan which is a component of the fungal cell wall. (This leads to depletion of beta(1,3) glucans in cell wall). This results in osmotic fragility.
65
What are echinicandin antifungals active against?
Candida species (including non-albicans isolates that are resistant to fluconazole). Aspergillus species (but NOT other moulds e.g. Fusarium, Zygomycosis). NO coverage for Cryptococcus neoformans.
66
What is the main polyene in polyene antifungals?
Amphotericin B
67
How does amphotericin B (antifungal) stored?
It is put into liposomes in a lot of different formulations to try and reduce toxicity and improve penetration. E.g. Ambisome has amphotericin within a phospholipid bilayer.
68
How is Amphotericin B produced?
It is a fermentation product of Streptomyces nodusus.
69
How does Amphotericin B work?
It is put into liposomes e.g. Ambisome has amphotericin within a phospholipid bilayer. Amphotericin B binds to ergosterol in the fungal cell membrane. This creates transmembrane channels leading to electrolyte leakage. This leads to fungal cell death.
70
What are polyene antifungals active against?
Active against most fungi except Aspergillus terreus and Scedosporium spp.
71
What is the original formulation of amphotericin B and why is it not used?
The original formulation of amphotericin B is amphotericin B deoxycholate (Fungizone). However, this has serious toxic side-effects (e.g. nephrotoxicity)
72
What are less toxic preparations of amphotericin B?
Liposomal amphotericin B, amphotericin B colloidal dispersion and amphotericin B lipid complex.
73
What should you be aware of with amphotericin?
1. Nephrotoxicity. Most significant delayed toxicity. 2. Renovascular and tubular mechanisms involved. Vascular - decrease in renal blood flow leading to a drop in GFR (azotaemia); and tubular - distal tubular ischaemia, wasting of sodium, potassium and magnesium. 3. Nephrotoxicity enhanced in patients who are volume-depleted or who are on concomitant nephrotoxic agents.
74
How does flucytosine work?
Restricted spectrum of activity. Inhibits DNA in the fungal cells.
75
What is resistance to flucytosine due to?
Decreased uptake (permease activity) and altered 5-FC metabolism (cytosine deaminase or UMP pyrophosphorylase activity).
76
What are clinical uses of flucytosine?
Monotherapy is now limited. Used in candidiasis and cryptococcosis (in combination with amphotericin B or fluconazole).
77
What are the side effects of flucocytosine?
Infrequent (D&V, changes in LFTs, blood disorders). Blood concentrations need monitoring when used in conjunction with amphotericin B.

MICRO - Abbie (19 decks)

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