Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology - Y5 > Introduction to Mycology > Flashcards

Introduction to Mycology Flashcards

1
Q

What are fungi?

A

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

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

What are yeasts?

A

Single celled, reproduce by budding

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

What are some examples of yeasts?

A

Candida

Cryptococcus

Histoplasma (dimorphic)

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

What are moulds?

A

Multicellular hyphae, grow by branching and extension

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

What are some examples of moulds?

A

Dermatophytes

Aspergillus

Agents of mucormycoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which is the commonest cause of fungal infections in human?

A

Candida spp

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

What is Candida Spp.?

A

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

Clinical manifestations:

  • Acute, subacute, chronic, episodic
  • Superficial or systemic/invasive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is this?

A

Oral candidiasis

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

What is this?

A

Candidal intertrigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are superficial Candida infections?

A
  • Oral thrush
  • Candida oesophagitis
  • Vulvovaginitis
  • Cutaneous – Localised or generalised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the topical management for Candida?

A

Oral thrush: Nystatin

Vulvovaginitis: Cotrimazole

Localised cutaneous: Cotrimazole

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

What is the oral management for Candida?

A

Vulvovaginitis: Fluconazole

Oesophagitis: Fluconazole

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

What are risk factors for Candidaemia?

A

Malignancies, esp haematological

Burns patients

Complicated post-op courses (e.g. Tx or GIT Sx)

Long lines

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

What is the general management for fungal infections?

A

Look for source and signs of dissemination:

  • Imaging
  • Serology for beta-D-glucan
  • ECHO
  • Fundoscopy

Antifungals for at least 2/52 (from date of first –ve blood culture): Echinocandin e.g. anidulafungin (whilst a/w identification and susceptibilities)

Blood culture every 48 hours

REMOVE ANY LINES/PROSTHETIC MATERIAL

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

What are some invasive Candida infections?

A

Candidaemia

CNS: Dissemination, trauma, Sx
Rx: Ambisome/voriconazole

Endocarditis: Abnormal valves/prosthetic valves, long lines, IVDU
Rx: Ambisome/voriconazole, Sx

Urinary tract: Vulvovaginits, catheters
Rx: Fluconazole

Bone and joint: Dissemination. Trauma
Rx: Ambisome/voriconazle, Sx

  • *Intra-abdominal:** Peritoneal dialysis, Sx, perforation
  • *Rx:** Echinocandin/Fluconazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Cryptococcus spp and how is it transmitted?

A

Encapsulated yeast:

  • Serotypes A&D = C neoformans (immunodeficient)
  • Serotypes B&C = C gattii (immunocompetent)

Transmission by inhalation of aerosolised organisms.

Chronic, subacute to acute pulmonary, meningitic or systemic disease.

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

Which animal is cryptococcus associated with?

A

Pigeons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are risk factors for cryptococcus?

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is C. Gatti?

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of ink is used for a cryptococcal stain?

A

India

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are appropriate investigations for cryptococcus?

A

Typical clinical history/features: Immunosuppressed host

Imaging

India ink staining of CSF

Serum/CSF cryptococcal Ag (CRAG)

Can culture from blood/body fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the management for cryptococcus?

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Aspergillosis?

A

A mould with worldwide distribution.

Causes a spectrum of disease in helath and immunocompromised patients:

  • 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.

Type of disease and severity depends upon the physiologic state of the host and the species.

24
Q

What is Aspergillosis associated with?

A

TB abscesses in the lung are most likely to be colonised by Aspergillosis.

25
What are appropriate investigations for Aspergillosis?
Imaging Sputum/BAL – MC&S, Ag testing Aspergillus Abs (precipitans) Galactomannan Bx – histology, MC&S
26
What is the management for Aspergillosis?
Voriconazole Ambisome Duration based on host/radiological/mycological factors – At least 6/52
27
What is Pneumocystis Jiroveci?
Ubiquitous in the environment and distributed worldwide. Lacks ergosterol in its cell wall. Acquisition by airborne route – Pneumonia. Extrapulmonary disease is very rare.
28
What are risk factors for Pneumocystis Jiroveci?
Immunodeficiency Immunosuppressive drugs Debilitated infants Severe protein malnutrition
29
What are appropriate investigations for Pneumocystis Jiroveci?
Microscopy PCR Beta-D-glucan
30
What is the management for Pneumocystis Jiroveci?
High dose cotrimoxazole 2-3/52 **Alternatives:** Atovaquone, clindamycin + primaquine Steroids if hypoxia present
31
Why might antifungals targeting the cell membrane not work in pneumocystis pneumonia (PCP)?
It lacks ergosterol in its cell wall
32
What is mucomycoses?
Clinical syndrome caused by a number of fungal species belonging to the order Mucorales e.g. Rhizopus, Rhizomucor, Mucor. Inoculation via inhalation of spores or primary cutaneous inoculation. Favours immunosuppressed/diabetic patients.
33
What are the clinical features of mucomycoses infection?
Rhinocerebral =\> CNS. * Cellulitis of the orbit and face progress with discharge of black pus from the palate and nose. * Retro-orbital extension produces proptosis, chemosis, ophthalmoplegias and blindness. * As the brain is involved, there are decreasing levels of consciousness. Pulmonary Cutaneous
34
What are appropriate investigations for mucomycoses?
Isolation from tissue Bx
35
What is the management for mucomycoses?
Ambisome/Posaconazole Symptomatic treatment guided by response
36
What are dermatophytes?
A group of fungi capable of ivading dead keratin of skin, hair and nails. Classified by site infected e.g. tinea capitis. Spread via contact with desquamated skin scales.
37
What are risk factors for dermatophytes?
Moisture Deficiencies in cell mediated immunity Genetic predisposition
38
On which sites do different tinea infections occur?
**Tinea pedis:** Foot **Tinea capitis:** Scalp **Tinea cruris:** Groin **Tinea corporis:** Abdomen
39
What are appropriate investigations for dermatophytes?
Skin scrapings, nail specimens and plucked hairs MC&S
40
What is the management for dermatophytes?
**Topical** e.g. Clotrimazole, ketoconazole **Oral** e.g. Griseofulvin, terbinafine, itraconazole
41
What are the side effects of azoles?
Abnormal LFTs
42
What are the side effects of polyenes?
Nephrotoxicity
43
What are the side effects of pyrimidine analogues?
Blood disorders
44
What are the side effects of echinocandins?
Relatively innocuous
45
What are the three common targets for antifungal therapy?
Cell membrane DNA synthesis Cell wall
46
Which antibiotics and antifungals target the cell membrane?
**Polyene antibiotics:** * Amphotericin B, lipid formulations * Nystatin (topical) **Azole antifungals:** * Ketoconazole * Itraconazole * Fluconazole * Voriconazole * Miconazole * Clotrimazole (and other topicals)
47
How do azoles work?
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. Some cross-reactivity is seen with mammalian cytochrome p450 enzymes: * Drug Interactions * Impairment of steroidneogenesis (ketoconazole, itraconazole)
48
How do polyenes (e.g. Amphotericin B) work?
Amphotericin B is a fermentation product of Streptomyces nodusus. It binds sterols in fungal cell membrane and creates transmembrane channel and electrolyte leakage. Active against most fungi except Aspergillus terreus, Scedosporium spp.
49
How do polyenes cause nephrotoxicity?
Most significant delayed toxicity. **Renovascular and tubular mechanisms:** * Vascular-decrease in renal blood flow leading to drop in GFR, azotemia (elevation of blood urea nitrogen (BUN) and serum creatinine levels). * Tubular-distal tubular ischemia, wasting of potassium, sodium, and magnesium. Enhanced in patients who are volume depleted or who are on concomitant nephrotoxic agents.
50
What can be done to mitigate the toxicity of Amphotericin B?
Classic amphotericin B deoxycholate (Fungizone™) formulation has serious toxic side effects. Less toxic preparations: * Liposomal amphotericin B * Amphotericin B colloidal dispersion * Amphotericin B lipid complex
51
Which antifungals target fungal cell walls?
Echinocandins e.g. Caspofungin acetate (Cancidas)
52
How do echinocandins work?
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.
53
What is the spectrum of echinocandins?
Candida species including non-albicans isolates resistant to fluconazole. Aspergillus spp. but not activity against other moulds (Fusarium, Zygomycosis). No coverage of Cryptococcus neoformans.
54
Which antifungals target DNA/RNA synthesis?
Pyrimidine analogues e.g. Flucytosine
55
Why does flucytosine have a restricted spectrum of activity?
**Acquired Resistance:** Result of monotherapy – rapid onset. **Due to:** * Decreased uptake (permease activity). * Altered 5-FC metabolism (cytosine deaminase or UMP pyrophosphorylase activity).
56
What are the uses and side effects of flucytosine?
**Limited:** Candida and cryptococcosis. In combination with Ambisome/fluconazole. Side effects: Infrequent – include D&V, alterations in liver function tests and blood disorders. Blood concentrations need monitoring when used in conjunction with Amphotericin B.

Pathology - Y5 (59 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions