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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.

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2
Q

What are yeasts?

A

Single celled, reproduce by budding

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3
Q

What are some examples of yeasts?

A

Candida

Cryptococcus

Histoplasma (dimorphic)

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4
Q

What are moulds?

A

Multicellular hyphae, grow by branching and extension

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5
Q

What are some examples of moulds?

A

Dermatophytes

Aspergillus

Agents of mucormycoses

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6
Q

Which is the commonest cause of fungal infections in human?

A

Candida spp

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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
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8
Q

What is this?

A

Oral candidiasis

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9
Q

What is this?

A

Candidal intertrigo

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10
Q

What are superficial Candida infections?

A
  • Oral thrush
  • Candida oesophagitis
  • Vulvovaginitis
  • Cutaneous – Localised or generalised
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11
Q

What is the topical management for Candida?

A

Oral thrush: Nystatin

Vulvovaginitis: Cotrimazole

Localised cutaneous: Cotrimazole

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12
Q

What is the oral management for Candida?

A

Vulvovaginitis: Fluconazole

Oesophagitis: Fluconazole

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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

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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

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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
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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.

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17
Q

Which animal is cryptococcus associated with?

A

Pigeons

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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.

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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.

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20
Q

What type of ink is used for a cryptococcal stain?

A

India

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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

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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.

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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
Q

What are appropriate investigations for Aspergillosis?

A

Imaging

Sputum/BAL – MC&S, Ag testing

Aspergillus Abs (precipitans)

Galactomannan

Bx – histology, MC&S

26
Q

What is the management for Aspergillosis?

A

Voriconazole

Ambisome

Duration based on host/radiological/mycological factors – At least 6/52

27
Q

What is Pneumocystis Jiroveci?

A

Ubiquitous in the environment and distributed worldwide.

Lacks ergosterol in its cell wall.

Acquisition by airborne route – Pneumonia.

Extrapulmonary disease is very rare.

28
Q

What are risk factors for Pneumocystis Jiroveci?

A

Immunodeficiency

Immunosuppressive drugs

Debilitated infants

Severe protein malnutrition

29
Q

What are appropriate investigations for Pneumocystis Jiroveci?

A

Microscopy

PCR

Beta-D-glucan

30
Q

What is the management for Pneumocystis Jiroveci?

A

High dose cotrimoxazole 2-3/52

Alternatives: Atovaquone, clindamycin + primaquine

Steroids if hypoxia present

31
Q

Why might antifungals targeting the cell membrane not work in pneumocystis pneumonia (PCP)?

A

It lacks ergosterol in its cell wall

32
Q

What is mucomycoses?

A

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
Q

What are the clinical features of mucomycoses infection?

A

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
Q

What are appropriate investigations for mucomycoses?

A

Isolation from tissue Bx

35
Q

What is the management for mucomycoses?

A

Ambisome/Posaconazole

Symptomatic treatment guided by response

36
Q

What are dermatophytes?

A

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
Q

What are risk factors for dermatophytes?

A

Moisture

Deficiencies in cell mediated immunity

Genetic predisposition

38
Q

On which sites do different tinea infections occur?

A

Tinea pedis: Foot

Tinea capitis: Scalp

Tinea cruris: Groin

Tinea corporis: Abdomen

39
Q

What are appropriate investigations for dermatophytes?

A

Skin scrapings, nail specimens and plucked hairs

MC&S

40
Q

What is the management for dermatophytes?

A

Topical e.g. Clotrimazole, ketoconazole

Oral e.g. Griseofulvin, terbinafine, itraconazole

41
Q

What are the side effects of azoles?

A

Abnormal LFTs

42
Q

What are the side effects of polyenes?

A

Nephrotoxicity

43
Q

What are the side effects of pyrimidine analogues?

A

Blood disorders

44
Q

What are the side effects of echinocandins?

A

Relatively innocuous

45
Q

What are the three common targets for antifungal therapy?

A

Cell membrane

DNA synthesis

Cell wall

46
Q

Which antibiotics and antifungals target the cell membrane?

A

Polyene antibiotics:

  • Amphotericin B, lipid formulations
  • Nystatin (topical)

Azole antifungals:

  • Ketoconazole
  • Itraconazole
  • Fluconazole
  • Voriconazole
  • Miconazole
  • Clotrimazole (and other topicals)
47
Q

How do azoles work?

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. Some cross-reactivity is seen with mammalian cytochrome p450 enzymes:

  • Drug Interactions
  • Impairment of steroidneogenesis (ketoconazole, itraconazole)
48
Q

How do polyenes (e.g. Amphotericin B) work?

A

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
Q

How do polyenes cause nephrotoxicity?

A

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
Q

What can be done to mitigate the toxicity of Amphotericin B?

A

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
Q

Which antifungals target fungal cell walls?

A

Echinocandins

e.g. Caspofungin acetate (Cancidas)

52
Q

How do echinocandins work?

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.

53
Q

What is the spectrum of echinocandins?

A

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
Q

Which antifungals target DNA/RNA synthesis?

A

Pyrimidine analogues e.g. Flucytosine

55
Q

Why does flucytosine have a restricted spectrum of activity?

A

Acquired Resistance: Result of monotherapy – rapid onset.

Due to:

  • Decreased uptake (permease activity).
  • Altered 5-FC metabolism (cytosine deaminase or UMP pyrophosphorylase activity).
56
Q

What are the uses and side effects of flucytosine?

A

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)

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