Exam #1: Clinical Mycology Flashcards

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1
Q

How many species of fungi infect humans?

A

150 of 200,000

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2
Q

How can fungi cause disease?

A
  • Intoxication i.e. through the production of microtoxins
    ○ Ergot alkaloids (bread fungi w/ ingestion leads to hallucinations)
    ○ Alfatoxin (peanut butter fungi that is hepatotoxic)
    ○ Stachybotrys (black mold in homes that produces neurotoxin)
    ○ Recreational “shrooms”
  • Allergens to mold spores
  • Colonization & Disease i.e. when fungi colonize us causing disease
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3
Q

Describe the general characteristics of Fungi.

A
  • Eukaryotic pathogen i.e. contains membrane bound organelles
  • Very similar to human cells, making fungi challenging to treat (fewer targets for therapy) w/ two important differences:
    ○ Cell wall (that is also different from bacteria)
    ○ Membrane sterol composition (ergosterol vs. cholesterol)
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4
Q

Which fungi contains a capsule?

A

Cryptococcus neoformas

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5
Q

What are the functions of the fungal cell wall?

A

To provide:

  • Shape
  • Rigidity
  • Strength
  • Protection from osmotic shock
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6
Q

Describe the structure of the fungal cell membrane.

A
  • Typical phospholipid bilayer
  • Unique sterol composition that contains “ergosterol (instead of cholesterol),” which serves as the chemotherapeutic target of antifungal drugs
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7
Q

What are the two general categories of fungi?

A
  • Yeast

- Molds (stuff growing on counter, refrigerator, strawberries)

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8
Q

Dimorphic

A

Fungi that can grow as both yeast & molds–many pathogenic fungi are dimorphic

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9
Q

List the characteristics of yeast.

A
  • Unicellular
  • Spherical or ellipsoid shape
  • Reproduce by budding (buds are called “blastoconidia”)
  • Some form pseudohyphae
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10
Q

What is a pseudohyphae?

A

Pseudohyphae= when yeast buds never really separate; chains of buds that look like hyphae in mold

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11
Q

What is a germ tube?

A

Germ Tube= a characterstics pseudophphae that looks like a bud w/ long extension or spoon
- Canida albicans can form a “germ tube” in the presence of serum

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12
Q

What are the different structures that mold can form?

A
  • Hyphae= individual strands of mold
  • Mycelium= a mass of intertwined hyphae
    ○ Can be vegetative or aerial
  • Septa= cross-walls that divide the hyphae into segments
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13
Q

How can mold reproduce?

A
  • Sexually= spores
  • Asexually= conidia
    ○ Micro= small
    ○ Macro= big
    ○ Chlamydo= spore formed in strand of hyphae
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14
Q

How are mold infections diagnosed?

A

Visually–there aren’t many biochemical tests for mold (vs. bacteria)

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15
Q

What are the different types of fungal infections?

A
  • Superficial mycoses= infection of the outermost layers of skin & hair
  • Cutaneous mycoses= infection which extends deep into the epidermis as well as invasive hair & nail infections
    ○ Most common
  • Subcutaneous mycoses= infections involving the dermis, subcutaneous tissues, muscle, & fascia
  • Systemic mycoses= infections that originate in the lung but may spread to any organ in the body
  • Opportunistic mycoses= infection associated with immunosuppressed individuals
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16
Q

What is the host response to fungal infection?

A
  • Innate immune system= generally sufficient to prevent infection
    ○ Intact skin
    ○ pH
    ○ Competition w/ normal bacterial flora
    ○ Epithelial turnover
    ○ Dissicated (dry) nature of stratum corneum
    ○ Mucous membranes have antimicrobial peptides & ciliated cells
  • Neutrophils & macrophages are both capable of destroying or damaging fungal spores or hyphae
17
Q

What is the role of the adaptive immune system to fungal infection?

A
  • Cell-mediated (T-cell) is important (esp. INF-gamma production)
  • Humoral (Antibody) plays a very small role
18
Q

How do antifungal drugs differ from antibacterial drugs?

A
  • Fewer antifungals available b/c of similarity to human cells
  • Drugs are more toxic
19
Q

What are some of the targets of antifungal drugs?

A

B-Glucan & Ergosterol (Cell wall & plasma membrane)

20
Q

What is Squalene epoxidase?

A

Squalene epoxidase= enzyme involved in ergosterol synthesis

21
Q

What class is amphotericin B?

A
  • Polyene (binds to ergosterol & directly disrupts by causing a pore to form in the membrane–>osmotic disruption)
  • Formerly the only polyene
22
Q

What is the mechanism of echinocandins?

A

Cell wall synthesis inhibitors (B-glucan)

23
Q

What is the limitation of the echinocandins?

A

Can only be used for fungi w/ a high concentration of B-glucan in cell wall

24
Q

What is the problem with visual diagnosis of fungal infections in the lab?

A

Lots of mold in the environment can lead to contamination of the sample

25
Q

How is the KOH prep used to identify fungi infection? What tissues is it good for?

A
  • Skin, nail, hair…etc.
  • KOH dissolves skin, hair…etc. cells at a greater rate than the fungal cells
    ○ Then add a dye to better visualize the actual fungi in the sample
26
Q

Do fungi stain gram negative or gram positive?

A

Gram positive

27
Q

What is the India ink stain used to identify? Why is this test important?

A

Cryptococcus neoformans, which is the cause of cryptococcal meningitis

28
Q

What is the germ tube test used to identify?

A

Candida albicans

29
Q

In the lab, can you use the same agar to grow bacteria to grow fungi?

A

No

30
Q

What are the two ways that fungal cells differ from human cells?

A

1) Presence of a rigid cell wall

2) Composition of the cell membrane (ergosterol)

31
Q

How does the composition of the fungal cell wall differ from the bacterial cell wall?

A
Bacteria= peptidoglycan & teichoic acid
Fungus= mannan, glucan, chitin
32
Q

What is the difference between septate & nonseptate?

A
Septate= segmented mold with septa 
Nonseptate= nonsegmented mold without septa i.e. aseptate mold
33
Q

What is the difference between conidia & spores?

A

Fungi reproduce both sexually & asexually.

  • Conidia= reproductive units produced asexually
  • Spores= reproductive units produced sexually
34
Q

What is the mechanism of action of the azoles?

A

Inhibit ergosterol synthesis, which has a fungistatic effect

35
Q

What is the mechanism of action of the nucleoside anagoles (5-flurocytosine)?

A

Inhibition of both RNA & DNA function & synthesis

36
Q

What family of antifungals is activate against most medically important yeast, but NOT mold or dimorphic fungi?

A

Nuceloside analogs (5-flurocytosine)

37
Q

What is the target of the Grisan family of antifungals? What type of infection would best be treated with a drug in the Grisan family?

A
  • Inhibits microtubular function

- Best for superficial mycoses esp. scalp infection

38
Q

What is the general mechanism of the Allylamines, Thiocarbamates, & Morpholines?

A

Inhibition of ergosterol synthesis

39
Q

What is the mechanism of Potassium Iodide?

A

Unknown