Mycology 1: Intro Flashcards

1
Q

What is fungal cell wall made of?

A

Polysaccharides beta-glucan and chitin

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2
Q

What stains in KOH prep?

A

Cell wall

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3
Q

What are the only 2 fungi that make up normal microbiota?

A

Candida albicans and Malassezia furfur

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4
Q

What parts of CMI aid in fungal host defense?

A

CD4 T cells and macrophages

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5
Q

What are 2 examples of fungi that exist only as yeast?

A

Cryptococcus neoformans and Candida glabrata

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6
Q

What 3 fungi exist purely as a mold?

A

Aspergillus, Dermatophytes, Zygomycetes

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7
Q

2 transition states

A

Germ tubes - elongation of yeasts into hyphae

Pseudohyphae - budding of yeast w/o fully separating.

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8
Q

Ascomycetes

A

2 compatible haploid nuclei fuse to form a diploid nucleus, followed by meiosis to form haploid progeny. Form spores w/in a sac called an ascus

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9
Q

Basidiomycetes

A

Similar to ascomycetes but early part occurs w/in a sac called the basidium, and then haploid progeny mature on the outer surface of that basidium (mushrooms).

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10
Q

Zygomycetes

A

Gametes fuse to form a zygote (similar to humans)

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11
Q

Deuteromycetes

A

No sexual stage has been identified

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12
Q

4 examples of mycotoxins

A
  • Aflatoxins – Aspergillus often grows on corn or peanuts. Does not affect humans due to food inspection, but may cause cirrhosis in poultry.
  • Ergot alkaloids from Claviceps purpurea in grains / breads cause vasoconstriction, peripheral necrosis, and gangrene
  • Fumonisins may cause neural tube defects
  • Trichothecenes from Stachybotrys or Fusarium
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13
Q

Top 2 outdoor allergens

A

Pollens and fungi

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14
Q

Top 2 indoor allergens

A

Dust mites and fungi

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15
Q

What causes cheese-washer’s disease?

A

Penicillium

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16
Q

What molecules are mycotoxins made of?

A

Low MW secondary metabolites

17
Q

General tx for superficial fungal infections

A

Topical / systemic antifungals for cosmetic reasons.

18
Q
Tinea / pityriasis versicolor
Causative fungus
Morphology
Requirement
Sxs
Mechanism
Tx
A

Malassezia furfur (normal microbiota)
Dimorphic. Mold is pathogenic. Yeast is commensal. Spaghetti and meatballs.
•Lipophilic – requires exogenous FA’s, from human sebaceous / oily skin
Causes flaking / scaling of skin w/ hyper / hypo pigmentation.
Mechanism - disordered host melanin production –> hyper pigmentation. Fungal metabolite azelaic acid –> hypopigmentation.
Tx w/ topical antifungals.

19
Q

3 other diseases caused by Malassezia

What type of pxs?

A

Often occurs in HIV pxs
•Seborrheic dermatitis – mainly affects face and axilla
•Dandruff / cradle cap – Scaling. Often affects newborns.
•Rare dissemination – mainly in premature infants receiving total parenteral nutrition (TPN). IV nutrition includes daily bolus of lipids, which is a good opportunity for Malassezia to enter blood stream

20
Q

What is the most common fungal infection?

A

Cutaneous mycoses (dermatophytes)

21
Q

What are the 3 genera of dermatophytes?

A

•Trichophyton, Microsporum, and Epidermophyton.

22
Q

3 characteristics of cutaneous mycoses

A

Keratinophilic w/ keratinases
Highly contagious (rare for fungus)
May be geophilic, zoophilic, or anthropomorphic.

23
Q

Tinea infections
Manuum
Fabis
Barbae

A
Manuum = hand (may be nodular)
Fabis = severe scalp infection w/ alopecia
Barbae = beared area
24
Q

Kerion

A

Superficial skin infection

Kerion = abscess that can be superinfected by skin bacteria such as staph or strep.

25
Q

What causes subcutaneous mycoses?

Which skin layers?

A

Trauma or mucus membranes (sinuses / eyes). Immunocompromise / diabetes may be present.
Involves epidermis, dermis, and subQ. Hydrolytic enzymes may cause destruction of fascia / bone.

26
Q

Sporothrix schenckii / Sporotrichosis
Morphology
Other names / associations
Diseases (3)

A
  • Dimorphic – Mold in soil (infectious form; mycelia and conidia). Yeast in host (pathogenic). Yeast are fusiform / cigar-shaped.
  • Asteroid body – central yeast cell surrounded by radiating red projections
  • Gardener’s / Rose picker’s disease, associated w/ potting soil / sphagnum moss.
  • Lymphocutaneous sporotrichosis – Most common manifestation. Small, hard, painless nodule develops, becomes fixed, and enlarged to form a fluctuant mass that eventually ulcerates. Nodules may “track” along lymphatics, but stays relatively regional.
  • Inhalation can cause pulmonary or disseminated sporotrichosis, mainly in immunocompromised pxs. Not actually subcutaneous.
  • Fixed cutaneous sporotrichosis – dry crusty surface lesion at site of infection w/o lymphatic progression. Often occurs in previously infected pxs who developed immune responses sufficient to contain the infection more quickly.
27
Q
Zygomycosis / mucormycosis
3 types of Mucorales
Morphology
General characteristics
Sites of infection
Mucor morphology
Risk factors for zygomycosis
Rhinocerebral zygomycosis
A

Rhizopus, Mucor, and Absidia
•Fast growing, saprobic, soil molds. Progressive tissue infection, often rapidly invasive / destructive
•Exist only as molds
•Enters via break in skin or inhalation. Lungs and sinuses are common spots of infection. Usually involves immunocompromise.
•Mucor - Broad, ribbon-like, aseptate hyphae. 90 degree branching
•Risk factors for zygomycosis – neutropenia, immunosuppressive therapy, iron chelation therapy, acidosis (low pH causes iron release from transferrin which is taken up by zygomycetes), diabetes (high glucose for nutrition and diminished phagocyte activity), DIABETIC KETOACIDOSIS
•Rhinocerebral zygomycosis – Sinus infection extending to brain. Rapidly progressive (hours / days), fulminant, and life threatening. Mainly seen in diabetic / acidotic pxs (diabetic ketoacidosis), neutropenic pxs, or those on immunosuppressive therapy.

28
Q

How are nail / hair dermatophyte infections treated differently than skin infections?

A

Nail / hair infections require oral azoles / terbinafine. Topical skin infections only require topical azoles / terbinafine.