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Microbiology by Bonnie > Fungi > Flashcards

Fungi Flashcards

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1
Q

Fungal versus mammalian plasma membrane sterols

A

Ergosterol (important target for antifungal therapy) versus cholesterol

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2
Q

Fungal cell wall composition

A

Glucan and chitin

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3
Q

Fungal virulence factors

A

Cell wall, exoenzymes/toxins

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4
Q

Fungi: Dimorphism two growth forms

A

Molds or yeasts

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5
Q

How do molds grow

A

Hyphae (Microscopic, branching, thread-like filaments) -> Mycelium

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6
Q

Hyphae two types

A

Septate (divided by cross walls)

Nonseptate and multinucleate

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7
Q

Yeast description

A

Single, ovoid, or spherical cells with a rigid cell wall

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8
Q

Candida morphogenesis

A

Present as yeast form but can elongate as hypha like structure (germ-tube)

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9
Q

Fungal virulence factors

A

Thermotolerance, cell wall components, exoenzymes, toxins

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10
Q

Host risk factors for fungal infection

A

Immunosuppression (neutropenia, cell-mediated immune dysfunction), previous antibiotic use, warm/wet environment, malnutrition, extremes of age, indwelling catheters/hardware

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11
Q

Fungal disease pathogenesis

A

Adherence, invasion, local tissue destruction, immunogenic cell wall (e.g. hypersensitivity to cell wall components)

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12
Q

What are the endemic fungi (with location)? Detection?

A

Histoplasma - Ohio-Mississippi River Valley
Blastomyces - North Central U.S.
Coccidioides - Southern U.S. and Latin America

Antigen detection helpful
Coccidioides still use serology (but generally not very useful)

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13
Q

What cause mild cutaneous fungal infections?

A

Trichophyton, Epidermophyton, Microsporum

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14
Q

What is KOH used for?

A

Body fluids, cervical/vaginal swab

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15
Q

Antifungal therapy

A

Polyenes - amphotericin B bind ergosterol (significant toxicity), currently enclosed in liposomes to make it safer, tends to be second-line

First line antifungal therapy - azoles inhibit ergosterol synthesis, rather safe

Allylamines - terbinafine topical antifungal, inhibits earlier step in sterol synthesis (has liver toxicity when taken orally)

Echinocandins - newest group, end in fungin, inhibit cell wall glucan synthesis, only IV use, predominantly used to treat candida (increasing azole resistance)

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16
Q

Fungal site of infections

A

Superficial, cutaneous, subcutaneous, pulmonary, bloodstream, meningitis

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17
Q

Superficial mycoses - where, what species

A

Involve stratum corneum, malassezia furfur

18
Q

Superficial mycoses - what does it cause, treatment

A

Chronic hypo or hyperpigmentation (pityriasis versicolor), superficial skin infection, generally treated with topical therapy

19
Q

Cutaneous mycoses - what does it cause

A

Tinea family (capitis, pedis, cruris, corporis, manus), dermatophytosis, onychomycosis

20
Q

Cutaneous mycoses treatment

A

Topical azoles, systemic azoles, terbinafine, griseofulvin

21
Q

Subcutaneous mycoses - species, what does it cause

A

Sporotrichosis - nodular lesion with lymphatic spread (“Rose gardener’s disease”)

22
Q

Subcutaneous mycoses treatment

A

Itraconazole

23
Q

Endemic mycoses causative agents

A

Thermally dimorphic fungi (hyphal form in environment, yeast form in tissue)

24
Q

How are endemic mycoses acquired

A

Inhalation -> pulmonary infection -> dissemination (potentially)

25
Q

Histoplasmosis - what does it cause

A

Vast majority of primary infection is subclinical

Complications - Pulmonary calcifications, mediastinal lymphadenitis, mediastinal fibrosis

26
Q

Histoplasmosis - characteristic tissue response

A

Caseating or noncaseating granulomas (also for TB)

27
Q

Histoplasmosis treatment

A

Amphotericin B, Itraconazole

28
Q

Blastomycosis - where does it disseminate

A

Skin and bone

29
Q

Blastomycosis - typical inflammatory response

A

Clusters of neutrophils and noncaseating granulomas

30
Q

Blastomycosis diagnosis

A

Broad-based budding yeast

31
Q

Candidiasis: Types of infections

A 
Mucocutaneous infection (thrush, vulvovaginal candidiasis, esophageal candidiasis)
Invasive infection (candidemia)
32
Q

What is candida auris associated with

A

Nosocomial transmission and outbreaks in healthcare settings, multi-drug resistance

33
Q

Cryptococcosis: What does it have a predilection for

A

CNS

34
Q

Cryptococcosis virulence factor

A

Polysaccharide capsule - produces brain edema, polysaccharide plug up arachnoid villi

35
Q

When use 5-flucytosine

A

Initial therapy for cryptococcosis (along with amphotericin B)

36
Q

How get cryptococcosis

A

Inhaled and disseminates

37
Q

How get aspergillosis

A

Inhaled

38
Q

What aspergillosis cause

A

Pneumonia, sinusitis, disseminated infection

39
Q

Aspergillosis histopathology

A

Septate hyphae, acute angle branching

40
Q

Mucormycosis - how get it

A

Environmental organisms get inhaled - right circumstances can cause disease

41
Q

Mucormycosis histopathology

A

Broad, non-septate, right-angle branching

42
Q

Mucormycosis - what does it cause

A

Pneumonia, rhino-orbital, cerebral disease

Microbiology by Bonnie (14 decks)

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