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Bloc G - Infection > May1 M1,2-Medical Mycology > Flashcards

May1 M1,2-Medical Mycology Flashcards

1
Q

(important) SE of voriconazole (an azole) that is important to know

A

visual hallucinations

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2
Q

(important) important pathogenic superficial and invasive yeast

A

candida albicans

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3
Q

(important) where candida is in the environment

A

lives in our intestines normally, are normal commensals of humans

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4
Q

(important) step that is required for candida albicans to become virulent

A

morphological switching

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5
Q

(important) resistance pattern (fluconazole, echinocandin) of candida albicans

A
  • fluconazole sensitive

- echinocandin sensitive

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6
Q

(important) resistance pattern (fluconazole, echinocandin) of candida glabrata

A
  • fluconazole resistant
  • echnicandin sensitive
  • echinocandin = tx*
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7
Q

(important) resistance pattern (fluconazole, echinocandin) of candida parapsilosis

A
  • fluconazole sensitive

- echinocandin sensitivie/intermediate

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8
Q

(important) resistance pattern (fluconazole, echinocandin) resistance of candida krusei

A
  • fluconazole resistant
  • echinocandin sensitive
  • tx=echinocandin*
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9
Q

(important) resistance pattern (azole, echinocandin and amphotericin B) of candida auris

A
  • fluconazole resistant
  • echinocandin R or S
  • amphotericin B resistant
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10
Q

(important) resistance pattern (fluconazole, echinocandin) main resistances to remember with candida

A
  • glabrata and krusei resistant to fluconazole

- auris resistant to fluconazole and amphotericin B

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11
Q

(important) treatment of choice for all candida infections

A
  • echinocandins IV

- for po, switch to fluco if it’s NOT glabrata or krusei (if it’s glabrata or krusei, switch to something else)

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12
Q

(important) necessary steps to increase the survival of patients with CANDIDEMIA (candidal blood infection) in the ICU

A

BOTH

  • anti-fungal in <24 hours
  • source control in <24 hrs (remove central vein catheter, surgical or radiological procedures to drain abscesses or fluid collections)
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13
Q

(important) other step of candidemia management after did anti-fungals + source control <24 hrs

A

assess for secondary sites of infection such a endophthalmitis, endocarditis, osteomyelitis

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14
Q

(important) cryptococcus spp (pathogenic yeast) 2 species

A
  • cryptococcus neoformans (from trees and poop)

- cryptococcus gatti (from eucalyptus trees)

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15
Q

(important) cryptococcus spp infection: most important thing to do in your patients

A

manage their ICP (intracranial pressure) because of the possible, underlying fungal meningitis

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16
Q

(important) in patients with a significant hematologic disease (like having received a HSCT, having AML, an acute leukemia, etc.), what’s the most important cause of death

A

invasive aspergillosis (invasive infection by aspergillus fumigatus), an invasive mold

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17
Q

(important) 3 levels of diagnosis for invasive aspergillosis

A
  • proven aspergillosis
  • probable aspergillosis
  • possible aspergillosis
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18
Q

(important) meaning of possible aspergillosis (dx)

A
  • the patient is immunosuppressed
  • one of these host factor criteria happened: neutropenia, persistant fever despite high-risk Abx, GVHD, prolonged CS use
  • you suspect aspergillosis
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19
Q

(important) meaning of probable aspergillosis (dx)

A

-1+ of the 4 host factor criteria + clinical feature + galactomannan evidence
OR
-culture from sputum or BAL in immunocompromised pts with clinical signs

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20
Q

(important) meaning of proven aspergillosis (dx)

A

Proven on either of

  • histopathology
  • growh in culture from tissue bx or sterile site aspirate
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21
Q

charact of fungal cell wall (which is on top of cell membrane)

A

beta-glucan and other polysaccharides

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22
Q

what’s a hyphae

A

multicellular form of fungi appearing as threadlike filaments (mycelium = group of hyphae, also means hyphae)

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23
Q

molecule used in fungal cell membrane instead of cholesterol (which is only in animals)

A

ergosterol

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24
Q

3 types of anti-fungals acting on the cell membrane

A
  • azoles (inhibit ergosterol synthesis)
  • allyamines (inhibits early step in ergosterol pathway)
  • polyenes (bind ergosterol and form MAC-like pores)
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25
Q

problem of polyenes

A

bind cholesterol too if no ergosterol around and this can be toxic

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26
Q

3 polyenes and their charact

A
  • nystatin (only topical, very toxic)
  • amphotericin B desoxycholate (binds cholesterol less)
  • lipid-based formulations of amphotericin (added lipid carrier to reduce toxicity)
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27
Q

azoles and their charact

A
  • fluconazole (most used): yeast only
  • itraconazole
  • voriconazole, isavuconazole, posaconazole = new and very good for mold (aspergillus included)
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28
Q

important SE of azoles

A

hallucinations (voriconazole)

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29
Q

allylamine used for what and why

A
  • usually superficial (dermato) fungal infections and used topically
  • because lipophilic and partition better to cells and keratin than blood
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30
Q

anti-fungal acting on DNA synthesis and action and used when

A

5-Flucytosine (5-FC)

  • inhibits DNA chain synthesis (chemo-like)
  • suppresses your BM and your microbiota
  • only used in combination therapy for cryptococcus
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31
Q

anti-fungal acting on the cell wall, mode of action, acts on what fungi and route of administration

A

echinocandins (end with fungin)

  • inhibits beta 1,3 glucan synthase
  • active on fungi with beta glucan so: yes = candida and ascomycetes no = cryptococcus, histoplasma, zygomycetes
  • IV only bc big molecule
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32
Q

hypersensitivity reactions to fungi (not anti-fungals): why happens and its charact + typical organism causing it

A
  • sensitized bc fungi pump out enzymes to eat us + we think they’re parasites (IgE, eosinophils, etc.)
  • mast cell degranulation, histamine release (asthma, rhinitis, pneumonitis, sinusitis)
  • aspergillus spp*
33
Q

how fungal disease is classified

A
  1. superficial by a. yeast or b. mold

2. invasive by a. yeast b. mold c. dismorphic

34
Q

types of diseases that yeast (unicellular fungi) cause

A

syndromes like bacterias cause: meningitis, fever, infection

35
Q

types of diseases that molds cause

A

focal local infections (lung or skin) and eat everything in their path leaving no cells alive. Then metastasize to seed elsewhere like a cancer

36
Q

(important) 2 pathogenic yeast

A
  • candida spp

- cryptococcus spp

37
Q

symptoms of superficial candidiasis

A
  • OPC (oropharyngial candidiasis = thrush) (T cell prob)
  • eosphageal candidiasis (T cell prob)
  • vaginitis (Abx impaired vaginal microbiome)
  • skin and nail infections
38
Q

invasive candidiasis symptoms

A

sepsis (after breaches in mucosal surfaces, chemo, IV catheters, intestinal surgery)

39
Q

(important) most common candida spp for deep infections

A

candida albicans

40
Q

antifungal used in candidemia (candida in the blood) treatment

A

caspofungin (an echinocandin. cell wall synthesis inhibition. works for candida but not cryptococcus)

41
Q

steps of infection and symptoms in a cryptococcus infection

A
  • pulmonary infection (asymptomatic)
  • then disseminates*
  • PRESENT AS MENINGITIS
42
Q

cryptococcus neoformans infections happen in who and present how

A
  • in T cell deficiency states (SOT, T cell modifying therapy, untreated HIV)
  • present as chronic meningitis
43
Q

cryptococcus gattii infections happen in who and present how

A
  • in immunosuppressed

- present as meningitis

44
Q

Vancouver cryptococcus outbreak was caused by what, symptoms and affects who

A
  • cause = combination of gattii from Australian eucalyptus and native BC gattii
  • immunocompetent patients
  • pneumonia and meningitis
45
Q

how to diagnose fungal (cryptococcus meningitis): best method, used now

A

Antigen testing

  • cryptococcal capsule sheds in serum and CSF
  • latex agglutination to check for them
46
Q

treatment of cryptococcus meningitis

A
  • liposomal (lipid) amphotericin (a polyene, ergosterol binding drug)
  • after weeks, downgrade to fluconazole (an azole, inhibits ergosterol synthesis)
47
Q

(important) 2 dimorphic fungi (invasive)

A
  • histoplasma casulatum

- blastomyces dermatidis

48
Q

difference between patients that have yeast infections (candida or cryptococcus spp) and dimorphic fungi infections

A

yeast = immunosuppressed patients

dimorphic fungi = healthy patients

49
Q

endemic mycoses stands for what

A

dimorphic fungi infections have specific endemic zones

  • histoplasma casulatum = histoplasmosis
  • blastomyces dermatiditis = blastomycosis
50
Q

2 forms of dimorphic fungi (endemic mycoses)

A
  • yeast form (in tissues) at 37C

- mycelial (saprophytic) form at 25C

51
Q

what infection do you get in bat caves

A

histoplasmosis

52
Q

reservoirs of histoplasma casulatum

A

nitrogen rich soils. includes

  • river valleys
  • bats and bat caves (because is in bat guano)
  • bird poop also
53
Q

tunnel construction associated with what infection in nearby communities and why

A

histoplasmosis (histoplasma casulatum). because stirring up the soil is the best way to infect people

54
Q

histoplasmosis symptoms and stages

A
  • inhale, stays in lungs and is latent or symptomatic with possible dissemination. calcified granulomas on CXR
  • latent can reactivate when T cell depleted (immunosuppressed)
55
Q

reservoir of blastomyces dermatiditis

A
  • trees

- rotten hard woods

56
Q

blastomycosis symptoms and stages

A
  • inhale, stays in lungs and is latent or symptomatic with possible dissemination.
  • latent can reactivate when T cell depleted (immunosuppressed) + can also disseminate (ON THE SKIN) when reactivated
57
Q

where blastomycosis relapses and typical specific location

A
  • on the skin. verrucous cryptic ulcer lesions

- usually testicles and male genitalia bc prefers cold places

58
Q

how to dx endemic mycoses (dimorphic fungi infections)

A
  • pulmonary syndrome = culture, bronchoalveolar lavage
  • disseminated disease = blood culture
  • Ag testing on urine is possible
59
Q

treatment of endemic mycoses

A
  • pulmonary syndrome = azole (itraconazole, voriconazole)
  • disseminated or severe = amphotericin B (a polyene)
  • no echinocandins, not much cell wall*
60
Q

superficial mold infections: think of what type of fungi usually

A

dermatophytes (molds)

61
Q

dermatophytes def + 3 genera

A

molds that only grow superficially on skin and eat keratin only

62
Q

some dermatophytes causing infections in humans

A
  • T rubrum
  • T mentagrophytes
  • E. floccosum
63
Q

tinea pedis (athletes foot) def + 2 types

A
  • dermatophyte infection (T rubrum, T mentagrophytes or E floccosum)
  • interdigital type or mocasin (plantar) type
64
Q

treatment of tinea pedis

A

topical azoles or allylamines

65
Q

tinea corporis (ringworm) def and tx

A
  • dermatophyte infection (T rubrum or T mentagrophytes) of the SKIN. round plaque
  • tx = topical azoles or topical terbinafine (an allylamine)
66
Q

tinea unguium (onychomycosis) def and tx

A
  • infection of the nail plate, common in elderly. nail looks yellow
  • tx = topical azole or terbinafine (an allylamine) for a year (to grow a whole nail bc Abx doesn’t reach penetrate the nail)
67
Q

diagnosis of dermatophytes (tinea pedis, corporis and tinea unguium)

A

scrape dead flakes of skin, calcofluor dye, look for hyphae

68
Q

who gets invasive mold infections (aspergillus and other molds)

A

immunosuppressed patients (chemo, BMT, organ transplant, high dose CS) OR LOCALLY immunocompromised

69
Q

invasive molds infect what regions of the body (typical syndromes)

A

pulmonary or sinonasal infection

dissemination follows

70
Q

aspergillosis on CXR

A

crescent sign (dead piece of lung)

71
Q

why aspergillosis dx is hard and has a specific diagnostic division (proven, probable, possible)

A
  • you can’t dx molds with blood cultures bc do local dissemination
  • 30% sensitivity BAL
72
Q

non culture diagnostic test for aspergillosis (only allows probable diagnostic (not proven) if positive)

A
  • galactomannan assay (a part of fungal cell wall)
  • check for a certain level of it in serum or BAL fluid (bc it sheds normally)
  • 75% sensitivity serum. 90% sensitivity BAL
73
Q

4 steps of management of IFI (invasive fungal infections)

A
  • prophylactic (asymptomatic high-risk)
  • empiric (high risk Abx + fever)
  • preemptive (high risk + novel dx with markers)
  • therapy (full blown disease). evidence of infection
74
Q

good and bad things with different steps of IFI management

A
  • early tx = better tx but tx more patient (prophylactic. asymptomatic high risk)
  • late tx = tx someone infected for sure and preserving the drugs but less successful in saving lives
75
Q

(important) treatment of invasive aspergillosis

A

voriconazole

76
Q

2 classical subcutaneous mycoses caused by local immune suppression and local inoculation due to trauma or wtv

A
  • chromoblastomycosis (multiple fungi, like dermatiaceous molds)
  • eumycotic mycetoma (caused by fungi and is not actinomycotic mycetoma caused by the bacteria actinomyces)
77
Q

treatment of chromoblastomycosis and eumycotic mycetoma

A

amphotericin B (polyene) and mold active azoles

78
Q

what’s sick building syndrome

A
  • chronic fatigue, resp illness and general malaise
  • caused by mycotoxins from fungi present in buildings and degrading their environment, making complex molecules
  • we inhale mycotoxins
79
Q

something that mycotoxins are 100% certainly associated with

A

allergies, asthma, rhinitis

not sick building syndrome

Bloc G - Infection (39 decks)

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