Mycology Flashcards

1
Q

What is the difference between yeast and mold?

A

yeast-single cells, reproduce by budding

mold-long filaments (hyphae) or a mat (mycelium)

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2
Q

What are some general characteristics of fungi?

A

larger than bacteria
eukaryotic
membrane-ergosterol
cell wall-chitin, glucan, mannan

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3
Q

What are some characteristics of yeast?

A

unicellular
oval to round on microscopic examination
colonies resemble bacteria

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4
Q

What are some characteristics of mold?

A

multicellular
surface texture-cottony, wooly, velvety, granular
pigmentation
hyphae and spores

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5
Q

How are hyphae classified? What are the different types of hyphae?

A

presence of septa
reproductive hyphae
vegetative hyphae
aerial hyphae

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6
Q

What is a mycelium?

A

intertwined mass of hyphae

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7
Q

What is dimorphism?

A

capable of growing in mold or yeast

form under different environmental conditions (temperature, nutrients)

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8
Q

How do fungi reproduce?

A

binary fission
sexual
asexual
without nuclear fusion-arthrospore, blastospore, conidia

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9
Q

What are the pathogenic factors of fungi?

A

adhesins
antiphagocytic capsule
ability to survive in macrophage by H. capsulatum
lack of host resistance

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10
Q

What is the host response to a fungal infection?

A

high innate immunity

humoral response is limited and not protective

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11
Q

What increases susceptibility to fungal infections?

A

intrinsic-age, stress, nutritional status, pregnancy, diabetes
extrinsic-burns, steroid, immunosuppressive therapy, antibiotics

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12
Q

What is a KOH mount?

A

10% KOH added to specimen

digests tissue so fungi can be observed (can stain the fungi)

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13
Q

What is a calcifluor white stain?

A

Binds to polysaccharides in cellulose and chitin

fluoresces under UV light

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14
Q

What is the PAS stain?

A

Periodic acid forms aldehyde with chitin monomer in fungal cell wall
forms a red dye

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15
Q

What is the methenamine silver stain?

A

silver stains all fungi strongly but only few tissue components are stained

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16
Q

What is the pH of Sabouraud’s agar?

A

Acidic (5.6)

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17
Q

When is Wood’s lamp used?

A

diagnosis of dermatophytes

fluoresce under UV light

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18
Q

What are the different kinds of fungal infections?

A

superficial
cutaneous-tinea (ring worm)
subcutaneous-sporotrichosis
systemic-coccidioidomycosis, paracoccidiodomycosis, blastomycosis, histoplasmosis (lung is most common site)

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19
Q

What antifungals inhibit cell wall synthesis?

A

glucan-echinocandins (capsofungin)

chitin-nikkomycin

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20
Q

What inhibits cell wall synthesis through ergosterol?

A

azoles

allylamines

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21
Q

What causes direct membrane damage?

A

Polyenes

amphotericin-B

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22
Q

What inhibits nucleic acid synthesis?

A

flucytosine

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23
Q

What inhibits microtubules halting mitosis?

A

griseofulvin

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24
Q

What inhibits protein synthesis?

A

sordarins

azosordarins

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25
Q

What opportunistic fungal infections are yeast?

A

candida (dimorphic)
malassezia furfur-lipophilic skin organism, mainly in neonates
cryptococcus (fungi with capsule)

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26
Q

What opportunistic fungal infections are molds?

A

aspergillus

zygomycetes

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27
Q

What fungi looks like protazoa?

A

pneumocystis carnii

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28
Q

What are the morphological characteristics of candida?

A

yeasts, pseudohyphae (elongated single cells with constricted ends), and true hyphae with septations
dimorphic

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29
Q

What are the risk factors for candida infection?

A
AIDS
diabetes
surgery, catheters, antibiotics
neutropenia
burns
dialysis
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30
Q

What contributes to the pathogenicity of candida?

A

adhesins
germ tube formation-hyphal formation associated with tissue invasion
gliotoxin-immunosuppressive toxin

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31
Q

What are the clinical syndromes caused by candida?

A

thrush-white patches on oral mucosa (can be scraped off-unlike oral hairy leukoplakia)
vaginal candidiasis-thick curd like discharge and burning
dermatitis-diaper rash, intertringinous (associated with moisture)
onychomycosis and paronychia-nails

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32
Q

How can candida be diagnosed?

A

stain from blood, tissue, sterile fluid, urine, CSF, skin, respiratory secretions
Germ tube test-incubated in serum or plasma after 3-5 hrs at 37

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33
Q

How is candida treated?

A

mucosal or cutaneous-azoles (fluconazole, itraconazole, voriconazole, posaconazole)
systemic-amphotericin B or flucytosine+ampho

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34
Q

What are morphological characteristics of aspergillus?

A
not dimorphic fungus
septate hyphae
conidial arrangement 
dichotomous branching
acute branching angle
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35
Q

What clinical syndromes can be caused by aspergillus?

A
allergy
sinusitis
aspergilloma
pulmonary aspergillosis
disseminated aspergillosis
36
Q

How is aspergillus treated?

A

amphotericin B

37
Q

What are morphological characteristics of zygomycetes?

A
large hyphae
grow rapidly
coenocytic lack septa 
appear as hollow tubes
resemble twisted ribbons
38
Q

When is rhinocerebral mucormycosis likely to occur?

A

terminal event in patient with acidosis or uncontrolled diabetes
invasive in severely burnt patients
proliferate in nasal sinuses and invade into facial soft tissue, nerve, blood vessel, and brain

39
Q

What are the symptoms of rhinocerebral mucormycosis?

A
facial pain
headache
persistent change in mental status
blood-tinged nasal discharge
bulging, discolored eye; fixed pupil
40
Q

How is mucormycosis treated?

A

amphotericin B

41
Q

What are characteristics of cryptococcus neoformans?

A
monomorphic
yeast form
acidic mucopolysaccharide capsule
phenol oxidase positive-blocks epinephrine 
found in pigeon poop
42
Q

What are the clinical syndromes from cryptococcus?

A

primary pulmonary infections-asymptomatic
solitary pulmonary nodule on chest x-ray
cryptococcal meningitis-hematogenous spread from lungs to meninges, symptoms of headache, mental status change, fever

43
Q

How is cryptococcus diagnosed?

A

India ink-CSF
capsular polysaccharide antigen
serological test-based on detection of antigen not antibody

44
Q

What are morphological characteristics of pneumocystis carini?

A

round cup shaped organism
lacks ergosterol (ribotyping and DNA homology)
obligate parasites-alveolar epithelium

45
Q

What clinical syndrome is caused by pneumocystis?

A

interstitial pneumonia-resembles mycoplasma pneumonia

frequent in AIDS patients

46
Q

How is pneumocystis diagnosed?

A

microscopy of BAL fluids

methenamine silver-stain reveals rounded cup shaped organism

47
Q

How is pneumocystis treated?

A

sulfamethoxazole or pentamidine isothionate

48
Q

Why have fungal infections increased?

A

advances in antibacterial therapies-resulting in fungal superinfections
predisposing procedures-indwelling catheters
predisposing treatments-chemo
predisposing diseases-leukemia, AIDS

49
Q

What is the MOA for amphotericin B?

A

binds to sterols (ergosterol) of the fungal plasma membrane
alters membrane permeability
results in leakage of essential cell contents
fungistatic or fungicidal depending on concentration

50
Q

Where does amphotericin B distribute?

A

poor CSF penetration-intrathecal administration

51
Q

What are the adverse effects of amphotericin B?

A

nephrotoxicity-vasoconstrictive effect on afferent renal arterioles (decrease GFR), potassium/bicarb/magnesium wasting, decrease EPO production (reversible)
hematologic-anemia

52
Q

What are the infusion related effects of amphotericin B?

A

shaking, chills, fever, myalgias, arthralgias

premedicate with NSAIDs, acetaminophen, antihistamines

53
Q

What is the spectrum of activity for amphotericin B?

A
aspergillosis
paracoccidioidomycosis
histoplasmosis
cryptococcus
blastomycosis
candida-topical use
coccidiodomycosis
54
Q

What is the importance of the liposomal formulations of amphotericin B?

A

decrease in nephrotoxicity, no loss in efficacy
higher dosing
ABLC-invasive aspergillosis
ABCD

55
Q

What is the mechanism of action for flucytosine?

A

penetrates fungal cell wall
deaminated to 5-fluorouracil by cytosine deaminase (specific to fungus)
5FU is an antimetabolite that competes with uracil and inhibits pyrimidine metabolism and RNA, DNA, protein synthesis

56
Q

Where is flucytosine distributed?

A

CSF penetration

57
Q

What are the adverse effects of flucytosine?

A

bone marrow hypoplasia (anemia, leukopenia, thrombocytopenia)
elevated serum levels of hepatic enzymes

58
Q

When should flucytosine be used and how?

A

serious candida and cryptococcus

never use alone due to resistance-synergistic with Amphotericin B

59
Q

What is the mechanism of action for azole antifungals?

A

interfere with fungal cytochrome P450 dependent enzyme (14 alpha sterol demethylase) for conversion of lanosterol to ergosterol

60
Q

What is the advantage of a triazole over a imidazole?

A

Triazoles have increased affinity for fungal CYPs rather than mammalian

61
Q

What are the adverse effects of azoles?

A

nausea/vomiting

hepatitis

62
Q

What can ketoconazole be used to treat?

A

Cushing syndrome
dose dependent depression of testosterone and adrenocorticotropic hormone
can result in gynecomastia, impotence, decreased libido

63
Q

What are the drug interactions for azoles?

A

antacids, H2 agonists, PPI decrease absorption
cycosporine and warfarin increased concentration
less drug interactions for fluconazole, voriconazole

64
Q

When is ketoconazole used?

A
histoplasmosis
blastomycosis
coccidioidomycosis
candidiasis
tinea/vaginal candidiasis-not FDA approved
65
Q

What is the spectrum of coverage for fluconazole?

A

cryotococcal infections-meningitis
coccidiodomycosis-excellent CSF penetration and less morbidity than intrathecal ampho B
Candidiasis (resistance amoung krusei, glabrata)

66
Q

Where does itraconazole distribute?

A

poor CSF penetration

not good for meningitis

67
Q

What is the spectrum of coverage for fluconazole?

A
aspergillosis
cryptococcal infections
coccidioidomycosis
histoplasmosis
blastomycosis
sporotrichosis
dermatophytosis
tinea unguium
68
Q

What are the advantages of itraconazole use in therapy?

A

oral therapy for histo/blasto

when clinical improvement from ampho B can be transitioned to itraconazole

69
Q

What is unique about the absorption of voriconazole?

A

decreased by high fat meals

high bioavailability

70
Q

What are the drug interactions for voriconazole?

A

Rifampin, carbamezepine/phenobarbital decreases voriconazole AUC
quinidine, sirolimus, ergot alkaloids increase drug concentrations

71
Q

What are the adverse effects of voriconazole?

A

visual disturbances-blurred vision, color changes

rash, increased liver enzymes

72
Q

When is voriconazole used?

A

invasive aspergillosis

candidiasis

73
Q

When is posaconazole used?

A

similar to itraconazole
can elevate LFTs
used for candida and aspergillus
inhibits CYP3A4

74
Q

What is the mechanism of action of capsofungin acetate?

A

echinocandin-blocks fungal wall synthesis

glucan synthesis inhibitor (B 1,3 D glucan)

75
Q

When is capsofungin used?

A

invasive aspergillosis

candida

76
Q

What are the adverse effects of capsofungin acetate?

A

phlebitis, headache, fever

increased LFTs, SrCr-monitor

77
Q

What is the mechanism of action for griseofulvin?

A

disrupts cell mitotic spindle structure

arrests cell division in metaphase

78
Q

How is griseofulvin administerd? What does it treat?

A

orally

treats dermatophytosis

79
Q

What are the side effects of griseofulvin?

A
nausea, vomiting, diarrhea
hypersensitivity/rash
hepatotoxicity
nephrotoxicity
P450 inducer-increase warfarin dose
80
Q

What is the mechanism of action for terbinafine?

A

allylamine derivative

inhibits squalene epoxidase-step in sterol biosynthesis in fungi

81
Q

What are the adverse reactions to terbinafine?

A
nausea/diarrhea
hypersensitivity-erythema multiforme
liver enzyme abnormalities
hematologic effects-neutropenia, pancytopenia
headache
82
Q

How does the clearance of other drugs change with terbinafine?

A

increased clearance for rifampin and cyclosporine

decreased clearance for cimetidine and warfarin

83
Q

When is terbinafine used?

A

onchomycosis-less drug interactions than itraconazole

84
Q

How is nystatin administered?

A

oral suspension-swish and swallow

not absorbed from GI tract

85
Q

What is the primary therapy for fungal infections?

A

creams, ointments, liquids

86
Q

When are powders used?

A

mild lesions and tinea pedis prevnetion