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microbiology > Antifungal Drugs & Fungi B- Exam IV > Flashcards

Antifungal Drugs & Fungi B- Exam IV Flashcards

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1
Q

Why are there fewer effective antifungal agents?

A

because of the similarity of human cells and fungal cells

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2
Q

It is easier to treat ___ fungal infections than ____ fungal infections

A

superficial mycoses; systemic infections

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3
Q

Sterol found in fungal cell membranes; human cells have cholesterol instead of tis:

A

ergosterol

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4
Q

Where is ergosterol found?

A

in fungal cell membranes

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5
Q

Antifungal treatment that binds ergosterol in fungal membranes:

A

polyene compounds

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6
Q

Give an example of a polyene compound that is used to treat systemic disease:

A

amphotericin B

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7
Q

Given an example of a polyene compound that is used to treat topical disease:

A

nystatin

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8
Q

Polyene compounds cause ___, leading to:

A

altered membrane permeability; leakage of cell constituents & cell death

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9
Q

Polyenes bind ____ in mammalian cells but this is less strongly than they bind ___

A

cholesterol; ergosterol

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10
Q

What is the basis for drug toxicity with the polyene compounds?

A

their ability to bind cholesterol in mammalian cells

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11
Q

Why is fillipin a potent but toxic anti-fungal agent?

A

due to the binding of cholesterol

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12
Q

Terbinafine (TBF) acts on the Ergosterol biosynthetic pathway at the ____ step.

A

squalene epoxidase

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13
Q

Itraconazole (ITZ) acts on the Ergosterol biosynthetic pathway at the ____ step.

A

C-14 demethylase

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14
Q

Function to block ergosterol synthesis by inhibiting squalene epoxidase activity:

A

Allylamines

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15
Q

Give an example of an Allylamine that functions to block ergosterol synthesis:

A

Terbinafine (TBF)

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16
Q

Allylamines are mainly effective on the:

A

dermatophytes

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17
Q

What form of allylamines are most effective on dermatophytes?

A

topical or tablet formulations

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18
Q

Function to block ergosterol synthesis by inhibiting cytochrome P450-dependent 14(alpha)-lanosterol demtheylation:

A

azoles

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19
Q

What was the first oral azole?

A

Ketoconazole

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20
Q

What are some downfalls to ketoconazole? (the first oral azole)

A

significant numbers of side effects and drug interactions

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21
Q

What was created to supersede/replace ketoconazole?

A

Itraconazole

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22
Q

Itraconazole is preferred over ketoconazole because:

A

active against many fungi and has improved safety profile

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23
Q

What fungal species is itraconazole effective against?

A
  1. candida species
  2. cryptococcus
  3. aspergillus
  4. endemic (systemic) fungi
  5. dermaphytes
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24
Q

antifungal agent that inhibits the synthesis of beta-(1,3)-D-glucan, an essential component of fungal cells walls

A

Echinochandins

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25
Q

What is the significant of Echinocandins inhibiting the synthesis of beta-(1,3)-D-glucan:

A

This is an essential component of fungal cell walls

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26
Q

Echinocandins are ___ compared to agents that target cell membrane components

A

more selective

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27
Q

Echinocandins can be considered ___ against aspergillus and candida species

A

narrow spectrum

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28
Q

Why are echinocandins considered “narrow spectrum” against aspergillus and candida species?

A

because these fungi have larger amounts of beta-(1,3)-D-glucans

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29
Q

A type of echinocandin that is administered intravenously and has minimal toxicity:

A

Caspofungin

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30
Q

Antifungal drug mechanism that interferes with fungal protein and DNA synthesis:

A

Pyrimidine inhibition

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31
Q

Pyrimidine inhibition interferes with:

A

fungal protein and DNA synthesis

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32
Q

antifungal drug mechanism “pyrimidine inhibition” is active against what species?

A

candida species and cryptococcus neoformans

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33
Q

Why must drugs using the mechanism “pyrimidine inhibition” be used in combination with another antifungal drug?

A

because resistance develops quickly if used alone

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34
Q

High risk categories for opportunistic mycoses:

A
  1. immunocompromised individuals
  2. burn victims
  3. long-term IV catheter users
  4. broad-spectrum antibiotic therapy
  5. DM
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35
Q

Candidiasis is caused by the fungal species: (3)

A
  1. candida albicans
  2. candida glabrata
  3. candida parapsilosis
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36
Q

Predominant species of candida colonizing humans and responsible for most candidiasis infections:

A

candida albicans

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37
Q

responsible for some candidiasis infections and often resistant to some anti-fungals:

A

candida glabrata

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38
Q

responsible for some candidiasis infections and common cause of catheter-related infections:

A

candida parapsilosis

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39
Q

What are two categories of diseases caused by candidiasis?

A

local disease vs. systemic invasive disease

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40
Q

Adequate ____ protects against invasive infection with candidiasis

A

neutrophil

41
Q

___ & ___ protects against mucosal candidiasis

A

local factors & T-cell mediated defense system

42
Q

What are some other host factors associated with protection against candida infections:

A
  1. salivary flow and constituents
  2. blood group & secretor status
  3. epithelial barrier
  4. presence of normal bacterial flora
43
Q

adequate neutrophil function protects against ____ while local factors & T-cell mediated defense system protects against ___.

A

invasive infection; mucosal candidiasis

44
Q

What are four oral candida infections?

A
  1. acute pseudomembraneous (acute erythematous)
  2. chronic palquelike/nodular
  3. chronic erythematous
  4. candida-associated angular chelitis
45
Q

Oral candida infection characterized by multiple removable white plaques:

A

acute pseudomembranous

46
Q

Oral candida infection characterized by generalized redness of tissue (antibiotic sore mouth):

A

acute erythematous

47
Q

Oral candida infection characterized by fixed white plaques on commissures:

A

chronic plaquelike/nodular

48
Q

Oral candida infection characterized by generalized redness of tissue on fitting surface of upper denture:

A

chronic erythmatous

49
Q

Oral candida infection characterized by bilateral cracks on angles of mouth:

A

candida-associated angular chelitis

50
Q

pseudomembranous candidiasis lesions on the palate, easily wiped off:

A

thrush

51
Q

form of candidiasis, cannot be easily removed:

A

chronic plaquelike/nodular candida infection

52
Q

Plaquelike/nodular candidiasis is also called (2):

A
  1. chronic hyperplastic candidiasis
  2. candida leukoplakia
53
Q

What is significant about plaquelike/nodular candidiasis:

A

up to 40% of lesions develop into oral cancer

54
Q

With angular chelitis, there is frequently a ___ component

A

bacterial component

55
Q

How is mucosal candidiasis diagnosed?

A

Scrape and look under microscope

56
Q

How is invasive candidiasis diagnosed?

A

biopsy of involved tissue (blood culture not sensitive)

57
Q

Staining methods to visualize fungi in clinical samples include:

A
  1. PAS
  2. KOH
  3. Grocott-Gomori methenamine silver
  4. Gridley’s method
  5. Calcofluor white
58
Q

Staining methods to visualize fungi in clinical samples that stains surface carbohydrate:

A

Periodic acid-schiff (PAS) & Grocott-Gomori methenamine silver

59
Q

Staining methods to visualize fungi in clinical samples that dissolves tissue but not the fungi due to chitin:

A

potassium hydroxide (KOH)

60
Q

Staining methods to visualize fungi in clinical samples that is a modification of PAS:

A

Gridley’s method

61
Q

Staining methods to visualize fungi in clinical samples that is a fluorescent probe for chitin:

A

calcofluor white

62
Q

a drug resistant germ that is spread in healthcare facilities:

A

candida auris

63
Q

Why is candida auris a problem?

A
  1. It causes serious infections
  2. Drug resistance
  3. Becoming more common
  4. Difficult to identify
  5. Spreads in healthcare settings
64
Q

Fungal species found worldwide in soil contaminated with bird excretions:

A

Cryptococcus neoformans

65
Q

C. neoformans is found worldwide in ___ contaminated with ___

A

soil; bird extreta

66
Q

___% of patients with cyptococcosis appear to be ___.

A

20%; immunocompetent

67
Q

Discuss the events that lead to cryptococcosis:

A

yeast cells are inhaled in alveoli and begin to produce a polysaccharide capsule

68
Q

The polysaccharide capsule produced in cryptococcosis inhibits ___ and ___

A

phagocytosis and intracellular killing

69
Q

What is crucial to control of infection with C. neoformans?

A

T-cell immunity

70
Q

What enhances virulence of C. neoformans?

A

Melanin production in cell wall

71
Q

C. neoformans resist ___ & ___

A

free radicals and enzyme degredation

72
Q

The primary pulmonary infection of C. neoformans is usually described as:

A

asymptomatic

73
Q

C. neoformans has a striking ____ with an unknown basis

A

neurotropism

74
Q

Describe what occurs with a CNS infection caused by cryptococcus neoformans:

A

minimal inflammatory response

75
Q

What might the clinical presentation of a patient with C. neoformans be?

A

worsening meningitis

76
Q

What is the diagnosis for cryptococcal meningitis?

A
  1. Examine CSF for encapsulated budding yeast
  2. latex agglutination test for capsular polysaccharide antigen (CSF and serum)
77
Q

What is the treatment of cryptococcal meningitis?

A

several months/lifelong therapy

78
Q

What fungal agents are responsible for causing aspergillosis?

A
  1. aspergillus fumigatus
  2. aspergillus favus
79
Q

Aspergillus species are acquired from:

A

the environment by inhalation of conidia

80
Q

Aspergillus species grow as ___ in immunosuppressed individuals

A

hyphae

81
Q

Aspergillus species grow as hyphae in:

A

immunosuppressed individuals

82
Q

What are the symptoms of aspergillosis?

A

Usually a pulmonary or sinus infection

83
Q

The growth of aspergillus through blood vessel walls causing tissue infarction, hemorrhage & necrosis:

A

angioinvasive growth

84
Q

Describe the diagnosis of aspergillosis:

A

culture on sabouraud’s agar (grows in a few days)

85
Q

Treatment of aspergillosis includes:

A

high mortality however expanded spectrum azole voraconazole may be effective

86
Q

Rhizopus and Nucor are the main genres of:

A

zygomycosis

87
Q

Describe Rhizopus and Mucor:

A

angioinvasive, aspettate, and broad hyphae

88
Q

In addition to standard risk groups, patients with ___ are at risk of zygomycosis

A

DM with ketoacidosis

89
Q

Why are patients with DM with ketoacidosis at an increased risk for zygomycosis?

A

because acidosis reduces neutrophil chemotaxis and phagocytosis

90
Q

The spread from nares/sinuses to palate, orbit, face, then to brain:

A

rhinocerebral zygomycosis

91
Q

Treatment of zygomycosis includes:

A

amphotericin B and aggressive surgical debridement

92
Q

Pneumocystosis is caused by the fungal species:

A

pneumocystis jiroveci

93
Q

Penuocystis jiroveci is an organism that has never:

A

been grown in vitro

94
Q

most people infected with pneumocystosis are infected:

A

early in life but disease only occurs due to immunosupression

95
Q

What is the biggest risk factor for disease symptoms associated with pneumocystosis?

A

T-cell deficiency (immunosupression)

96
Q

Most common opportunistic infection in AIDS patients before antiviral therapy:

A

pneumocystis pneumonia

97
Q

Pneumocystis jiroveci is and organism rarely found:

A

outside lungs

98
Q

Treatment of pneumocystosis includes:

A

Trimethoprim-sulfamethoxazole (used prophylactically)

99
Q

What is the target for treatment with Trimethoprim-sulfamethoxazole for pneumocystosis?

A

target folic acid synthesis and utilization

P. Jiroveci lacks ergosterol

microbiology (24 decks)

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