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Microbiology > Fungi B & Antifungal Treatments (EXAM IV) > Flashcards

Fungi B & Antifungal Treatments (EXAM IV) Flashcards

1
Q

Why are their fewer effective antifungal agents?

A

Because of the similarity of fungal cells & human cells

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2
Q

It is easier to treat ______ fungal infections vs. ____ 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 this:

A

Ergosterol

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4
Q

Where is ergosterol found?

A

In fungal cell memrbanes

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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 used to treat systemic disease:

A

Amphotericin B

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7
Q

Give an example of a polyene compound used to treat topical disease:

A

Nystatin

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8
Q

Polyene compounds cause ______ leading to:

A

Altered membrane permeability; leading to 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 use of polyene compounds?

A

Their ability to bind cholesterol in mammalian cells

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11
Q

Why is Filipin a potent but toxic antifungal agent?

A

Due to the binding of cholesterol

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12
Q

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

A

Squaline Epoxidase

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13
Q

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

A

C14-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 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 demethylation:

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 & 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 & 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 cell walls:

A

echinocandins

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25
Q

What is the significance 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 & Candida species

A

Narrow spectrum

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28
Q

Why are echinocandins considered narrow spectrum against Aspergillus & Candida species?

A

Because these fungi have larger amounts of Beta-(1,3)-D-glucans

(and this is the target of these agents)

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29
Q

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

A

Pyrimidine inhibition

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30
Q

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

A

Caspofungin

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31
Q

Pyrimidine inhibition interferes with:

A

Fungal protein & DNA synthesis

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32
Q

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

A

Candida species & cryptococcus neoformans

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33
Q

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

A

Because resistance develops quickly if used alone

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34
Q

High risk categories for opportunistic mycoses include:

A
  1. Immunocompromised individuals
  2. Burn victims
  3. Long-term IV catheter users
  4. Broad-spectrum antibiotic therapy
  5. Diabetes mellitus
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35
Q

Candidiasis is caused by the fungal species (3):

A
  1. Candida albicans
  2. Candid glabrata
  3. Candida parapsilosis
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36
Q

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

A

Candida albicans

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37
Q

Responsible for some candidiasis infections & often resistant to some antifungals:

A

Candida glabrata

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38
Q

Responsible for some candidiasis infections & 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 of candidiasis:

A

Neutrophil function

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 & 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 pseudomembranous (acute erythematous)
  2. Chronic plaquelike/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 erythematous

49
Q

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

A

Candida-associated angular chelitis

50
Q

Psuedomembranous candidiasis lesions on the palate; easily wiped off:

A

Thrush

51
Q

Form of candidiasis that cannot be easily removed by scraping:

A

Plaquelike/nodular Candidiasis

52
Q

Plaquelike/nodular candidiasis is called: (2)

A
  1. Chronic hyperplastic candidiasis
  2. Candidal leukoplakia
53
Q

What is the significance of plaquelike/nodular candidiasis?

A

Up to 40% of lesions develop into oral cancer

54
Q

With angular chelitis there is frequently:

A

A bacterial component

55
Q

How is mucosal candidiasis diagnosed?

A

Scrape & 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. Calofluor white
58
Q

Staining methods to visualize fungi in clinical sample that stain surface carbohydrate:

A

Periodic acid-Schiff (PAS) & Grocott-Gomori mehenamine 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 spreads in healthcare facilities:

A

Candida auris

63
Q

Why is candida auras 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 excreta:

A

Cryptococcus neoformans

65
Q

C. Neoformans is found worldwide in ______ contaminated with ____

A

Soil; bird excreta

66
Q

___% of patients with cryptococcosis appear to be _____

A

20% ; immunocompetent

67
Q

Discuss the events that lead to cryptococcosis:

A

Yeast cells are inhaled in alveoli & begin to produce a polysaccharide capsule

68
Q

The polysaccharide capsule produce in cryptococcosis inhibits ______ and _____

A

Phagocytosis & 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 resists ____ & ____

A

Free radicals & enzyme degradation

72
Q

The primary pulmonary infection of Cryptococcus 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 patient of 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 fluid & serum)
77
Q

What is the treatment of cryptococcal meningitis?

A

Several months/lifelong therapy required

78
Q

What fungal agents are responsible for causing Aspergillosis?

A
  1. Aspergillus fumigatus
  2. Aspergillus flavus
79
Q

Aspergillus species are acquired from:

A

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

immunocompromised 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 Sabourad’s agar (grows in a few days)

85
Q

What is the treatment of Aspergillosis?

A

High mortality however it may be treated with expanded spectrum Azole Voraconazole

86
Q

Rhizopus & Mucor are the main genera of:

A

Zygomycosis

87
Q

Describe Rhizomes & Mucor:

A

Angioinasive; aseptate & brand hyphae

88
Q

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

A

Diabetes mellitus with ketoacidosis

89
Q

Why are patients with diabetes mellitus in 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 may be seen in:

A

Rhinocerebral zygomycosis

91
Q

Treatment of zygomycosis includes:

A

Amphotericin B & aggressive surgical debridement

92
Q

Pneumocystosis is caused by the fungal species:

A

Pneumocystis jiroveci

93
Q

Pneumocystis jiroveci is an organisms that has never:

A

Been grown in itro

94
Q

Most people infected with pneumocystosis are infected:

A

early in life, but disease only occurs due to immunosuppression

95
Q

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

A

T cell deficiency (immunosuppression)

96
Q

Most common opportunistic infection in AIDS patients before effective antiviral therapy:

A

Pneumocystic pneumonia

97
Q

Pneumocystis jiroveci is a fungal 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 of pneumocystosis with Trimethoprim-sulfamethoxazol?

A

Target folic acid synthesis & utilization

(Jiroveci lacks ergosterol)

Microbiology (22 decks)

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