Mycoses Flashcards

0
Q

This group of fungi includes cryptococcus neoformans

A

Basidiomycota

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1
Q

What is the largest group of fungi, which includes pathogens Aspergilllus and Candida. Sexual structures are asci, sacs of ascospores…

A

Ascomycota

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2
Q

Most medically important fungi are (Non/Motile)

A

NON-MOTILE

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3
Q

The main distinguishing factor of fugal cell membranes from humans is the presence of:

A

ERGOSTEROL

instead of cholesterol = good drug target

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4
Q

Describe the cell wall of a fungus in 3 basic layers (outside to in)

A
  1. Outer dense glycoprotein layer
  2. Inner glucan layer (Chitin in bottom of this layer)
  3. Cytoplasmic membrane (contains ergosterol)
    * polysaccharides account for 90% of a fungal cell wall mass *
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5
Q

______________ is an important target of innate immunity to fungi

A

Beta 1,3 Glucan of the cell wall

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6
Q

Anti-fungal therapy: What to AZOLES do?

A

target the fungal Cytochrome P450 Erg11A needed for ERGOSTEROL SYNTHESIS.

Drugs include: flucanazole, voriconazole

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7
Q

Anti-fungal therapy: What do polyenes do?

A

Target ERGOSTEROL DIRECTLY

Drugs include: Amphotericin B, Natamycin A

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8
Q

Anti-fungal therapy: What do Echinocandins do?

A

Target fungal BETA GLUCAN SYNTHESIS

Drugs: Caspofungin

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9
Q

Amphoterecin B is fungi(cidal/static)

A

FungiCIDAL

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10
Q

Nystatin is fungi(cidal/static)

A

FungiSTATIC

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11
Q

T/F: Polyenes are poorly absorbed by the GI tract

A

True

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12
Q

T/F: Amphotericin B CAN be used systemically

A

True, it is toxic but can be used systemically

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13
Q

T/F: Nystatin CAN be used systemically

A

False, nystatin is too toxic and can only be used as a topical/oral agent. (‘swish and swallow’ is safe because polyenes are not absorbed by GI tract)

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14
Q

T/F: Azoles CAN be used systemically

A

True, these are used for systemic mycoses.

They can cause hepatotoxicity in 0.01% of patients.

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15
Q

Azoles are fungi(cidal/static)

A

Fungistatic; they inhibit ergosterol synthesis.

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16
Q

Echinocandins are fungi(cidal/static)

A

FungiCIDAL; these inhibit 1,3 beta-D-glucan Synthase

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17
Q

Flucytosine
Drug class?
Cidal/static?

A

The only ANTIMETABOLITE antifungal drug. Inhibits fungal protein synthesis by replacing uracil with 5-fluorouracil in fungal RNA.

It can be BOTH fungicidal and static, depending on the fungus.

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18
Q

You have a fungus from a patient with a glucuronoxylomannan capsule. What is it??

A

Most likely Cryptococcus Neoformans.

This is the most common capsular fungus in medicine. Capsule may be found in urine, blood, CSF, etc.

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19
Q

What is Sabouraud’s agar and why is it used

A

An agar with acidic pH; used for fungi because they are acid tolerant and it enriches their cultures.

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20
Q

Aseptate or Coenocytic means:

A

Lack of Hyphae

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21
Q

Define: Spitzenkorper

A

Collection of vesicles near the tip specific to hyphal growth

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22
Q

What type of hyphal growth produces spores that are easily airborne?

A

Arial (as opposed to submerged, which is under the growth media)

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23
Q

Dimorphism means

A

growth in 2 different forms - hyphal or yeast, depending on environment.

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24
Q

The most common fungal infections are ________ infections and are cause by _________

A

Skin infections

Caused by Dematophytes

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25
Q

The dermatophytoses are caused by 3 fungal genera:

A
  1. Epidermophyton
  2. Trichophyton
  3. Microsporum
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26
Q

Disease caused by dermatophytes are termed

A

Tinea (body part)

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27
Q

Fungi that infect hair from the outside are termed ______

While those that infect hair from the inside are termed ________

A

Ectothrix

Endothrix

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28
Q

Tinea Versicolor is caused by the organism ______

A

Malassezia Furfur

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29
Q

Clinical picture of Tinea Versicolor infection

A

Hypopigmented areas appear on skin.

Is dimorphic in infected tissue

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30
Q

Tinea Nigra is caused by the organism __________

A

Cladosporium werneckii

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31
Q

Clinical picture of Tinea Nigra

A

Brown spots on skin cause by fungal melanin production.

Is dimorphic in infected tissue

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32
Q

How to diagnose Cutaneus fungal infection

A

KOH mount specimen

Culture only for ID of specific macroconidia

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33
Q

What are microconidia?

Macroconidia?

A

Microconidia are asexual spores that are small and airborne, often the infectious form of the fungus.

Marcoconidia are the large spores useful for identification

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34
Q

Subcutaneaus mycoses often come from fungi found __________

A

In soil or vegetation

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35
Q

Sporotrichosis:
Introduced by?
Clinical picture?

A

A subcutaneaus mycoses that is caused by sporothrix shenkii. It is introduced via puncture wound. Demonstrates classi dimorphism; budding yeast @ 37C and hyphae @ 25C.

Causes nodular lesions under skin from site of inoculation. Can disseminate if immunocompromised.

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36
Q

Chromoblastomycosis

A

Subcutaneaus mycoses that cause slow growing wart-like lesions with brown fungal cells.

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37
Q

Treatment for CUTANEOUS mycoses

A

Topical antifungal cream

Tineas

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38
Q

Treatment for SUBcutaneous mycoses

A

Oral azole therapy. Surgery may be needed.

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39
Q

At room temperature, Candida albicans would appear as a ______ _________

A

Budding Yeast

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40
Q

At 37C, Candida appears as:

A

Producing germ tubes, which become vegetative hyphae in culture. Arial hyphae are NOT formed.

41
Q

What part of the human body is colonized by Candida Albicans at birth?

A

The GI tract.

42
Q

The source of most Candida infections is:

A

The patients own endogenous flora; person to person can also happen.

43
Q

Which form of Candida Albicans is more adherent and invasive?

A

The Hyphal form (as opposed to the yeast form)

44
Q

Which form of Candida Albicans is believed to promote escape from biofilms?

A

The yeast form.

45
Q

What is a virulence ‘property’ of Candida Albicans

A

The ability to interconvert between the yeast and hyphal morphologies.

46
Q

Those who suffer from chronic mucocutaneous candidiasis have a genetic deficiency in:

A

Th17 Cell immunity

47
Q

What is the second most prevalent yeast pathogen after Candida albicans?

A

Candida Glabrata

48
Q

Among Candidia Glabrata and Candida Albicans, which is most resistant to azoles?

A

C. Glabrata is MORE RESISTANT

49
Q

Diagnosis of Candida

A

Culture! on blood or Sabauraud’s agar = smooth white colonies after 2 days

50
Q

Dectin-1

A

A host pattern recognition receptor that initiates immune response against fungi.

51
Q

Th17 cells have been found to play a critical role in fungal immunity. What does IL-17 do?

A

IL-17, which is secreted by Th 17 cells, recruits NEUTROPHILS and activates epithelial cells to initiate anti fungal defences.

52
Q

What stains would one use to visualize fungi histologically?

A

Periodic acid schiff
methanamine silver
GMS

53
Q

Coccidioidomycosis is endemic in:

Is more prevalent in:

A

Coccidioidomycosis is endemic in North, Central, and South America.
It is most prevalent among DARK SKINNED MEN

54
Q

The two species that can cause coccidiomycosis (Valley Fever) are:

A

Coccidioides Immitis and Posadasii

55
Q

Pathogenesis of coccidiomycosis:

A
  1. Inhaled arthroconidia lodge in the alveoli -> form spherules in tissue
  2. Rupture of spherule -> endospore release -> new spherule formation
  3. Initial response by host macrophage and neutrophil; but spherules are resistant to neutrophil
56
Q

T/F: Coccidiomycosis infection is often asymptomatic

A

True; 40% do have symptoms similar to lower resp. infection - cough, sputum, chest pain, malaise, fever, chills, anorexia, arthralgia.

57
Q

How long does Valley Fever last?

A

2-6 weeks. (coccidiomycosis)

58
Q

10% of coccidiomycosis patients may experience Erythema Nodosum (EN); what is EN and what does it indicate?

A

Erythema Nodosom is the formation of nodules that do not contain organisms. They are NOT indicative of disseminated disease, and INDICATE PROTECTIVE IMMUNITY

59
Q

The onset of cell-mediated immunity to Coccidiomycosis may take _______ days/weeks/months and is indicated by:

A

2-4 weeks. This is indicated by use of a DTH skin test, which indicates protective immunity.

60
Q

To diagnose coccidiomycosis:

A

detect spherules with KOH mount
Sarubouraud’s Agar
IgM Ab @ 2-4 weeks

Caution - arthrospores are hazardous to lab techs!

61
Q

Histoplasmosis is caused by what organism?

A

Histoplasma Capsulatum

62
Q

T/F: Histoplasma Capsulatum produces a capsule

A

FALSE - No capsule. They may look capsular due to staining but they are not.

63
Q

The tissue growth form (37C) of histoplasma capsulatum is:

A

Yeasts (ovoid, 1.5 - 2.0 micron)

64
Q

Name one important virulence property of H. Capsulatum

A

Ability to grow within macropahges

65
Q

Histoplasma capsulatum is highly endemic in ____ and ______

Also is found in __________

A

Endemic in Ohio and Mississippi valley regions.

Found in Bird shit.

66
Q

Histoplasmosis Pathogenesis:

After spores are inhaled into bronchioles and alveoli….

A
  • > germinate after 2-3 days
  • > proliferate in macrophage
  • > migrate to MEDIASTINAL LYMPH NODES
  • > cell mediated response in 9-15 days
67
Q

How do H. Capsulatum yeasts survive in marcopahges?

A

They increase the pH of phagolysosome by Bicarbonate and Ammonia production -> inactivates degradative enzymes.

68
Q

T/F: most histoplasmosis infections are asymptomatic

A

True; acute pulmonary histoplasmosis is self-limiting in immunocompetent,, often unoticed

69
Q

Chronic Pulmonary histoplasmosis is often mistaken for ______
and is opportunistic due to ______

A

Mistaken for TB

Often opportunistic due to structural lung defects which allow colonization in abnormal lung spaces.

70
Q

Your patient has Disseminated Histoplasmosis! What test should you perform that is (almost) always positive for intracellular yeasts within macrophages?

A

Wright stained smear of peripheral blood!

Also can use:

  • Culture lung tissue organisms -> need to demonstrate dimorphism
  • Histoplasma Ag urine test
  • Serology
71
Q

Why cant you use a skin test to confirm a H. Capsulatum infection?

A

Cross reactivity with Blastomyces Dermatitidis

72
Q

You see 5 - 30 micron yeast with SINGLE BUDS and BROAD BASES and maybe a PEAR SHAPED CONIDIA in the mold form. You’re lookin at:

A

Blastomyces Dermatitidis

73
Q

Blastomycosis is a common infection in ______

A

Doggies

74
Q

What is Bad1?

A

A surface protein on blastomyces dermatitidis required for virulence -> it PROMOTES UPTAKE BY MACROPHAGES where yeasts then multiply and are carried to other organs.

75
Q

Blastomycosis has tissue tropism for ____ and _____

A

Skin and bone

76
Q

Acute blastomycosis usually resolves spontaneously, but progressive disease can occur, involving:

A

The lungs + other organs. Often an influenza-like syndrome.

77
Q

You see large yeasts at 37C with THICK WALLS, MULTIPLE BUDS, and WAGON WHEEL appearance; you are looking at:

A

Paracoccidioides Brasiliensis

The cause of ‘south american blastomycosis’ - paracoccidioidomycosis

78
Q

How to treat a sick dude with any systemic fungal infection

A

Probably do nothing, most resolve by themselves.

If severe; Amphotericin B or azoles

79
Q

A key distinguishing feature of cryptococci is:

A

A prominent polysaccharide capsule composed of glucuronoxylomannan (GXM). No capsule = No virulence.
SUGAR COATED KILLA

80
Q

All pathogenic fungi are Urease (+/-) and grow at ____C

A

Urease +

Grow at 37C

81
Q

The disease caused by cryptococcus is:

A

Meningoencephalitis. Cryptococcci cause more life-threatening infection than any other fungus.

82
Q

Cryptococcus Neoformans grows abundantly in ____

A

Soil with bird droppings

83
Q

Cryptococcus gatti is found in the environment associated with

A

TREES…southwest canada

84
Q

The most common route of infection for Cryptococcus is

A

Inhalation of spores

85
Q

Cryptococcus has phenol oxidases which use ______ to make __________, which protects them from oxidative damage elicited by the host response.

A

Uses DOPAMINE to make MELANIN -> protection

86
Q

The cryptococcus fungus has a preference for invading:

It gets there by:

A

Preference for the CNS (meningoencephalitis)

It gets there thru the micro capillaries of the BBB or by phagocyte delivery.

87
Q

Diagnosis of C. Neoformans:

A

Capsular Ag in CSF

88
Q

T/F: Aspergillus fumigatus and flavus exhibit classic dimorphism

A

FALSE; aspergillus grow in the myocelial (mold) form ONLY and are NOT DIMORPHIC

89
Q

Mystery organism forms aerial hyphae in culture and in host tissue shows septate hyphae with V shaped branches…What is the mystery organism?

A

ASSPERGILLUS

90
Q

Aspergillus is an endemic or opportunistic infection?

A

aspergillus is an opportunistic fungus - it occurs in immunsupressed

91
Q

A common finding of aspergillosis after trauma or TB is the development of:

A

Aspergillomas, fungal balls

92
Q

The best way to diagnose aspergillosis is

A

Galactomannan ELISA

93
Q

organisms that form ‘right-angle’ branching in tissue and are not dimorphic are probably

A

mucormycoses/zygomycoses

94
Q

Increased susceptibility to mucormycoses/zygomycoses might occur in:

A

Diabetic Ketoacidosis

95
Q

The incidence of mucormycosis is increasing due to:

A

Prophylactic azole administration

96
Q

T/F: Pneumocystis Carinii can be cultured on Saurbaraud’s agar only

A

FALSE Pneumocystis CANNOT BE CULTURED ON ANYTHING EVER

97
Q

Each form of pneumocystis has a ‘specific form’ for each animal it infects; what is the human form called?

A

Pneumocystis Carinii

98
Q
Pneumocystis Carinii (jiroveci) is susceptible to:
It is NOT susceptible to:
A

Susceptible to antiparasitic drugs pentamidine and Trimethoprim sulfamethoxazole.

It is NOT susceptible to Amphotericin B

99
Q

UNLIKE most fungi, P. Carinii has ______ in its cell membrane instead of the usual _______ that appears in fungal cell walls.

A

P. Carinii has CHOLESTEROL in the cell membrane; most other fungi have ERGOSTEROL

100
Q

Pneumocystis pneumonia is often associated with early recognition of:

A

AIDS prior to the discovery of HIV
or
immunosuppressive therapies

101
Q

Loss of ________ immunity (specificly) leads to pneumocystis pneumonia

A

CD4+ immunity.

transmission is thru aerosols.