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Respiratory 2 > Fungal Pathogens & Anti-Fungals > Flashcards

Fungal Pathogens & Anti-Fungals Flashcards

1
Q

Why have fungal infections become more prominent in the last several years?

A

1) Patients are living longer (more older people)

2) Immunosuppression therapies for other illnesses make patients more prone to opportunistic fungal infections

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2
Q

Who are susceptible to fungal infections?

A

Primary immunodeficiencies (CGD, other immune defects)
Acquired immunodeficiencies (HIV/AIDs, Cancer, transplant, immune modulating drugs)
Mech. Ventilation
Catheters
Organ dysfunction
ICU-acquired sepsis

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3
Q

Cells involved in immunity against fungal infections

A

Innate: neutrophils and band cells (immature)
Adaptive: CD4+ Th1 cells

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4
Q

Why are fungal infections so evenly spread across in HIV patients with low CD4+ T lymphocyte counts?

A

The lower the # of CD4+ cells, the more likely to get fungal infections since there is no adaptive cells to fight the fungal pathogens.

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5
Q

Examples of opportunistic fungi

A

1;. Yeast (Candida, cryptococcus, pneumocystis)

  1. Molds (aspergillus, mucor & rhizopus)
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6
Q

Examples of yeasts (3 total)

A

Candida
Cryptococcus
Pneumocystis

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7
Q

Examples of molds (3 total)

A

Aspergillus

Mucor & Rhizopus (zygomycetes)

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8
Q

Examples of dimorphic (systemic or endemic mycoses) fungi (4 total)

A

Histoplasma
Blastomyces
Coccidioides
Paracoccidioides

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9
Q

Examples of branching bacteria (2 total)

A

Actinomyces

Nocardia

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10
Q

How is mold transmitted?

A

through inhalation of airborne CONIDIA

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11
Q

What happens to conidia in absence of sufficient pulmonary defenses?

A

conidial germination occurs

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12
Q

What are the two possible outcomes of conidial germination if it successfully occurs?

A
  1. If Neutropenia: excessive hyphal growth and dissemination

2. In corticosteroid-induced immunosuppression: PMN recruitment and tissue damage

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13
Q

Mold that exists as septate hyphae in tissue with V-shaped branching

A

Aspergillus fumigatus

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14
Q

What are examples of respiratory tract infections caused by Aspergillus?

A
  • sinusitis
  • ABPA
  • Aspergilloma
  • Chronic necrotizing aspergillosis,
  • invasive aspergillosis
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15
Q

What is the exaggerated response of the immune system that is caused by Aspergillosis and associated with asthma and CF? What is the treatment?

A

Allergic Bronchopulmondary Aspergillosis (ABPA)

Itraconazole; maybe corticosteroids

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16
Q

What is the fungus ball that grows inside lung cavities, often from TB? What is the treatment?

A

Aspergilloma (aka mycetoma)

surgery + antifungal

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17
Q

Treatment for invasive Aspergillus

A

azoles (Voriconazole)
Amphotericin B
Echinocandins

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18
Q

Imaging, microscopy/histopathology, culture, and fungal antigen tests, and NAAT are diagnostic tests for

A

Apergillus

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19
Q

Fungal antigen detection test targets what in Aspergillus?

A

Galactomannan or B-D-glucan in the cell wall

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20
Q

What Aspergillus structure will be identified in lab-grown cultures but not in tissues (infected cells)?

A

Conidia structure

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21
Q

What type of mold is becoming increasingly resistant to azole?

A

pan-resistant Aspergillus

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22
Q

Aseptate mold with wide angle branching; causes Rhinocerebral (sinus infection spreading to brain), GI, and cutaneous infections

A

Mucor & Rhizopus species

aka. Zygomycetes

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23
Q

Hallmark of mucor & Rhizopus species

A

Necrosis following angioinvasion (hemoptysis)

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24
Q

How is Mucor & Rhizopus diagnosed?

A

Direct observation in tissue

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25
Q

Treatment for Mucor & Rhizopus species (Zygomycetes)

A

Amphotericin B

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26
Q

“dimorphic” fungi means what?

A

Fungi is in the mold form in the environment (25 celcius) and in the yeast form in the body (37 celcius)

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27
Q

Oval yeast cells INSIDE macrophages; fungal homolog of MTB and can cause pneumonia with cavitary lesions

A

Histoplasma capsulatum

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28
Q

Possible dissemination to liver, spleen, bone marrow can occur with

A

Histoplasma capsulatum

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29
Q

How is Histoplasma capsulatum diagnosed?

A

Direct observation is tissue, culture, URINE antigen test

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30
Q

Treatment for Histoplasma capsulatum

A
  1. No txt if asymptomatic/mild

2. Itraconazole or Amphotericin if serious

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31
Q

Thick-walled extracellular yeast with broad-based budding (looks like a dumbbell); commonly infects skin, bones and joints

A

Blastomyces dermatitidis

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32
Q

How does Blastomyces dermatitidis act in acute or chronic pneumonia setting?

A
  1. Acute pneumonia: looks like bacterial, but doesn’t respond to antibacterial therapy; may progress to ARDS
  2. Chronic Pneumonia: looks like TB and Histo
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33
Q

How is Blastomyces dermatitidis diagnosed?

A

Direct observation in tissue and culture

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34
Q

Treatment for Blastomyces dermatitidis

A

Itraconazole or Amphotericin B (even for asymptomatic)

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35
Q

Difference between Histoplasma and Blastomyces mold (conidia) forms

A

Histoplasma: bumpy cones
Blastomyces: smooth cones

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36
Q

If you have step 1 question, and it asks how you would treat a fungal infection and you don’t know the answer, your best bet is…

A

Amphotericin B (it’s toxic though, so be careful in the real world)

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37
Q

fungal infection with spherules (w/ endospores inside) in tissue and barrels in environment; often disseminates to skin, lymph nodes, bones, and joints

A

Coccidioides immitis (Valley Fever)

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38
Q

Causes erythema nodosum (desert bumps)

A

Coccidioides immitis (Valley Fever)

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39
Q

How is Coccidioides immitis diagnosed?

A

Direct observation in biopsy, culture (BAL or tissue) or skin test

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40
Q

Fungal infections that can be observed with lavage (BAL)

A

Pneumocystis jirovecii

Coccidioides immitis

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41
Q

Treatment for Coccidioides immitis

A

Fluconazole
Amphotericin B

  • if persistent or disseminating
42
Q

Fungal infection that can be diagnosed with urine antigen test

A

Histoplasma

43
Q

fungal infection that is endemic to Central and South America (Brazil); associted with outdoor work in rural areas

A

Paracoccidioides braziliensis

44
Q

Budding yeasts of Paracocciodioides are often described as __________ and may resemble the conidia of Histo

A

Ship’s Wheels

45
Q

Treatment for Paracoccidioides

A

azoles, Amphotericin B, or TMP-SMX

  • Long-term (1 year) needed
46
Q

Budding yeasts and/or pseudohyphae in tissues

A

Candida species (C. albicans)

47
Q

How is Candida diagnosed?

A

requires culture on Sabrouraud agar and germ-tube formation @37 degrees

48
Q

Candida pneumonia is rare except in

A

neutropenic patients

49
Q

Extrapulmonary infections (Chronic mucocutaneous candidiasis, candidemia) caused by Candida are

A

common

50
Q

Treatment for invasive candida infections

A

Echinocandins
Amphotericin B

*if invasive

51
Q

If a question stem involves “Sabouraud agar”, that implies that the infective agent is probably…

A

fungal

52
Q

heavily encapsulated yeast; meningitis is most common manifestation; usually with non-specific pulmonary symptoms (cough, fever, malaise)

A

Cryptococcus neoformans

53
Q

How is Cryptococcus diagnosed?

A

diagnose with direct visualization (india ink) with halo, culture or antigen detection

54
Q

With a cryptococcus neoformans infection with suspected meningitis, you also want to evaluate for…

A

pneumonia (and vice versa)

55
Q

Treatment for cryptococcus neoformans

A

Amphotericin B + Flucytosine

56
Q

Disc-shaped (cyst-like) yeast in lung tissue

A

Pneumocystis jirovecii

57
Q

Extrapulmonary infections are rare in Pneumocystis except in

A

AIDS

58
Q

What can be seen on CXR of Pneumocystis jirovecii?

A

diffuse interstitial pneumonia with “ground glass” infiltrates

59
Q

How is Pneumocystis diagnosed?

A

direct visualization in lung tissue, lavage (BAL), or sputum to diagnose

60
Q

Stain used to diagnose Pneumocystis

A

Silver Stain

61
Q

Treatment for Pneumocystis jirovecii

A

TMP-SMX

62
Q

Pneumocystis jirovecii is resistant to

A

most antifungals

63
Q

branching bacteria with “beaded” filaments; gram + aerobe that is weakly acid fast; pulmonary disease is typical, along with brain abscesses

A

Nocardia asteroides

64
Q

What pulmonary disease is typically caused by Nocardia?

A

pneumonia or lung abscess w/ cavity formation

65
Q

What other serious condition can be caused by Nocardia in immunocompromised patients?

A

Brain abscess

66
Q

How is Nocardia diagnosed?

A

Direct observation, culture

67
Q

Treatment for Nocardia asteroides

A

TMP-SMX

68
Q

branching bacteria, gram + anaerobe; normal oral flora that can lead to oral abscesses and PID w/ IUD

A

Actinomyces israelii

69
Q

How is Actinomyces diagnosed?

A

Direct observation is tissue biospy

70
Q

Treatment for Actinomyces israelii

A

Penicillin

71
Q

What are the three antifungal agents?

A
  1. Cell wall active agents
    - Polyenes (Amphotericin B)
    - Azoles
  2. B-Glucan synthesis inhibitors
    - Echinocandins (-fungin)
  3. DNA & Protein Synthesis Inhibitor
    - Pyrimidine analogue (5-Flucytosine)
72
Q

How does fungal antigen detection tests work?

A

Samples of urine, serum, BAL fluid, or CSF are used to detect fungal polysaccharides or proteins that have shed into body fluids during infection

73
Q

What does fungal antigen detection test look for in cryptococcus species? What sample is used?

A
  • Detects mannose-containing capsular polysaccharides

- serum or CSF

74
Q

What does fungal antigen detection test look for in Aspergillus? What sample is used?

A
  • Galactomannan released by growing hyphae

- Serum or BAL

75
Q

What does fungal antigen detection test look for in Histoplasma? What sample is used?

A
  • Different galactomannan polysaccharide

- URINE or Serum

76
Q

What fungal pathogen can cross react with other endemic fungi?

A

Histoplasma

77
Q

Penicillium which is the microbial source penicillin is now called

A

Talaromyces

78
Q

What is the MoA of Amphotericin B (polyene)?

A

Binds ergosterol and forms holes in the fungal cell membrane

79
Q

What is the molecular structure of Ampho B?

A

It has one hydrophilic face and one hydrophobic face

80
Q

How can fungal cells become resistant against Amphotericin B?

A
  1. reduce concentration of ergosterol in the membrane

2. modification of ergosterol to inhibit AmpB binding

81
Q

How is AmpB administered?

A

I.V. due to poor GIT absorption

  • oral only for lumenal GI infections
82
Q

Since AmpB is amphipathic, it is insoluble in water and must be formulated with _______ to keep it soluble in the plasma

A

lipids

83
Q

toxicities of Amphotericin B that occurs in nearly 100% after IV administration but abate in 30-45 minutes

A

“Shake and Bake” (fever, chills, muscle spasms)

84
Q

more severe toxicities of Amphotericin B

A

Nephrotoxicity (DCT damage)

  • especially in immunosuppressants patients, renal toxicities could be additive if they are taking other drugs with nephrotoxicity
85
Q

Amphotericin B pregnancy risk

A

Category B (safest anti-fungal during pregnancy)

86
Q

Azole antifungals inhibit fungal

A

ergosterol synthesis (inhibit lanosterol demethylase enzyme)

87
Q

Azole toxicity associated with heart

A

prolonged QT interval

88
Q

Azole pregnancy risk category

A

Category D (positive evidence of risk, but some situations may dictate)

89
Q

Azole toxicity associated with drug interaction

A

azole Inhibits a handful of CYP enzymes, decreasing the metabolism and increasing the serum conc. of other drugs (increase their toxicities)

  • especially for HIV drugs
90
Q

Azole toxicity associated with hormones

A

ketoconazole inhibits androgen synthesis and cause gynecomastia (breast enlargement in men) erectile dysfunction

91
Q

fungal mechanism of resistance against azoles

A

mutations of lanosterol demethylase

92
Q

why azoles and ampB should not be used together

A

azoles will cause less ergosterol in the cell membrane leading to reduced binding of ampB

93
Q

Why is Pneumocystis jirovecii resistant to anti-fungals?

A

Most anti-fungals target ergosterol, and pneumocystis doesn’t have it (uses cholesterol from host) and the lanosterol enzyme has natural resistance mutations

94
Q

SMX/TMP is used primarily for what fungal infection

A

Pneumocystis jirovecii

95
Q

Sulfonamides and Trimethoprim are folate synthesis inhibitors that target what enzymes?

A

Sulfonamides: Pteroate Synthase

Trimethoprim: DHFR

96
Q

Pneumocystis can become resistant against SMX/TMP by

A

mutations of pteroate synthase and DHFR

97
Q

PABA (intermediate product of SMX) can overwhelm both SMX/TMP drugs (True or False)

A

True

98
Q

SMX toxicities

A

Stevens-Johnson syndrome

99
Q

TMP toxicities

A

Hematologic (megaloblastic anemia, leukopenia, granulocytopenia)

  • due to folate deficiency
100
Q

SMX/TMP pregnancy categories

A

SMX: Category B
TMP: Category C

Respiratory 2 (6 decks)

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