Invasive Fungal Infections Flashcards

1
Q

Unicellular, reproduce by budding

A

yeasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

multicellular, filamentous colonies

A

molds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Yeast classification

A
  1. candida spp

2. cryptococcus spp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Molds classifcation

A
  1. aspergillus spp
  2. coccidioidomycoses
  3. histoplasmosis
  4. blastomycosis
  5. mucormycosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

most common cause of invasive fungal infections especially in hospitals and ICU

A

candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are healthcare associated infections of candida (4)?

A
  1. broad spectrum antibiotic exposure
  2. corticosteroids
  3. dialysis
  4. prolonged use of intravascular catheters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are 5 different species of candida?

A
  1. candida albicans
  2. candida glabrata
  3. candida parapsilosis
  4. candida tropicalis
  5. candida krusei
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most common and susceptible candida

A

candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common candida in immunocompromised patients and organ transplant recipients

A

candida glabrata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A multi drug-resistant germ that spreads in healthcare facilities and behaves more like Nosocomial Bacteria than traditional Fungi (i.e., it is more difficult to contain and decontaminate than most Fungi)

A

candida auris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Challenges of Diagnosing Invasive Candidiasis (IC)

A
  • nonspecific clinical signs and symptoms
  • colonization vs infections
  • candida endopthalmitis
  • skin lesions
  • muscle soreness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Risk factors for getting candida (8)

A
  1. ICU stay of 7 or more days
  2. central IV lines
  3. neonates
  4. broad spectrum abx
  5. hemodialysis
  6. glucocorticoid use
  7. IV drugs use
  8. abdominal surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gold standard for diagnosing candida

A

blood cultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 disadvantages of blood cultures for candida

A
  1. slow turn around time 2-3 days
  2. antifungal sensitivities can takes 7 or more days
  3. false negatives occur in 40-75% of cultures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Disseminated candida

A

Candida likes to travel to highly perfused organs such as the Liver, Kidneys, and the Spleen, resulting in nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Problems with Diagnosing Invasive Fungal Infections

A
  1. Poor Diagnostic Tools with long turnaround times
  2. Empiric Antifungal Therapy is often delayed, putting patients at a
    heightened risk for mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

low resistance to Fluconazole (Diflucan®), making Fluconazole the drug of choice for this candida infection

A

candida albicans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What has an Acquired Resistance to

Triazoles like Fluconazole (Diflucan®)

A

candida glabrata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What has the highest rate of resistance to Fluconazole (above 80%),
but its’ high resistance does NOT confer cross-resistance to other Triazoles

A

candida krusel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2nd most common Fungi seen in hospitals

A

Aspergillosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

universal and occurs via inhalation

A

Aspergillosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

found in soil, plants, and indoors (i.e., black mold in showers)

A

Aspergillosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

most common invasive mold infection

A

Aspergillosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Aspergillosis resistant to amp B

A

A. terreus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ubiquitous in the environment, disease is most frequently seen in Immunocompromised patients

A

Aspergillosis

26
Q

Aspergillosis Disease Presentation in Immunocompetent Hosts

A

Allergic Reaction, specifically

Allergic Bronchopulmonary Aspergillosis (ABPA)

27
Q

Aspergillosis Disease Presentation in Patients with Immune Impairment

A
  1. Chronic Necrotizing Pulmonary Aspergillosis, or a
    “Fungal Ball”
  2. Fibrocavitary Aspergillosis
  3. Aspergilloma (i.e., Fungal Ball)
28
Q

Risk Factors for Invasive Aspergillosis (4)

A
  1. Prolonged Neutropenia
  2. Recipients of Hematopoietic Stem Cell Transplants (or Solid Organ Transplants)
  3. HIV Stage 3 (AIDS)
  4. Chronic Granulomatous Disease (i.e., COPD)
29
Q

Radiographic Findings of aspergillosis

A

halo sign

air crescent sign

30
Q

A Dimorphic Endemic Fungi

A

Coccidioidomycosis

31
Q

typically peaks in the fall (October) and late spring (May)

A

Coccidioidomycosis

32
Q

Five Main Clinical Manifestations of Coccidioidomycosis

A
  1. Acute Pneumonia
  2. Chronic Progressive Pneumonia
  3. Pulmonary Nodules and Cavities
  4. Extrapulmonary Non-CNS (Non-Meningeal) Disease
  5. Meningitis
33
Q

Coccidioides – Acute Pneumonia

A
  1. Onset: 1–3 weeks after exposure
  2. Severe Headache (may be indicative of Meningitis), Severe Pleuritic Chest Pain, Fatigue lasting several weeks to months, Hilar or Paratracheal Adenopathy seen on Chest X-Ray
34
Q

Sites of dissemination with coccidioides

A
  1. extra pulmonary disease

2. meningitis

35
Q

Extra-Pulmonary Disease

A
  • Occurs in less than 5% of immune-competent patients
  • Patients of African or Filipino ancestry are at an increased risk
    (possible genetic predisposition)
  • Pregnant women are also at an increased risk
36
Q

Meningitis

A

-more commonly seen

in Stage III HIV (AIDS) patients

37
Q

dismorphic fungi endemic to Ohio and Mississippi river valleys

A

histoplasmosis

38
Q

histoplasmosis

A
  • grows in rich soil in bird and bat droppings

- most common endemic mycosis causing human infection

39
Q

Disseminated histoplasmosis

A
  • symptomatic pts usually immunocompromised
  • chills, fever, anorexia, weight loss
  • GI tract, diffuse ulcerations of the mucosa
  • CNS involvement not common
40
Q

histoplasmosis chronic or mild to moderate infection treatment

A
  1. itraconazole preferred for non-severe infections

2. alt: amp b or fluconazole

41
Q

histoplasmosis moderately severe to severe or CNS disease

A

lipid formulation of amp B followed by intraconazole

42
Q

yeast with a thick polysaccharide capsule that blunts a

patients’ immune response

A

Cryptococcus

43
Q

Epidemiology Cryptococcus neoformans

A
  • Immune Compromised

- Clinical manifestations: Pulmonary Disease and Meningitis

44
Q

Epidemiology Cryptococcus gatti

A
  • Immune Competent

- Clinical manifestations: Cryptococcomas, Neurological involvement, Prolonged therapy

45
Q

“Necrotizing Fasciitis of the Fungal World”

A

Mucormycosis

46
Q

one fungal infection that can affect Immune Competent patients, as well as Immunocompromised patients

A

Mucormycosis

47
Q

Mucormycosis Risk Factors in Immune Competent Individuals

A
  1. Major Trauma / Inoculation and Contaminated Lacerations
  2. Surgery and Use of Contaminated Materials
  3. ICU Stay with High Acuity
  4. Iron Chelation Therapy, specifically with Deferoxamine
  5. Burns
48
Q

Mucormycosis Risk Factors in Immunocompromised Individuals

A
  1. Diabetes, specifically Diabetic Ketoacidosis (DKA)
  2. Uremia / Metabolic Acidosis
  3. Hematological Malignancies, particularly Leukemias
  4. Stem Cell Transplant
  5. Solid Organ Transplant
  6. Immunosuppressive Drugs (i.e., Corticosteroids)
49
Q

Mucormycosis clinical presentation

A

-Infarction and Necrosis of Host Tissue
- usually begins in Nasal Turbinates (i.e., the Rhino-Orbital-Cerebral) or
Alveoli (Pulmonary)

50
Q

Management of Candidemia Preferred Initial Therapy

A

Echinocandins (may be Oral Therapy if isolates are

susceptible to oral Antifungal agent) At least 2 weeks if no dissemination has occurred to other sites

51
Q

Management of Candidemia Alternative Therapy

A

Fluconazole (Diflucan®) may be considered in non-

critically ill patients who are unlikely to have Fluconazole-Resistant Candida spp.

52
Q

Management of Candidemia precautions

A

i. Remove Central Venous Catheters if possible
ii. A Dilated Ophthalmological Examination should be performed prior to initiating
therapy to look for sites of dissemination
iii. Repeat blood cultures daily to establish Clearance

53
Q

Aspergillosis Treatment

A

-Voriconazole
- If an Aspergillosis patient cannot tolerate Voriconazole, we may deescalate to
Amphotericin B

54
Q

Coccidioides Treatment

A

-the drug of choice is Fluconazole
(Diflucan®), 400 mg or more IV (or PO) daily
- alt: itraconazole po only

55
Q

Cryptococcal Treatment Mild-to-Moderate Pulmonary Disease

A

Fluconazole (Diflucan®) Oral Therapy

56
Q

Cryptococcal Treatment Severe Pulmonary Disease OR Cryptococcal Meningitis

A
  • Amphotericin B IV PLUS 5-Flucytosine for 2 wks. Minimum

- Maintenance Therapy – Fluconazole (Diflucan®) 12 mg / kg initially, then 6 mg / kg for 6–12 months

57
Q

Mucormycoses Treatment

A
  • Liposomal Amphotericin B (L-AmB®), 5–10 mg / kg / day

- Alt: Posaconazole (Noxafil®) PO tablets or Isavuconazole (Cresemba®)

58
Q

Mechanism of Action – Decrease Ergosterol Synthesis by inhibiting Fungal Cytochrome P450 enzymes (i.e., Lansterol14 Demethylase). This prevents Fungal Cells from incorporating Ergosterol into the plasma membranes of newly formed Fungal Cells, drastically reducing their growth

A

triazole

59
Q

Mechanism of Action – Bind to Ergosterol in Fungal Plasma Membrane and
forms “Pores” in the Fungal Cell Membranes. These pores disrupt membrane
permeability, allowing intracellular molecules to “leak out”

A

Polyenes (Amphotericin B)

60
Q

Mechanism of Action – Inhibit Fungal Cell Wall Synthesis by inhibiting Beta-(1,3)- D-Glucan Synthesis; Beta-(1,3)-D-Glucan Synthesis is a polysaccharide component of Fungal Cell Walls

A

Echinocandins

61
Q

Mechanism of Action – 5-Flucytosine (5-FC) gets converted into 5-Fluorouracil
(5-FU), which gets incorporated into Fungal RNA to inhibit Fungal Protein
synthesis

A

5-Flucytosine (5-FC) – DNA / RNA Synthesis Inhibitor