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invasive fungal infections Flashcards

1
Q

where is fungi freely present?

A

the environment ( soil)
some parts of the normal flora in humans/ animals

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2
Q

what are 3 endemic fungi (not part of the normal human flora)

A

histoplasmosis
blastomycosis
coccidiomycosis

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3
Q

what are the 4 opportunistic fungi (part of the normal human flora ( microbiota))

A

candidiasis
aspergillosis
mucormycosis
cryptococcosis

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4
Q

what is the primary defense mechanism against endemic and opportunistic fungi ?

A

innate immunity

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5
Q

why are fungi increasingly recognized as a major pathogen

A

intentional immunosuppression
-cancer treatments, immunosuppressive agents

use of broad spectrum antibiotics
-imbalances normal flora
-increast risk of opportunistic fungi

general advances in medical care
-surgery, aggressive treatment, organ treatment, HIV/AIDS

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6
Q

invasive infections

A

high mortality
disseminated, deep organ

effects blood, heart, brain, lungs, eyes, bones

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7
Q

esgrosterol inhibitors/binders class includes

A

polyenes
azoles
allylamines (terbinafin)

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8
Q

cell wall active agents include

A

echinocandins

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9
Q

intracellular active agents include

A

flucytosine

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10
Q

MOA of Polyenes

A

intercalate the cell membrane by directly binding to ergosterol –.> leakage of intracellular contents

concentration- dependent

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11
Q

spectrum of activity for polyenes : AMB

A

all candida
aspergillus terreus
some mucorales
some fusarium
all endemic

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12
Q

what is the formulation of amphoterin B

A

IV

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13
Q

conventional amphotericin B

A

amphotericin B deoxylate (AmB-d, fungizone)

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14
Q

lipid amphotericin B

A

amphotericin B lipid complex ( ABLC, abelcet)

liposomal amphotericin B (L-AmB, AMbisome)
- more favorable
- more expensive for dose escalations

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15
Q

amphotericin B ADME

A

A; poor, all formulations are IV products
D: tissue, blood, liver, body fluid,urin, CSF (poor, best L-AmB)
M; none
E: feces/ urine (AmB-d)

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16
Q

amphotericin B side effects

A

infusion-related reactions
-preventable: pre-medication, slow infusion, pre-hydration

nephrotoxicity
-tubular damage, vasoconstriction

electrolyte abnormalities
-hypokalemia
-hypomagnesemia

thrombophlebitis

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17
Q

monitoring parameters for amphotericin B

A

signs and symptoms of nephrotoxicity , potassium (4) , magnesium (2)

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18
Q

MOA of -azoles

A

Bind to 14 alpha-demethylase, a fungal CYP450, which subsequently depletes ergosterol in the cell membrane, leading to:

(1) impaired membrane fluidity
(2) accumulation of toxic 14 alpha-methylated sterols intracellularly
(3) collateral inhibition of human CYP enzymes leading to DDIs

AUC:MIC ratio dependent killing

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19
Q

what azole drugs have >90% bioavailability

A

fluconazole
voriconazole
isavuconium

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20
Q

what azole drugs have 50% bioavailability

A

itraconazole

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21
Q

what azole drugs unpredictable bioavailability

A

posaconazole

-especially unpredicatble if pt has poor appetite due to N/D, mucositis, GvHD invoking gut/colon

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22
Q

formulation and specific instructions for fluconazole

A

IV and PO
take with or without food

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23
Q

formulation and specific instructions for voriconazole

A

IV and PO
take on empty stomach

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24
Q

formulation and specific instructions for isavunconazonium

A

IV and PO
take with or without food

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25
formulation and specific instructions for itraconazole
PO only - caps: take with high fat meal or acidic beverages -OS take on empty stomach
26
formulation and specific instructions for posaconazole
PO only -OS: the with high fat meal - devide dosed to improve absorption -
27
metabolism and drug interactions of azoles
inhibit CYP2C19, 2C9, and 3A4 to varying degree
28
azoles that are strong inhibitors of CYP3A4
itraconazole posaconazole
29
azoles that are strong inhibitors of CYP2C19
Voriconazole
30
fluconazole SE
QT prolongation GI, rash, hepatotoxicity
31
Itraconazole SE
QT prolongation; Contraindication in CHF GI, rash, hepatotoxicity
32
Voriconazole SE
QT prolongation photosensitivity, visual changes GI, rash, hepatotoxicity
33
Posaconazole SE
, QT prolongation GI, rash, hepatotoxicity
34
Isavuconazonium SE
elevated LFTs, hypokalemia, peripheral edema, infusion related reactions, shortening of QT GI, headache
35
MOA of each echinocanins
Competitive inhibition of ß-1,3-D-glucan polymers (the crosslinking structural components of fungal cell walls) AUC:MIC ratio dependent killing
36
echinocanins ADME
A: poor; IV only D: Blood, liver, kidneys, large intestines, spleen, and lungs - Minimal or undetectable in urine, CSF, eye -Highly protein bound M: hepatic (C, M) E: Caspofungin (Urine); Micafungin and Anidulafungin (feces)
37
SE of echinocandins
GI, headache, flushing, infusion-related pruritus, increased LFTs
38
monitoring of echinocandins
LFTs, Hypersensitivity
39
echinocandins drug interactions
minimal
40
what is the most common invasive fungal infection
invasive candidiasis
41
clinical presentation of invasive candidiasis
-Single or multi-organ involvement -Kidney, brain, myocardium, skin, eye, bone / joints  --Liver and spleen (common in patients undergoing chemotherapy for acute leukemia, lymphoma) -Symptoms: acute onset fever, tachycardia, tachypnea, chills, hypotension -Diagnosis: --Cultures: blood culture sensitivity ~ 50 % ----Lung, urine, GU/GI: Sometimes can be difficult to discern whether colonization or pathogen if there are co-infections w bacteria, etc.
42
what is the 1st line treatment for Candidemia/Disseminated Candidiasis
1st line: echinocandins
43
what is the alternative empiric treatment for noncritical ill pts & without azole exposure for Candidemia/Disseminated Candidiasis
azole used once culture / susceptibility data known & patients are clinically sta
44
what is the alternative agent if intolerance or antifungal resistance develops for Candidemia/Disseminated Candidiasis
Amphotericin B Lipid formulation preferred to minimize side effects, toxicities
45
what is the duration for treatment of candidemia and Disseminated candidiasis
Candidemia: 14 days from negative blood cultures, symptom resolution (repeat blood cultures q24-48h)​ Disseminated candidiasis: weeks to months until lesions have resolved on imaging​
46
clinical presentation of invasive aspergillosis
Single or multiorgan involvement Sites: -Common: lung ,sinuses -Other: CNS, skin, liver, spleen, heart, pericardium (uncommon) Symptoms: -pleuritic chest pain, fever, wheezing, hemoptysis; stuffiness, runny nose, headache Diagnosis -->Challenging -Cultures & histopathology Imaging: CT 
47
what is first line for invasive aspergillosis
Voriconazole
48
what are second line options for invasive aspergillosis
-AmB deoxycholate / lipid derivatives -Isavuconazole: newer agent, indicated for Invasive Aspergillosis; less data compared with voriconazole, AmB -Echinocandins: effective in salvage therapy; not recommended routinely as monotherapy for primary treatment -Posaconazole: only suspension studied in treatment/prophylaxis studies -Itraconazole: rarely recommended, reserved for less severe disease
49
what is the treatment duration for invasive aspergillosis
a minimum of 6–12 weeks, and suppression therapy may follow if immunosuppression state persists 
50
what class covers dimorphic/ endemic fungi ?
Polyene: AMB trizoles
51
epidemiology of blastomycosis
MS and OH river valleys; great lakes region Found in moist soils, decomposing matter (wood, leaves) Higher risk in persons participating in outdoor activities in wooded areas (forestry work, hunting, camping)
52
etiology of blastomycosis
Inhalation of conidia from air
53
risk factors of blastomycosis
Travel to/residence in an endemic area Occupational soil exposure Immunocompromised host
54
Presentation and diagnosis of blastomycosis
Clinical presentation --Asymptomatic infection, acute/chronic pneumonia, disseminated disease ---Fever, cough, night sweats, myalgias, arthalgias, chest pain --Disseminated blastomycosis ---Skin, bone / joint, or genitourinary tract ---Cutaneous blastomycosis reported in 40-80 % of cases, marker for multi-organ involvement Diagnosis -HISTORY, including travel -Direct visualization in cytology/histologic specimens -Culture (respiratory) -Urine antigen; may cross-react w/ H. capsulatum
55
epidemiology of histoplasmosis
MS and OH river valleys; Central/South America; Asia; Africa Organism grows best in soil containing bird/bat droppings (accelerate sporulation)
56
etiology of histoplasmosis
Inhalation of microscopic fungal spores
57
risk factors of histoplasmosis
Travel to/residence in an endemic area Occupational soil exposure, chicken coops, areas with bird droppings, cave exposure, demolition of old buildings Immunocompromised host
58
presentation and diagnosis of histoplasmosis
Clinical presentation depends on comorbidities, immune status, previous exposure  --Environment: duration, enclosed area, inoculum size Sites: --Disseminated disease: pulmonary, liver, spleen, GI, bone marrow, CNS, ocular, pericarditis (rare) Symptoms: --fever, malaise, headache, weakness, myalgias; cough, chest pain Diagnosis: Medical/travel history Cultures/histopathology, direct Antigen detection (serum, urine); antibody assays Imaging (pulmonary)
59
epidemiology of Coccidioidomycosis (valley fever)
San Joaquin Valley, CA SW US, N. Mexico, Central / S. America Organism grows best in soil
60
etiology of of Coccidioidomycosis (valley fever)
Inhalation of conidia
61
risk factors of Coccidioidomycosis (valley fever)
Travel to/residence in an endemic area Race: African-American, Filipino; Asian, Hispanic, Native Americans Pregnancy (especially 3rd trimester) Immunocompromised host
62
presentation & diagnosis of Coccidioidomycosis (valley fever)
Clinical presentation --Variable; majority of patients are asymptomatic ---Fever, cough, chest pain --> may mimic CAP --Sites: primarily pulmonary ---Disseminated (skin, bone/joints, CNS) Diagnosis HISTORY, including travel! Imaging (CXR, CT scans) Cultures/histopathology/direct microscopy Serologic (EIAs), PCR, and/or antigen testing

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