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(C) CM 1B: ID/EENT > Lecture 8: Fungal Diseases > Flashcards

Lecture 8: Fungal Diseases Flashcards

1
Q

What are the classes of antifungals?

A

Azoles
Polyenes
Echinocandins
Mitotic inhibitors
Allyamines
Flucytosine (Ancobon)
Ibrexafungerp (Brexafemme)

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2
Q

What are the two types of azoles?

A

Triazoles (for systemic or cutaneous infections)

Imidazoles (topicals mainly)

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3
Q

What falls under triazoles?

A

Fluconazole
Itraconazole
Voriconazole
Posaconazole
Isavuconazole

FIVPI (No letters overlap with the imidazoles)

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4
Q

What is the MOA of an azole?

A

Inhibit synthesis of ergosterol

Systemic resistance is increasing!!

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5
Q

Which azole tends to have less DDI than any other?

A

Fluconazole

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6
Q

What can slow azole metabolism?

A

Grapefruit juice
Alcohol (binge)
Some abx and some GERD meds

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7
Q

What can increase azole metabolism?

A

Alcohol (chronic), several anticonvulsants

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8
Q

What are the minor SE of azoles?

A

GI UPSET (N/V/D, abd pain) HA; taste changes

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9
Q

What are the major SE of azoles?

A

Hepatotoxicity, QT prolong, seizures, leukopenia, thrombocytopenia

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10
Q

What are the CIs of azoles?

A

Similar SE drugs

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11
Q

What kind of patients should not take azoles?

A

Caution in hepatic/renal impairment
Pregnancy (mainly systemic in 1st tri)

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12
Q

What is the prototype of the azoles?

A

Fluconazole (narrow range but covers the common)

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13
Q

When is fluconazole indicated?

A

C. albicans
Cryptococcus
The FCC

CSF (superficial or uncomplicated systemic)

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14
Q

What is itraconazole the DOC in?

A

Histoplasmosis
Sporotrichosis
Blastomycosis

BISH

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15
Q

What is Voriconazole the DOC in?

A

Invasive aspergillosis (mold)

Vacuum the mold

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16
Q

What are posaconazole and isavuconazole the DOC in?

A

Invasive infections in immunocomped or resistant infections.

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17
Q

What is the key diff between posa and isavu azoles?

A

Posa gets into CSF well.
Isavu gets into brain tissue well, not CSF. (i save ur brain)

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18
Q

What azoles are the broadest spectrum?

A

Posa and Isavu

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19
Q

Which topical azoles can be QD instead of BID?

A

Eco
Keto

Eko friendly

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20
Q

What are the cheapest OTC topical azoles?

A

Clotrim
Micon

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21
Q

What is the MOA of a polyene?

A

Bind to ergosterol in the membrane, creating pores and leaking cell contents.
Polyenes have high affinity for fungal ergosterol.

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22
Q

What should you avoid using nystatin for?

A

Systemic therapy.

Nystatin has severe SE with systemic administration.

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23
Q

When do we use amphotericin B? Why?

A

For severe, disseminated mycotic infections. It is often the initial tx while we wait for culture results.

It has very broad spectrum activity.

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24
Q

What are the adverse effects of ampho B?

A

Infusion-related: fever, chills, N/V, HA
Renal: IMPAIRMENT, NEPHROTOXIC
Electrolytes: HypoK, HypoM, HyperC acidosis
Others: Anemia, hypotension

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25
Q

When do we use nystatin?

A

Non-invasive candidal infections. (It is topical and oral rinse form)

Oral, vulvovaginal, intertrigo

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26
Q

What are the adverse effects of Nystatin?

A

Topical: Local irritation
Oral Rinse: Local irritation, GI upset

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27
Q

What are the echinocandins?

A

Caspofungin
Anidulafungin
Micafungin

All IV.

Echidnas are candid fun guys

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28
Q

What is the MOA of the echinocandins?

A

Inhibits synthesis of beta-(1,3)-d-glucan, needed in cell walls.

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29
Q

When are echinocandins used?

A

Invasive fungal infections:

Disseminated candidiasis
Aspergillosis (esp HIV pts)

DEA

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30
Q

What are the adverse effects of echinocandins?

A

Infusion-related: dyspnea, flushing, hypotension
Common: GI upset, HA, fever, insomnia
Serious: HEPATOTOXICITY, HypoK, anemia

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31
Q

What is the mitotic inhibitor and its MOA?

A

Griseofulvin.

Acts on cell wall and DNA synthesis, no clear.

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32
Q

What is unique about the admin of griseofulvin?

A

Greasy griseo.

Oral absorption best with a fatty meal.

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33
Q

When do we use griseo?

A

Dermatophyte/tinea infections of hair and skin.

Greasy skin, greasy hair

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34
Q

What are the DDIs of griseo to be worried about?

A

Alcohol (di-sulfiram like)
Contraceptives
Warfarin
Barbs

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35
Q

What are the CIs of griseo?

A

Liver failure
Porphyria
PREGNANCY (Absolute CI)

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36
Q

What are the main AE of griseo?

A

HA, GI upset, skin rashes, dizziness

Serious: GRANULOCYTOPENIA, hepatotoxicity, teratogenic.

Need weekly CBCs.

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37
Q

What drug is an allylamine? MOA?

A

Terbinafine

Interferes with ergosterol synthesis.

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38
Q

What is important regarding terbinafine administration?

A

Irritating to mucous membranes

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39
Q

When is oral terbinafine used?

A

Onychomycosis
Dermatophyte/tinea infections of hair and skin

DOT

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40
Q

When is topical terbinafine used?

A

Dermatophyte/tinea infections of hair and skin

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41
Q

What are the DDIs of terbinafine?

A

BBs
TCAs
Tamoxifen
Tramadol

T and B

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42
Q

What is the main CI for terbinafine use?

A

Liver disease

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43
Q

What are the AE of terbinafine?

A

HA, GI upset, rashes, taste disturbances

Serious:
Hepatoxicity
Neutropenia

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44
Q

What is the MOA of flucytosine?

A

converted to 5-FU upon entering a cell, which is an antimetabolite.

Inhibits fungal RNA and protein synthesis.

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45
Q

When is flucytosine used?

A

Adjunct for amphotericin B in cryptococcal meningitis
Severe candidal or cryptococcal infections (IC pts)

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46
Q

What are the AE of flucytosine?

A

BBW: Renal impairment use

Renal: Renal failure, increased need for BMPs
Hepatic: injury, toxicity, GI upset
Heme: Pancytopenia/aplastic anemia
CNS: peripheral neuropathy, confusion, psychosis, dizziness, ataxia

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47
Q

What is ibrexafungerp’s MOA? drug class?

A

Inhibits glucan synthase, used to make part of cell wall.

New class: triterpenoids

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48
Q

What is ibrexafungerp indicated for?

A

Vulvovaginal candidiasis (Single day tx)

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49
Q

What is ibrexafungerp CId in?

A

pregnancy

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50
Q

What are the AE of ibrexa?

A

GI: Abd pain, N/D
Rare GI: elevated AST/ALT, flatulence, V

GU: vaginal bleeding, dysmenorrhea
Other: Rash, dizziness, back pain

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51
Q

What are the other topical antifungals for tineas only?

A

Butenafine (OTC)
Tolnaftate (OTC)
Naftifine (RX only)

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52
Q

What are the other topical antifungals for onychomycosis only?

A

Ciclopirox
Tavaborole
Efinaconazole (not a real azole) (no generic)

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53
Q

What is the main superficial candidiasis strain?

A

Candida albicans

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54
Q

What increases risk of candidiasis?

A

Chronic disease: CKD, cancer, HIV, DM
Meds: Steroids, immunosupps, broad-spectrum abx
Vascular access: IVDU, IV catheters
Other: recent abd surgery, prolonged neutropenia, organ transplant.

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55
Q

What is candidiasis of the mouth and esophagus or lower respiratory indicative of?

A

AIDS-defining conditions.

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56
Q

What kind of pts usually get oral candidiasis?

A

Infants
Elderly
DM
Immunodef
Post med use

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57
Q

What does oral candidiasis present as?

A

Beefy red, edematous mucosa of oral cavity.

+/- white plaques on tongue, palate, buccal, oropharynx
SCRAPABLE PLAQUES

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58
Q

How do we Dx oral candidiasis?

A

Clinically is OK

KOH prep: bud yeasts, pseudohyphae
Culture: checking which species.

59
Q

How do we Tx oral candidiasis?

A

Topically:
Nystatin
Clotrimazole
Miconazole

Systemic:
Fluconazole

1-2 weeks for all tx.

60
Q

What is the alternate tx to oral candidiasis that we avoid?

A

Gentian violet x3 days
(faster tx but stains everything violet)

61
Q

How does esophageal candidiasis present?

A

Odynophagia
Nausea
Reflux
+/- oral thrush

62
Q

How do we actually Dx esophageal candidiasis?

A

Endoscopy

63
Q

How do we Tx esophageal candidiasis?

A

Systemic only!

Oral:
Fluconazole (2-3 weeks)
Itraconazole (if failed flu)

IV:
Fluconazole (2-3 weeks)
Vori, Posa, Enchinocandin (if failed flu)

64
Q

What ups the likelihood of vulvovaginal candidiasis?

A

HIV
Pregnancy
ABX use
Uncontrolled DM

65
Q

What are the S/S of vulvovaginal candidiasis?

A

Discomfort: pruritis, burning, pain, dyspareunia
Discharge: thick, white, malodorous, cottage cheese

66
Q

What PE findings suggest vulvovaginal candidiasis?

A

Erythematous, edematous mucosa
+/- erythema, edema, excoriations
Thick, white, curdy, cottage cheese easily removed by swab.

67
Q

How do we Dx vulvovaginal candidiasis?

A

Clinically.

KOH prep
Culture

68
Q

How do we Tx vulvovaginal candidiasis topically?

A

Topical:
1,3,7 day regimens of micon, clotrim, tercon azoles.

69
Q

How do we tx vulvovaginal candidiasis systemically?

A

Fluconazole 1 dose
Ibrexafungerp 2 doses 1 day

70
Q

How do we tx recurrent/prophylaxis for vulvovaginal candidiasis?

A

Azoles: topical PV or flu x1 week
Probiotics: maybe

71
Q

What is the alternative tx for vulvovaginal candidiasis?

A

Gentian violet
Boric acid PV

72
Q

Where does candidal intertrigo usually appear?

A

Skin folds

73
Q

What increases the risk of candidal intertrigo?

A

Obesity
Tight clothing
Sweating
Incontinence
DM
Immunosupps
Meds

74
Q

How does candidal intertrigo present?

A

Erythematous, macerated, well-defined plaques
Satellite erythematous papules and pustules

75
Q

How do we Dx candidal intertrigo?

A

Clinically.

KOH prep (skin scrapings)
Culture

76
Q

How do we tx candidal intertrigo?

A

Correct underlying factors. use drying agents (talc, nystatin powder)

Topical azoles/nystatin

Systemic fluconazole

77
Q

What are the 6 tineas?

A

Tinea capitis (scalp)
Tinea corporis (ringworm/body)
Tinea cruris (Jock itch/groin)
Tinea pedis (Athlete’s foot)
Tinea unguium (Nail/onych)
Tinea versicolor (Body/pityriasis versicolor)

78
Q

Which tinea is a fake one?

A

Tinea versicolor

79
Q

What is the etiology and diagnostic technique for tineas?

A

Etiology: dermatophytes eat keratin sources.
Species: epidermophyton, trichphyton, microsporum

Diagnostic technique: KOH prep should show segmented hyphae.

80
Q

How does tinea capitis present?

A

Single/multiple scaly, circular patches on scalp.
Alopecia, black dots at follicles.
Enlarging patches.

81
Q

Who is tinea capitis most common in and how do I Dx?

A

Children primarily, seen in child-to-child contact.

Clinical Dx, KOH prep/culture only for ambiguous/refractory.

82
Q

How does tinea corporis (ringworm) present?

A

Early: Pruritic, erythematous, scaling, circular, or oval plaque.

Later: spreads outward. Central clearing with raised, scaly border.

83
Q

Who is tinea corporis most common in and how do I Dx?

A

Person to person
Infected animal

Clinical Dx

KOH only for ambiguous/refractory.

84
Q

How does tinea cruris (Jock itch) present?

A

Asymptomatic or itchy
GROIN and GLUTEAL CLEFT
Erythematous lesions with scaly, sharp, spreading margins. May have central clearing.

85
Q

Who is tinea cruris most common in and how do I Dx?

A

Males

Risk factors: Obesity, DM, immunodeficiency, sweating

Clinical Dx

KOH only for ambiguous/refractory.

86
Q

How does tinea pedis (athlete’s foot) present?

A

Itching, burning, stinging of toes and feet.
Erythematous bullae (acute) => scaling, fissuring, macerated skin, thickened papules

Acute exacerbations are self-limiting, often triggered by sweat.
Continues indefinitely without treatment.

87
Q

Who is tinea pedis most common in and how do I Dx?

A

Teens and adults, esp. MALES and ATHLETEs.
Contact via shower spores, poools, etc…
Often have cruris, manuum, and unguium also.

Clinical Dx.

KOH only for ambiguous/refractory and can be false-negative if skin was macerated.

88
Q

How does tinea unguium (onychomycosis) present?

A

Thickened nail with yellowish or brownish discoloration, may separate from nail bed.

89
Q

Who is tinea unguium most common in and how do I Dx?

A

Elderly
Swimmers
Tinea pedis people
Immunocompromised
DM
Psoriasis

KOH prep/culture recommended to r/o other nail disorders. NOT CLINICAL DX.

90
Q

How do I treat tinea capitis?

A

Systemic only. Can use griseofulvin.

Terbinafine, fluconazole, itraconazole.

91
Q

How do I treat tinea corporis, tinea cruris, and tinea pedis?

A

Topically or systemically.

92
Q

What can I recommend for tinea cruris besides an oral antifungal?

A

Drying powder: Talc or nystatin powder.

93
Q

How do I treat tinea unguium?

A

Topically or systemically.
Systemic: terbinafine

94
Q

What topical antifungal is specifically not effective for dermatophyte infections?

A

Topical Nystatin is a nono

95
Q

What are the main risk factors for disseminated candidiasis?

A

Severely immunocomped
Nosocomial

96
Q

How does disseminated candidiasis present?

A

Minimal fever to septic shock.
Skin lesions from pustules to nodules
May involve liver, kidney, spleen, eyes, and heart.

97
Q

How do I diagnose disseminated candidiasis?

A

Blood cultures. Only 50% positive ):

98
Q

What is first-line treatment for disseminated candidiasis?

A

IV echinocandins: Caspofungin with loading dose.
(Good for critically ill or non-albicans strain)

99
Q

What is the other treatment for disseminated candidiasis and how long?

A

Mild-moderate = fluconazole with loading dose.
2 weeks past the last positive blood culture.

100
Q

In WV, what are the two main fungal strains to be worried about?

A

Histoplasmosis
Blastomycosis

101
Q

How is histoplasmosis transmitted? What is the nickname?

A

Inhaled spores via bird and bat droppings.

Batman and robin disease

102
Q

What is the organism that causes histoplasmosis and where does it usually begin in the body?

A

Histoplasma capsulatum

Lungs, spreading to the body.

103
Q

What are the 4 major presentations of histoplasmosis?

A

Asymptomatic
Acute pulmonary histoplasmosis
Progressive disseminated histoplasmosis (HIV+ or TNF-blockers)
Chronic pulmonary histoplasmosis

104
Q

How does asymptomatic histoplasmosis present?

A

Incidental CXR showing pulmonary or splenic calcifications.
Often described as EGG SHELL lymph node calcification.

105
Q

How does acute pulmonary histoplasmosis present?

A

Fever, cough, myalgia, minor chest pain.
Mild FLS to severe pna for 1 wk to 6 mo.

CXR shows miliary infiltrates and mediastinal LAN.

Often in land development when soil is disturbed that has droppings.

106
Q

How does progressive disseminated histoplasmosis present?

A

Fever, cough, dyspnea, weight loss, prostration, oropharyngeal ulcers.
Multiple organ system involvement.

CXR shows miliary infiltrates and mediastinal LAN.

Can also have a fulminant, septic shock presentation.

107
Q

How does chronic pulmonary histoplasmosis present?

A

CXR shows apical cavities, chronic infiltrates, and pulmonary nodules.

Often in older pts with chronic underlying disease.

Presents like a chronic lung disease, but complications of granulomatous mediastinitis can occur.

108
Q

What is granulomatous mediastinitis?

A

Persistent mediastinal LAN leading to fibrosis.

109
Q

What are the complications of granulomatous mediastinitis?

A

SVC syndrome
Esophageal constriction

110
Q

What diagnostic studies should you order for histoplasmosis and what would they show?

A

CMP: elevated AST
LDH: elevated
Ferritin: elevated
CBC: Pancytopenia possible

Sputum culture (chronic); Blood culture (Disseminated)
Bronchoscopy + biopsy.

CXR and CT Chest vary depending on presentation

111
Q

What is the treatment for mild-moderate histoplasmosis?

A

Itraconazole (HIV/AIDS needs it lifelong)

112
Q

What is the treatment for severe histoplasmosis?

A

Amphotericin B

113
Q

What is the treatment for granulomatous mediastinitis?

A

Itraconazole +/- rituximab +/- corticosteroids.

Consider surgery

114
Q

What causes coccidioidomycosis and what is its nickname?

A

Coccidioides immitis
Coccidioides posadasii

Valley fever

115
Q

How is valley fever transmitted? MC demographics?

A

Inhaled spores.

Arid soil in southwest US, mexico, central america.
Immunocomped and elderly and endemic areas.

Responsible for 15-30% of CAP in endemic areas.

116
Q

What are the 3 possible presentations of valley fever?

A

Asymptomatic (60%)
Primary
Disseminated

117
Q

How does primary valley fever present?

A

INcubation of 10-30 days, followed by FLS.
Arthralgia and joint edema in knees and ankles.
Erythema nodosum may appear (bilateral shin rashes)

CXR shows INFILTRATE, cavities, abscesses, nodules, bronchiecstasis (5%)

118
Q

How does disseminated valley fever present?

A

Worsened pulmonary s/s: mediastinal LAN, cough, sputum, abscesses
Multiorgan involvement: skin, bones, pericadium/myocardium, meningitis

Fungemia possible, death imminent.

CXR shows LOCALIZED INFILTRATE, thin-walled cavities, etc
Local valley

119
Q

What ethnicities are MC for disseminated valley fever?

A

Non-white:
Filipino
Black

Also pregnant women and immunosuppressed.

120
Q

What will I see in diagnostic studies for valley fever?

A

CBC: Leukocytosis, eosinophilia (you can test for IgM and IgG complement fixation titer (sometimes neg)

Cultures: Blood cultures are rarely positive

Bronchoscopy: with biopsy and culture. MOST RELIABLE.

CXR: patchy, nodular, upper lobe infiltrates are MC.

121
Q

How do I treat mild-moderate valley fever?

A

Fluconazole or itraconazole

122
Q

How do I treat severe/disseminated valley fever?

A

Amphotericin B followed by an azole.

123
Q

When do AIDS pts get prophylaxis for valley fever?

A

CD4 < 250 with azole.

124
Q

What causes blastomycosis? What is the nickname?

A

Blastomyces dermatitidis

Woodsman disease

125
Q

How is woodsman disease transmitted and where is it most common?

A

Inhaled spores found in moist soil with decomposing organic matter.

MC in outdoors men.
South central and midwestern US + Canada

Often occurs in immunoCOMPETENT pts.

126
Q

What are the 3 presentations of woodsman disease?

A

Asymptomatic
MC: Chronic pulmonary infection
Disseminated

127
Q

How does chronic woodsman disease present?

A

FLS
Wart-like skin lesions

S/S may become pneumonia like.

128
Q

How does disseminated woodsman disease present?

A

Rare, only immunocompromised generally.

Bone pain: ribs and vertebrae MC
GU: epididymitis, prostatitis, bladder irritation
Skin: nodular lesions.

Often a DDx for UTI in men.

Morning wood => epididymitis

129
Q

How do diagnostic studies present for woodsman disease?

A

CBC: Leukocytosis, anemia
Urine antigen: cross-reacts with histoplasma
Cultures: sputum or blood.
Bronchoscopy: with biopsy and culture (most specific?)
CXR: Consolidation or masses (a forest consolidates)

urine antigen: his wood

130
Q

How do I treat mild-moderate woodsman disease?

A

Itraconazole (2-3 months)

131
Q

How do I treat Severe/CNS involvement woodsman disease?

A

Amphotericin B

132
Q

What causes cryptococcosis?

A

Crytococcus neoformans (worldwide)
Cryptococcus gattii (tropical regions and pacific NW)

133
Q

How is cryptococcosis transmitted?

A

Inhaled spores via soil and PIGEON dung.

Clinically significant in immunocompromised pts.

C. gattii is more likely to infect regular people and cause severe disease.

134
Q

How does pulmonary cryptococcosis present?

A

Mild to resp failure.
Simple nodules or fever, infiltrates, dyspnea

135
Q

How does Cryptococcal meningitis present?

A

MC cause of Fungal meningitis

HA followed by AMS, fever, CN abnormalities.

Often NO MENINGEAL SIGNS in HIV+ esp.

136
Q

How does skin cryptococcosis present?

A

Nodular lesions
Mimics bacterial cellulitis

Mainly in immunocompromised pts

137
Q

What diagnostic study results would I expect in cryptococcosis?

A

Serum: cryptococcal antigens
Cultures: Sputum, blood, urine
Bronchoscopy: Sputum
CSF: Budding, encapsulated yeast; + cryptococcal antigen

138
Q

What is the treatment for pneumonia cryptococcosis?

A

Fluconazole for 6-12 months.

139
Q

What is the treatment for cryptococcal meningitis?

A

Amphotericin B + Flucytosine (2 weeks
Followed by 8 weeks of fluconazole

Possible LP or CSF shunting for high CSF pressure

140
Q

What is the main cause of pneumocystosis?

A

Pneumocystis jirovecii (previously named carinii)

PJP or PCP

141
Q

How is PCP transmitted?

A

Airborne.

Most pts had an asymptomatic infection when younger.

Epidemics occur among preemies or debilitated infants in underdeveloped countries.

Sporadic in older people with impaired immunity, esp AIDS.

142
Q

How does PCP/PJP present?

A

Abrupt onset of fever, tachypnea, SOB, non-productive cough
+/- bibasilar crackles on exam
Spontaneous pneumothorax possible.
Rapid deterioration and death if not treated.

143
Q

What do diagnostic studies show for PCP?

A

CXR: diffuse interstitial infiltration. (5-10% normal CXR)
Cultures: CANNOT CULTURE
Bronchoscopy: special testing of respiratory specimens required (giemsa, methenamine silver, PCR, MAB testing)

144
Q

What is the treatment for PCP?

A

TMP-SMZ first line. CD4 < 200 need prophylaxis.

Second: primaquine/clindamycin, trimethoprim-dapsone

(C) CM 1B: ID/EENT (27 decks)

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