Fungal Infections Flashcards

1
Q

What are two major risk factors for Aspergillus infection?

A

Neutropenia, chronic granulomatous disease, lung dysfunction (asthma, emphysema)

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2
Q

Which species of Aspergillus is most commonly pathogenic in humans?

A

A. fumigatus

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3
Q

What is the infectious agent of Aspergillus?

A

The spores, or conidia

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4
Q

Describe the three steps in the pathogenesis of Aspergillus.

A

(1) Germination of the spores, (2) hyphal extension, (3) mold extension into vasculature

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5
Q

What is the presentation and the worst course of invasive aspergillosis?

A

It presents with respiratory symptoms and fever like a primary pulmonary infection, but can worsen to organ dissemination and can even spread to the CNS

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6
Q

What sorts of patients usually develop chronic aspergillosis?

A

Patients with altered anatomy (e.g. emphysema patients) but intact immune systems

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7
Q

What is an aspergilloma and why can it develop?

A

It is a fungal ball and can develop when patients have lung cavities (sometimes due to past TB)

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8
Q

How is allergic bronchopulmonary aspergillosis treated and why is it different from the usual tx?

A

It is treated with anti-inflammatories because it is an allergic reaction to the mold in asthma patients, and there is minimal hyphal extension

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9
Q

What are two crucial antigens in blood/BAL that can indicate Aspergillus?

A

Galactomannan and β-D-glucan

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10
Q

What is the appearance of Aspergillus under the microscope?

A

Regular, septate hyphae with acute angle branching

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11
Q

What is the radiographic appearance of invasive aspergillosis?

A

“Air crescent” sign of lungs, which forms as dead tissue is expectorated

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12
Q

What is the best treatment for aspergillosis?

A

Due to diagnostic challenges, empiric tx for this disease is crucial; mold-active azoles (voriconazole is the best), amphotericin B, echinocandins are less effective; surgical debridement can be indicated

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13
Q

What are two morphological characteristics of mucorales or zygomycete fungi?

A

Rapidly growing hyphal molds (grow on bread), broad hyphal diameter, few septa, ribbon-like folding in tissue

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14
Q

What is the classic (and most deadly) presentation of mucormycosis?

A

Rhinocerebral infection that spreads from the sinuses into other facial structures and even into the brain

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15
Q

What is the critical sign of rhino cerebral mucormycosis?

A

Palatal eschar, a necrotic lesion on the hard palate

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16
Q

What are alternate (less common) presentations of mucormycosis?

A

Pulmonary or GI infection

17
Q

What is the most effective diagnostic tool for mucor infection? What is ineffective?

A

Radiography is not effective because it is not specific; culture is a terrible idea because of contamination risk; histopathology is the move because you can see the ribbon-like, aseptate hyphae

18
Q

What is the treatment for mucormycosis?

A

Surgical debridement is really the only effective therapy; antifungals are not effective; Fe modulation has been approached as a potential therapy

19
Q

What is a major endemic fungus of the Southwest USA?

A

Coccidioides immitis/posadasii

20
Q

Distinguish the primary and chronic infections in coccidiomycosis/“valley fever.”

A

The primary infection is a self-limiting respiratory infection, while the secondary causes chronic pneumonia, skin, or eosinophilic meningeal infections

21
Q

Name the two different structures present in the tissue vs environmental forms of Coccidioides.

A

The tissue form contains spherules, or sacs of yeast cells while the environmental form has hyphae with many arthroconidia

22
Q

What is a major endemic fungus of the Ohio/Mississippi River valleys?

A

Histoplasma spp.

23
Q

Distinguish the primary and chronic infections in histoplasmosis.

A

The primary infection is a self-limiting respiratory infection, while the secondary causes chronic pneumonia, hiding in macrophages and DCs for years until it emerges, causing infections in AIDS or anti-TNF patients

24
Q

What is a major endemic fungus of the Great Lakes region?

A

Blastomyces spp.

25
Q

Distinguish the primary and chronic infections in blastomycosis.

A

The primary infection is a self-limiting respiratory infection, while the secondary causes chronic pneumonia, skin/bone lesions, and male GU tract issues.

26
Q

What is the defining characteristic of paracoccidiomycosis?

A

The captain’s wheel form in culture

27
Q

Describe the course of Sporothrix infection.

A

Primary skin inoculation followed by proximal spread via lymphatics causing “nodular lymphangitis”

28
Q

What is the mechanism of amphotericin B?

A

It binds ergosterol and forms pores in membrane, which disrupts the structure and causes cell death

29
Q

What are two major adverse effects of amphotericin B?

A

Renal toxicity and electrolyte changes; ototoxicity, altered vestibular function causing hearing loss and ringing in ears

30
Q

Which formulation of amphotericin B minimizes adverse effects?

A

Lipid associated amphotericin B

31
Q

What is the spectrum of amphotericin B?

A

Cryptococcal meningitis (induction phase); systemic mold infections (mucormycosis); serious endemic fungal infections; resistant Candida infections

32
Q

What is the mechanism of triazoles?

A

Inhibit the Erg11 protein in the ergosterol synthesis pathway

33
Q

What are two major adverse effects of triazoles?

A

P450 enzyme inhibition can cause liver and drug metabolism issues; QT prolongation

34
Q

Which azoles are mold-active and which are yeast-active?

A

Fluconazole is yeast-active and voriconazole, itraconazole, and posaconazole are mold-active

35
Q

What is the usage of fluconazole?

A

Candida, Cryptococcus neoformans maintenance-phase therapy

36
Q

What is the usage of the mold-active azoles?

A

Systemic infections of Aspergillus fumigatus; invasive yeast infections; endemic fungal infections

37
Q

What is the mechanism of echinocandins?

A

Inhibit β-glucan synthesis

38
Q

What is the usage of echinocandins?

A

Serious Candida infections like candidemia; second-line therapy for Aspergillus

39
Q

What is the usage of flucytosine?

A

C. neoformans meningitis, induction phase in combination with amphotericin B; never alone