Fungal Pathogens - Hill Flashcards

1
Q

Describe the bimorphic behavior exhibited by most pulmonary mycoses.

A

At room temperature, exist as molds (mycelia); at body temperature, exist as yeasts.

“Yeast in the heat, mold in the cold”.

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2
Q

Who is susceptible to infection by pulmonary mycoses?

A

The immunocompromised at at greater risk, but these can cause illness in the immunocompetent!

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3
Q

Describe the natural setting and distribution of Histoplasma.

A

Found in rich, moist soil (with bird & bat feces) in the Mississippi and Ohio river valleys.

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4
Q

Distinguish a Histoplasma mold from a Blastomyces mold.

A

Both form branched hyphae, but histoplasma is multinucleate while blastomyces is uninucleate.

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5
Q

Which are more infectious, microconidia or macroconidia? Why?

What occurs upon inhalation of the infectious agent?

A

Microconidia–smaller, so better alveolar penetration.

Upon inhalation, microconidia are phagocytized (via CD2/18 antigens) and transform into yeasts.

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6
Q

Distinguish Histoplasma, Blastomyces, and Coccidiodes based on their appearance at body temperature.

A

Histoplasma forms yeast with narrow bud necks.

Blastomyces forms much larger yeast with broad bud necks.

Coccidioides forms spherules filled with endospores.

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7
Q

Describe the time progression of pulmonary infection in the three major mycoses

A

Histoplasma and Coccidiodes cause pulmonary illness about 1-3 weeks following exposure. Blastomyces takes about 4-6 weeks.

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8
Q

What are the pulmonary symptoms of histoplasmosis?

What does imaging reveal?

A

Non-specific flu-like syndrome.

Resembles miliary TB. Latent infection yields multiple calcified lesions & granulomas.

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9
Q

What complications can be seen in severe histoplasmosis?

A

Pericarditis, ocular fibrosis, and fibrosing mediastinitis (causes SVC syndrome, cor pulmonale, and mitral stenosis).

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10
Q

What are the treatment indications for Histoplasma?

A

Often, no treatment is necessary. Itraconazole can be given as an adjunct.

If severe/disseminated, give Itraconazole + Amphotericin B.

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11
Q

Describe the natural setting and distribution of Blastomyces.

A

Found in rich/moist and acidic soil along rivers. Prevalent in mississippi & Ohio river valleys (like Histo), but also around the Great Lakes.

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12
Q

How does primary Blastomyces infection occur?

What doesn’t occur in the lung?

A

Inhalation of microconidia.

Unlike histo, Blasto microconidia do not require phagocytosis to transform. They form yeasts extracellularly, and are too large to be phagocytosed.

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13
Q

What are the most common clinical syndromes seen in Blastomycosis?

A

Flu-like pulmonary infection (usually benign & self-limiting, sometimes granulomatous)

Sometimes skin infection (primary or disseminated) yielding SubQ nodules or papules.

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14
Q

What are the treatment indications for Blastomyces?

A

Treat with Itraconazole; add Amphotericin B if severe/disseminated.

More aggressive therapy than with Histo?

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15
Q

Describe the natural setting and distribution of Coccidioides.

When are flares of infection seen?

A

Found in mineral-rich soils in hot & arid climates (San Joaquin valley).

Incidence highest in late summer & autumn (driest season). Spikes with storms, construction, or anything that can kick up the mold.

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16
Q

Describe the two morphs of Coccidioides.

A

Outside: Multicellular hyphae form barrel-shaped arthroconidia.

Inside: Spherules with endospores.

17
Q

What special populations must be considered in evaluating Coccidioides infection?

A

Pregnant women, construction workers, agricultural workers, ranchers.

Note: Incidence higher in darker-skinned ethnicities.

18
Q

What are the treatment indications (and CONTRAINDICATIONS) for Coccidioides?

A

Usually no antifungals necessary. If severe: Itraconazole + Amphotericin B.

Note: Azoles are TERATOGENIC

19
Q

Which mycosis is often coincident with bronchogenic carcinoma, TB, and other severe pulmonary diseases?

A

Blastomyces

20
Q

Recall the mechanism of action of Itraconazole and Amphotericin B.

A

Itraconazole (and most azoles) block ergosterol synthesis from lanosterol by blocking 14a-demethylase.

Amphotericin B binds Ergosterol in the cell wall.