Fungal Infections Flashcards

(26 cards)

1
Q

What are the clinical forms of Candida albicans infections?

A

Superficial (e.g., thrush on mucosal surfaces) and invasive (e.g., heart, CNS, eye, liver).

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2
Q

How does Candida albicans appear morphologically at 20°C vs. 37°C?

A

20°C: Yeast with pseudohyphae.

37°C: Germ tube formation.

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3
Q

What is a common superficial infection caused by Candida albicans?

A

Thrush (white patches on mucosal surfaces, e.g., mouth, vagina).

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4
Q

What type of patients are most at risk for Cryptococcus neoformans infections?

A

Immunocompromised patients (e.g., HIV/AIDS, transplant recipients).

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5
Q

What are the primary clinical forms of Cryptococcus neoformans infection?

A

Pulmonary (lungs, primary site)

CNS (meningitis, encephalitis)

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6
Q

How does Cryptococcus neoformans appear microscopically?

A

Yeast with a thick gelatinous capsule, staining PAS+ and mucicarmine+.

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7
Q

What are the key histopathological findings in:
a) Immunocompromised patients?
b) Immunocompetent patients?

A

a) Soap-bubble lesions (capsule-filled spaces)

b) Granulomas/suppuration

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8
Q

What is the primary site of Cryptococcus neoformans infection before dissemination?

A

The lungs (pulmonary infection).

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9
Q

Which patient population is most at risk for Pneumocystis jirovecii pneumonia (PJP)?

A

AIDS patients (severely immunocompromised).

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10
Q

What are the classic clinical features of PJP?

A

Rapidly progressive bilateral pneumonia.

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11
Q

What is the preferred specimen for diagnosing PJP?

A

Bronchoalveolar lavage (BAL) fluid (shows organisms/exudate).

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12
Q

How does Pneumocystis jirovecii appear on Gomori methenamine silver (GMS) stain?

A

Cup-shaped or oval yeast with a central dot (GMS+).

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13
Q

What histologic finding is classic for PJP in lung tissue?

A

Eosinophilic honeycomb exudate in alveolar spaces.

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14
Q

What lab marker supports PJP or invasive fungal infection?

A

Elevated 1,3-β-D-glucan in serum or BAL.

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15
Q

Match the yeast to its morphologic hallmark:
a) Blastomyces dermatitidis
b) Coccidioides immitis
c) Paracoccidioides brasiliensis

A

a) Broad-based budding

b) Spherules

c) Mariner’s wheel (multiple budding).

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16
Q

What are the three clinical forms of aspergillosis?

A

Allergic bronchopulmonary aspergillosis (ABPA)

Colonizing aspergillosis (fungus balls in lung cavities)

Invasive aspergillosis (lungs, heart valves, brain).

17
Q

How does Aspergillus appear microscopically?

A

Septate hyphae branching at acute angles (45°).

18
Q

What are the tissue findings in:
a) Colonizing aspergillosis?
b) Invasive aspergillosis?

A

a) Fungus ball with sparse/chronic inflammation

b) Angioinvasion → vasculitis, hemorrhagic necrosis.

19
Q

Which Aspergillus species produces aflatoxin, and what is its complication?

A

Aspergillus flavus → increased risk of hepatocellular carcinoma.

20
Q

What is the hallmark of invasive aspergillosis on histopathology?

A

Angioinvasion leading to vasculitis and necrotizing lesions.

21
Q

Which patients are at highest risk for colonizing aspergillosis?

A

Those with pre-existing lung cavities (e.g., from TB, emphysema).

22
Q

Which patient populations are at highest risk for mucormycosis?

A

Immunocompromised or diabetic patients.

23
Q

What are the three clinical forms of mucormycosis?

A

Pulmonary

Gastrointestinal

Rhinocerebral (nasal eschar → brain/orbit invasion).

24
Q

How does Mucor appear microscopically?

A

Non-septate hyphae branching at right angles (90°).

25
What is the hallmark histopathologic feature of invasive mucormycosis?
Angioinvasion → vasculitis & hemorrhagic necrosis.
26
What is the classic presentation of rhinocerebral mucormycosis?
Nasal eschar → rapid spread to orbit and brain.