8.3-ASPERGILLOSIS+MUCORMYCOSIS Flashcards

1
Q

What is the causative agent of Aspergillosis?

A

Aspergillus spp

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2
Q

What are the five most common Aspergillus species causing disease?

A

A. fumigatus (most common)
A. flavus
A. niger
A. terreus
A. lentulus

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3
Q

What is the mode of transmission (MOT) for Aspergillus?

A

Inhalation of conidia (spores)

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4
Q

What kind of fungi are Aspergillus species?

A

Ubiquitous saprobes (colonizing soil, plants, grains)

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5
Q

What type of immune reaction can Aspergillus cause in atopic individuals?

A

Severe allergic reactions to conidial antigens

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6
Q

What happens when immunocompromised patients inhale Aspergillus conidia?

A

Conidia germinate, forming hyphae that invade the lungs and other tissues

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7
Q

What is the causative agent of Aspergillosis?

A

Aspergillus spp.

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8
Q

What are the five most common Aspergillus species causing disease?

A

A. fumigatus (most common); A. flavus; A. niger; A. terreus; A. lentulus

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9
Q

What is the mode of transmission (MOT) for Aspergillus?

A

Inhalation of conidia (spores)

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10
Q

What kind of fungi are Aspergillus species?

A

Ubiquitous saprobes (colonizing soil, plants, grains)

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11
Q

What type of immune reaction can Aspergillus cause in atopic individuals?

A

Severe allergic reactions to conidial antigens

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12
Q

What happens when immunocompromised patients inhale Aspergillus conidia?

A

Conidia germinate, forming hyphae that invade the lungs and other tissues

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13
Q

Which Aspergillus species is the most common cause of aspergillosis?

A

A. fumigatus

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14
Q

What is a key morphological feature of A. fumigatus?

A

Sporulation occurs only from the upper half or two-thirds of the vesicle

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15
Q

What does an A. niger colony look like?

A

White with black pepper-like growth → Forms a radiate head

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16
Q

What does an A. flavus colony look like?

A

Yellow to yellow-green → Phialides cover the entire vesicle, pointing in all directions

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17
Q

What does an A. terreus colony look like?

A

Brown colonies → Phialides cover the entire vesicle

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18
Q

What is the first line of defense against Aspergillus conidia?

A

Alveolar macrophages engulf and destroy conidia

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19
Q

What happens if conidia survive in the lungs?

A

Conidia swell and germinate; Hyphae invade lung tissue and blood vessels; May cause aspergilloma (fungus ball) in preexisting lung cavities

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20
Q

What are the hallmark features of allergic bronchopulmonary aspergillosis (ABPA)?

A

Asthmatic reaction; Recurrent chest infiltrates; Eosinophilia; Type I (immediate) & Type III (Arthus) hypersensitivity

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21
Q

What symptoms are common in ABPA?

A

Difficulty breathing; Sputum with Aspergillus; Serum precipitins; Lung scarring

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22
Q

What can exposure to massive doses of conidia cause in normal hosts?

A

Extrinsic allergic alveolitis

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23
Q

Aside from the lungs, what other infections can Aspergillus cause?

A

Keratitis (eye); Nail infections; Endocarditis (heart); CNS infections

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24
Q

What is aspergilloma, and how does it form?

A

Fungus ball in preexisting lung cavities; Forms when inhaled conidia germinate & produce hyphae

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25
Q

What lung condition increases the risk for aspergilloma?

A

Cavitary diseases (e.g., tuberculosis, lung abscesses)

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26
Q

What are the symptoms of aspergilloma?

A

Cough; Dyspnea; Weight loss; Fatigue; Hemoptysis (coughing up blood)

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27
Q

How is aspergilloma usually treated?

A

Lobectomy (surgical removal of affected lung area)

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28
Q

Who is at highest risk for developing aspergilloma?

A

Immunocompromised patients (e.g., diabetics, corticosteroid users, AIDS patients)

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29
Q

What noninvasive Aspergillus infections can occur?

A

Localized colonization in: Nasal sinuses; Ear canal; Cornea; Nails

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30
Q

What is invasive aspergillosis?

A

Acute pneumonia with or without dissemination

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31
Q

What organs can invasive Aspergillus spread to?

A

Gastrointestinal tract; Kidney; Liver; Brain; Other organs

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32
Q

What patients are at highest risk for invasive aspergillosis?

A

Lymphocytic or myelogenous leukemia; Lymphoma patients; Stem cell transplant recipients; Patients on corticosteroids; AIDS patients (CD4 <50 cells/uL)

33
Q

What is the main risk factor for invasive aspergillosis in stem cell transplant patients?

A

Allogeneic transplants (higher risk than autologous transplants)

34
Q

What are the symptoms of invasive aspergillosis?

A

Fever; Cough; Dyspnea; Hemoptysis; Thrombosis, infarction, necrosis

35
Q

What is the gold standard for diagnosing Aspergillus infections?

A

Culture & histopathology

36
Q

What are the specimen types used for diagnosis?

A

Sputum; Bronchoalveolar lavage (BAL); Tissue biopsy; Blood (for disseminated infection)

37
Q

What is the key histopathological feature of Aspergillus?

A

Septate hyphae with acute-angle branching (45° angle)

38
Q

What serologic test is used to detect Aspergillus antigen?

A

Galactomannan antigen test

39
Q

What is the first-line treatment for invasive aspergillosis?

A

Voriconazole

40
Q

What are alternative antifungal treatments for Aspergillus?

A

Amphotericin B; Echinocandins (Caspofungin, Micafungin, Anidulafungin)

41
Q

Is aspergilloma (fungus ball) treated with antifungal drugs?

A

No, it requires surgical removal (lobectomy)

42
Q

Where is Aspergillus found in the environment?

A

Soil, decaying plants, grains, air

43
Q

What group of people should be extra cautious about Aspergillus exposure?

A

Immunocompromised individuals (e.g., transplant recipients, HIV/AIDS patients, plant enthusiasts in high-risk groups)

44
Q

What are the common specimen types used for Aspergillus diagnosis?

A

Sputum, respiratory tract specimens, lung biopsy tissue, blood samples

45
Q

What is the key microscopic feature of Aspergillus hyphae?

A

Hyaline, septate, uniform width (~4 µm), and dichotomous branching

46
Q

How quickly do Aspergillus species grow on culture media?

A

Within a few days at room temperature

47
Q

How are Aspergillus species identified?

A

By the morphology of their conidial structures

48
Q

What serologic test is positive in 80% of patients with aspergilloma or allergic aspergillosis?

A

ID test for precipitins to A. fumigatus

49
Q

What serologic marker is used for diagnosing invasive aspergillosis?

A

Circulating cell wall galactomannan

50
Q

What additional fungal marker helps diagnose invasive aspergillosis and candidiasis?

A

β-glucan detection

51
Q

What are the treatment options for aspergilloma?

A

Itraconazole or amphotericin B + surgery

52
Q

What is the first-line treatment for invasive aspergillosis?

A

Amphotericin B (native/lipid formulation) or voriconazole

53
Q

What adjunct therapy is often given for invasive aspergillosis?

A

Cytokine immunotherapy

54
Q

What antifungal is used for Amphotericin B-resistant Aspergillus species?

A

Posaconazole (for A. terreus, A. flavus, A. lentulus)

55
Q

What is the treatment for less severe chronic necrotizing pulmonary aspergillosis?

A

Voriconazole or itraconazole

56
Q

How are allergic forms of aspergillosis treated?

A

Corticosteroids or disodium cromoglycate

57
Q

What is the main preventive strategy for individuals at high risk for invasive aspergillosis?

A

Avoid exposure to Aspergillus conidia

58
Q

What prophylactic antifungal therapy is given to high-risk patients?

A

Low-dose amphotericin B or itraconazole

59
Q

What is another name for mucormycosis?

A

Zygomycosis

60
Q

What fungal order causes mucormycosis?

61
Q

What phylum and subphylum do Mucorales belong to?

A

Phylum Glomerulomycota, Subphylum Mucoromycotina

62
Q

What type of fungi are Mucorales?

A

Ubiquitous, thermotolerant saprobes

63
Q

What are the leading genera of fungi causing mucormycosis?

A

Rhizopus, Rhizomucor, Lichtheimia, Cunninghamella, Mucor

64
Q

What are the major risk factors for mucormycosis?

A

Acidosis, leukemia, lymphoma, corticosteroid treatment, severe burns, immunodeficiencies, dialysis with deferoxamine

65
Q

What is the major clinical form of mucormycosis?

A

Rhinocerebral mucormycosis

66
Q

What are the symptoms of rhinocerebral mucormycosis?

A

Edema of the involved facial area, bloody nasal exudate, orbital cellulitis

67
Q

How does thoracic mucormycosis develop?

A

Inhalation of sporangiospores with invasion of lung parenchyma and vasculature

68
Q

What causes massive tissue destruction in thoracic mucormycosis?

A

Ischemic necrosis

69
Q

What has thoracic mucormycosis been associated with?

A

Contaminated wound dressings and other situations

70
Q

What is the colony appearance of Mucorales?

A

Coarse, wooly, fluffy, white to gray or brown sporangium

71
Q

How fast do Mucorales hyphae grow?

A

Within 1–3 days, rapidly covering the agar surface

72
Q

What is the characteristic appearance of Rhizopus?

A

Large, broad, non-septate hyphae that produce horizontal runners (stolons), rhizoids at contact points, and sporangiospores in clusters

73
Q

How does Absidia differ from Rhizopus?

A

Sporangiospores arise between nodes from which rhizoids are formed

74
Q

What is the defining feature of Mucor?

A

No rhizoids (root-like structures)

75
Q

What are the key microscopic features of Mucorales?

A

Broad hyphae (10–15 µm), uneven thickness, irregular branching, sparse septations

76
Q

How do Mucorales colonies grow in culture?

A

Rapidly, producing abundant cottony colonies

77
Q

What is the basis for identification of Mucorales?

A

Sporangial structures

78
Q

What are the key treatment strategies for mucormycosis?

A

Aggressive surgical debridement, rapid administration of amphotericin B, control of underlying disease

79
Q

What residual effects may occur after treatment of rhinocerebral mucormycosis?

A

Partial facial paralysis or loss of an eye