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Infectious Disease 1 > JITT Fungals > Flashcards

JITT Fungals Flashcards

1
Q

How are fungi defined?

A

They’re heterotrophs (they eat dead material); they’re mostly aerobic (some facultative anaerobes); can be uni or multicellular

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2
Q

What kind of organisms are fungi?

A

Eukaryotes with active cytoskeleton

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3
Q

What is the predominant sterol in the fungi cell membrane?

A

ergosterol

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4
Q

What do polyenes do?

A

target ergosterol in the cell membrane, altering cell permeability and causing cell death

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5
Q

What do allylamines do?

A

block ergosterol synthesis (inhibits squalene epoxidase)

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6
Q

What do azoles do?

A

block ergosterol synthesis (inhibits 14 alpha demethylase)

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7
Q

What is the fungi cell wall composed of?

A

chitin, mannoprotein, and glucan

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8
Q

What do echinocandins do?

A

block glucan linkage (glucans can’t link into polymers within the cell wall)

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9
Q

How do fungi reproduce? What does it yield?

A

Asexual reproduction yields conidia; Sexual reproduction yields spores

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10
Q

What are the two fungi morphologies? What do they yield?

A

Yeasts and molds; Yeasts reproduce via budding; Molds reproduce via hyphae

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11
Q

How is a mycelium formed?

A

Hyphae create an intertwined mass

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12
Q

What is a dimorphic species?

A

interconvert between yeasts and molds: dimorphic species exist as molds in temperatures below 37 degrees and yeasts above 37

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13
Q

What is the heat shock response?

A

Conversion of dimorphic species from mold to yeast

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14
Q

What are superficial fungi?

A

usually direct inoculation from environment

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15
Q

What are endemic fungi?

A

Dimorphic species (Coccidiomycosis, Blastomycosis, Histoplasmosis)

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16
Q

What are opportunistic fungi?

A

part of native flora, require breach in host defense (crypto, asperg)

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17
Q

How does the host respond to fungi?

A

First defense is PMN-mediated killing; Macrophages active against local infections that have escaped PMNs; T cell response necessary to prevent systemic spread; Humoral response limited

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18
Q

What causes histoplasmosis?

A

HIstoplasma capsulatum var. capsulatum, the most prevalent endemic fungi, is a thermally dimorphic organism that grows in acidic, humid soil enriched with bat or bird droppings, in the Mississippi or Ohio River Valleys

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19
Q

What are exposure risks for histoplasmosis?

A

caves, chicken coops, old buildings or dead trees

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20
Q

What is the pathogenesis for histoplasmosis?

A

Microconidia are inhaled into alveoli and phagocytosed by macrophages. Yeast inhibit the phagolysosome complex, and survive inside the macrophage. The yeast evoke a granulomatous response. Some spread by traveling within the macrophage throughout the reticuloendothelial system (lymph nodes, spleen, bone marrow, peripheral blood, etc). Granulomas undergo fibrocaseous necrosis and calcification.

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21
Q

What are the 4 presentations of histoplasmosis?

A
  1. asymptomatic to mild cough (most immunocompetent individuals); 2. acute histoplasmosis (flu-like); 3. chronic cavitary (occurs in patients with preexisting lung disease); 4. disseminated (sepsis, multi-organ system dysfunction including adrenal failure or respiratory failure)
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22
Q

How is histoplasmosis diagnosed?

A

Gold standard is culture (50% sensitivity in disseminated disease, less in acute histoplasmosis), but fungal stains also used to support diagnosis. Urine and serum antigen tests are most sensitive (95% in disseminated, 80% in acute).

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23
Q

How is histoplasmosis treated?

A

Itraconazole. Longer courses needed to treat chronic cavitary disease. For severe acute histoplasmosis +/- CNS involvement or disseminated disease, use amphotericin B first and then switch to itraconazole

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24
Q

What causes blastomycosis?

A

Blastomycosis dermatidis is a thermally dimorphic organism that is endemic to the southeastern, southcentral, Midwestern and some northeastern states, particularly in areas with decomposing materials (eg, beaver dams)

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25
Q

What is the pathogenesis of blastomycosis?

A

Microconidia are inhaled into alveoli, phagocytosed and killed. Those that escape convert into thick walled, large yeasts with broad based buds that can survive in the extracellular space. Adehesins on their surface result in a pyogranulomatous response.

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26
Q

How does blastomycosis present?

A
  1. asymptomatic to mild cough (most immunocompetent individuals); 2. acute histoplasmosis (flu-like); 3. chronic (Looks similar to TB or malignancy; CXR may show cavitation, mass lesions or fibronodular infiltrates); 4. disseminated (diffuse lung involvement that leads to respiratory failure; also common in skin or bone)
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27
Q

How is blastomycosis diagnosed?

A

Gold standard is culture, but fungal stains are more sensitive. No widely accepted antigen or DNA probes are available.

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28
Q

How is blastomycosis treated?

A

Itraconazole. For severe acute blastomycosis +/- CNS involvement or for disseminated disease, use amphotericin B first and then switch to itraconazole. For refractory blasto or brain abscesses, fluconazole or voriconazole (which each have better CNS penetration) are appropriate options

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29
Q

What causes coccidiodomycosis?

A

There are two species, but one genus of this soil-dwelling thermally dimorphic fungi that grows in the Southwest US. Increased exposure occurs during archeological digs, after earthquakes, and during construction

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30
Q

What is the pathogenesis of coccidiomycosis?

A

Arthroconidia are aerosolized into the bronchioles, where they either mature to become very large spherules or undergo PMN mediated phagocytosis and death. Mature spherules rupture and release many endospores. Killing endospores requires a TH1 driven, adaptive immune response, which results in necrotizing granuloma formation. Endospores that escape can mature and become spherules.

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31
Q

What are the clinical presentations of coccidiomycosis?

A
  1. Asymptomatic: 60% of exposure; 2.Acute Pulmonary Coccidioidomycosis: 40% of exposures. 2-6 weeks after inoculation, develop a constellation of symptoms very similar to CABP. CXR reveals focal opacities and adenopathy, but 10% may develop effusions; 3. Extrapulmonary: 10% experience cutaneous symptoms (lower extremity erythema nodosum, necklace distribution of erythema multiforme, or rarely erythema toxicum). May also have MSK involvement; 4. Chronic Pulmonary Coccidioidomycosis:
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32
Q

How is coccidiomycosis treated?

A

Mild infection does not require treatment. Moderate disease may be treated with itraconazole or fluconazole. Severe, chronic or disseminated disease is treated first with amphotericin B, and then a prolonged course with an azole to prevent relapse. CNS involvement requires lifelong treatment with fluconazole to prevent relapse.

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33
Q

How is coccidiomycosis diagnosed?

A

Gold standard is culture, but fungal stains revealing pomegranate-shaped spherules are also used to support diagnosis. Coccidioides serologies are very sensitive and specific. Serologies become negative following infections, and so a positive serology is always clinically relevant. Skin tests remain positive for life.

34
Q

What causes aspergillosis?

A

Infection from genus aspergillus (A. fumigatus, flavus, nidus, terreus, nidulans, niger, others) usually in immunocompromised individual

35
Q

What are the forms of aspergillosis?

A

1) invasive (pulmonary, sinusitis, disseminated),
2) chronic (pulmonary, sinusitis, aspergillomas), or
3) allergic (allergic bronchopulmonary, allergic sinusitis) disease

36
Q

What is the etiology of aspergillosis?

A

Ubiquitous molds (average exposure of millions/day) with aerosolizable terminal conidia. Extreme exposure (moldy hay, construction work) can (rarely) cause disease in immunocompetent. Yeast are narrow, septate hyphae branching at 45 degrees

37
Q

What are risk factors for the development of aspergillosis?

A

Poor PMN function (congenital, HIV/AIDS, transplant, glucocorticoid use, hematologic malignancy). Pre-existing pulmonary parenchymal disease is a risk factor for chronic disease. Genetic polymorphisms and heterozygosity of CFTR gene are risk factors for allergic disease.

38
Q

What is the pathogenesis for aspergillosis?

A

Conidia reach alveoli, adhere to ECM, produce proteases to invade, and disseminate in mold form hematogenously (or via direct invasion). Macrophages are first-line defense, but PMNs needed to kill mold forms.

39
Q

What are aspergillomas?

A

static or very slowly growing fungal balls usually in cavities larger than 2.5 cm in the lungs or sinuses; associated with chronic aspergillosis

40
Q

How is aspergillosis diagnosed?

A

Histopathology is the gold standard. Culture is less reliable. The aspergillus antigen test (for galactomannan) is 70% sensitive, 90% specific and is useful in diagnosing chronic disease (along with elevated IgE). CT may reveal a “halo sign” (ground glass around hyperintense nodule) which is 60-70% sensitive but non-specific. ABPA is diagnosed with elevated IgE levels and positive skin-prick tests.

41
Q

How is aspergillosis treated?

A

Invasive disease is treated with voriconazole. Chronic and allergic disease are treated with itraconazole. Other active agents include amphotericin and echinocandins. Aspergillomas requires surgical debridement.

42
Q

What causes mucormycosis?

A

Life-threatening infection caused by molds from the order mucorales. They are thick-walled, ribbon-like, aseptate molds that branch at 90 degree angles. They cause superficial disease in immunocompetent individuals and invasive disease (rhinocerebral, pulmonary, GI, disseminated) in individuals with defects in immunity.

43
Q

What are risk factors for mucormycosis?

A

1) Defect in PMN function (DM, neutropenic)
2) Elevated serum iron (End Stage Renal Disease)
3) Acidosis (Diabetics (DM), Diabetic ketoacidosis (DKA), serious infections)
4) Hyperglycemia (DM in DKA)

44
Q

What is rhinocerebral mucormycosis?

A

Infection of the ethmoid and/or maxillary sinuses. Occurs most commonly in DM patients in DKA. Present with eye/facial swelling and pain, followed by numbness and vision changes. May spread to mouth, the orbit or cavernous sinus. External exam may reveal chemosis, erythema or eschars.

45
Q

What is pulmonary mucormycosis?

A

Most common presentation in hematologic malignancies (2nd most common overall). Present with cough, dyspnea, chest pain, and may eventually have severe hemoptysis. Imaging reveals infiltrates and numerous nodules (>10).

46
Q

What is GI mucormycosis?

A

Premature neonates. Very high mortality

47
Q

How is mucormycosis diagnosed?

A

Requires high index of suspicion. Histopathology remains most sensitive and specific. Culture aids in diagnosis, but given the urgency of treatment initiation histology is preferable. CT or MRI may aid in diagnosis and prognosis.

48
Q

How is mucormycosis treated?

A

Surgical treatment. Steps of treatment: 1) early diagnosis 2) reverse risk factors 3) surgical debridement 4) AmB 5) follow with radiographic imaging to ensure no disease
progression. Posaconazole also has activity.

49
Q

What causes Cryptococcosis?

A

Infection from a genus of yeast with two species (C. neoformans and C. gattii). Large capsuled yeast whose capsule excludes ink. Causes pulmonary, CNS or disseminated disease.

50
Q

What is the epi of cryptococcosis?

A

C. neoformans causes disease exclusively in individuals with impaired immunity. It is found in soils contaminated with avian excreta (especially pigeons). AIDS patients make up the majority of cases. Roughly 1/3 of AIDS patients in the world have cryptococcal meningitis,
causing 600,000 deaths a year. C. gattii is found in certain tree species, can cause disease in immunocompetent individuals, and is common in the Pacific Northwest

51
Q

How is cryptococcosis treated?

A

fluconazole (amp b either before or in synergy for serious cases)

52
Q

What is candidiasis considered?

A

opportunistic

53
Q

What causes candidiasis?

A

In genus, Candida albicans is the most important, but non-albicans species cause 50% of disseminated disease. Exist as small round blastospores in flora, but in disease state candida exist as pseudohyphae/hyphae.

54
Q

How does immunology affect candidiasis?

A

Innate immunity is most important. PMNs phagocytose yeast; are more efficient in the presence of complement/antibody. PMNs kill hyphae with oxidative bursts and prevent dissemination. T cells are needed to prevent chronic mucocutaneous disease.

55
Q

What is the pathogenesis of candidiasis?

A

Candidiasis results from a change in the host (allowing fungi proliferation) and organism (changing from yeast to virulent hyphal forms).

56
Q

Where can candidiasis be found?

A

cutaneous, mucosa, disseminated

57
Q

What is a particular concern with disseminated candidiasis?

A

Endopthalmitis requires urgent treatment to prevent blindness, and is almost always indicative of severe
systemic disease.

58
Q

How is candidiasis diagnosed?

A

Gold standard is visualization of hyphae. Because candida are abundant in flora, with positive cultures
it is often difficult to differentiate between colonization and true disseminated disease; A Beta-D-Glucan test is non-specific, but has a high NPV (90%); Endophthalmitis or macronodular skin lesions are almost always indicative of systemic spread.

59
Q

How is candidiasis treated?

A

Treatment for Mucocutaneous Candidadias: *Must repair defect in mechanical defenses
Cutaneous: Topical azoles
Oral (thrush): Nystatin (swish and swallow)
Esophageal/GI involvement: Oral fluconazole
Vulvovaginitis/balanitis: Topical azole vs. oral azole (eg, fluconazole)

60
Q

How is candidiasis prophylaxed?

A

Practice varies center to center.

Transplant patients: Fluconazole (most common), vs. newer azole vs. echinocandin

61
Q

What is amphotericin?

A

first available anti-fungal class; binds to ergosterol in cell membrane and makes channels, cations leak, leads to cell death; only available in IV

62
Q

What are side effects of amphotericin?

A

infusion reaction, nephrotoxicity, anemia

63
Q

What are the formulations of amphotericin B? Which is more commonly used?

A

conventionla vs lipid - we use lipid formulations because they are better tolerated

64
Q

When is amphotericin b used?

A

broad spectrum; used for disseminated superficial infections, endemic fungi, opportunistic fungi, or severe fungal infections

65
Q

What is nystatin’s class and use?

A

polyene - used as “swish and swallow” for mucocutnaeous infections; can be used as suppository or topical

66
Q

What are side effects of nystatin?

A

Few

67
Q

What are the class side effects of azoles?

A

inhibition of CYP450, suppression of corticosteroid axis, hepatotoxicity

68
Q

When is fluconazole used?

A

excellent CNS and ocular penetration; oral and IV; excellent for candidiasis; preferred agent for crypt and cocc meningitis

69
Q

What are side effects of fluconazole?

A

azole class side effects, alopecia, dry mouth

70
Q

When is itraconazole used?

A

poor CNS penetration, but reaches high levels in adipose and keratinized tissue; broader spectrum than fluconazole, treatment of choice for mild-moderate endemic infections, sporotrichosis, some activity in aspergillosis, sometimes used for more severe tinea versicolor and dermatophytosis

71
Q

When is voriconazole used?

A

All species of candida and very active against aspergillosis

72
Q

What are the side effects of voriconazole?

A

visual disturbances, hallucinations, class side effects

73
Q

What is distinct about voriconazole?

A

Metabolized by CYP2C19 - genetic polymorphisms can cause 4x difference in metabolism

74
Q

When is posaconazole used?

A

rarely - can be used as prophylaxis or in refractory candidiasis; available orally but must be given with food

75
Q

What can posaconazole cause?

A

QT prolongation

76
Q

When are echinocandins used?

A

candidiasis; some activity against aspergillus

77
Q

When is flucytosine used?

A

in combo with amp b for crypt meningitis - never used as a single agent

78
Q

How does flucytosine work?

A

Interferes with DNA synthesis

79
Q

What are side effects of flucytosine

A

It’s a chemotherapy agent, so chemo toxicities

80
Q

When is terbinafine used?

A

dermatophytosis and onchomycosis - can be oral or topical

81
Q

What are side effects of terbinafine?

A

diarrhea and taste disturbances

Infectious Disease 1 (10 decks)

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