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Microbiology & Infectious Diseases > 25: Fungals & Antifungals > Flashcards

25: Fungals & Antifungals Flashcards

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Biology 101 flashcards
1
Q

Describe the fungal structure.

A
  • Defined by heterotrophy (eat dead material).
  • Ergosterol predominant in cell membrane.
  • Azoles and allylamines inhibit ergosterol synthesis (both static).
  • Polyenes bind this sterol which causes cell leaking, death (cidal).
  • Note: All bind cholesterol in humans cells, therefore toxic.
  • Wall contains mannin, beta-glucan and chitin.
  • Echinocandins block the enzyme linking beta-glucan in the cell wall.
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2
Q

Describe fungal reproduction and morphology.

A
  • Asexual reproduction yields conidia.
  • Sexual reproduction yields spores.
  • Yeast reproduce by generating buds.
  • Molds reproduce by forming parallel walls that form hyphae and are subdivided into subunits by septa.
    • A mycelium is an interwined hyphae that behaves like a root.
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3
Q

Describe dimorphic fungi.

A
  • Can form either yeast or mold.
  • If less than 37C, mold
  • If more than 37C, yeast (more metabolically active)
  • Conversion = heat shock response
  • 37C = body temp
  • Mold are more immunogenic; yeast in human body better at evading immune response
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4
Q

What is the gold standard for diagnosing fungal infections?

A
  • Micrscopic observation: GS, KOH prep, silver stain
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5
Q

How can fungal infections be divided?

A
  • Anatomic location (superficial, mucocutaneous, deep)
  • Epidemiology (opportunistic or endemic)
  • Morphology (yeast, mold, dimorphic)
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6
Q

What are the superficial and subcutaneous fungal infections?

A
  • Tinea versicolor (M)
  • Dermatophytes (Y)
  • Sporotrichosis (D)

NB: Inoculation via direct environmental exposure.

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7
Q

What are the endemic mycosis?

A
  • Blastomycosis
  • Histoplasmosis
  • Coccidioidomycosis

NB: All dimorphic.

NB2: Pathogenesis resembles TB; conidia enter lung, cause system spread response in attempt to contain infx.

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8
Q

What are the opportunistic fungal infections?

A
  • Cryptococcosis (Y)
  • Aspergillosis (M)
  • Mucormycosis (M)
  • Candida (Y)

NB: Cause disease mostly in immunocompd pt.

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9
Q

What is the immunology of fungal infections?

A
  • First defense is PMN-mediated killing
  • Macrophages are then active against infx that escaped PMNs
  • T cell response necessary to prevent systemic spread
  • Humoral response limited
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10
Q

Where do superficial fungal infections occur?

A
  • Stratum corneum, hair and nails
  • Tinea versicolor and dermatophytosis are both superficial fungal infections.
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11
Q

For tinea (pityriasis) versicolor:

  1. Genus
  2. Source
  3. Epidemiology
  4. Pathogenesis
  5. Clinical
  6. Diagnosis
  7. Treatment
A
  1. Malassezia furfur, lipophilic dimorphic yeast
  2. Normal skin flora of 78-98% pop.
  3. Humid/tropic climates, young adults
  4. Converts from yeast to pathologic mold; metabolic side products block UV light, inhibit tyrosinase (melanin synthesis)
  5. Hypo/hyperpigmeted skin
  6. Clinical, Wood’s Lamp (yellow-orange fluorescence); KOH prep to confirm; histo: “spaghetti & meatballs”
  7. Topical treatment first (selenium sulfide, ketoconazole or terbinatine), then oral (fluconazole or itraconazole) if recurrence or systematic.
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12
Q

For dermatophytes:

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. 3 genera molds (trichophyton, microsporum, epidermophyton); invade keratinized structures in epidermis and feed on keratin; high tropism for specific tissues
    • capitis = head
    • corporis = body
    • barbae = beard
    • cruris = crotch
    • unguium = nails
    • pedis = feet
  2. More common in men (progesterone inhibits); transmitted person-to-person, via fomites, animal-to-person, or soil-to-person.
  3. Enzymes adhere to skin, invade surrounding tissues, incite immune response; need cellular immunity to prevent wide spread.
  4. Corporis: serpiginous/annular rash with curcumferential erythematous plaques and central clearing; capitis: inflammatory, non-inflammatory or chronic; barbae: superficial or inflammatory; cruris: well marginated, bilateral with scales; pedis: interdigital, sesiculobullous with bullae at varying stages of healing; unguium: refractory to tx
  5. Clinical, Wood’s Lamp, KOH
  6. Topical first (selenium sulfide, allylamines, azoles); for refractory infx, capitis or unguium, oral therapy (fluconazole or itraconazole)
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13
Q

For sporotrichosis:

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. Sporothrix schenkii, thermally dimorphic fungi found in soil
  2. Geophilic transmission; often occurring in gardeners.
  3. Trauma allows direct inoculation of conidia; germinates in lymphatics; rare presentations: osteoarticular form in joint space of middle-aged male alcoholics, pulmonary form in lung parenchyma in COPD patients, disseminated form in immunocompd.
  4. Single papule at inoculation site, later ulcerates; papule, nodule and ulcerative spread along lymphatic tracts.
  5. Clinical, culture of mold forms at room temp, biopsy revealing granulomatous/pyogenic process with scant, cigar-shaped yeasts.
  6. Itraconazole for 2-4 weeks (if severe, AmpB)
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14
Q

For Histoplasmosis:

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. Histoplasma capsulatum var. capsulatum; thermally dimorphic organism
  2. Grows in acidic, humid soil enriched with bat/bird droppings, in MS/OH river valleys; risks include caves, chicken coops, old buildings or dead trees
  3. Microconidia inhaled into alveoli, phagocytosed by macrophages; yeast inhibit phagolysosome complex, survive inside macrophage; evoke granulomatous response; spread by traveling within macrophage through reticuloendothelial system (lymph nodes, spleen, bone marrow, peripheral blood); granulomas undergo fibrocaseous necrosis and calcification.
  4. Asymptomatic to mild cough; flu-like illness in acute histoplasmosis; sequelae = great vessel/airway compression, fistula formation, fibrosing mediastinitis; chronic cavitary histoplasmosis = pts w/ pre-existing lung disease; looks like TB in presentation and on CXR; disseminated = sepsis, MOSD including adrenal & respiratory failure
  5. Culture (gold standard), fungal stains, urine/serum antigen tests most sensitive.
  6. Itraconazole; AmpB first if severe acute or disseminated.
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15
Q

For Blastomycosis:

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. Blastomycosis dermatidis; thermally dimorphic
  2. Endemic to SE, SC, MW, some NE states, particularly in areas of decomposing materials (e.g., beaver dams).
  3. Micrconidia inhaled into alveoli, phagocytosed and killed; those that escape convert into thick-walled, large yeasts with broad based buds that survive in EC space; adhesins on surface result in pyogranulomatous response.
  4. Four types:
    1. Asymptomatic to mild cough
    2. Acute: flu-like illness, limited spread
    3. Chronic: similar to TB or malignancy; CXR may show cavitation, mass lesions or fibronodular infiltrates
    4. Disseminated: immunocomp’d pts; diffuse long involvement leading to respiratory failure; skin: verrucous, nodular or ulcerative lesions; bone; GU tract; CNS with brain abscesses or meningitis.
    5. Culture (gold standard), but fungal stains more sensitive.
    6. Itraconazole; AmpB for severe acute or disseminated; fluconazole or voriconazole for refractory or brain abscesses.
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16
Q

For coccidioidomycosis (Valley Fever):

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. Soil-dwelling dimorphic fungus
  2. Southwest US; archeological digs, afer earthquakes, construction.
  3. Arthroconidia aerosolized into bronchioles, where they mature to become very large spherules; rupture and release endospores; endospore death requires TH1 driven, adaptive immune response, which results in necrotizing granuloma formation; endospores that escape mature and become spherules.
  4. Five types:
    1. Asymptomatic (60%)
    2. Acute Pulmonary: Sx similar to CABP; CXR reveals focal opacities and adenopathy, 10% effusions.
    3. Extrapulmonary: cutaneous sx, MSK involvement.
    4. Chronic pulmonary: in pts w/ pre-existing lung disease; looks like TB or malignancy.
    5. Disseminated: in immunocompd pts., diffuse lung involvement w/ variable extrapulm. manifestations.
  5. Culture (gold standard); fungal stains with pomegrante-shaped spherules; serologies.
  6. Moderate: itraconazole or fluconazole; severe, chronic or disseminated: AmpB then azole; CNS involvement requires lifelong tx with fluconazole.
17
Q

For Aspergillosis:

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. A. fumigatus; opportunistic fungus; ubiquitous molds with aerosolizable terminal conidia; yeast are narrow, septate hyphae branching at 45 degrees.
  2. Moldy hay, construction work (can rarely cause infx in immunocompetent); risk if poor PMN function, pre-existing pulmonary parenchymal disease, genetic polymorphisms and heterozygosity of CFTR (allergic disease)
  3. Conidia reach alveoli, adhere to ECM, produce proteases to invade, disseminate in mold form hematogenously.
  4. Three types:
    1. Invasive: pulmonary disease (acute/subacute), asymp to fever w/ hemoptysis and cough; may involve sinuses; disseminated may involve brain (cutaneous sx indicate dissemination)
    2. Chronic: pulmonary disease (mimick TB); chronic sinusitis destroys ethmoid and sphenoid sinuses, may cause loss of sense of smell, headache, vision changes or blindness; aspergillomas are static/slow growing balls in cavities.
    3. Allergic: asthma exacerbations, bronchial obstruction, recurrent pneumonia
  5. Histopathology gold standard; antigen test; CT may reveal “halo sign” (ground glass around hyperintense nodule); allegic diagnosed with elevated IgE and positive skin-prick test
  6. Voriconazole for invasive; itraconazole for chronic/allergic.
18
Q

For mucormycosis:

  1. Etiology
  2. Epidemiology
  3. Clinical
  4. Diagnosis
  5. Treatment
A
  1. Molds from order mucorales; thick-walled, ribbon-like, aseptate molds that branch at 90 degree angles
  2. Pts w/ risk factors (DM in DKA, transplant, neutropenic pts, hematologic malignancies), may occur in pts on azole prophylaxis.
  3. Three types:
    1. Invasive: rhinocerebral (sinuses, eye/facial swelling, pain, numbness and vision changes; chemosis, erythema or eschars); pulmonary (hematologic malignancies, cough, dyspnea, chest pain, severe hemoptysis; CXR = infiltrates, nodules); GI (premature neonates, high mortality)
    2. Disseminated: commonly to brain; high mortality
    3. Cutaneous: infx of subcutaneous tissue, muscle, fascia, bone; may lead to necrotizing fasciitis
  4. Histopathology; culture (but urgency); CT or MRI
  5. Surgical; AmpB
19
Q

For cryptococcosis:

  1. Etiology
  2. Epidemiology
  3. Pathogenesis
  4. Clinical
  5. Diagnosis
  6. Treatment
A
  1. C. neoformans and C. gattii; large capsuled yeast whose capsule excludes ink
  2. Individuals with impaired immunity (AIDS patients); found in soils contaminated with avian excreta (especially pigeons); C. gattii found in certain tree species common in Pacific NW.
  3. Yeast enters lungs, easily cleared by intact immunity (TH1 response); yeast have anti-phagocytic capsule, convert catecholamines to melanin (dampen immune response), use macrophage to enter CNS.
  4. Pulmonary: asymp or with painful cough, sputum; CNS: HA, fever, lethargy, neck stiffness, focal deficits; disseminated: MODS, highly variable skin lesions.
  5. Histology gold standard; India ink; CSF exam reveals mononuclear pleocytosis, increased serum protein, increaed opening pressure; imaging.
  6. Non-severe: fluconazole; severe: AmpB; NS: AmpB + flucytosine
20
Q

For Candiasis:

  1. Etiology
  2. Pathogenesis
  3. Clinical
  4. Diagnosis
  5. Treatment
A
  1. Candida albicans; small round blastspores in flora, but in disease state exist as pseudohyphae/hyphae
  2. Host change: Abx alter flora, disrupted mechanical barrier exposes new ECM binding sites, indwelling catheter/device allows candida to form biofilm; organism changes: blastospores transform to hyphae, which form strong attachments to epithelium, secrete proteinases/phospholipases and invade.
  3. Cutaneous: erythematous macerated patches with satellite vesiculopustules that form in areas of skin breakdown; macronodular lesions indicate disseminated disease; mucosa: white patches on buccal mucosa, tongue, palate, GI tract, glans penis, vulva or vagina; may reveal bleeding base; thrush in those with debilitating illness, immunocompd, inhaled steroid use; nausea, GI ulceration/perforation, vulvovaginitis common; balanitis in uncircumcised; disseminated: fever, leukocytosis, MODS.
  4. Visualization of hyphae from smear; because abundant in flora, hard to differentiate between colonization and dissemination via cultures; Beta-D-Glucan test
  5. Must repair defecet in mechanical defense:
    • Cutaneous: topical azole
    • Oral: Nystatin
    • GI: Oral fluconazole
    • Vulvovagnitis/balanitis: Topical azole or oral fluconazole
    • Hematogenous: AmpB, fluconazole, voriconazole, echinocandin (when high rate of C. glabrata)
    • Ppx: fluconazole for transplant; posaconazole for neutropenic pt
21
Q

List the anti-fungals.

A
  1. Polyenes (AmpB, Nystatin)
  2. Azoles (Fluconazole, itraconazole, voriconazole)
  3. Echinocandins (micafungin, caspofungin)
  4. Flucytosine
  5. Allylamines (terbinafine)
22
Q

For polyenes:

  1. Types
  2. Mechanism
  3. Indications
  4. Toxicity
A
  1. AmphotericinB and Nystatin
  2. Binds sterols and causes leakage, death
  3. AmpB: resistant, severe or disseminated fungal infections; Nystatin: mucocutaneous infx (thrush - candida)
  4. AmpB: renal tube toxicity, hypokalemia, hypermagnesium
23
Q

For azoles:

  1. Types
  2. Mechanism
  3. Indications
  4. Toxicity
A
  1. Fluconazole Itraconazole Voriconazole Posaconazole
  2. Inhibit ergosterol synthesis (CYP450)
  3. Flu: Crypto/Coccidio meningitis, candida prophylaxis; Itra: non-severe endemic infx, sporotrichosis, severe tinea versicolor, severe dermatophytosis; Vor: Aspergillosis; Posa: refractory candida, 2nd-line mucormycosis
  4. Vor: hallucinations, Asians slow metabolizers; Posa: QT prolongation
24
Q

For echinocandins:

  1. Type
  2. Mechanism
  3. Indication
  4. Toxicity
A
  1. Caspofungin
  2. Inhibit cell wall synth
    3.

Microbiology & Infectious Diseases (26 decks)

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