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13 Cards in this Set
- Front
- Back
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When are you likely to see a fungal infection? |
In the immunocompromised, after organ transplant, steroid use, after antibiotic use. Most fungi are benign, but are opportunistic. |
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3 unique fungal structures |
Chitinous/glucan cell wall (virulence factor)
Plasma membrane with ergosterol (instead of cholesterol-- key diff!)
Exoenzymes/toxins (secreted)
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5 Fungi vs bacteria differences |
Fungi bigger (5um), bacteria (<2um)
Fungi both sexual + asexual
Fungi can form multicellular structures (merging)
Eukaryotic fungi have nucleus, mitochondrion, ER,
chitinous cell wall vs murein cell wall in bacteria. Polysaccharides (glucans) in cell wall vs LPS outer membrane |
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Fungi life cycle |
Spore -> hyphae -> mycelium -> spore (repeat, or bud asexually) |
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What is the pathogenesis of 4 fungal virulence factors? |
Going from cold forest to warm human requires adaptations. These adaptations are virulence factors!
Host is warm with lots of defenses. Fungi convert from mycelia to yeast/spore form, which is the form that causes disease. Thermal dimorphism/tolerance is a virulence factor.
Hydrolytic exoenzymes: proteases, lipases, phospholipases damage barriers/host cells, to generate nutrition and allow entry. If you have collagenases/elastases, even more invasive.
Cell wall has alpha (1,3)- glucans. Thick sugar coats, heavily glycosylated prots resist phagocytosis, mask antigens. Also help with adhesion to epithelia/ECM
Aflatoxin (carcinogenic, leads to liver failure) |
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Mycoses (fungal disease) five basic characteristics. Who is susceptible? |
Chronic, relapsing Non-contagious cell-mediated immunity (bad if youre IC'd) delayed type hypersensitivity (mount response at distal location- ex: ringworm on arm leads to finger blistering from t-cells) Tissue tropism
IC, elderly, newborn, malnutrition, warm/moist env, previous Ab use |
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5 ways to diagnose fungal infection? |
Culture (4 weeks) Gram stain with KOH/peroxide Fluorescence under Wood Lamp Biomarkers (like galactomannan, sugars we don't have) DTH skin test for fungal sensitivity |
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6 Antifungal agents and their mechanisms |
Polyenes- Amphotericin B. Bind ergosterol, disrupt membranes
Azoles (keto-, flucon-, itraconazole): inhibit fungal cytochrome P-450 to interrupt ergosterol syn.
Allylamines: inhibit earlier step in squalene syn
5-fluorocytosine: converted to 5-fluorouracil by cytosine permease (gets in, we don't have it). Put into RNA miscodes protein syn and into DNA inhibits replication.
Echinocandins (capsofungin, micafungin): inhibit beta- 1,3 glucan syn. Impaired tolerance of osmotic or mechanical stress.
Griseofulvin: interrupts mitoic spindle assembly via binding tubulin. Accumulates in hair/nails by forming complex with keratin-producing cells.
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Superficial mycoses example, clinical |
Malassezia spp
Pityriasis versicolor (ash-like rash). |
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Cutaneous mycoses examples, clinical |
Dermatophytes (trichophyton, microsporum, epidermophyton)
Dermatophytids (distal vesicles) manifestation of hypersensitivity. Tineae ("ringworm") on head, body, inguinal region, foot (athletes foot) nails. |
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Subcutaneous mycoses example, clinical |
Sporothrix schenkii
Sporotrichosis: Granulomatous lesions (dark nodules) spreading via lymphatics |
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Systemic fungal pathogens (name four major diseases) and general characteristics |
Dimorphic fungi found in nitrogen-enriched soil. Spores inhaled, start as pulmonary focus, then spread.
Coccidioidomycosis (immitis)- Beaver dams. Self-limiting shitton of pulmonary spherules/endosomes, proteinases VF, dissemination in IC
Histoplasmosis (capsulatum)- midwest, farms, looks like TB, has pulmonary nodules, TB-like lesions. Reside in alveolar macrophages.
Blastomycosis (dermatitidis)- similar to histo, but not in macrophages. Fungus ball in lung. Skin lesions common with dissemination.
Paracoccidioidomycosis (brasiliensis)- long dormant phase. male predominance. Pulmonary infection with chronic cutaneous ulcers. |
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Opportunistic mycoses (usually co-exist with host, only progress during IC) |
Candidiasis (albicans): mucosal surfaces (thrush, vagina), can spread to retina, kidneys, CNS
Cryptococcosis (neoformans): pidgeon feces. Pulmonary infection spreads to CNS, meningitis.
Aspergillosis (fumigatus): wet basement, rotting wood. Asthma-like hypersensitivity. Common nosocomial in IC
Mucormycosis: diabetic acidosis. Rhinocerebral disease (eats away face). From zygomycosis, rhizomucor, and mucor.
Pneumocystosis (jiroveci): creates a diffusion barrier at surfactant layer in lungs, causing hypoxemia (diffuse looking pneumonia) |
