Mycology 1 Flashcards

1
Q
  1. Identify the crucial structural feature distinguishing eukaryotic fungi from prokaryotic bacteria.
A

fungi rarely have obligate interaction with host; saprobic (obtain nutrients from dead organic material) or symbiont–heterotrophic, absorptive and non motile, no diaminopimelate in cell wall

virtually ubiquitous, free-living

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2
Q
  1. Identify the components of fungal cell membranes and walls that distinguish them from mammals and provide therapeutic targets.
A

fungal membranes: ergosterol instead of cholesterol (target of amphotericin B or azoles)

fungal cell surrounded by cell wall: carbohydrate polymers including chitin, B-glucan (echinocandins)

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3
Q
  1. Describe the yeast and mold morphologies of fungi; explain dimorphism; identify each fungal pathogen discussed as “yeast” “mold” or “dimorphic.
A

dimorphic: may grow as a yeast, a mold depend ending on conditions (Malassezia fufur, Sporothrix schenkii, Candida albicans, Histoplasma capsulatum, Blastomyces dermatitidis, Coccidiodes)
yeast: unicellular oval structure that divides by budding (ie. Cryptococcus neoformans, Candida glabrata Histoplasma capsulatum- yeast is pathogenic)
molds: filamentous hype or mycelia growing by apical extension (ie. aspergillus, Dermatophytes, zygomycetes, Candida albicans, only hyphae are invasive although yeast can also cause disease)
pseudohyphae: cell reproducing as a yeast by mother daughter cells remain attached and elongate

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4
Q

Discuss two antifungals and their how their mechanisms exploit human/fungal differences

A

amphotericin B binds to ergosterol, damages membrane

azoles: inhibit ergosterol synthesis by lanosterol demthylase

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5
Q
  1. Describe the 3 principle mechanism that fungi cause disease in humans.
A

infection (fungi adhere or invade host tissue- superficial, cutaneous, subcutaneous or systemic)
allergy (hypersensitivity to fungal antigen)
mycotoxins (fungal products with deleterious effects on humans)

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6
Q

Contrast fungal allergen and toxin mediated disease based on their mechanism and time course.

A

allergen response damage is mediated by host immune response to HMW glycoproteins that occurs rapidly presuming sensitizing exposure (IgE mediated)

toxin damage is mediated by toxic activity and occurs in hours to days caused by LMW secondary metabolites (no essential role in primary metabolism required for growth of fungus)

note mold is #2 for indoor and outdoor allergies

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7
Q

Give some examples of mycotoxins, and their mechanism of damage to cells.

A

aflatoxins: Aspergillus in raw or processed seeds or nuts causing hepatotoxicity and liver cancer

ergot alkaloids: Claviceps purpurea in grains and breads, causing vasoconstriction, peripheral necrosis and gangrene

trichothecens: from Stachybotrys on building materials or Fusarium sp. in grains, breads causing cytotoxicity an systemic effects

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8
Q

Describe the four categories of medically important fungi base on their sexual reproductive stage.

A

zygomycetes: 2 compatible gametangia
ascomycete: 2 compatible haploid nuclei fuse
basidiomycetes: similar to ascomycetes, and the early part of the process occurs in a basidium (sac)
deuteromycetes: no sexual stage identified

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9
Q
  1. Malassezia fur fur: describe this organism’s morphology, risk factors and infections. (spaghetti and meatballs)
A

infections: tinea versicolor (oil loving) often resulting in hyper/hypo pigmentation of the skin; dandruff, cradle cap, seborrheic dermatitis

dimorphic, morphogenesis is poorly understood, hyphal form associated with pathogenesis, yeast commensal

risk: immunocompromised, infants with TPN at risk for disseminated disease

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10
Q

Briefly discuss the capabilities of the human immune system to fight fungal infection (re: blocking and containment of infection).

A

host defenses for the most part are very effective
innate and nonspecific factors are very important in blocking initial infection, final clearance, or containment requires effective adaptive specific CMI (specific CD4 T lymphocyte activation of macrophage)

impairment of cellular defenses is associated with increased susceptibility to fungal infection and increased severity

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11
Q
  1. Describe the clinical syndromes caused by the dermatophytes.
A

infections: dermatophyotoses, tineas(captitis, varbae, manuum, corporis, cruris, pedis, unguium, paranychomycosis) or ringworm
agents: Trichophyton, microsporum and epidermophyton are very contagious; **are kartinophilic, very contagious

disease produced by metabolic products and allergic inflammatory host response, fungal spores viable for mo-yrs via indirect passage through environment

dx.: KOH prep, UV woods lamp or culture on selective media

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12
Q

Name common causes of infection in subcutaneous mycoses.

A

agents found in soil or decaying organic material; restricted geo distribution ie. tropical

lesions develop at or near the site of infection, usually by traumatic implantation, can present similar to actinomycetes or streptomycetes

difficult to treat without surgical intervention, destructive and may compromise vascular, vary in intensity and length

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13
Q
  1. Sprothrix schenkii: describe how this organism exists in human tissue v. the environment, associated risk factor sn clinical syndromes. (astroid body, fusiform yeast)
A

dimorphic fungus that exists as a mold in environment and a yeast in tissues at 37 deg. (gardener’s disease)

lymphocutaenous sporotrichosis: traumatic implantation results in small, hard, painless nodule, which becomes fixed over time and enlarges to form fluctuant mass that ulcerates; infection can extend along lymphatics

pulmonary sporotrichosis: inhalation of spores, primary disease similar to TB

fixed cutaneous, mucocutaneous and extracutaenous disseminated sporotrichosis

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14
Q
  1. Zycomycosis: describe the risk factors and clinical manifestations associated with this syndrome. (absidia, rhizomes, mucor- ribbon like hypahe)
A

rapidly invasive cutaneous, mucocutaneous, subcutaneous or disseminated

lungs and nasal sinus are common initial sites of infection, burn and trauma patients also susceptible via skin to spore infection

rhino cerebral zygomycosis- life threatening fulminant infection, often in (DKA) acidotic individuals but also neutropenics or iron chelation, acidosis or DM

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