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Amy Somerville > INF1 - E. FUNGI AND ANTIFUNGALS-COVERED > Flashcards

INF1 - E. FUNGI AND ANTIFUNGALS-COVERED Flashcards

1
Q

what type of cells are fungi cells and how are they different

A
  • eukaryotic cells
  • haploid: single set of chromosomes
  • cell wall is rigid and made of chitin, mannan, glucan
  • cytoplasmic membrane contains ergosterol
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2
Q

what are the 3 classes of fungi

A
  1. moulds
  2. yeasts
  3. mushrooms
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3
Q

explain what hypae are

A
  • networks of filaments which form in the environment
  • can spread for long distances
  • can grow in our body as a from of a fungal infection
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4
Q

what 2 classes exist as multicellular (have hyphae)

A

moulds
mushrooms

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5
Q

what class exists as unicellular organisms

A

yeasts
live naturally in environment but can cause infection in our body

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6
Q

explain dimorphic behaviour

A
  • when fungi convert from hyphae to yeast forms and vice versa (ie: hyphal form - produces spores - inhale - germinate - yeast form in body)
  • dependent on temperature
  • pathogenic dimorphic fungi grow as one form in outside environment and a different form in body of a host
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7
Q

explain sporulation

A
  • fungi form spores
  • allows fungi to spread, maintain genetic diversity and survive adverse conditions
  • spores are airborne
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8
Q

how do fungal infections arise (aka mycoses)

A
  • overgrowth of normal flora (yeasts - oral and vaginal thrush and dermatophytes on skin ie, nails - athletes foot and ringworm)
  • inhalation of fungal spores
  • traumatic implantation of fungal spores from a sharp nail and hence germination and growth in tissues
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9
Q

what are fungal pathogenicity factors

A
  • adhesion to host cells (proteins etc) - TROPISM
  • capsules to prevent phagocytosis
  • enzymes to facilitate tissue invasion and suppress immune system
  • don’t produce/release exotoxins or endotoxins
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10
Q

what are superficial infections

A
  • on surface layers
  • hair shaft, dead layer of skin
  • piedras - pityriasis versicolor
  • skin blemishes/weakened hair shafts
  • yeast or fungi
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11
Q

what are cutaneous infections

A
  • in deeper layers
  • epidermis, nails
  • tineas - athletes foot and ringworm
  • fungi
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12
Q

what are subcutaneous infections

A
  • in muscle layers - spores implanted in deeper layers
  • dermis, subcutis
  • mycetoma, chromoblastomycosis, sporotrichosis
  • deep, tissue damaging (traumatic implantation)
  • fungi
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13
Q

what are systemic infections

A
  • in bloodstream (lungs, internal organs)
  • blastomycosis, cryptococcal meningitis, histoplasmosis, coccidioidomycosis
  • inhalation of spores
  • grow as hyphae, become more like yeast, get into blood
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14
Q

what are opportunistic infections

A
  • mucosal tissues, internal organs, systemic
  • live in one environment but can exploit an opportunity and cause a more serious infection
  • candidosis, aspergillosis - environmental infection, Farmers lung - hyphae to spores to hyphae
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15
Q

what causes poisoning/allergies

A

fungal toxins (mycotoxins)
ie - ergot in wheat, peanuts, mushrooms

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16
Q

examples of hyphal forms to yeast-like forms

A

Cryptococcosis - causes fungal meningitis (fungi in grown bird/bat droppings, release spores, inhaled)

Coccidioidomycosis - skin, meningitis, bone

17
Q

example of yeast-like form to hyphal form

A

Candida albicans - part off microbiome, can cause thrush and maybe systemic infections)

18
Q

what are superficial mycoses

A
  • harmless, minimal destructive damage
  • white pier: infection of hair shaft, white nodules cause thinning and breakage of hair
  • pityriasis versicolor: red/brown blemishes
  • topical treatment:
  • selenium-based shampoo
  • ketocanazole body wash
19
Q

what are cutaneous mycoses

A
  • dermatophyte fungi digest keratin found in hair, nails, skin
  • tinea capitis: infection of hair and scalp
  • tinea corporis: infection of trunk, arms, legs
  • tinea pedis: athletes foot
  • tinea cruris: genital itch
  • tinea unguium: nail infection
  • contagious
  • topical agents or systemic therapy for extensive infection
20
Q

what are subcutaneous mycoses

A
  • fungi introduced by trauma, wounds, splinters, thorns
  • amputations/surgical extension?
  • chromoblastomycosis
  • mycetoma
21
Q

what are systemic mycoses

A
  • often opportunistic pathogens ie - candida
  • infection by spore inhalation ie - cryptococcosis, aspergillosis
  • spread from mucosal infections ie - candidiosis
  • often caused by dimorphic behaviour
  • aggressive therapy
22
Q

what are opportunistic infections

A
  1. Candida albicans
    - part of mucosal and cutaneous microflora, live on moist regions of body
    - oral thrush (antibiotic use/immunocompromised state)
    - vaginal thrush (change in vaginal pH)
    - candidiosis common in diabetes (poor blood circulation), cancer, HIV, burns patients, post surgery infection
    - systemic infection
    - dimorphic (yeast to hyphae)
  2. Candida auris
    - superbug - major cause of hospital-acquired infections
  3. Aspergillus fumigatus
    - found in wet soil/damp surfaces
    - spore inhalation, drowns as hyphal form in lung tissue
    - release toxins like phospolipases, haemolysins - damage lungs, facilitate spread
    - pulmonary aspergillosis: farmers lung
  4. Cryptococcus neoformans (Crytpococcosis)
    - found in soil contaminated with bird dropping
    - inhalation of spores
    - immunocompromised patients and cause for meningitis in AIDS patients
    - surrounded by capsules - infection and immune invasion
    - phagocytoses by macrophages, surviving and multiplying within macrophage and trafficked around body
23
Q

what does a fungal cell consist of

A

nucleus
mitotic spindle
endoplasmic membrane (synthesis of ergosterol)
membrane (ergosterol)
cell wall

24
Q

why are there fewer systemic fungal treatments

A
  • less common than bacterial infections
  • fungal cells are eukaryotic - difficult to make compounds specific and non-toxic to host cells
  • poor solubility, absorption, stability
25
Q

what do polyenes target and how do they act

A
  • bind to ergosterol in cell membrane
  • therefore preference for fungal cells rather than human cells
  • dosing important so cholesterol not targeted
  • fungicidal
  • causes leakage of cell contents
  • renal toxicity is a side effect
  • IV injection: lipid complex or liposome delivery
  • drug molecules orient themselves parallel to side chains of CM to form cylindrical channel/pores, cell death
  • Amphotericin B and Nystatin
26
Q

what do azoles target and how do they act

A
  • target sterol synthesis
  • inhibit precursor stage of ergosterol biosynthesis
  • bind to fungal P450 enzyme (haem group) which makes ergosterol (14 alpha-sterol demethylase) so membrane stability disrupted
  • fungistatic: stop cell growing but still remains live
  • reaction dependent on cytochrome P450
  • can interfere with mammalian sterol metabolism (testosterone)
  • Ketoconazole, Fluconazole, Itraconazole (imidazoles, triazoles)
27
Q

what do nucleoside derivatives target and how do they act

A
  • block DNA/RNA synthesis
  • relies on selective uptake (ie - mechanisms that don’t exist in our cells)/metabolic activation in fungal cell
  • active uptake, converted to 5-flurouracil (fungal selectivity)
  • further converted to 5-fluorouridylic acid monophosphate (FUMP - inhibits RNA synthesis) or 5-fluorodeoxyuridine monophosphate (inhibits DNA synthesis)
  • Flucytosine
28
Q

what do echinocandins target and how do they act

A
  • block cell wall synthesis by blocking beta 1-3 glucan polymer synthesis
  • cyclic lipopeptides that non-competitively inhibit 1,3-beta-D glucan synthase
  • this integral membrane exports glucan polymer
  • Caspafungin
29
Q

what do grisans target and how do they act

A
  • inhibit microtubule functions by interfering with tubulin and therefore mitosis and cell division
  • may affect cell wall synthesis by inhibiting chitin synthesis
  • Griseofulvin
30
Q

what do allylamines target and how do they act

A
  • target squalene epoxidase (enzymes in ergosterol synthesis)
  • Naftifine, Terbinafine
31
Q

what do morpholines target and how do they act

A
  • target ergosterol synthesis by inhibiting reductase and isomerase
  • Amorolfine
32
Q

why does resistance to polyenes occur

A
  • usually primary resistance (naturally)
  • lower production of sterols
  • altered sterols which bind drug with lower affinity
  • reorientation/masking of existing ergosterol to limit polyenes binding
33
Q

why does resistance to nucleosides (pyrimidine analogues) occur

A
  • usually secondary resistance
  • decreased uptake
  • loss of enzymatic activity responsible for conversion to FUMP by loss of cytosine permease/deaminase
34
Q

why does resistance to azoles occur

A
  • usually secondary resistance
  • increase content of target enzymes by gene amplification/upregulation of encoding gene
  • mutations in 14-alpha lanosterol demethylase enzyme
  • active efflux (ABC transporters which use energy to pump out drug molecules)
  • resistance has risen due to use in HIV patients with mucosal fungal infections
35
Q

why does resistance to enchinocandins occur

A
  • mutations in glucan synthase target (acquired/secondary resistance)
36
Q

other resistance mechanisms

A
  • formation of biofilms
  • anti fungal drug has poor penetration in biofilm and efflux pumps in fungal biofilms are unregulated

Amy Somerville (70 decks)

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