MYCOLOGY 5 - CLIMATE CHANGE Flashcards

1
Q

what are the two parts of fungi that differentiate from human cells and that are used as targets for antifungals?

A

fungi have ergosterol and not cholesterol in their membrane
fungi also have a cell wall and we don’t

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2
Q

what do the three main families of antifungals that were developed target?

A

2 against ergosterol
1 against the cell wall

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3
Q

where else is chitin present other than fungi?

A

present in exoskeletons of insects

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4
Q

how do echinocandins work?

A

cell wall enzyme inhibitors
newest family of drugs (2001)
first line of defense against yeast
fungicidal on yeast
fungistatic on mold

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5
Q

what is the function of ergosterol?

A

insures fungal plasma membrane fluidity

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6
Q

what are the 2 main families of antifungals that target ergosterol?

A

polyenes
azoles
target different parts of the synthesis pathway

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7
Q

how does polyene work?

A

used as a last resort, only for invasive infections because it is very toxic to us
ergosterol and cholesterol have similar structures
the max dose is 1mg/kg/day over 2-4 hours
the way it works:
the hydrophobic part of the molecule interact with the ergosterol
this forms a sort of channel, which creates a hole in the membrane and kills the fungus

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8
Q

what functional groups do azoles have?

A

imidazole (2 nitrogens) or triazole group (3 nitrogens)

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9
Q

how do azoles infect fungi?

A

fungicidal for mold
fungistatic for yeast
why it is important to know which type of infection patients have

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10
Q

how can fungi increase their resistance to drugs?

A

make a biofilm

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11
Q

how do biofilms contribute to resistance?

A

can increase the resistance to a drug by 1000 fold
the biofilm is a self made matrix made of polysaccharides and proteins, protects fungus from the outside environment

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12
Q

what are the limitations of azoles?

A

azoles are used in agriculture, and those are the same azoles used in clinic
means that we are selecting for the fungi that are resistance to azoles, and then when we get infected the fungi are already resistant

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13
Q

what is the hypothesis for the rapid spread of Candida auris?

A

global warming allowed for the strain to be resistant to higher temperatures
gained salinity tolerance as the wetlands ecosystems changed
persistence was facilitated by plastic pollutants
possibility of an intermediate animal reservoir (birds)

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14
Q

how does valley fever work?

A

dimorphic fungi
lives as a mycelium in the environment, and then as spherules and endospores in humans
symptoms: pneumonia like symptoms, dissemination to skin, lymph nodes, bone, joints, CNS
40% of people inhaling spores will get symptoms
different risks based on the population (most vulnerable are filipino)

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15
Q

what conditions does the valley fever fungus like?

A

low humidity and high temperature
climate change increases the geographical range that they can tolerate

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