Control of Microbial Population 2 Flashcards

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1
Q

type of microbial drug that is effect on both protozoa and fungi

A

azoles

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2
Q

why are sulfonamides so important

A

they can be used to treat both prokaryotes and eukaryotes

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3
Q

what are aminoglycosides not effective against and why

A

not effective against anaerobes because of absent oxidative phosphorylation due to lack of oxygen

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4
Q

what are glycopeptides not effective against and why

A

gram negative bacteria because they are too large and can’t penetrate through outer membrane

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5
Q

what are nitroimidazoles not effective against and why

A

aerobes because they require activation by flavodoxin which is found only in anaerobes

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6
Q

what are penicillins and cephalosporins not effective against and why

A

these things target particular structure which is the cell wall

mycoplasma because it lacks cell wall
mycobacteria because cell wall impenetrable

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7
Q

what are some challenges with fungi infections?

A

harder to treat, usually chronic, longer tx time, recurrence is common, eukaryotes so similar to humans

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8
Q

what was the first antifungal and are there many antifungals

A

azoles

not many because of challenge when it comes to treating fungi infections

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9
Q

what are some sites of target for antifungal agents

A

nucleic acid synthesis (flucytosine)
cell membrane
direct membrane

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10
Q

what do antifungal agents that target nucleic acids do

A

inhibits synthesis of DNA, RNA, and proteins

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11
Q

what antifungal targets nucleic acid and what is its mechanism?

A

cytosine analogue 5-fluorocytosine (uses fungal enzyme) –> 5-fluorouracil –> 5-fluorouridyllic acid –> blocks synthesis of p nucleic acids that the fungi is going to need to replicate

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12
Q

what is the difference between narrow and broad spectrum compounds

A

narrow - only treat one type of bacteria or fungi or virus

broad - treat several types of bacteria, fungi, or virus or even some cross over and treat both prokaryotes and eukaryotes

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13
Q

name of antifungal that targets cell membrane

A

polyenes e.g. amphotericin B

specifically ergosterol

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14
Q

what is the mechanism of polyenes (amphotericin B)

A

lipid loving compound that binds to ergosterol that create pores in the membrane causing leakage of ions out of the fungi –> cell lysis

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15
Q

which antifungal compound is fungicidal

A

polyenes (amphotericin B) because it actually kills the fungi

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16
Q

how does allylamines work

A

they are antifungals that interrupt the formation of ergosterol which is needed for cell membrane

it targets squalene epoxidase which turns squalene to lanesterol

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17
Q

example of allylamines

A

terbinafine

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18
Q

how do azoles work

A

they are antifungals that interrupt the formation of ergosterol which needed for cell membrane

it targets 14 alpha demethylase which turns lanesterol to ergosterol

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19
Q

example of azoles

A

fluconazole (triazole)

20
Q

what are the two groups of azoles

A

imidazoles (two nitrogens)

triazoles (three nitrogens)

21
Q

effects of azoles on fungal growth

A

fungistatic and fungicidal depending on species and specific compound

22
Q

advantage of azoles

A

250 fold more effective against fungi sterols than against mammalian sterols

23
Q

what antifungal targets cell wall

A

echinocandins eg caspofungin

24
Q

mechanism of caspofungin

A

blocks (1,3) -beta-D-glucan synthetase –> prevents formation of chitin for cell wall

25
Q

what antibiotics target metabolism

A

sulfonamides (inhibitors of metabolism or nucleic acid synthesis)

26
Q

sulfonamides are derived from

A

prontosil

27
Q

mechanism of sulfonamides

A

blocks folic acid synthesis

since bacteria synthesize their own antibiotics using PABA, sulfonamides are analogues of PABA so if taken up halts the production of folic acid

28
Q

what two drugs synergistically inhibit the synthesis of folic acid in fungi

A

sulfamethoxazole and trimethoprim

TMP-SMX/SMZ

29
Q

which antibiotics target protein synthesis in bacteria

A

tetracyclines, streptomycin, erythromycin, chloramphenicol

30
Q

what antibiotics target cell wall of bacteria

A

beta lactams

31
Q

what drugs fall under beta lactam and why? also how do these drugs work

A

penicillin, cephalosporins, monobactams, carbapenems – all have beta lactam ring

active only on growing cells

32
Q

what drugs inhibit the formation of cell wall of bacteria by attacking cytoplasm and cytoplasmic membrane respectively

A

cytoplasm - cycloserine

cytoplasmic membrane - bacitracin glycopeptides

33
Q

cross linking of NAM molecules in peptidoglycan is carried out by and this process is interfered with by what?

A

transpeptidases aka penicillin binding proteins

beta lactams

34
Q

what happens to cell wall when beta lactams comes in and interferes with the cross linking of NAM molecules

A

they continue to grow (though they do not have the cement) but will eventually lyse since nothing is keeping it together

35
Q

mechanisms in which bacterias use to resist against antibiotics

A

altered uptake - decrease/block uptake of antibiotic or as soon as antibiotic gets into the bacteria is as soon as bacteria pumps it back out

altered target - change in receptor affinity through mutation

drug inactivation: beta lactamases, chloramphenicol, acetyltransferases

36
Q

most commonly used antifungal

A

azoles

37
Q

which drug is susceptible to all resistance mechanism of bacteria: altered target, altered uptake, drug inactivation

A

beta lactam

38
Q

which resistance mechanism by bacteria is mostly used against antibiotics

A

drug inactivation

39
Q

sources of resistance by bacteria

A

chromosomal mutation
genes on transmissible plasmids
genes on transposable elements (transposons)

40
Q

how does beta lactamase inactivate beta lactams

A

it cleaves the antibiotic at the beta lactam ring hence inactivating it

41
Q

most common beta lactamase

A

TEM beta lactamase

42
Q

confers resistance to all beta lactam anitibiotics and many other classes of antibiotics like aminoglycosides and fluoroquinolones

A

extended spectrum beta lactamases (ESBL)

43
Q

exception to ESBL

A

cephamycin (cefoxitin and cefotetan), carbapenems

44
Q

main producers of ESBL (extended spectrum beta lactamases) and KPC

A

enterobacteriacae particularly e. coli and klebsiella species

45
Q

KPC (klebsiella pneumoniae carbapenemases) are resistant to what

A

all beta lactams, fluoroquinolones, aminoglycosides

associated with high therapeutic failure and high mortality rate

46
Q

Actions YOU as a healthcare practitioner can take to help limit the spread of resistance and selection of resistant strains

A
  1. Wash your hands thoroughly between patient visits.
  2. Do not give in to patients’ demands for unneeded antibiotics.
  3. When possible, prescribe antibiotics that target only a narrow range of bacteria.
    – Sensitivity testing
  4. Isolate hospital patients with multi drug‐resistant infections.
  5. Familiarize yourself with local data on antibiotic resistance.