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Microbiology > Mechanisms of Antimicrobial Action and Resistance 2 > Flashcards

Mechanisms of Antimicrobial Action and Resistance 2 Flashcards

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0
Q

What does vancomycin bind to?

A

D Ala - D Ala substrate

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1
Q

What does vancomycin do? Is it a different mechanism than penicillin?

A

Inhibits peptidoglycan synthesis

Yes

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2
Q

Is vancomycin resistant to beta-lactamases?

A

Yes

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3
Q

Vancomycin: depsipentapeptide vs pentapeptide

A

Pentapeptide is vancomycin sensitive (binds to D alanyl - D alanine)
Depsipentapeptide is vancomycin resistant (can’t bind to D alanyl - D lactate)

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4
Q

What did vancomycin used to be considered as?

A

Last resort

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5
Q

Vancomycin resistant bacteria do what?

A

Synthesize D-Ala - Lactate substrate and the depsipentapeptide
Destroy the D-Ala - D-Ala substrate and pentapeptide

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6
Q

What is single-gene resistance used for?

A

Screening

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7
Q

The bla gene encodes what?

A

Beta-lactamase enzyme

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8
Q

mecA gene encodes what?

A

PBP 2A - methicillin resistance

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9
Q

How many separate van genes are there?

A

5 - multiple gene resistance

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10
Q

Drugs that act on ribosomes do what?

A

Act on subunits of bacterial ribosome to disrupt translation

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11
Q

What do aminoglycosides do?

A

Affect the 30S subunit of ribosomes and are bactericidal (gram positives and negatives)

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12
Q

What does tetracycline do?

A

Affects 30S subunit and is bacteriostatic

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13
Q

Which drugs affect the 50S subunit?

A

Chloramphenicol, macrolides, clindamycin

Bacteriostatic

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14
Q

Gentamicin (aminoglycoside) inhibits what?

A

30S ribosomal subunit and mitochondrial ribosomes

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15
Q

What acts as a barrier to gentamicin?

A

Mammalian cells and mitochondrial membranes

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16
Q

Mechanism of resistance to gentamicin?

A

Proteins modify and inactivates gentamicin and other aminoglycosides
Resistance is additive
Proteins encoded on plasmids

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17
Q

Can there be resistant ribosomal proteins?

A

Its very rare but when it happens it is highly resistant

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18
Q

Types of kanamycin inactivation?

A

N-acetyl transferases
O-acetyl transferases
O-adenyl transferases
O-phosphatases

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19
Q

Chloramphenicol binds to what, inhibits and does not inhibit what?

A

Binds to 50S
Inhibits mitochondrial 70S
Does not inhibit mammalian 80S

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20
Q

Chloramphenicol can cause what, in what percent of cases?

A

Aplastic anemia in 1/25k-40k administrations

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21
Q

Erythromycin is what type of antibiotic?

A

Macrolide

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22
Q

Erythromycin inhibits, doesn’t inhibit, doesn’t cross?

A

Does not inhibit mammalian 80S
Inhibits mitochondrial 70S
Doesn’t cross mitochondrial membrane

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23
Q

Mechanism of resistance to erythromycin?

A

Resistance by rRNA methylation

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24
Q

Erythromycin is often used as an alternative to what?

A

Penicillin because of allergies

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25
Q

Clindamycin has a similar spectrum as what? Binds to what?

A

Binds to 50S

similar spectrum as erythromycin

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26
Q

Clindamycin is frequently associated with what?

A

Bowel superinfection with clostridium difficile colitis

AKA pseudomembranous colitis

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27
Q

What is clindamycin used for?

A

Used to treat anaerobic infections

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28
Q

What are tetracyclines?

A

Bacteriostatic inhibitors with broad spectrum

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29
Q

What are tetracycline mechanism of action?

A

Block binding of aminoacyl-tRNAs to A site of 30S

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30
Q

Resistance to tetracyclines due to what?

A

Efflux and insensitive ribosomes

31
Q

Quinupristin/Dalfopristin do what?

A

Act synergistically on the ribosome to prevent protein synthesis

32
Q

Quinupristin/Dalfopristin are active against what?

A

VRSA and VRE (E. faecium not E. faecalis)

33
Q

Quinupristin/Dalfopristin used often? Why?

A

No, lots of side effects and must be given IV

34
Q

Linezolid (zyvox) mechanism of action? What bacteria does it work against?

A

Inhibits protein synthesis at the ribosome

Bacteriostatic against staphylococci and enterococci, VRSA and VRE (E. faecium not E. faecalis)

35
Q

Linezolid (zyvox) is administered how? How is it tolerated?

A

Orally or IV

Generally well-tolerated

36
Q

Telithromycin (ketek) is structurally related to what?

A

Macrolides, which include erythromycin

37
Q

How does telithromycin work? Treats what?

A

Blocks protein synthesis

Treats gram positive staph aureus (not VRSA) and s. pneumoniae

38
Q

Telithromycin (ketek) problem?

A

Reports of serious hepatotoxicity

39
Q

Tigecycline (Tygacil) is active against what?

A

MRSA and probably VRE in vitro

40
Q

Is tigecycline (tygacil) broad spectrum?

A

Yes

41
Q

Is tigecycline a substrate for tetracycline antiporters?

A

No

42
Q

What is tigecycline approved to treat? Administration?

A

Complicated intra-abdominal and skin suture infections.

IV, bacteriostatic

43
Q

Nystatin binds to what?

A

Binds to ergosterol (found in fungi membranes)

44
Q

Nystatin mechanism of action?

A

Forms pores, leading to potassium efflux, depolarization, and cell death

45
Q

Nystatin used to treat what?

A

Mold and yeast infections

46
Q

Polymyxins effective against what gram?

A

Gram negative but not gram positive

Bactericidal, affecting outer membrane

47
Q

Polymyxins are used as what?

A

Topical creams because they are too toxic for systemic use

48
Q

Daptomycin (cubicin) is what?

A

lipopeptide

49
Q

Daptomycin: how does it work, what is it effective against?

A

Binds to membrane of gram positives and depolarizes it

Effective against VRSA and VRE

50
Q

How is daptomycin administered and what is it approved for?

A

IV

Treatment of complicated skin and skin suture infections

51
Q

What is sulfanilamide?

A

First sulfonamide discovered 4 years after penicillin (1932)

Red dye that cured strep/staph in mice

52
Q

Sulfonamide antagonizes what?

A

para-aminobenzoic acid (PABA)

53
Q

Sulfonamides vs PABA (compete for uptake by bacteria)

A

PABA is 1000 times more effective
Small amounts PABA negate sulfonamides
Not a problem because we don’t get a lot of PABA in our diets and it is rapidly excreted

54
Q

We lack dihydropteroic acid synthase, so we require what in our diet?

A

Folic acid

55
Q

How are bacteria different from humans when it comes to folic acid?

A

Bacteria must synthesize it with dihydropteroic acid synthase
They can’t use an external source

56
Q

Are sulfonamides effective in the presence of folic acid?

A

Yes

57
Q

What happens when sulfonamides are used?

A

There is a deficit in tetrahydrofolic acid

58
Q

Sulfonamides bacteriostatic or bactericidal?

A

They are bacteriostatic if they block RNA/protein synthesis
They are bactericidal if RNA/protein synthesis continues (if there are methionine and purines in the environment such as in blood or urine)

59
Q

Why are sulfonamides ineffective in purulent lesions?

A

Rich in methionine, purines, and thymidine from lysed cells so RNA/DNA/protein synthesis can continue

60
Q

Sulfonamides introduced the problem of what?

A

Bacterial resistance to drugs

61
Q

Sulfonamides were introduced to treat what?

A

Bacterial dysentery in WWII

62
Q

How many years did it take for bacteria to become resistant to sulfonamides?

A

4 years

And about 10% of cases were resistant to other drugs

63
Q

True/False: resistance to multiple drugs is more common than resistance to a single drug. Why?

A 
True
R factors (transposons) carry multiple resistance genes
64
Q

What are three mechanisms of resistance to sulfonamides?

A

Reduced uptake (antiporter)
Altered dihydropteroic acid synthase
Increased synthesis of PABA (rare)

65
Q

Trimethoprim: what does it do?

A

Trimethoprim blocks a step in biosynthesis of tetrahydrofolic acid
It is a competitive inhibitor of dihydrofolic acid reductase

66
Q

Trimethoprim is a competitive inhibitor of dihydrofolate reducate: do humans or bacteria have this?

A

Both humans and bacteria have dihydrofolate reductase

67
Q

If humans have dihydrofolate reductase, which trimethoprim is a competitive inhibitor for, how is it ok for us to use it?

A

The human dihydrofolate reductase is 60k fold less sensitive to trimethoprim than the bacterial dihydrofolate reductase

68
Q

Resistance to trimethoprim?

A

Dihydrofolate reductases with reduced sensitivity to trimethoprim
It is not a mutant form of the bacterial enzyme, but a new gene

69
Q

How do sulfonamides and trimethoprim work together?

A

They are synergistic, meaning you can use smaller doses.

Use of the drugs together (5 parts sulfamethoxazole: 1 part trimethoprim) reduces the frequency of resistance

70
Q

What is bactrim?

A

5 parts sulfamethoxazole: 1 part trimethoprim

71
Q

Which drug was the first quinolone?

A

Naldixic

72
Q

Naldixic was used for what?

A

Treatment of UTIs

Rapidly excreted in urine but too toxic for systemic use

73
Q

How does naldixic work?

A

Inhibits A subunit of DNA gyrase - rapidly inhibits DNA synthesis
The human analog (topoisomerase II) is several hundred fold less sensitive
Bactericidal unless growth is prevented

74
Q

What are three mechanisms of resistance to quinolones?

A

Missense mutations in DNA gyrase subunit A
Reduced uptake
Plasmid-encoded resistance genes that reverses the inhibition of DNA gyrase subunit A

75
Q

Ciprofloxacin (a quinolone) resistance stats in nosocomial infections
Why did resistance increase so quickly?

A

Between 1989 and 1992 resistance among S. aureus increased 123%
1/4 of all S. aureus were resistant
Drug was used at levels close to MIC

Microbiology (10 decks)

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