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Microbiology > Mechanisms of Antimicrobial Action and Resistance 2 > Flashcards

Mechanisms of Antimicrobial Action and Resistance 2 Flashcards

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
Erythromycin is often used as an alternative to what?
Penicillin because of allergies
25
Clindamycin has a similar spectrum as what? Binds to what?
Binds to 50S | similar spectrum as erythromycin
26
Clindamycin is frequently associated with what?
Bowel superinfection with clostridium difficile colitis | AKA pseudomembranous colitis
27
What is clindamycin used for?
Used to treat anaerobic infections
28
What are tetracyclines?
Bacteriostatic inhibitors with broad spectrum
29
What are tetracycline mechanism of action?
Block binding of aminoacyl-tRNAs to A site of 30S
30
Resistance to tetracyclines due to what?
Efflux and insensitive ribosomes
31
Quinupristin/Dalfopristin do what?
Act synergistically on the ribosome to prevent protein synthesis
32
Quinupristin/Dalfopristin are active against what?
VRSA and VRE (E. faecium not E. faecalis)
33
Quinupristin/Dalfopristin used often? Why?
No, lots of side effects and must be given IV
34
Linezolid (zyvox) mechanism of action? What bacteria does it work against?
Inhibits protein synthesis at the ribosome | Bacteriostatic against staphylococci and enterococci, VRSA and VRE (E. faecium not E. faecalis)
35
Linezolid (zyvox) is administered how? How is it tolerated?
Orally or IV | Generally well-tolerated
36
Telithromycin (ketek) is structurally related to what?
Macrolides, which include erythromycin
37
How does telithromycin work? Treats what?
Blocks protein synthesis | Treats gram positive staph aureus (not VRSA) and s. pneumoniae
38
Telithromycin (ketek) problem?
Reports of serious hepatotoxicity
39
Tigecycline (Tygacil) is active against what?
MRSA and probably VRE in vitro
40
Is tigecycline (tygacil) broad spectrum?
Yes
41
Is tigecycline a substrate for tetracycline antiporters?
No
42
What is tigecycline approved to treat? Administration?
Complicated intra-abdominal and skin suture infections. | IV, bacteriostatic
43
Nystatin binds to what?
Binds to ergosterol (found in fungi membranes)
44
Nystatin mechanism of action?
Forms pores, leading to potassium efflux, depolarization, and cell death
45
Nystatin used to treat what?
Mold and yeast infections
46
Polymyxins effective against what gram?
Gram negative but not gram positive | Bactericidal, affecting outer membrane
47
Polymyxins are used as what?
Topical creams because they are too toxic for systemic use
48
Daptomycin (cubicin) is what?
lipopeptide
49
Daptomycin: how does it work, what is it effective against?
Binds to membrane of gram positives and depolarizes it | Effective against VRSA and VRE
50
How is daptomycin administered and what is it approved for?
IV | Treatment of complicated skin and skin suture infections
51
What is sulfanilamide?
First sulfonamide discovered 4 years after penicillin (1932) | Red dye that cured strep/staph in mice
52
Sulfonamide antagonizes what?
para-aminobenzoic acid (PABA)
53
Sulfonamides vs PABA (compete for uptake by bacteria)
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
We lack dihydropteroic acid synthase, so we require what in our diet?
Folic acid
55
How are bacteria different from humans when it comes to folic acid?
Bacteria must synthesize it with dihydropteroic acid synthase They can't use an external source
56
Are sulfonamides effective in the presence of folic acid?
Yes
57
What happens when sulfonamides are used?
There is a deficit in tetrahydrofolic acid
58
Sulfonamides bacteriostatic or bactericidal?
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
Why are sulfonamides ineffective in purulent lesions?
Rich in methionine, purines, and thymidine from lysed cells so RNA/DNA/protein synthesis can continue
60
Sulfonamides introduced the problem of what?
Bacterial resistance to drugs
61
Sulfonamides were introduced to treat what?
Bacterial dysentery in WWII
62
How many years did it take for bacteria to become resistant to sulfonamides?
4 years | And about 10% of cases were resistant to other drugs
63
True/False: resistance to multiple drugs is more common than resistance to a single drug. Why?
``` True R factors (transposons) carry multiple resistance genes ```
64
What are three mechanisms of resistance to sulfonamides?
Reduced uptake (antiporter) Altered dihydropteroic acid synthase Increased synthesis of PABA (rare)
65
Trimethoprim: what does it do?
Trimethoprim blocks a step in biosynthesis of tetrahydrofolic acid It is a competitive inhibitor of dihydrofolic acid reductase
66
Trimethoprim is a competitive inhibitor of dihydrofolate reducate: do humans or bacteria have this?
Both humans and bacteria have dihydrofolate reductase
67
If humans have dihydrofolate reductase, which trimethoprim is a competitive inhibitor for, how is it ok for us to use it?
The human dihydrofolate reductase is 60k fold less sensitive to trimethoprim than the bacterial dihydrofolate reductase
68
Resistance to trimethoprim?
Dihydrofolate reductases with reduced sensitivity to trimethoprim It is not a mutant form of the bacterial enzyme, but a new gene
69
How do sulfonamides and trimethoprim work together?
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
What is bactrim?
5 parts sulfamethoxazole: 1 part trimethoprim
71
Which drug was the first quinolone?
Naldixic
72
Naldixic was used for what?
Treatment of UTIs | Rapidly excreted in urine but too toxic for systemic use
73
How does naldixic work?
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
What are three mechanisms of resistance to quinolones?
Missense mutations in DNA gyrase subunit A Reduced uptake Plasmid-encoded resistance genes that reverses the inhibition of DNA gyrase subunit A
75
Ciprofloxacin (a quinolone) resistance stats in nosocomial infections Why did resistance increase so quickly?
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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