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Owenbacteria Block 2 > Antibiotics and Resistance > Flashcards

Antibiotics and Resistance Flashcards

1
Q
  1. What are some examples of B-lactam antibiotics?
  2. What are they effective against?
A
  1. Penicillins, Cephalosporins, Carbapenems, Monobactams
  2. Gram negative & Gram positive
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2
Q
  1. How do B-lactams like Penicillins and Cephalosporins work?
  2. What are the benefits of B-lactams like Penicillins and Cephalosporins?
  3. What is the primary drawback?
A
  1. Inhibition of PDG cross-linking by binding PBP’s (Penicillin Binding Proteins)
  2. High specificity for bacteria and low toxicity
  3. High incidence of hypersensitivity reactions.
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3
Q
  1. How do bacteria primarily develop resistance to B-lactam antibiotics like penicillins and cephalosporins?
  2. Which type of bacteria typically express this?
  3. What are two other methods of B-lactam resistance?
  4. Which type of bacteria utilize the third method? What is the most famous of these bugs?
A
  1. Expression of beta-lactamase which cleaves the lactam ring.
  2. Gram negative
  3. Porin modification which prevents entry of drug and mutation in PBPs
  4. Gram positive bugs, MRSA
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4
Q

How do we overcome B-lactamase resistance in bugs?

A

Combine a B-lactamase inhibitor with the antibiotic. Like Clavulanic acid, Sulbactam, or Tazobactam

These form a complex with B-lactamase and only release it slowly. This gives the anti-biotic time to work.

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5
Q
  1. What is the primary example of a Glycopeptide Class antibiotic?
  2. What type of bacteria is it effective against?
  3. Why isn’t it effective for the other type?
A
  1. Vancomycin
  2. Gram positive
  3. Not effective for Gram negative because of limited permeability.
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6
Q

How does a Glycopeptide like Vancomycin create its effect?

A

It binds to the D-Ala D-Ala segment which blocks PBPs from catalyzing crosslinking and synthesis of PDG.

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7
Q

What are two benefits for a glycopeptide antibiotic like Vancomycin?

A
  1. It is good for B-lactam resistant organisms
  2. It is good for patient’s with B-lactam allergies
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8
Q

How does an organism create resistance to a glycopeptide like Vancomycin?

What is the most famous of these bugs?

A

It modifies the target for Vanco binding. D-Ala D-Ala becomes D-Ala D-Lac. Vanco therefore can’t bind.

Vancomycin Resistant Enterococcus which can transfer its resistance to staph and create VRSA.

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9
Q

What is a second line TB drug that demonstrates a two step inhibition of PDG?

A

Cycloserine

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10
Q

What PDG inhibitor is effective against Group A Strep (*S.pyogenes) *but can only be used topically as it is too toxic for systemic use?

A

Bacitracin

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11
Q

What drug is bactericidal against Gram positive bacteria that works by disrupting the cytoplasmic membrane?

A

Daptomycin (2003) of the Lipopeptide class

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12
Q

What is the benefit of a lipopeptide like Daptomycin?

A

It is good for resistant Gram positive bacteria due to its novel mechanism

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13
Q

What are two lipopeptide drugs that are bactericidal against gram negative bacteria?

How is it that they are effective against gram negative when Daptomycin, another lipopeptide is not?

A

Poly B and Colistin, both considered Polymyxins

They bind to LPS in the outer membrane of gram negative bugs.

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14
Q

What is the drawback to lipopeptide polymyxins like Poly B and Colistin?

A

They are very toxic which limits their use to topical use or as final resort against resistant bacteria.

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15
Q

What broad spectrum, bacteriostatic drugs bind the 30S subunit and stop tRNA binding?

A

Tetracycline class: Tetracycline, Doxycycline, Minocycline

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16
Q

How do bacteria develop resistance to Tetracyclines like Doxycycline and Minocycline?

A

Development of a Tetracycline efflux pump or mutation of the ribosome to prevent binding to the 30S subunit.

17
Q

What broad spectrum, bactericidal drugs bind the 30S subunit irreversibly and cause premature release from mRNA?

A

Aminoglycoside Class: Gentamycin, Amikacin, Kanamycin, Tobramycin

18
Q
  1. What are the benefits of Aminoglycosides like Gentamycin and Tobramycin?
  2. What are the drawbacks of Aminoglycosides like Gentamycin and Tobramycin?
A
  1. They are good for resilient Gram negative bugs like P. Aeruginosa
  2. They aren’t very good for gram positive bugs and they can result in ototoxicity and nephrotoxicity.
19
Q

How do bacteria become resistant to Aminoglycosides like Gentamycin and Tobramycin?

A

Enzymatic modification of the antibiotic prevents binding.

20
Q
  1. What type of bacteria are the macrolide class of Erythromycin, Azithromycin, and Clarithromycin good for? Are they -static or -cidal?
  2. How do they work?
A
  1. They are good for gram positive and are bacteriostatic.
  2. They bind to the 50S subunit and block elongation
21
Q

How do bacteria develop resistance to Macrolide antibiotics like Erythromycin and Azythromycin?

A

Enzyme modification of the rRNA and development of macrolide efflux pumps

22
Q
  1. What class is the MOA of Chloramphenicol similar to?
  2. Why should it be limited in its use?
  3. What two illnesses should it be used for?
A
  1. It is similar in MOA to Macrolides like Erythro and Azithro.
  2. It has toxic effects of aplastic anemia
  3. It should be used for Typhoid and RMSF.
23
Q

How do bacteria develop resistance to Chloramphenicol?

A

Enzyme addition of acetyl group to drug which prevents binding.

24
Q
  1. Clindamycin has the same MOA and same resistance mechanism as what other drugs?
  2. What is it good for?
  3. What is it not good for?
A
  1. Erythromycin and Azithromycin
  2. MRSA and Toxin producing S.Aureus
  3. Gram negative bacteria
25
Q
  1. What is linezolid best used for?
  2. -Static or -Cidal?
  3. What is the MOA?
  4. Drawbacks?
A
  1. Staph. aureus, Strep pyogenes, Strep agalactiae
  2. -static
  3. Binds unique site on 50S to prevent formation of 70S
  4. Expensive, Not good for gram negative
26
Q

What is the mechanism for resistance to linezolid?

A

Point mutations in ribosome components to prevent drug binding. No cross resistance.

27
Q
  1. What broad spectrum, bactericidal drugs bind DNA gyrase or topoisomerase resulting in DNA damage?
  2. How does resistance develop against these drugs?
A
  1. 2nd Generation Fluroquinolones: All the -floxacins
  2. Point mutations in DNA gyrase prevent binding. Occasionally efflux pumps can develop
28
Q

What drug is good for Anaerobic bacteria like C. diff.?

How does it work?

A

Metronidazole

A radical is produced in the anaerobic environment which is a toxic metabolite that damages bacterial DNA

29
Q
  1. What bactericidal drug binds B subunit of bacterial RNA polymerase?
  2. What problem does it have?
A
  1. Rifampin
  2. Rapid selection for resistant mutants
30
Q

What bactericidal drug is a noncompetitive inhibitor of RNA synthesis and binds RNA polymerase?

A

Fidaxomicin

31
Q

How do sulfonamides work against bacteria?

A

They are a metabolic analogue of p-aminobenzoic acid and works as an anti-metabolite

32
Q

How does Trimethoprim work?

How does resistance develop?

A

It is a metabolic analogue of dihydrofolate and works as an anti-metabolite.

Acquisition of another gene encoding dihydrofolate reductase creates resistance.

33
Q

What are three examples of synergism?

A
  1. Sulfonamides and Trimethoprim have sequential actions.
  2. Penicillins enhance the uptake of Aminoglycosides like Gentamycin and Tobramycin
  3. Clavulanic acid prevents inactivation of B-lactams like amoxicillin.
34
Q

What are two examples of Antagonism in drug therapy?

A
  1. Static and Cidal combination because cidal works against rapidly proliferating bacteria and static inhibits this.
  2. Combining B-lactams: Ampicillin induces AmpC B-lactamase which degrades many penicillins

Owenbacteria Block 2 (12 decks)

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