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Week 2-Day 2 > Antimicrobial Agents & Microbial Resistance > Flashcards

Antimicrobial Agents & Microbial Resistance Flashcards

1
Q

Major Inhibition Mechanisms of Antibacterials

A
  1. Cell Wall Synthesis
  2. Membrane Structure
  3. Folate Synthesis
  4. DNA Synthesis
  5. DNA Damage
  6. mRNA Synthesis
  7. Protein Synthesis
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2
Q

Minimum Inhibitory Concentration (MIC)

A

The lowest drug concentration that inhibits VISIBLE growth.

*Every drug has a MIC and MBC

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3
Q

Minimum Bactericidal Concentration (MBC)

A

The lowest drug concentration that kills bacteria.

*Every drug has a MIC and MBC

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4
Q

MIC & MBC

A
  • The lower the number, the more susceptible the bacteria (easily dies).
  • The higher the number, the less susceptible the bacteria (more resistant).
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5
Q

Bacteriostatic

A
  • The drug that prevents the growth of bacteria

- Bacteriostatic MBC&raquo_space; MIC

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6
Q

Bactericidal

A
  • The drug that kills bacteria

- Bactericidal MBC ~= MIC

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7
Q

Pharmacodynamics (PD)

A

The biological effects of the drug ON the BODY.

  • Time, drug concentration, and side effects are important factors.
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8
Q

Pharmacokinetics (PK)

A

The body’s effects ON the DRUG.

  • Time of absorption, distribution, metabolism, excretion are things to be considered.
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9
Q

Time-Dependent Killing (TDK)

A

It is the duration of exposure in which T>MIC for plasma concentration.

Ex. (Wall Inhibitors): Penicillins & Cephalosporins
Ex. (Protein Inhibitors): Macrolides & Clindamycin

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10
Q

Concentration-Dependent Killing (CDK)

A

It is the maximum plasma concentration and therefore the Area Under Curve.

Ex. (DNA Inhibitors): Fluoroquinolones
Ex. (Protein Inhibitors): Aminoglycosides

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11
Q

Post-Antibiotic Effect (PAE)

A

The time it takes bacteria to return to LOG-PHASE growth following removal of antibiotic.

  • CDK drugs have longer PAE than TDK drugs.
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12
Q

Cell Wall Synthesis Inhibitors

A
  • B-lactams

- Glycopetides

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13
Q

Cell Membrane Disrupting Drugs

A
  • Lipopeptides
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14
Q

Subclasses of B-lactams

A
  • Penicillins
  • Cephalosporins (aka. cephamycins)
  • Monobactams
  • Clavams
  • Carbapenems
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15
Q

Peptidoglycan Structure

A
  • Alternating NAM and NAG sugar chains are cross-linked by polypeptide (AAs) bonds.
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16
Q

Transglycosylation

A

Glycosidic bond formation between NAM and NAG sugars.

  • The process is carried out by Transglycosylase.
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17
Q

Transpeptidation

A

Peptide bond formation by removing D-Ala-D-Ala.

  • The process is carried out by Transpeptidase.
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18
Q

Penicillin-Binding Proteins

A

Bacterial proteins that bind to B-lactam antibiotics.

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19
Q

B-lactamases

A

Breaks a bond in the B-lactam ring to disable the antibiotics.

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20
Q

Extended Spectrum B-lactamases (ESBL)

A
  • Most derived from active site mutations in TEM/SHV.

- Results in activity against cephalosporins.

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21
Q

New Delhi Metal-Dependent B-lactamase (NDM-1)

A

One type of B-lactamase I need to know

22
Q

Clavulanic Acid (Generic Name)

A
  • B-lactamase INHIBITOR

- Belongs to Clavams

23
Q

3 Main Antibiotic Resistance Mechanisms

A
  1. Enzymatically Inactivate Drug
  2. Alter Drug Target
  3. Alter Drug Exposure
24
Q

Subclass of Glycopeptides

A

Vancomycin

  • Primarily used to treat Gram +
25
Q

Glycopeptides Inhibition

A

Inhibits Transglycosylation by binding to D-ala-D-ala directly.

26
Q

B-lactam Inhibition

A

Inhibits Transglycosylation by binding to transpeptidase that is suppose to bind to D-ala-D-ala.

** only work on actively dividing cells (D-ala-D-ala).

27
Q

Anti-Mycobacterial Drugs

A
  1. Isoniazid: Inhibits mycolic acid synthesis.

2. Ethambutol: Inhibit arabinotransferases.

28
Q

Lipopeptides Generic Drug

A

Generic Name: Daptomycin

29
Q

Lipopeptide Inhibition

A
  • Antibacterial drug against Gram +.
  • Binds to phosphatidyl-glycerol in bacterial cell membrane and pokes a hole.
  • Gram - outer membrane protects against lipopeptides.

** Lipopeptides are not used to treat pneumonia (because lung surfactant layer is rich in phosphatidyl-glycerol) to not damage your lungs.

30
Q

Sulfonamides

A
  • Bacteriostatic drugs against G+ and G- and some protozoa.
  • Inhibit folate synthesis precursor (DHPS)
  • Generic Name: sulfamethoxazole (smx)
31
Q

Trimethoprim (tmp)

A
  • Bactericidal
  • Inhibit folate synthesis precursor (DHFR)
  • synergistic with smx (becomes bactericidal) in low concentrations against resistance.
32
Q

Fluoroquinolones/Quinolones

A
  • Bactericidal against G- more than G+
  • Inhibit DNA Gyrase & topoisomerase IV
  • Generic Name: Ciprofloxacin
33
Q

DNA Gyrase

A

Topoisomerase II (releasing knots)

34
Q

Topoisomerase IV

A

Helps newly replicated chromosomes separate into daughter cells.

35
Q

Rifamycins

A
  • Can be bactericidal or bacteriostatic depending on concentration.
  • Inhibit mRNA synthesis by binding to bacterial DNA-dp RNA polymerase.
  • Generic Name: Rifampin
36
Q

Nitroimidazoles

A
  • Bactericidal against anaerobes and some protozoa.
  • Its prodrug must be converted to active form by bacterial enzyme.
  • Activated form produce toxic free radicals that damage DNA.
  • Generic Name: metronidazole
37
Q

Drug Classes Inhibiting Protein Synthesis

A
  1. 30S
    - Aminoglycosides
    - Tetracyclines
  2. 50S
    - Chloramphenicol
    - Macrolides
    - Lincosamides
    - Streptogramins
    - Oxazolidinones
38
Q

Aminoglycosides

A
  • Bactericidal against Gram - and mycobacterium by binding to 30S subunit.
  • Produced by streptomyces spp.
  • Generic Name: Streptomycin & Gentamicin
  • Anaerobes are intrinsically resistant to aminoglycosides
39
Q

B-lactams & Aminoglycosides

A

They are often prescribed together in combination for synergistic treatment.

40
Q

Tetracyclines

A
  • Bacteriostatic
  • Bind to 30S subunit.
  • Generic Name: Tetracycline & Doxycycline
41
Q

Tetracycline & B-lactams

A

They are combinations to AVOID; Antagonistic

42
Q

Chloramphenicol

A
  • Bacteriostatic (cidal against encapsulated ones)

- Inhibits protein synthesis by binding to 50S subunit.

43
Q

Macrolides

A
  • Bacteriostatic against G+ by binding to 50S subunit.
  • Produced by streptomyces spp.
  • Generic Names: Erythromycin & Azithromycin
44
Q

Lincosamides

A
  • Bacteriostatic against G+ and G- anaerobes by binding to their 50S subunit.
  • Produced by streptomyces spp.
  • Generic Name: Clindamycin
45
Q

Streptogramins A & B

A
  • Individually bacteriostatic, bactericidal together.
  • Produced by streptomyces spp.
  • Bind to 50S subunit.
46
Q
  • mycin drugs
A

Drugs whose generic names end in -mycin are produced by soil bacteria.

  • erythromycin/azithromycin (macrolides)
  • clindamycin (lincosamides)
  • streptomycin/gentamycin (aminoglycosides)
  • streptogramins (깍두기)
47
Q

Resistance to MLSB

A

Cross-resistance to Macrolides, Lincosamides, and Streptogramins B. and can lead to multi-drug resistance.

  • Clindamycin resistance is INDUCIBLE (detected using Disk test) in presence of other drug
48
Q

Resistance to B-lactam

A
  1. Enzymatically Inactivate Drug
    - Inhibitory enzyme B-lactamase
  2. Alter Drug Target
    - Mutation & Horizontal Genetic Exchange
  3. Alter Drug Exposure
    - Decreased Uptake (in Gram - by altering membrane porins)
    - Increased Efflux
49
Q

Resistance to Fluo/Quinolones

A
  1. Altered Drug Target
    - Mutations in gyrase (gyr A) and topoisomerase (parC) genes
  2. Altered Drug Exposure
    - Decreased uptake & increased efflux
    - Cross-resistance between quinolones and other drugs causing multi-drug resistance
50
Q

Resistance to Rifamycins

A

Altered Drug Target

- Mutations in RNA polymerase gene

51
Q

Oxazolidinones

A
  • Bacteriostatic against G+ by binding to 50S subunit.

- Generic Name: linezolid

Week 2-Day 2 (3 decks)

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