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MBIO 3010 > Dr. Zhanel's Lectures > Flashcards

Dr. Zhanel's Lectures Flashcards

1
Q

What does the ideal antimicrobial do?

A

Eradicates the infectious organism without damaging the host

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2
Q

Are antibiotic and antimicrobial synonymous?

A

Yes

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3
Q

What are antibiotics?

A

Drugs naturally produced by bacteria and fungi

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4
Q

Which species produce the majority of available antibiotics?

A
  • Streptomyces species
  • Bacillus species
  • Molds
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5
Q

What is selective toxicity?

A

The ability of an antimicrobial to selectively act on the pathogen and not on the human cell

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6
Q

What is selective toxicity often expressed as?

A

Therapeutic index, ratio, or window

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7
Q

What does a large therapeutic window indicate?

A

Safe

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8
Q

What does a small therapeutic window indicate?

A

Toxic

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9
Q

When would you use a drug with a small therapeutic window?

A

When nothing else works

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10
Q

What does broad spectrum mean?

A

Antimicrobials that work against different kinds of pathogens

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11
Q

When are broad spectrum antimicrobials used?

A

When you don’t know what is causing an infection

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12
Q

When are narrow spectrum antimicrobials used?

A

When you know what is causing the infection

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13
Q

Why aren’t broad spectrum antimicrobials used all the time?

A

Because they kill pathogens as well as normal flora

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14
Q

What does bactericidal mean?

A

The ability of an antibiotic to kill (more than 3 logs in 24 hours) an organism

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15
Q

When are bactericidal antibiotics used?

A
  • Immunocompromised individuals
  • Infections in the brain
  • Infections of the heart valves/tissues
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16
Q

In immunocompotent patients, are bactericidal or bacteriostatic antibiotics better and why?

A

They are the same because the immune system works with the antibiotic

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17
Q

What does bacteriostatic mean?

A

Reversibly inhibiting growth (less than 3 logs in 24 hours)

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18
Q

Are the majority of antibiotics bacteriostatic or bactericidal?

A

Bacteriostatic

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19
Q

What is MIC?

A
  • Minimum inhibitory concentration

- The lowest concentration of an antibiotic that prevents growth of the pathogen

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20
Q

Do you want a low or high MIC?

A

As low as possible

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21
Q

What is MBC?

A
  • Minimum bactericidal concentration

- Lowest concentration that kills an organism

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22
Q

Do you want the MBC/MIC ratio to be small or large?

A

Small

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23
Q

What is the typical MBC/MIC ratio of a bactericidal agent?

A

2-4

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24
Q

What is the typical MBC/MIC ratio of a bacteriostatic agent?

A

Very high, if it kills at all

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25
Q

How is antibiotic susceptibility determined?

A

Dilution or diffusion tests

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26
Q

What is a dilution test?

A
  • A series of test tubes with broth or plates with agar with different antibiotic concentrations are set up
  • The lowest concentration of antibiotic that inhibits growth after 16-24 hours is the MIC
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27
Q

What are disk tests?

A
  • Antibiotic-impregnated disks are placed on freshly streaked plates containing the organism
  • A zone of inhibition occurs are the disk, and the zone width is the MIC
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28
Q

What does a big zone of inhibition mean?

A

The antibiotic is good for that pathogen

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29
Q

What does a small zone of inhibition mean?

A

The pathogen is resistant to that antibiotic

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30
Q

What are the 4 common methods of action of antibiotics?

A
  • Damage bacterial cell wall (peptidoglycan) synthesis
  • Inhibit microbial protein and nucleic acid synthesis
  • Disrupt microbial membrane structure and function
  • Block metabolic pathways through inhibition of enzymes
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31
Q

When would 2 antibiotics be used together?

A

If you don’t know what the pathogen is and a secondary infection is possible

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32
Q

What are the 3 possible outcomes of antimicrobial combination and which is the most important in practice?

A
  • Indifference (most important)
  • Synergy
  • Antagonism
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33
Q

What is indifference?

A

Slightly more killing than one antibiotic alone

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34
Q

What is synergy?

A

Way more killing together than each separately

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35
Q

What is antagonism?

A

Less killing together than each separately

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36
Q

Which outcome is the most common in antimicrobial combination?

A

Indifference or additivity

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37
Q

Where are NAM and NAG synthesized?

A

In the cytoplasm

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38
Q

How is the pentapeptide chain formed?

A

Amino acids are sequentially added to UDP-NAM

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39
Q

____ is added to UDP-NAM as a dipeptide

A

2 terminal D-alanines

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40
Q

Where is the NAM-pentapeptide transported?

A

From UDP to a bactoprenol phosphate carrier at the cell membrane surface

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41
Q

What is the function of UDP-NAG?

A

Add NAG to the NAM-pentapeptide to form the peptidoglycan repeat unit

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42
Q

What is special about the peptidoglycan repeat unit in gram positives?

A

A pentaglycine interbridge is required, so glycines are added by glycyl-tRNA molecules

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43
Q

Where is the NAM-NAG peptidoglycan repeat unit transported?

A

Across the cell membrane to the outer surface by the bactoprenol pyrophosphate carrier

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44
Q

What are the last few steps of peptidoglycan synthesis, after all transportation has occurred?

A
  • New peptidoglycan unit is attached to the existing peptidoglycan chain
  • Bactoprenol carrier returns to inside of cell
  • Phosphate is released to bactoprenol phosphate so it can accept a new NAM-pentapeptide
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45
Q

What does transpeptidation create?

A

Peptide cross-links between the peptidoglycan chains

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46
Q

What enzyme performs transpeptidation?

A

Transpeptidase

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47
Q

What is transpeptidase called in gram negatives and positives?

A

Penicillin binding protein (PBP)

48
Q

What are the categories of cell wall active antibiotics?

A
  • Penicillins
  • Cephalosporins
  • Glycopeptides/lipopeptdes
  • Bacitracin
49
Q

What are penicillins and cephalosporins referred to as?

A

Beta-lactams

50
Q

Are penicillins broad or narrow spectrum?

A

Both

51
Q

Do penicillins have a small or large therapeutic window?

A

Large

52
Q

Do cephalosporins have a small or large therapeutic index?

A

Large

53
Q

Are cephalosporins broad or narrow spectrum?

A

Broad

54
Q

Are glycopeptides broad or narrow spectrum?

A

Narrow

55
Q

Do glycopeptides have a small or large therapeutic index?

A

Small

56
Q

Which type of cell wall active antibiotics inhibit cell wall synthesis?

A
  • Beta lactams and beta-lactam like agents
  • Glycopeptides
  • Bacitracin
57
Q

What does inhibition of cell wall synthesis cause?

A

Osmotic instability, which causes cell death

58
Q

Are beta-lactams bactericidal or bacteriostatic?

A

Bactericidal

59
Q

Are glycopeptides bactericidal or bacteriostatic?

A

Bactericidal

60
Q

Is bacitracin bactericidal or bacteriostatic?

A

Bactericidal

61
Q

What are the terminal AA residues on the precursor NAM/NAG peptide subunits?

A

D-alanyl-D-alanine

62
Q

What facilitates the binding of beta-lactams to the active serine site of PBPs?

A

D-alanyl-D-alanine

63
Q

What prevents the final crosslinking of a new peptidoglycan layer?

A

The binding of the beta-lactam nucleus to the serine residue of the PBP active site

64
Q

What is the consequence of beta-lactams binding to PBPs?

A

Inhibition of peptidoglycan synthesis, which causes autolysin activation, which breaks down existing peptidoglycan, causing cell death

65
Q

Where do glycopeptides bind to an peptidoglycan?

A

The terminal D-ala-D-ala residues

66
Q

How does bacitracin work as an antibiotic?

A

Blocks the dephosphorylation of bactoprenol pyrophosphate

67
Q

What is important to note about bacitracin?

A
  • Very toxic, so only used topically

- Good at killing staph and strep, which are most common in skin infections

68
Q

What are mechanisms of resistance that pathogens use?

A
  • Beta-lactamases
  • Alteration of PBPs
  • Reduction in antibiotic uptake
  • Antibiotic efflux
69
Q

What do beta-lactamases do?

A

Break the beta-lactam ring

70
Q

How can beta-lactamases be inhibited?

A

By binding irreversibly to beta-lactamase inhibitors

71
Q

Do beta-lactamases cause a large or small increase in MIC?

A

Large

72
Q

Does alteration of PBPs cause a large or small increase in MIC?

A

Small

73
Q

What type of ribosomes do prokaryotic cells have?

A

70S ribosomes, with 50S and 30S units

74
Q

What type of ribosomes do eukaryotes have?

A

80S ribosomes, with 60S and 40S units

75
Q

What does the ribosomal structural difference between prokaryotic and eukaryotic cells account for?

A

The selective toxicity of antibiotics that affect protein synthesis

76
Q

What type of ribosomes are mitochondrial ribosomes?

A

70S

77
Q

How do antibiotics that inhibit protein synthesis generally work?

A

Interacting with the prokaryotic ribosome at the 30S site or the 50S site

78
Q

Which types of antibiotics interact with the 30S site of a prokaryotic ribosome?

A
  • Aminoglycosides

- Tetracyclines

79
Q

Which types of antibiotics interact with the 50S site of a prokaryotic ribosome?

A
  • Chloramphenicol
  • Clindamycin
  • Macrolides
  • Ketolides
  • Oxazolidinones
80
Q

Are antibiotics that inhibit protein synthesis bacteriostatic or bactericidal?

A

Bacteriostatic, except aminoglycosides are bactericidal

81
Q

What is the most important aminoglycoside?

A

Gentamicin

82
Q

Are aminoglycosides bactericidal or bacteriostatic and why?

A

Bactericidal because they bind to mRNA

83
Q

Are aminoglycosides broad or narrow spectrum?

A

Broad

84
Q

Do aminoglycosides have a large or small therapeutic index?

A

Small

85
Q

When are aminoglycosides used?

A

When other things aren’t working

86
Q

What are the 2 most important macrolides?

A
  • Erythromycin

- Clindamycin

87
Q

Are macrolides bacteriostatic or bactericidal?

A

Bacteriostatic

88
Q

Are macrolides broad or narrow spectrum?

A

Broad

89
Q

Do macrolides have a large or small therapeutic index?

A

Large

90
Q

What are macrolides used to treat?

A

RTI’s

91
Q

What is the most important tetracycline?

A

Tetracycline

92
Q

Are tetracyclines bacteriostatic or bactericidal?

A

Bacteriostatic

93
Q

Are tetracyclines broad or narrow spectrum?

A

Very broad

94
Q

Do tetracyclines have a large or small therapeutic index?

A

Medium

95
Q

What is important to note about tetracyclines?

A

Can’t be used in women that can potentially become pregnant

96
Q

Do oxazolidinones have a large or small therapeutic index?

A

Medium

97
Q

Are oxazolidinones broad or narrow spectrum?

A

Very narrow, only staph and strep

98
Q

What is the general mechanism of resistance in gram-negative bacteria?

A

Reduce antibiotic uptake

99
Q

What is the mechanism of resistance against aminoglycosides?

A
  • Plasmid and chromosomally encoded inactivating enzymes modify the antibiotic so that it can’t bind to ribosomal sites
  • Alteration in bacterial ribosomes
100
Q

What is the mechanism of resistance against macrolides?

A

Plasmid mediated mono or di-methylation of adenine of the 23S rRNA, causing reduced affinity between the antibiotic and ribosome

101
Q

What is the mechanism of resistance against tetracyclines?

A

Tetracycline efflux across the cytoplasmic membrane

102
Q

How can resistance to tetracyclines be overcome?

A

Using tigecycline

103
Q

What is the mechanism of resistance against chloramphenicol?

A

Plasmid or chromosomally encoded enzyme (chloramphenicol acetyltransferase) modifies the antibiotic

104
Q

What is the mechanism of mechanism against oxazolidinones?

A

Mutations of 23S rRNA

105
Q

What do fluoroquinolones contain?

A

A 4-quinolone ring

106
Q

Are fluoroquinolones bacteriostatic or bactericidal?

A

Bactericidal

107
Q

What is the mechanism of action of fluoroquinolones?

A

Inhibition of bacterial DNA gyrase

108
Q

What is DNA gyrase?

A

An enzyme that introduces negative twists in DNA and helps separates its strands

109
Q

What is a generalization about fluoroquinolones?

A

They disrupt all cell processes that involve DNA

110
Q

What are the 3 mechanisms of resistance against fluoroquinolones and which is the most important?

A
  • Reduced uptake through altered outer-membrane proteins or LPS
  • Spontaneous single step mutations involving DNA gyrase leading to reduced antibiotic binding (*most important)
  • Antibiotic efflux across the cell membrane
111
Q

Which mechanism of resistance against fluoroquinolones occurs in gram-negatives?

A

Reduced uptake through altered outer-membrane proteins or LPS

112
Q

What do sulfonamides do?

A

Interfere with different steps of the metabolic pathways that synthesize folic acid

113
Q

What are sulfonamides structurally similar to and why is this important?

A
  • Para-aminobenzoic acid (PABA)

- PABA is required by bacteria for folic acid synthesis

114
Q

What is the outcome of sulfonamide action of inhibiting folic acid synthesis?

A

Decrease in bacterial purines, which subsequently inhibits bacterial growth

115
Q

What are the 3 mechanisms of resistance against sulfonamides?

A
  • Reduced accumulation (preventing uptake of the drug or effluxing the drug out of the cell)
  • Drug inactivation through chemical modification
  • Target site modification

MBIO 3010 (17 decks)

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