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MICROM 442 > Exam 1 Lecture 7 and 8 > Flashcards

Exam 1 Lecture 7 and 8 Flashcards

Principles of Antimicrobials

1
Q

What is the effect of timing antibiotics on survival?

A

In sepsis patients, early antimicrobial initiation correlated with higher survival fraction. Every hour counts!

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2
Q

Potential antibiotic targets

A
  1. Cell wall
  2. Cell membrane
  3. DNA replication
  4. Transcription
  5. Protein Synthesis
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3
Q

Which bacterial target is least toxic to humans?

A

Cell wall

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4
Q

Selective toxicity

A

Increasing toxicity to bacteria while having the least effect on our cells

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5
Q

Selective toxicity contributes to:

A

Side effects and therapeutic index

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6
Q

What is therapeutic index?

A

Toxic dose/therapeutic dose

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7
Q

Therapeutic index for penicillins:

A

High (low toxicity and can be administered in high amounts)

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8
Q

Therapeutic index for aminoglycosides:

A

Low (lower dose can be toxic, so blood level of aminoglycosides must be monitored actively)

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9
Q

Therapeutic drug monitoring must be done for:

A

(example) Aminoglycosides and Vancomycin

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10
Q

Sources of antimicrobials

A

Naturally occurring, semi-synthetic, synthetic

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11
Q

Absorption

A

Oral vs IV

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12
Q

Oral (absorption)

A

Not all becomes bioavailable, not absorbed as well as a result

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13
Q

IV (absorption)

A

Becomes available to all sites at a high rate, including blood and soft tissues

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14
Q

Pharmacology impacts on drug choice (5 things)

A
  1. Absorption
  2. tissue distribution
  3. metabolism/excretion
  4. time-dependent killing (half life)
  5. concentration-dependent killing
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15
Q

What does a bactericidal drug do?

A

Inhibits growth and kill bacterial cells

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16
Q

Examples of bactericidal drug

A

Beta lactams, aminoglycosides

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17
Q

When would you want to administer a bactericidal drug?

A
  1. immunocompromised patient (who would have decreased response to bacteriostatic)
  2. Very severe infection

Overall, if there’s a choice, often go for bactericidal

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18
Q

What does a bacteriostatic drug do?

A

Inhibits bacterial growth but does not kill; relies on host immune system to help clear out the bacteria

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19
Q

Examples of bacteriostatic drug

A

Macrolides, tetracyclines

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20
Q

What is MIC?

A

Minimum inhibitory concentration; clinically, all susceptibility testing goes back to MIC

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21
Q

What is combination therapy?

A

Administering 2 (or possibly more) drugs at the same time

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22
Q

Why is combination therapy helpful sometimes?

A

Helps to reduce chance of developing resistance over time

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23
Q

When do you want to give combination therapy?

A
  1. Empiric therapy
  2. Polymicrobial Infection
  3. Prevent resistance
  4. Enhanced efficacy (synergy, additive)
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24
Q

What is empiric therapy?

A

Used when the exact causative agent is not known or are hard to predict, yet antimicrobials are administered to cover those potential bacteria; “educated guess”

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25
Q

How do providers make antimicrobial decisions before we give them a final report?

A

Physician sees patient; makes clinical diagnosis; and prescribes empiric antimicrobials

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26
Q

1st generation cephalosporins are great for…

A

MSSA

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27
Q

Example of 1st generation cephalosporin

A

Cefazolin

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28
Q

Vancomycin is great for…

A

Emperic coverage (both MSSA and MRSA are susceptible)

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29
Q

In vitro susceptibility testing examples

A
  1. Broth Dilution
  2. Diffusion tests (Kirby-Bauer, ETEST)
  3. Beta lactamase test
  4. Molecular test
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30
Q

Broth or ETEST provides ____

A

MIC

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31
Q

Kirby Bauer provides ___

A

mm inhibition

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32
Q

MIC and KB must be ______

A

correlated with clinical breakpoints

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33
Q

What are the three clinical breakpoints?

A

Resistant, Intermediate, Susceptible

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34
Q

Names of cell wall antibiotics

A
  1. Beta lactams (penicillins and cephalosporins)

2. Glycopeptides (vancomycin)

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35
Q

Name of cell membrane antibiotics

A

Polymixins

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36
Q

Name of DNA antibiotics

A
  1. [Fluoro]quinolones (e.g. ciprofloxacin)

2. Sulfonamides and trimethoprim (e.g. Bactrim)

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37
Q

Name of transcription antibiotics

A

Rifampin

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38
Q

Name of protein synthesis antibiotics (4 classes)

A
  1. Aminoglycosides (e.g. gentamycin)
  2. Macrolides (e.g. azithromycin, “Z-pack”)
  3. Tetracyclines
  4. Lincosamides (e.g. clindamycin)
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39
Q

Lincosamide drug name example

A

Clindamycin

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40
Q

Aminoglycosides drug name example

A

Gentamycin

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41
Q

Macrolides drug name example

A

Azithromycin

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42
Q

General mechanisms of resistance

A
  1. Efflux
  2. Target site alterations
  3. Inactivating enzymes
  4. Restricted access to target
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43
Q

What is meant by restricted access to target?

A

Inherent structures in the bacteria that makes it harder for drug penetration (e.g. physical barrier, porins)

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44
Q

What is the biggest concern for infection control?

A

Mobile genetic elements that contribute to transformation of bacterial populations, allowing them to acquire resistance genes and for resistance mechanism to spread

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45
Q

How are resistance determinants encoded/expressed?

A
  1. Intrinsic (chromosomal)
  2. De novo mutations
  3. Acquired (plasmids, transposons, integrons, natural transformation, bacteriophage)
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46
Q

Why are infections of mechanical heart valves and prosthetic joints “surgical solutions”?

A
  1. biofilms provide physical barriers to antimicrobials

2. organisms are often not rapidly growing, reducing the efficacy of many antimicrobials

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47
Q

What does a mucoid isolate imply?

A

slows diffusion and ability of drugs to get into the cell

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48
Q

2 examples of restricting access to target

A
  1. biofilms

2. impermeability (porins, LPS)

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49
Q

Direct interactions with antibiotics

A
  1. Inactivation by hydrolysis (ex. beta lactamase)

2. Inactivation by steric hindrance (ex. aminoglycoside-modifying enzymes)

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50
Q

Mutation of target site example

A

Mutations in topoisomerase confer fluoroquinolone resistance

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51
Q

Target site protection example

A

Methylation of 16S rRNA alters binding of erythromycin to ribosome

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52
Q

Upregulation of efflux pumps can lead to:

A

Multidrug resistance

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53
Q

True or false: efflux pumps can be broad or narrow spectrum

A

true

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54
Q

How do we end up with multi-drug resistant strains?

A
  1. encode multiple genes (ex. on a plasmid)
  2. encode a gene that can target multiple antibiotics
  3. selective pressure
55
Q

Beta lactams are ____ cell ____ agents

A

cidal; wall

56
Q

4 categories of beta lactams:

A
  1. penicillin
  2. cephalosporins
  3. monobactams
  4. carbapenems
57
Q

Beta lactams bind ____ which _____ cell growth

A

PBPs (penicillin binding proteins); inhibits

58
Q

Why are beta lactams cidal?

A

weakens integrity of cell wall, leading to osmotic instability and lyses the cell

59
Q

Lower generations of cephalosporins generalizations:

A

narrow spectrum (primarily gram positives); not as good for resistant strains

60
Q

Which cephalosporin covers MRSA?

A

Ceftaroline (5th generation)

61
Q

Ceftriaxone is a ____ cephalosporin

A

3rd generation

62
Q

What are 3 general mechanisms of resistance to Beta lactams?

A
  1. decreased penetration to the target site
  2. Inactivation of antibiotic by bacterial enzyme
  3. alteration of target site
63
Q

Where are beta lactamases localized in Gram - cells?

A

periplasmic space (higher level resistance)

64
Q

Where are beta lactamases localized in Gram + cells?

A

secreted (often lower level resistance)

65
Q

AmpC beta lactamases are ______ encoded and _____ for several Enterobactericeae

A

chromosomally; inducible

66
Q

When does AmpC become a problem?

A

When it is overexpressed

67
Q

AmpC

A

encodes for beta-lactamase enzyme

68
Q

AmpR

69
Q

AmpD

A

regulator that detects small cell wall fragments

70
Q

True or false: you must treat a SPICEM organism with a 1st, 2nd, or 3rd generation cephalosporin

A

False –> this can lead to quick resistance

71
Q

Carbapenem mechanism of resistance (3 things)

A
  1. decreased penetration to the target site (efflux)
  2. inactivation of the antibiotic by a bacterial enzyme (carbapenemase in KPC)
  3. Enzymatic degradation plus decreased uptake (beta lactamase AmpC plus porin mutation)
72
Q

Alterations of ____ may influence their binding affinity for beta lactam antibiotics. This mechanism is responsible for ___ ____ ____.

A

PBP’s; methicillin resistance in staphylococci (MRSA)

73
Q

How is PBP2a acquired?

A

Through mobile element called SCCmec, mecA gene encodes for PBP2a

74
Q

What are some lab methods to detect methicillin resistance?

A
  1. susceptibility to methicillin, cefoxitin, or oxacillin (disc diffusion, MICs)
  2. detection of mecA gene through PCR
  3. detection of PBP2a through lateral flow/latex agglutination
75
Q

Vancomycin blocks peptidoglycan crosslinks of _____ only.

A

gram positive bacteria

76
Q

What forms hydrogen bonds with D-ala-D-ala?

A

vancomycin

77
Q

Vancomycin is used for ____ treatment against ____.

A

empiric; MRSA

78
Q

True or false: vancomycin can treat C. diff and can be administered orally

79
Q

True or false: vancomycin can be nephrotoxic

A

True; MIC and therapeutic drug monitoring are used together to facilitate dosing and prevent toxicity

80
Q

True or false: In MSSA, vancomycin works better than a beta lactam

A

False: vancomycin be suboptimal

81
Q

Vancomycin acquired resistance:

A

Altered peptidoglycan precursors, tolerance

82
Q

Vancomycin resistance mechanism in Enterococci?

A

Altered terminal peptide is D-lactate, therefore vancomycin cannot H bond

83
Q

What is the most common mechanism for E. faecalis and E. faecium resistance?

A

Van A and Van B; transferable due to being encoded on mobile genetic elements

84
Q

Best therapy for E. faecalis

A

Ampicillin

85
Q

True or false: E. faecalis is usually resistant to vancomycin

A

False; rarely resistant

86
Q

True or false: E. faecium is frequently resistant to ampicillin and vancomycin

87
Q

Which antibiotic targets cell membrane?

A

Polymyxins

88
Q

Polymyxins are ____ polypeptides with ___ ___ effect

A

large; cationic detergent

89
Q

True or false: Polymyxins are relatively toxic

A

true; primarily for multi-drug resistant Gram -

90
Q

DNA replication antibiotics

A

Fluoroquinolones, sulfas/trimethoprim, metronidazole

91
Q

Fluoroquinolones that are targeted towards Gram -:

A
  1. Ciprofloxacin

2. Levofloxacin

92
Q

Fluoroquinolones that are targeted towards Gram +:

A

Moxifloxacin

93
Q

How do fluoroquinolones work?

A

Inhibit DNA gyrase +/- topoisomerase IV

therefore inhibits chromosomal replication -> cidal

94
Q

Fluoroquinolones stand out for:

A

high bioavailability (oral almost as good as IV)

95
Q

How do sulfas/trimethoprim work?

A

Inhibits folate synthesis, thereby inhibiting purine metabolism

96
Q

Do mammals synthesize folic acid?

97
Q

Sulfas/trimethoprim spectrum

A

Broad spectrum against many G+ and G-, also some parasites

98
Q

Sulfonamides target:

A

dihydropteroate synthetase

99
Q

Trimethoprim targets:

A

Dihydrofolate reductase

100
Q

Metronidazole requires reduction of ___ ___ under ____ conditions

A

nitro group; anaerobic

101
Q

Metronidazole only effective against ___ and ___

A

Anaerobes; protozoa

102
Q

True or false: metronidazole causes breaks in the RNA

A

false –> DNA

103
Q

Transcription antibiotic name

104
Q

Rifampin inhibits ____ ____, and therefore inhibits _____

A

RNA polymerase; transcription

105
Q

In ribosomes, resistance can be conferred by __ __ in ___

A

point mutations; rpoB

106
Q

T or F: With rare exceptions, rifampin must be used in combination therapy

A

Tru; rapid selection for resistance

107
Q

Antibiotics against protein synthesis names

A
  1. Aminoglycosides
  2. Tetracyclines
  3. Macrolides
  4. Clindamycin
108
Q

How do aminoglycosides work?

A
  1. Binds irreversibly to bacterial 30S and 50S
  2. prevents formation of initiation complexes
  3. Cidal
109
Q

What are aminoglycosides effective against?

A

Gram negatives

110
Q

Aminoglycosides are ___ with beta lactams

A

synergistic

111
Q

Tetracyclines spectrum

112
Q

Tetracycline mechanism

A

bind irreversibly to 30S ribosomal subunits, preventing attachment of aminoacyl-tRNAs to ribosomal acceptor

113
Q

True or false: tetracyclines are bactericidal

A

false; bacteriostatic

114
Q

Macrolides drug names examples

A

erythromycin, azithromycin, clarithryomycin

115
Q

Macrolides mechanism

A

bind reversibly to 23S, blocks translocation of tRNA acceptor to donor site

116
Q

Macrolides spectrum

A

Broad -

  1. gram +, some gram -
  2. anaerobes
  3. Atypical mycobacteria
  4. atypical respiratory pathogens
117
Q

Clindamycin mechanism

A
  1. binds 50S ribosomal subunit, prevents elongation of peptide chains
  2. Bacteriostatic or bactericidal
118
Q

Clindamycin has poor penetration into the ___

119
Q

Clindamycin is frequently used for ____ ____ and ____

A

gram + cocci; anaerobes

120
Q

_____ can be used to suppress toxin formation and can cause inducible resistance

A

Clindamycin

121
Q

Erythromycin & Clindamycin mechanisms of action (3 things)

A
  1. inhibit protein synthesis at 50S ribosome
  2. prevent transpeptidation and chain elongation
  3. have a common binding site at 23S rRNA component of the 50S ribosome
122
Q

Erythromycin mechanisms of resistance

A

Efflux, Methylation of ribosome

123
Q

Clindamycin mechanisms of resistance

A

Methylation of ribosome

124
Q

What coverage difference is there between ciprofloxacin/levofloxacin and moxifloxacin?

A

Moxifloxacin is mainly for G+

Cipro/levofloxacin is mainly for G-

125
Q

Name two drugs where both MIC and therapeutic drug monitoring are used

A

Vancomycin and Aminoglycosides

126
Q

What are 4 general categories of resistance?

A
  1. Efflux
  2. Target site alteration
  3. Drug alteration/degradation
  4. Physical barrier
127
Q

How would you treat a patient with an Enterococci infection prior to having susceptibility results back?

A

E. faecium = vancomycin

E. faecalis = ampicillin

128
Q

What 2 drugs have the same target and are concerning for cross resistance?

A

Erythromycin and Clindamycin

129
Q

Why do you not want to treat Enterobacter with ceftriaxone?

A

It’s a 3rd gen cephalosporin (need 4th or 5th gen) - resistance can quickly develop, especially AmpC resistance

130
Q

What are the 2 most common mechanisms for resistance to beta-lactams?

A
  1. Beta lactamase

2. PBP2A (altered target site)

131
Q

Name 2 classical side effects that can occur with both vancomycin and aminoglycosides

A
  1. Ototoxicity (ear)

2. Nephrotoxicity (kidney)

132
Q 
Which of the following is the best drug for mycoplasma?
A. Penicillin
B. Ceftriaxone
C. Vancomycin
D. Azithromycin
A

D - Azithromycin

133
Q

Name 2 drugs commonly used for anaerobes

A

Clindamycin and metronidazole

MICROM 442 (26 decks)

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