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Bacteriology > Antimicrobial Susceptibility Testing > Flashcards

Antimicrobial Susceptibility Testing Flashcards

1
Q

Antibiotic

A

a substance produced by a microorganism that kills or inhibits other microorganisms

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2
Q

Antimicrobial agent

A

a substance that kills or inhibits a microorganism (can be natural like an antibiotic or synthetic)

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3
Q

Antibacterial agent

A

an antimicrobial that affects bacteria

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4
Q

Bactericidal

A

agents that kill bacteria

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5
Q

Bacteriostatic

A

agents that inhibit bacteria

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6
Q

Spectrum of activity

A

the range of organisms that are adversely affected by an antimicrobial agent

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7
Q

Plasmid

A

extrachromosomal DNA that can replicate and may carry resistance genes that can be transferred among organisms

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8
Q

Additive drug interaction

A

the antimicrobial agent effect is the sum of the activity of the individual antimicrobial agents (drugs work together but the effect is not amplified)

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9
Q

Synergy drug interaction

A

the effect of the antimicrobial agents is greater than the sum (amplified)

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10
Q

Antagonism drug interaction

A

one antimicrobial agent interferes with the activity of another (two drugs are less effective than one)

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11
Q

Indifferent drug interaction

A

the antimicrobial agents are independent of one another

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12
Q

Intrinsic resistance

A

inherent/it is a characteristic of a species, genus, or group
Ex: GNRs being resistant to vancomycin because it cannot cross the outer membrane

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13
Q

Acquire resistance

A

a change in a bacterial strain’s susceptibility from gene mutation and transfer of resistance genes

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14
Q

Enzyme inactivation resistance mechanism

A

produce enzymes that inactivate antimicrobial agents
Ex: penicillinase

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15
Q

Permeability barriers

A

unable to reach their intended target sites

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16
Q

Drug efflux

A

use an energy-dependent system to pump an antimicrobial agent out of the bacterial cell

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17
Q

Low-affinity target sites

A

the drug binds poorly or not at all to its target site

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18
Q

Bypass mechanisms

A

able to circumvent the metabolic block caused by an antimicrobial agent

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19
Q

Constitutive resistance expression

A

the microorganism is constantly expressing the resistance mechanism

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20
Q

Inducible resistance expression

A

the microorganism expresses the resistance mechanism only when exposed to the appropriate antimicrobial agent

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21
Q

Constitutive-inducible resistance expression

A

constantly expresses resistance at a low level and a high level when the antimicrobial agent is present

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22
Q

B-lactam agents

A

inhibit cell wall synthesis by binding to enzymes involved in peptidoglycan production (penicillin-binding proteins); bactericidal

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23
Q

Penicillin-binding proteins (PBPs)

A

enzymes involved in the formation of peptidoglycan cross-links

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24
Q

Acyl-D-alanyl-D-alanine

A

the normal substrate required for synthesis of the linear glycopeptide in the bacterial cell wall; the ring for beta-lactams are similar to this ring

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25
Q

B-lactamases

A

enzymes that inactivate B-lactam agents by cleaving the B-lactam ring
Includes: penicillinases and cephalosporinases

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26
Q

Which antimicrobial agents are B-lactams?

A

Penicillins, cephems, carbapenems, and monobactams

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27
Q

Which staphylococci are resistant to B-lactams

A

Methicillin-resistant staphylococci are resistant to all B-lactam agents

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28
Q

What are the key steps for antimicrobial action?

A
  1. The agent must be in an active form
  2. It must be able to achieve sufficient levels at the site of infection
  3. It must be able to inhibit growth or kill the bacteria
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29
Q

Which antibacterial agents inhibit cell wall synthesis?

A

Beta-lactams, fosfomycin tromethamine, glycopeptides, and lipoglycopeptides

30
Q

Fosfomycin tromethamine

A

inhibits cell wall formation by inactivating enzymes involved in the first step of peptidoglycan synthesis; generally used for uncomplicated UTIs caused by Enterococcus faecalis and E. coli

31
Q

Glycopeptides

A

inhibit bacterial cell wall synthesis by binding to the end of peptidoglycan interfering with transpeptidation (cross-linking); Ex: vancomycin
Effect for GP organisms, but too big for GN ones

32
Q

Lipoglycopeptides

A

structurally similar to vancomycin but they have hydrophobic chemical groups to increase cell permeability and causes depolarization of the cell membrane potential

33
Q

Which agents inhibit cell membrane function?

A

Lipopeptides: daptomycin and polymyxins
Lipopeptides bind to and disrupt the cell membrane

34
Q

Daptomycin

A

binds to the cytoplasmic membrane and inserts its hydrophobic tail into the membrane, increasing its permeability
For GP bacteria but should not be used for lung infections because it can cause eosinophilic allergic pneumonia

35
Q

Polymyxins

A

cyclic lipopeptide agents that act as detergents, interacting with phospholipids in the cell membrane to increase permeability; most effect on GN bacteria, but it can be a neutrotoxin and nephrotoxin so it is a last resort for MDRO

36
Q

Which agents inhibit protein synthesis/ disrupt cellular metabolism?

A

Aminoglycosides, Macrolide-Lincosamide-Streptogramin group, ketolides, oxazolidinones, chloramphenicol, tetracyclines, and glycylglycines

37
Q

Aminoglycosides

A

inhibit bacterial protein synthesis by irreversibly binding to protein receptors on the organism’s 30S ribosomal subunit; this interrupts formation of the protein synthesis complex, reading of mRNA, and formation of the ribosomal-mRNA complex

38
Q

What drugs are aminoglycosides and which bacteria do they work on?

A

Gentamicin, amikacin, streptomycin, and tobramycin; used in combination with cell-wall antibiotics like beta-lactams or vancomycin; cannot be used on anaerobic bacteria; can be a nephrotoxin and auditory or vestibular toxin

39
Q

Macrolides

A

the most common MLS; inhibits protein synthesis by binding to the 23S rRNA on the bacterial 50S ribosomal subunit, disrupting the growing peptide chain by blocking translocation

40
Q

What drugs are macrolides and which bacteria do they work on?

A

Erythromycin, azithromycin, and clarithromycin; effective against GP, mycoplasmas, treponemes, and rickettsiae

41
Q

Lincosamides

A

bind to the 50S ribosomal subunit and prevent elongation by interfering with peptidyl transfer during protein synthesis

42
Q

What drugs are lincosamides and which bacteria do they work on?

A

Clindamycin and lincomycin; Clindamycin works on anaerobic GP and some anaerobic GN while lincosamides work on GPC; increase the risk of C. diff. associated disease after use

43
Q

Streptogramins

A

enter bacterial cells by passive diffusion and bind irreversibly to the 50S subunit, induing a conformation change that interferes with peptide bond formation; effective against GP and some GN

44
Q

Ketolides

A

same mechanism as macrolides, but maintains activity against most macrolide-resistant GP organisms; particularly effective against Mycoplasma, Mycobacteria, Chlamydia, Rickettsia, and Francisella tularensis; includes telithromycin

45
Q

Oxazolidinones

A

interact with the 23S rRNA in the 50S ribosomal subunit, inhibiting 70S initiation complex formation and blocking translation of any mRNA; effect against most GP and mycobacteria; includes linezolid and tedizolid

46
Q

Chloramphenicol

A

inhibits the addition of amino acids to the growing peptide chain by reversibly binding to the 50S ribosomal subunit, inhibiting transpeptidation; has bone marrow toxicity, which can lead to aplastic anemia

47
Q

Tetracyclines

A

inhibit protein synthesis by binding reversibly to the 30S ribosomal subunit, interfering with the binding of the tRNA-amino acid complexes to the ribosome; can treat GP and GN, some intracellular pathogens, some protozoa, N. gonorrhoeae, mycoplasma, and spirochetes; effects upper GI and has cutaneous phototoxicity

48
Q

Glycylglycines

A

tetracyline derivatives that work against the most common tetracycline-resistant bacteria; includes tigecycline

49
Q

Which agents inhibit DNA and RNA synthesis?

A

Fluoroquinolones, Metraonidazole, and Rifamycin

50
Q

Fluoroquinolones

A

bind to and interfere with DNA gyrase enzymes involved in the regulation of DNA supercoiling; some also inhibit topoisomerase

51
Q

What drugs are fluoroquinolones?

A

Ciprofloxacin, levofloxacin, ofloxacin, and moxifloxacin; can lead to tendinitis and rupture of the Achilles tendon

52
Q

Metronidazole

A

contains a nitro group that is reduced by nitroreductase in the bacterial cytoplasm, generating cytotoxic compounds and free radicals; most potent against GN anerobes and microaerophilic bacteria and protozoans

53
Q

Rifamycin

A

bind to the enzyme DNA-dependent RNA polymerase and inhibit synthesis of RNA; includes rifampin and is frequently used with other agents

54
Q

Which agents inhibit other metabolic processes

A

Sulfonamides, Trimethoprim, and nitrofuratoin

55
Q

Sulfonamides

A

bind to dihydropteroate synthase, disrupting the folic acid pathway, which produces precursors required for DNA synthesis; active against GP and GN but not P. aeruginosa; can be antagonistic for other medications

56
Q

Trimethoprim

A

targets the folic acid pathway by inhibiting dihydrofolate reductase; combined with sulfamethoxazole

57
Q

Nitrofuratoin

A

converted by bacterial nitroreductases to reactive intermediates that bind ribosomal proteins and rRNA, disrupting synthesis of RNA, DNA, and proteins; used to treat uncomplicated UTIs; can lead to chronic pulmonary conditions like irreversible pulmonary fibrosis

58
Q

What are the three resistance pathways for beta-lactams?

A
  1. Enzymatic disruption: beta-lactamase enzymes that destroy the beta-lactam ring; Ex: penicillin resistance
  2. Altered target: mutational changes to PBPs or PBPs that do not bind to beta-lactams; Ex: MRSA
  3. Decreased uptake: porin channels change in # or character so beta-lactams cannot cross the outer membrane; Ex: imp. resistance
59
Q

What are the two resistance pathways for glycopeptides?

A
  1. Altered target: alteration in the molecule structure of cell wall precursor components, decreasing vanc. binding
  2. Target overproduction: excess peptidoglycan
60
Q

What are the three resistance pathways for aminoglycosides?

A
  1. Enzymatic modification: enzymes modify sites on the aminoglycoside molecule
  2. Decreased uptake: porin channels change in # or character so uptake is diminished; Ex: GN resistance
  3. Altered Target: mutational changes in ribosomal binding sites; Ex: enterococci resistance to streptomycin
61
Q

What are the two resistance pathways for quinolones?

A
  1. Decreased uptake: alteration in outer membrane diminish uptake of drug and/or activation of an efflux pump that removes drugs before sufficient intracellular concentration; Ex: GNR and Staph resistance
  2. Altered target: changes in DNA gyrase subunits decreases ability of drugs to bind to the enzyme
62
Q

What are the two resistance pathways for macrolides?

A
  1. Efflux: pumps drug out of cell before target binding; Ex: some staph and strep
  2. Altered target: enzymatic alteration of ribosomal target reduces drug binding; Ex: some staph and strep
63
Q

Anaerobic bacteria resistant to aminoglycosides

A

lack of oxidative metabolism to drive uptake of aminoglycosides = resistance

64
Q

Gram positive bacteria resistant to aztreonam

A

lack of PBP targets that bind this antibiotic = resistance

65
Q

Gram negative bacteria resistant to vancomycin

A

Lack of uptake resulting from inability of vancomycin to penetrate outer membrane

66
Q

P. aeruginosa resistant to sulfonamides, trimethoprim, tetracycline, or chloramphenicol

A

lack of uptake resulting in ineffective intracellular concentrations = resistance

67
Q

Klebsiella spp. resistant to ampicillin

A

production of beta-lactamases destroy ampicillin before it reaches its PBP target = resistance

68
Q

Enterococci resistant to aminoglycosides

A

lack of sufficient oxidative metabolism to drive uptake of aminoglycosides

69
Q

Enterococci resistant to all cephalosporins

A

lack PBPs that effectively bind

70
Q

STENMA resistant to imipenem

A

production of enzymes that destroy imipenem before it reaches PBP targets

Bacteriology (9 decks)

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