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50 Cards in this Set
- Front
- Back
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1. What two antibiotics block cell wall synthesis at the cytoplasmic steps?
What antibiotic blocks cell wall synthesis at the membrane step? What two antibiotics block cell wall synthesis at the wall steps? |
1. D-cycloserine
2. Phosphonomycine Bacitracin 1. Glycopeptides (vancomycin) 2. β-lactams |
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2. What are β-lactam antibiotics?
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1. Penicillin
2. Cephalosporin 3. Clavems carbapenems 4. Monobactams |
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3. What two antibiotics block folic acid biosynthesis?
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1. Trimethoprim
2. Sulfonamides -sulfisoxazole -sulfamethoxazole -sulfamethizole -sulfasalzine |
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4. What antibiotic target cell membrane?
What antibiotic causes DNA breakage? What two antibiotics target DNA replication (DNA gyrase) |
Polymyxins
Metronidazole 1. Quinolones 2. Floroquinolones |
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5. What three antibiotics target DNA-dependent RNA polymerase?
What antibiotic targets protein synthesis? |
1. Rifampicin
2. Rifamycin 3. Rifampin Oxazolidinones |
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6. What two antibiotics inhibit the 50S subunit of bacterial ribosomes?
What two antibiotics inhibit the 30S subunit of bacterial ribosomes? |
1. Marcrolides
2. Lincosamides 1. Tetracycline 2. Aminoglycosides |
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7. What are the characteristics of a good antibiotic?
Eight characteristics.... |
1. Broad spectrum
2. Does not affect the normal flora 3. Ability to penetrate bacterial cells and eukaryotic cells **some pathogens are intracellular 4. Low bacterial resistance 5. Low toxicity to host 6. Non-allergenic w/ minimal side effects 7. Be able to reach the site of infection 8. Inexpensive and easy to produce |
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8. Why should a good antibiotic be broad spectrum?
What can be bad about broad spectrum antibiotics? (two things) |
Need to have a balance between rapid and accurate diagnosis and need for treatment
**Takes 48 hours to get lab results back to confirm diagnosis 1. Damage normal flora 2. Create antibiotic resistance |
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9. What do an antibiotic need in order to be able to reach the site of infection?
Three characteristics.... |
1. Be administered IV and orally
2. Chemical stability 3. Serum stability |
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10. What are three sources of antibiotics?
What are the uses of antibiotics? (three uses) |
1. Synthetic
2. Natural 3. Semisynthetic 1. Treatment of human diseases 2. Treatment of animals 3. Food preservation **treating animals w/ antibiotics is problematic b/c animal strands become resistant and the resistance is horizontally transferred to human strand |
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11. What are the three possible outcomes when an antibiotic is added to bacteria?
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1. Resistance
-bacteria are resistant and continues to grow 2. Bacteriostatic 3. Bactericidal -bacteria are killed |
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12. What is meant by bacteriostatic?
If an antibiotic is bacteriostatic what does the killing of the bacteria depend upon? |
Bacterial growth stops but the bacteria are not killed and growth will resume after removal of the antibiotic
Depends on the immune system **adaptive immune system should have taken over **if patient is immuno-compromised then bacteria will grow again |
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13. What is the minimum inhibitory concentration (MIC) of an antibiotic?
Which antibiotics have MICs? |
The lowest concentration at which bacterial growth is inhibited
Both bacteriostatic and bactericidal antibiotics |
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14. What is the minimal bactericidal concentration (MBC)?
How is the MBC determined? Which antibiotics have MBCs? |
Lowest concentration at which bacteria are killed
Determined by removing an aliquot of bacteria from MIC assay and determining if the bacteria will resume growth in the absence of antibiotics Only bactericidal antibiotics |
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15. What do disk diffusion assays do?
What does a small zone indicate? What does a large zone indicate? How does the exact size of resistant zones varies? On a disk diffusion assay how is the MIC determined? |
Assess how large of a zone of clearing surrounds an antibiotic-impregnated disk
Small = resistant **need more antibiotic Large = sensitive **need less antibiotic Exact size varies depending on the antibiotic Point where strip starts to inhibit growth |
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16. What does the size of the zone correlate to?
How is resistance determined? What is a sensitive antibiotic? What is an intermediate antibiotic? What is a resistant antibiotic? |
Correlates to the antibiotic concentration
(differ between antibiotics) Resistance is determined by the achievable clinical dose Inhibited or killed by 1/4 of the achievable clinical dose Inhibited or killed by 1/2 of the achievable clinical dose Cannot be killed by an achievable clinical dose **can still be killed by drug even if resistant but not at a clinically achievable dose |
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17. What are the three major antibiotic resistance mechanisms?
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1. Natural (intrinsic)
2. Acquired 3. Mutational |
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18. What are natural resistance mechanisms?
What are some examples? |
Properties that make the bacteria more resistant
1. Gram-negative membrane -permeability barrier causing inaccessibility of target 2. Efflux pumps (Type I secretion) **non-specific 3. Proteases that destroy drugs **drug inactivation |
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19. How are acquired resistance mechanisms acquired?
How can they be spread? |
Acquired on mobile genetic elements from other bacteria
1. Spread of resistance bacteria 2. Spread of resistant gene **harder to control b/c they are a mobile genetic element |
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20. How do mutational resistance mechanisms arise?
How is the spread of them? |
Arise from mutation of the chromosome
Spread is clonal *through spreading the resistant strain **easier to control b/c mutation comes from chromosome |
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21. How do efflux pumps provide bacteria w/ resistance to antibiotics?
What type of resistance mechanism are efflux pumps? Efflux pumps are only active for what type of drugs? Are efflux pumps specific or non-specific? |
Efflux pumps remove the drug from the bacteria
**prevent accumulation in the cytoplasm Can be intrinsic, acquired, or mutational Only active for drugs that affect cytoplasmic functions (i.e. protein synthesis) Some are narrow spectrum and some confer multi drug resistance |
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22. What do β-lactamases do?
Which type of bacteria produce them? |
Inactivate penicillin by cleaving the β-lactam ring
**penicillin will inhibit cell wall synthesis b/c it's a β-lactam Both gram-negative and positive bacteria produce β-lactamases |
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23. What can be administered w/ penicillin?
What do these do? |
β-lactamase inhibitors
Bind and significantly reduce the rate of cleavage causing the β-lactamase to be less effective **β-lactamase resistant forms of β-lactam antibiotics |
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24. What are ESBLs?
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Extended Spectrum β-Lactamases
These are emerging β-lactamases that destroy resistant forms of β-lactam antibiotics Cleave the β-lactamase resistant drugs |
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25. What is fosomycin cleaved by?
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Fosfomycinases
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26. What three basic modifications will inactivate aminoglycosides?
How can chloramphenical be inactivated? |
1. N-acetylation
2. O-phosphorylation 3. O-adenylation Inactivated by acetylation (acetyl transferase) |
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27. What will target site modification prevent?
What is an example of target site modification? |
Prevent antibiotic action
**modifies a site to prevent interaction w/ the antibiotic These include mutation to specific targets that are either acquired or mutational Example - penicillin binding protein |
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28. What is methicillin resistant staphylococcus aures (MRSA)?
What is the mecA gene? How is the mecA gene carried? |
Methicillin - modified β-lactam that is relatively resistant to β-lactamases
A gene that encodes a new β-lactam resistant PBP (PBP2a) ***PBP does not bind essentially all β-lactam antibiotics mecA gene is carried on mobile elements |
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29. What is β-lactam resistan streptococcus pneumonia?
What is PBP2X? What is PBP2B? |
Low-level resistance
(have to increase clinical dose to affect growth) PBP2X - low level resistance PBP2B - low and high level resistance |
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30. What do MLS (macrolide-lincosamide-streptogramnin) strains have?
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A erthromycin methyltransferase gene that methylates 23S rRNA preventing the interaction of macolides and lincosamindes/clindamycin w/ the 23S rRNA and the 50S ribosomal subunit
**target side modification by methylation of 23S rRNA |
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31. What will changes in RNA polymerase structure via target site modification prevent?
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Prevent interaction of rifampicins w/ RNA polymerase
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32. How is vancomycin resistance obtained?
How is the resistance conferred? |
Acquired and encoded by 7 genes
The genes change the D-Ala-D-Ala pentapeptide to D-Ala-D-Ser or D-Ala-D-Lac **this changed pentapeptide isn't recognized by vancomycin so subunits for cell wall can be added |
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33. What are the three types of vancomycin resistance operons?
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1. VanA
-induced by vancomycin 2. VanB -induced by vancomycin and teichopanin **seen in Europer 3. VanC -produces a D-Ala-D-Ser substitution |
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34. What is metabolic bypass?
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Either modification or complete substitution of dihydropteroic acid synthetase and dihydrofolate reductase
**These mutations or unique enzymes prevent drug binding |
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35. What type of antibiotic are β-lactams?
What do they target? What is a resistance mechanism for them? (five) |
Cell wall
PBPs 1. Variable outer membrane penetration 2. Efflux 3. β-lactamases 4. PBP mutants 5. Extended Spectrum β-lactamases |
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36. What type of antibiotic is bacitracin?
What do they target? What is a resistance mechanism for them? |
Cell well
Undecaprenyl carrier |
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37. What type of antibiotic vancomycin?
What do they target? What is a resistance mechanism for them? (two things) |
cell wall
D-Ala-D-Ala 1. D-Ala-D-Ala to D-Ala-D-Ser/Lac 2. Efflux |
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38. What type of antibiotic is fosfomycin?
What do they target? What is a resistance mechanism for them? (two things) |
Cell wall
NAM biosynthesis 1. Reduced transport 2. Fosfomycinases |
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39. What type of antibiotic are macrolides/streptogramins?
What do they target? What is a resistance mechanism for them? (four things) |
Protein synthesis
50S subunit ribosome 1. Variable outer membrane penetration 2. Methylation 23S rRNA subunit 3. Efflux pumps 4. 50S subunit mutations |
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40. What type of antibiotic are Lincosamides?
What do they target? What is a resistance mechanism for them? (two things) |
Protein synthesis
50S subunit ribosome 1. Efflux pumps 2. Methylation 23S rRNA subunit |
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41. What type of antibiotic is chloramphenical?
What do they target? What is a resistance mechanism for them? |
Protein synthesis
50S subunit ribosome Acetylation |
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42. What type of antibiotic are tetracyclines?
What do they target? What is a resistance mechanism for them? |
Protein synthesis
30S subunit Efflux pumps |
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43. What type of antibiotic are aminoglycosides?
What do they target? What is a resistance mechanism for them? (three things) |
Protein synthesis
30S subunit 1. Acetylation 2. Phosphorylation 3. Adenylation |
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44. What type of antibiotic are (fluro)quinolones?
What do they target? What is a resistance mechanism for them? (two things) |
DNA replication
DNA gyrase 1. Efflux pump 2. Permeability mutations |
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45. What type of antibiotic are rifampicin?
What do they target? What is a resistance mechanism for them? |
DNA transcription
RNA polymerase AA changes in RNA polymerase |
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46. What type of antibiotic are sulfonamides?
What do they target? What is a resistance mechanism for them? (two things) |
Folic acid metabolism
PABA analog 1. Alternate dihydropterate synthetase 2. Efflux |
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47. What type of antibiotic are trimethoprim?
What do they target? What is a resistance mechanism for them? (two things) |
Folic acid metabolism
Dihydrofolate reductase 1. Dihydrofolate reductase mutants 2. Efflux |
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48. How quickly do bacteria become resistant to antibiotics?
What is essential to prevent the further spread and reduce resistance development? |
Rapidly
Prudent use of antibiotics |
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49. What does the prudent use of antibiotics include?
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1. Appropriate antibiotics use
2. Public education **using full antibiotic regime **virus vs. bacteria 3. Selective removal, control, or restriction of antimicrobial agents or classes **new antibiotics used only for resistant bacteria **use of antibiotics in cyclic patterns |
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50. What does the prudent use of antibiotics include?
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4. Use of combination therapies to reduce likelihood of resistance emergence
5. Use of physical means to prevent spread of resistance organisms *handwashing |
