Micro test3 1st

  1. How does a bacteria achieve resistance to Aminoglycosides?
    • They make enzymes that add a functional group to the aminoglycoside. The possible changes are
    • Adenylation
    • Phosphorylation
    • Acetylation
  2. What does the gentamycin assay show you?
    Intracellular bacteria concentration (all extracellular are killed by the gentamycin, but the intracellular survive)
  3. Which antibiotics inhibit tRNA Binding?
    • Aminoglycosides
    • Tetracyclines
    • Spectinomycin
  4. What are four important factors regarding Aminoglycosides?
    • Require Oxygen for uptake (not effective on anaerobes)
    • Do not enter mammalian cells
    • Toxic concentration can easily be reached
    • Synergistic with beta lactams
  5. What classification of drug are Streptomycin, Neomycin, Gentamicin, Tobramycin, and Amikacin? What are they used for?
    • They are all aminoglycosides
    • Streptomycin – TB and plague
    • Neomycin – topical component of 3 in one ointment
    • Gentamycin – Broad spectrum IV
    • Tobramycin – Broad spectrum IV
    • Amikacin – reserved for resistant strains
  6. Are aminoglycosides bacteriocidal or bacteriostatic?
    • Bacteriocidal
    • They stop 85% of protein synthesis, and the remaining 15% of proteins are incorrectly made
    • These faulty proteins kill the cells
  7. What class drug works synergistically with Aminoglycosides?
    Beta lactams because they weaken the cell wall allowing aminoglycoside entry
  8. Is spectinomycin bacteriocidal or bacteriostatic?
  9. How do cells become resistant to Tetracycline? (3 mechanisms)
    • “tet” protein on plasmid: mediates pumping tetracycline out of cells
    • Ribosome protection: gene on plasmids produce RPP that binds to 30S preventing tetracycline binding
    • Uncommon method: plasma coded enzyme that oxidizes tetracycline
  10. What drug was designed to combat the resistance to tetracycline?
    Tigecycline overcomes ribosome protection and has efflux resistance
  11. What drugs bind to the 30s subunit of RNA? (prevent tRNA binding)
    • Aminoglycosides
    • Spectinomycin
    • Tetracylcines
  12. What drugs bind to the 50s RNA subunit? (prevent peptide bond formation)
    • Chloramphenicol
    • Lincosamines
    • Synercid
    • Retapamulin
  13. What is Chloramphenicol used for? What drug is sometimes paired with it?
    • Broad spectrum, static on most bacteria, but cidal for agents of meningitis
    • Paired sometimes with Rifampin to prevent resistant population
  14. What side effect was observed with chloramphenicol use?
    Enters cells and disrupts mitochondria resulting in lethal anemia
  15. How do cells become resistant to Chloramphenicol?
    Chloramphenicol Acetyl Transferase (CAT) acetylates Chloramphenicol
  16. What is Lincomycin used for? What is its mechanism of action?
    • Gram +
    • Good for penicillin allergic patients
    • It binds to the 50s ribosomal subunit
  17. What is Clindamycin used for? What is its mechanism of action?
    • Gram + as well as anaerobes like Bacteroides
    • It binds the 50s Ribosomal subunit
    • Very similar to Lincomycin
  18. What is a side effect of long courses of Clindamycin?
    Overgrowth of C. difficile – antibiotic associated enterocolitis
  19. What drugs make up Synercid and what are their mechanisms?
    • Dalfopristin – blocks peptide bond formation
    • Quinupristin – releases incomplete peptide
    • Both drugs are binding to the 50s subunit
  20. What is Synercid used for and what is it not good for?
    • Cidal for VR MRSA
    • Static for Enterococcus faecium
    • Not effective for Enterococcus fecalis
    • Care must be taken because it is toxic to blood vessel it is injected in – use a large vein
  21. What are the three mechanisms for Synercid resistance?
    • Drug efflux reaction
    • Enzymes, either acetyl transferase or lyase
    • Methylation of ribosome (“D” reaction)
  22. What are the rare side effects of Synercid?
    Hypotension or GI hemorrhage
  23. What is Retapamulin used for? What is the mechanism?
    • Used topically for impetigo or to eliminate staph carrier state
    • Bacteriostatic – binds unique site on 50s
  24. What class are the drugs erythromycin, clarithromycin, and azithromycin in? What step do they block?
    • Macrolide antibiotics
    • They block translocation
  25. What class of drug are minocycline, doxycycline, and tigecycline?
    • Tetracyclines
    • They bind the 30s subunit
  26. What is the drug of choice for Legionella, Mycoplasma pneumoniae, and Campylobacter?
    Macrolide antibiotics
  27. What is a “D” reaction? What is the example we have for it?
    • Erythromycin induces the ribosome to methylation for resistance. The methylated ribosome is then resistant to Clindamycin or Lincomycin
    • On a plate it makes the clindamycin or lincomycin disk look like a “D” instead of a circle of killed cells
  28. How does Linezolid function? How is resistance achieved?
    • Binds to the 50s subunit (specifically the 23s portion) and stops it from assembling with the 30s to form the 70s
    • Resistance can be from a point mutation in the 23s subunit
    • Works on gram +
  29. What is the rare side effect of Linezolid?
    It reacts with mitochrondria, especially in nerve cells causing “LION” – linesolid induced optic neuropathy
  30. What is Nalidixic Acid?
    • Quinolone (not fluoroquinolone) used for E. Coli UTI
    • Rapid resistance so not very good
  31. What is the method of action of the Fluoroquinolones?
    • Inhibit DNA gyrase (esp. in gram -)
    • Inhibit DNA topoisomerase IV (esp. in gram +)
  32. What should you not use Fluoroquinolones for?
    • Strep
    • Anaerobes
    • Gonococcus
  33. What generation Fluoroquinolone is Levofloxacin?
    Third, also known as extended spectrum
  34. What generation Fluoroquinolone are Moxifloxacin and Gatifloxacin?
    • Fourth
    • Good for most everything
  35. Which antibiotic class can induce tendon damage?
    • Fluoroquinolones
    • Other side effects of Fluoroquinolones –
    • Rare CNS disturbances
    • Photosensitization (sun damage)
    • Not for most children
  36. What is a drug targeted at Clostridium difficile but not normal gut flora?
    • Fidaxomicin
    • Binds to RNA polymerase
  37. Why is Sulfa-Trimethoprin static in tissues but cidal in urine?
    Urine lacks exogenous folic acid that can “rescue” bacteria found in tissues
  38. What Is the mechanism of action of Polymyxin?
    • Polymyxin has a hydrophilic head and a hydrophobic tail
    • It inserts into bacterial membranes causing cidal leakage
    • It binds to LPS so effective for gram negative
    • Mainly topical use because it is toxic
  39. What is the mechanism of Daptomycin?
    • Binds Ca++ in the membrane of gram + bacteria
    • Produces holes that kill bacteria
    • ***not effective for pneumonia b/c binds to surfactant in lungs
  40. What is the mechanism of Metronidazole?
    Converted to a poison under strict anaerobic conditions
  41. What is Nitrofurantoin used for?
    • Broad spectrum bacteriostatic, mechanism unclear
    • E coli, KES, staph, and enterococcus susceptible (not pseudomonas or proteus)
    • Resistance is very rare (good for long term usage)
  42. What is the mechanism of Mupirocin?
    • Blocks binding of Isoleucine to tRNA
    • Bacteriostatic for gram + strep or staph (impetigo)
    • Topical (Bactroban)
  43. A sample of drug susceptible Pseudomonas organisms were
    placed on top of a monolayer of tissue culture cells and
    incubated for 30 minutes at 37°C before gentamicin was added
    (50 µ/ml). After incubating for an hour, the cells were removed
    from the monolayer, washed, and then diluted. Then 500 cells
    were inoculated onto a blood agar plate and incubated. The
    next day, 40 Pseudomonas colonies were found on the plate.
    Which of the following best explains these findings?

  44. An E. coli isolated from a urinary track infection was found to
    be resistant to multiple antibiotics, but susceptible to trimethoprim.
    Another lab found that the organism was resistant to trimethoprim.
    The labs used the same methods except the one that found it
    resistant to trimethoprim used a medium enriched with yeast
    extract. Which of the following explains the findings?
    a. Medium without yeast extract was nutritionally weak and
    increased the susceptibility of the organism
    b. Medium with yeast extract provided the end product of the
    pathway blocked by trimethoprim
    c. Yeast extract inhibited DNA gyrase so the organism was
    more susceptible to trimethoprim
    d. Yeast extract reacted with trimethoprim thus protecting the
  45. What is the mechanism of Isoniazid?
    • First it binds to Catalase and then to NAD-Mycolic Acid Synthetase
    • The inactive Mycolic acid synthetase prevents building of mycolic acids
    • Catalase-deficient mutants are INH resistant*****
  46. What is the mechanism of Pryazinamide?
    • Converted by bacterial enzyme pyrazinamidase at low pH into pyrazinoic acid which kills the cell
    • Mutants that lack pyrazinamidase are resistant
    • Side effect of liver damage
  47. What is the mechanism of Ethambutol?
    • Inhibits arabinosyl transferase, thus blocking synthesis of arabinoglycan
    • Bacteriostatic
    • Resistance occurs by mutation in arabinosyl transferase enzyme
    • Side effect of neurotoxicity – especially optic nerve
  48. What are Macrolides good for?
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Card Set
Micro test3 1st
Micro test3 1st