Micro Bio Session 4

  1. Describe the most important mechanism explaining how bacteria become antibiotic resistant.
    • Transferring of plasmid - bacteria become resistant to abx by transferring plasmid called "R factors"
    • R is for resistanceit can code for all kind of things that help it become resistant
    • enzymes to break down the drugs
    • pumps to pump out abx
  2. what are other mechanim beside (transferring of plasmid)of antibiotic resistance?
    • a. Bacteria forms biofilm to become resistant. Bugs at bottom of biofilm cannot be reached by abx.
    • b. Bacteria can mutate their genes in way that it can survive the abx. When you take too much drugs, you are selecting the ones that are resistant to it.
    • c. Change structures abx targets. Some just don't make cell wall for a certain time.
    • d. Metabolic pathways - bug might be able to live w/o the metabolic pathways
  3. state where antibiotics were first isolated from and how semi-syntethic and synthetic agents improve on these antibiotics.
    • where abx isolated from: anti (against) biotic (life), made by other bacteria and fungi (original source)
    • i. take "natural" abx and modify them to "semi-synthetic" 2nd generation
    • ii. want to expand to broader spectrum or narrow spectrum (gentler on pt flora, have to crrectly identify organism ), stability, can kill better
  4. Define bactericidal, bacteristatic, and bacterilytic agents. Describe broad spectrum vs. narrow spectrum antibiotics and advantage and disadvantages of each.
    • broad spectrum - can kill more type of bacteria. Can be given to an unknown cause. Can damage other normal flora.
    • narrow spectrum - gentler on body if we know the ID of the bacteria. if you don't ID the correct bacteria, then the bacteria has another week to grow.
  5. Differentiate between chemotherapeutic agents and antiseptics, disinfectants, and sterilants.
    • chemotherapeutic agents - can be use internally. ex. antibiotics.
    • anitseptics - use externally ex. mouthwash
    • disinfectants - don't use on patient but on equipment (dental chair)
    • sterilants - anything that comes in contact with pt ( pt contact instruments )
  6. Describe the MIC test. Is a higher or a lower MIC test desirable? How does this compare with an agar diffusion method? the MBC test?
    • Abx susceptibel testing: MIC or MBC
    • i. MIC: how much abx to inhibit growth. 1. serial dilution and put bug 2. which conc wher you don't see any growth
    • ii. MBC: tubes from MIC and put them in rich media 1. if abx is bactericidal, MIC = MBC 2. BUT if ab was bacterialstatic, MBC >MIC because bacteria will start growing. a. larger means that at a more dilute tube, you will still see growth. use less abx if bacterialstatic.
  7. What is Kirby-Bauer test?
    • agar diffusion
    • streak bacteria and get a lawn of bugs. Plop on Ab disk and then look for clearing around the disk.
    • 1. clearing = zone of inhibition
    • 2. If see dots on tope of antibiotic disk, they are drug resistant.
  8. What are the 9 desirable properties of antibiotics?
    • 1. soluble: can it "get to" infection?
    • 2. slow breakdown and excretion - pts are better of taking it once a day then many more time, better compliance
    • 3. selectively toxic - leaves flora alone
    • 4. pH stable
    • 5. NOT allergy - pt that will nto be allergic to it
    • 6. Drug resistance: RARE
    • 7. small dose - want one that pt can just sit there and take it and that will be it. Pt tends to stop taking it when they feel better.
    • 8. bactericidal/bacteristatic? depending on the pt
    • 9. want it active and stable in pus because infection in mouth are usually pus.
  9. How to choose an antibiotic? and the risk and reasons an antibiotic might not work for your patient.
    • might not work if you didn't ID it
    • know activity of Abx: tetracycline is inhibited by milk and others. Birth controls are inhibited by tetracycline and erythromycin.
    • drug history, allergy, immunosuppressed
    • did they take it? did you the complete the course?
    • possibly didn't drain the absess (bacteria wall off)
  10. Define synergistic and antagonistic effects of antibiotics and selective toxicity.
    • Synergy: 2 things working together to get more effect than just 1 by itself. Use 2 abx at the same time.
    • Antagonistic: 2 abx cancelling each other out
    • Dentist should avoid combination therapy because it will hasten the process when it's not needed yet. use to combat drug resistance in certain strains.
  11. How can you, a future healthcare provider, help stop the spread of antibiotic resistance?
    • not over prescribe
    • save serious Abx for last
    • EDUCATE your patient
    • i. save a little for next time just in case
    • ii. save for someone else for family member
  12. What are the cell wall synthesis inhibitors?
    • beta-lactams
    • non-beta lactams
    • bacitracin
  13. What is beta lactams, it's structure, and give examples of beta lactams of cell wall synthesis inhibitors.
    • structure - all share this ring structure
    • function - stop cross linking of peptidoglycan
    • ex. penicillin, cephalosporin's
    • resistance by enzyme beta - lactamase which cut the beta lactams ring where it can't do it anymore
    • now they have inhibitors of enzyme that come with the inhibitors
  14. What are examples of non-beta lactams? What is VRE and why is it important?
    • isoniazide for TB
    • vancomycin - with a lot of resistance
    • VRE (vancomycin resistant enterococci) with enterococci pass it to staph
  15. What is bacitracin use for?
    • on SKIN only
    • staph and strep
  16. What is an example of a cell membrane inhibitors?
    • Polymyxin - has detergent action
    • use topically
  17. Is transcription inhibitor broad spectrum or narrow? Give an example of this.
    • BROAD spectrum
    • 2 examples -
    • 1. Quinolones - DNA gyrase. These are modified to be fluoroquinolones.
    • 2. Rifamycin - for TB - liver toxic
  18. Is translation inhibitor relatively broad or narrow spectrum? Give 4 examples.
    • relatively BROAD spectrum
    • 1. aminoglycosides = streptomycin
    • 2. macrolides = erythromycin (2nd common use next to penicillin)
    • bind to prokaryotic ribosomes
    • obligate anaerobes are not affected
    • use when pt are allergic to penicillin
    • 3. lincosamides = clindamycin - for serious anaerboic infection but has a nasty GI complications called pseudomembranous colitis
    • 4. tetracyclines - BROAD spectrum
    • cause brown stain on teeth in kids (younger than 8) or adults. Use for dermatology
  19. What are metabolic inhibitors? Give 1 example.
    • Pick pathway that bug has but person does not
    • ex. sulfonamides - stop folate synthesis (DNA synthesis pathway)
    • ok for us because we eat folic acid, not make it
  20. Define penicillin G in terms of mode of action, method of administration and risks.
    • Mode of action - cell wall synthesis inhibitors. bacteria can surfive in presence of this but it won't when it is making cell wall.
    • acid sensitive so can't take it orally
    • use IV or IM
  21. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as penicillin V.
    Pennicillin V - oral form use for dentistry. Use for prophylaxis, infection in mouth, extraction. Warning: allergy. some has beta-lactamase in bacteria.
  22. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as methicillin.
    • narrower spectrum
    • use for staph until MRSA arrived so we don't use methicillin very often
  23. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as ampicillin.
    • related to amoxicillin
    • broad spectrum
    • beta-lactam type
    • use of prophylaxis when scaling and root planning
    • have affect on gram - as well
  24. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as cephalosporin.
    • beta - lactam
    • multiple generation: each generation gets better with gram - and worse with gram +
    • warning: 10% of penicillin allergic patients are allergic to cephalosporin
    • cross-reactivity: if they are allergic to one, don't give them the other because of those 10%
  25. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as monobactam.
    • narrow spectrum
    • active only against aerobic, gram - bacteria
    • not widely used
  26. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as isoiazid.
    • inhibit mycolic acid synthesis
    • bactericidal against actively replicating mycobacteria
  27. Contrast the mode of action of penicillin G with semi-synthetic penicillins such as carbapenems.
    • broad spectrum
    • bind Penicillin Binding Proteins (PBPs) and enzymes responsible for peptidoglycan synthesis (same with cephalosporin, monbactam, penicillin)
    • resistant for oxacillin - resistant staphylococci, selected gram - rods, enterococcus
  28. How do bacteria devlop resistance to beta-lactam antibiotics?
    resistance by enzyme beta-lactamase which cut the beta lactams ring where it can't inhibit anymore
  29. Classify the mode of action of vancomycin and contrast with bacitracin and penicillin.
    • Penicillin - binds PBPs and enzymes responsible for peptidoglycan synthesis
    • Vancomycin - inhibits cross-linking of peptidoglycan layers
    • Bacitracin - inhibits bacterial cytoplasmic membrane and movement of peptidoglycan precursors
  30. What is the mechanism of action of polymyaxin? what is the significant risk of polymyxin use. What do we use polymyxin for?
    • mechanism - inhibit bacterial membranes
    • Use for detergent and is use only topically
  31. What is the mechanism of action of clindamycin? what is the risk?
    • mechanism - prevent polypeptide elongation at 50S ribosome
    • risk - nasty GI complications called pseduomembranous colitis
  32. What are the risks of tetracyclin use?
    colored teeth of kids who are under 8
Card Set
Micro Bio Session 4
micro bio session 4, rabbe