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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
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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
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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
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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.
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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 )
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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.
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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.
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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.
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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)
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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.
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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
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What are the cell wall synthesis inhibitors?
- beta-lactams
- non-beta lactams
- bacitracin
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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
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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
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What is bacitracin use for?
- on SKIN only
- staph and strep
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What is an example of a cell membrane inhibitors?
- Polymyxin - has detergent action
- use topically
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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
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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
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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
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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
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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.
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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
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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
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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%
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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
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Contrast the mode of action of penicillin G with semi-synthetic penicillins such as isoiazid.
- inhibit mycolic acid synthesis
- bactericidal against actively replicating mycobacteria
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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
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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
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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
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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
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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
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What are the risks of tetracyclin use?
colored teeth of kids who are under 8
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