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
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
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
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.
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 )
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.
What is Kirby-Bauer test?
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.
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.
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)
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.
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
What are the cell wall synthesis inhibitors?
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
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
What is bacitracin use for?
on SKIN only
staph and strep
What is an example of a cell membrane inhibitors?
Polymyxin - has detergent action
Is transcription inhibitor broad spectrum or narrow? Give an example of this.
2 examples -
1. Quinolones - DNA gyrase. These are modified to be fluoroquinolones.
2. Rifamycin - for TB - liver toxic
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