Microbiology Antimicrobial Susceptibility Testing Test Questions – Flashcards
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| Antibiotic therapy |
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| use of chemical compounds to treat diseases caused by microorganisms |
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| Antibiotic |
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| produced by organism |
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| Antimicrobial agent |
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| synthetic compounds |
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| Bactericidal |
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| Kills organism |
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| Bacteriostatic |
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| inhibit growth to allow immune system to fight off bacteria |
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| Combination therapy |
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| additive, indifferent, synergistic, and antagonistic |
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| Additive |
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| each kills a certain amount of bacteria |
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| indifferent |
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| each kills the same amount of bacteria |
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| synergistic |
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| work together to kill more bacteria |
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| antagonistic |
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| antibiotic interefere with one another |
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| Factors affecting Antimicrobial activity |
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| environment and concentration |
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| environment |
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| state of metabolic activity (microorganisms are dormant or live), distribution of drug in body tissue, location of organisms, interfering substances (food, alcohol) |
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| concentration |
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| absorption (depends on route of administration), distribution (varies within tissues), and variability of concentration (dosing schedule to keep in therapeutic range) |
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| Intrinsic resistance |
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| known, no susceptibility testing |
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| Aminoglycosides do not work on anaerobic bacteria or Enterococcus |
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| because anaerobes do not use oxidative phosphorylation which takes up the Aminoglycosides |
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| Aztreonam (beta lactam) doesn’t work on gram positive bacteria |
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| because it doesn’t have the protein binding site |
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| Vancomycin doesn’t work on gram negative rods |
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| because of their complicated cell wall thorough which complex vancomycin cannot penetrate |
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| SXT, tetra and chloramphenicol doesn’t work on P. aeruginosa |
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| because it lacks the means of uptake and the antibiotics can never reach the concentration to work |
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| Ampicillin doesn’t work on Klebsiella |
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| because Klebsiella produces beta lactamase which destroys ampicillin before it reaches the binding site |
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| Metronidazole doesn’t work on aerobic bacteria |
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| because they cannot reduce |
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| All cephalosporins cannot be used against Enterococcus |
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| because they do not have the penicillin binding sites |
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| Lactobacilli and leuconostoc |
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| do not have vancomycin binding site |
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| S.maltophilia produces an enzyme |
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| that destroys imipenem |
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| Acquired resistance (5) |
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| • Enzymatic degradation/modification of agent • Decreased uptake • Altered agent • Circumvention of consequences of antimicrobial action • Uncoupling of antibiotic-target interactions |
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| emergence of resistance (4) |
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| • Old genes to new hosts • New genes • Mutations of old genes to become more potent • Intrinsically resistant opportunistic bacteria due to inappropriate and widespread use of antibiotics |
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| Mechanisms of action (5) |
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| • Effect cell wall integrity • Effect cell membrane structure and function • Inhibit protein synthesis • Inhibit essential metabolites • Interefere with nucleic acid metabolism |
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| Beta-Lactams |
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| cell wall integrity, inhibit cell wall synthesis by binding to transpeptidase (penicillin binding protein), bactericidal in actively growing organisms |
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| Penicillins |
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| beta lactam ring with one place for modification, differ in R group |
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| Penicillin G |
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| strep, clost, aerobic GPR |
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| Ampicillin |
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| strep, clost, aerobic GPR and some enterococci |
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| Methicillin |
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| act against beta lactamase, staph |
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| Ticarcillin, pipercillin |
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| pseudomonas |
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| Cephalosporins |
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| two places for modification, 4 generations |
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| 1st generation cephalosporins |
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| GP cocci (not Enterococcus) anaerobic cocci |
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| 2nd generation cephalosporins |
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| GP cocci (not Enterococcus) anaerobic cocci and Enterobacteriaceae, ceftetan: bacteroides |
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| 3rd generation cephalosporins |
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| lose GP cocci, GNRs, pseudomonas, penetrate CNS |
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| 4th generation |
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| enhanced enteric |
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| Monobactams |
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| no secondary ring, no GPC, GPR or anaerobes |
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| Carbapenems |
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| extended spectrum of activity, aerobic, anaerobic strep, enterics, pseudomonas |
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| Penicillin and Cephalosporin resistance due to |
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| enzymatic destruction- beta lactamase, altered target-altered penicillin binding protein, decreased uptake- change in porin number and character |
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| Glycopeptides |
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| vancomycin and daptomycin, |
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| vancomycin and daptomycin |
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| gram positive, Inhibit the 2nd stage of cell wall synthesis, bactericidal, for gram positive only |
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| resistance to glycoproteins due to |
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| Resistance due to altered target-cell wall precursor structure to decrease binding, and target overproduction- excess peptidoglycan |
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| Polymyxins |
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| bind to cell membrane phospholipids, destroys active transport and membrane permeability barrier, bactericidal, |
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| polymyxins effective against |
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| gram – aerobic bacilli (pseudomonas and Serratia) |
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| Toxicity of polymyxins |
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| neurotoxin and poor distribution |
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| Aminoglycosides |
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| bind to 30s ribosomal unit, bactericidal |
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| aminoglycoside Resistance due to |
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| altered target-deficiency of ribosomal receptor, enzyme modification- enzymatic destruction of drug and decreased uptake- lack of permeability to drug molecule |
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| aminoglycoside toxicity |
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| ototoxic (hearing loss) and nephrotoxic (kidney |
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| Streptomycin |
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| aminoglycoside, TB |
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| kanamycin |
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| aminoglycoside, topical antibiotic |
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| gentamicin/tobramycin/amikin |
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| gram + (not strep), gram – pseudo, not anaerobes, does not penetrate CNS |
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| Tetracyclines |
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| inhibit protein synthesis by reversibly binding to 30S subunit, Bacteriostatic |
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| Tetracyclins Resistance due to |
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| efflux system, altered/protected ribosomal target, enzyme inactivation |
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| Macrolides |
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| : attach to receptor of 50S subunit, interefere with translocation reactions, Bacteriostatic, works on gram positive and a few gram negative (Legionella, Moraxella, and campy) |
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| macrolides resistance due to |
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| efflux (pump drug out of cell before target binding), altered target (enzymatically alter ribosomal target to reduce binding) |
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| Clindamycin |
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| attach to 50S subunit and interferes with translocation, Bacteriostatic, works on aerobic gram + and anaerobic bacteria (bacteroides) |
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| Chlororamphenicol |
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| reversible binding of 50S subunit blocks bond formation, Bacteriostatic |
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| Chlororamphenicol Resistance due to |
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| by Chlororamphenicol acetyltransferase, decreased uptake |
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| Chlororamphenicol toxicity |
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| problems with RBC maturation, and rarely aplastic anemia |
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| Sulfonamides |
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| interefere with folic acid pathway by competitively inhibiting bacterial dihydropteroate synthetase |
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| Trimethoprim |
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| : interferes with folic acid pathway by competitively inhibiting bacterial dihydrofolate reductase |
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| Sulfonamides and Trimethoprim |
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| • Bacteriostatic • Used in combination against gram + and many gram – but no pseudomonas • Resistance due to altered enzyme targets |
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| resistance of Sulfonamides and Trimethoprim |
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| altered enzyme targets |
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| Rifampin |
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| binds DNA dependent RNA polymerase |
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| Rifampin Resistance due to |
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| change in RNA polymerase target |
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| Rifampin used on |
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| mycobacterium, never taken alone always in combination (only alone for prophylaxis |
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| Quinolones |
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| all come from nalidixic acid, block DNA gyrase, bactericidal, used against gram + and gram – |
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| resistance of Quinolones |
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| decreased uptake-alteration in outer membrane to reduce uptake or activation of efflux pump or altered target, change in DNA gyrase subunits to decrease FQ binding |
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| Metronidazole |
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| disrupts DNA by making it unstable, must be partially reduced to become active so only works in anaerobic organisms, bactericidal |
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| Effects on cell wall integrity |
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| Beta lactams, glycopeptides |
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| Effects on cell membrane structure and function |
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| polymyxins |
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| Inhibition of protein synthesis |
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| Aminoglycosides, tetracyclines, and Macrolides |
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| Inhibition of essential metabolites |
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| sulfonamides |
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| Interference with nucleic acid metabolism |
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| quinolones |
