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use of chemical compounds to treat diseases caused by microorganisms |
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inhibit growth to allow immune system to fight off bacteria |
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additive, indifferent, synergistic, and antagonistic |
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each kills a certain amount of bacteria |
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each kills the same amount of bacteria |
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work together to kill more bacteria |
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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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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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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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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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• 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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• 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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cell wall integrity, inhibit cell wall synthesis by binding to transpeptidase (penicillin binding protein), bactericidal in actively growing organisms |
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beta lactam ring with one place for modification, differ in R group |
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strep, clost, aerobic GPR |
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strep, clost, aerobic GPR and some enterococci |
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act against beta lactamase, staph |
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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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no secondary ring, no GPC, GPR or anaerobes |
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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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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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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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neurotoxin and poor distribution |
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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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ototoxic (hearing loss) and nephrotoxic (kidney |
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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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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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: 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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attach to 50S subunit and interferes with translocation, Bacteriostatic, works on aerobic gram + and anaerobic bacteria (bacteroides) |
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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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interefere with folic acid pathway by competitively inhibiting bacterial dihydropteroate synthetase |
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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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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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mycobacterium, never taken alone always in combination (only alone for prophylaxis |
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all come from nalidixic acid, block DNA gyrase, bactericidal, used against gram + and gram – |
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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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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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Inhibition of protein synthesis |
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Aminoglycosides, tetracyclines, and Macrolides |
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Inhibition of essential metabolites |
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Interference with nucleic acid metabolism |
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