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52 Cards in this Set

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what are the main modes of action for antibacterial agents? (6)
1. inhibit cell wall syn
2. disrupt PM
3. inhibit protein syn
4. inhibit nucleic acid syn
5. antimetabolites
6. target regulatory mol
what is the BEST mode of action for antibacterial agents and why?
inhibit cell wall syn; b/c not targeting a process that is used by host cells (less side effects, toxic)
"highly selective toxicity"
why is targeting protein syn also a good mxn?
bacteria use different ribosomes (30,50S) than eukaryotes (40,60S)
selective toxicity
if a drug prevented cell wall syn would it be considered bactericidal or bacteriostatic?
bacteriostatic b/c preventing formation of new microorganisms
if a drug caused the break down of bacterial cell walls would it be considered bactericidal or bacteriostatic?
bactericidal because it is causing bacterial cell death
what are some drugs that inhibit cell wall syn? (4)
1. penicillin (Penicillin binding protein)
2. cephalosporins
3. bacitracin
4. vancomycin
drugs that inhibit protein syn? (4)
1. chloramphenicol
2. erythromycin (macrolide)
3. tetracyclin (bacteriostatic)
4. streptomycin (aminoglycoside)
also, oxazolidones
drugs that inhibit syn of metabolites (2)
what metabolite?
1. sulfanilamide
2. trimethoprim
target folic acid syn
drugs that inhibit nucleic acid replication, transcription (3)
quinolones, rifampin and metronidazole
drug that causes injury to PM
polymyxin B
(also, lipopeptides and bacitracin)
what are some methods by which bacteria become resistant to antibiotics? (5)
1. alter target
2. active efflux
3. inactivate drug
4. decr uptake of drug
5. prod decoys
why do bacteria become resistant to antibiotics? where are these genes found?
bacteria have a high rate of replication and accumulate many mutations that can lead to drug resistance.
most antibiotic resistance genes are found on plsmids;
overuse of one antibiotic will result in proliferation of only bacteria that are resistant to that antibiotic
how do bacteria decrease uptake of antibiotics?
accumulate mutations in permeases and porins
what are characteristics of antibacterial agents? (4)
1.selective toxicity
2.cidal v. static
3.spectrum of activity
4. adverse host rxn (some)
what is selective toxicity? what is an example?
ablity to kill pathogen before/without killing host cell
most often in antibacterial b/c can target prokaryotic structures,fxns
ex: penicillin targeting PG in the cell wall
how does vancomycin cause adverse host reaction?
what is important about this example?
targets PG but also causes nephrotoxicity in pts with underlying renal disease
ADVERSE RXN MAY BE UNRELATED TO MXN OF ACTION OF THE DRUG!
what is an ex of a bactericidal and a bacteriostatic agent?
cidal: penicillin- decr # CFU and viable organisms
static: tetracycline-# org stays the same
what is minimum inhibitory concentration?
lowest concentration of a drug that stops GROWTH
what is therapeutic index?
ratio: drug toxic dose/MIC
imp for use and dosage
why are antibiotics used in combination?
to overcome bacterial resistance to the drugs
what is an example of 2 antagonistic antibiotics
penicillin and tetracyclin;
tetracyclin prevents growth and therefore prevents cell wall syn which is where penicillin would normally act (PBP, in log phase);
penicillin doesnt work on stationary cells
what are inhibitors of cell wall syn (5)
beta-lactams
glycopeptides
bacitracin
isoniazid (acid fast)
ethambutol (acid fast)
what is the mxn of action of beta-lactams?
inhibit cell wall syn
block PBP
what is the MOA of glycopeptides?
inhibit cell wall syn
block tetrapeptide linkage
what is the mxn of action of bacitracin?
inhibits cell wall syn
blocks recycling of transport proteins
(also interferes with cytoplasmic mbr integrity)
what is the mxn of action of isoniazid?
inhibits acid fast cell wall syn
blocks syn mycolic acid
what is the mxn of action of ethambutol?
block syn of arabinogalactan; acid fast cell wall inhibitor
what is significant abt Augmentin?
combination drug that fxns as beta-lactam and includes clavulanic acid which inhibits beta-lactamase
what are the properties of cell wall inhibitors? (5)
1. bind bacteria
2. penetrate outer mbr, periplasmic space of G-
3. interact with PBP on cytoplasmic mbr
4. upregulate autolysin-degrade muramic acid, PG of cell wall
5. bactericidal
resistance to cell wall inhibitors (2)
inactivate antibiotic (beta-lactamase)
alter target
inhibitors of protein syn (4)
aminoglycosides
tetracyclines
macrolides
oxazolidones
mxn of aminoglycosides
inhibit protein syn
interfere with f-met tRNA
cidal
mxn tetracyclines
inhibits protein syn
inhibit elongation (tRNA to acceptor site)
static
mxn macrolides
inhibit protein syn (CLEan TAG)
block translocation
(ex: Erythromycin)
mxn oxazolidones
inhibits protein syn
bind 50S; block ribosome assembly (initiation)
properties of protein syn inhibitors (3)
penetrate outer mbr G- (porins and permeases)
transported in via active transport system in cell mbr
bind ribosome, translation factors
bacterial resistance to protein syn inhibitors (5)
mutation of target
alter antibiotic
decr uptake (via porins, permeases)
active efflux
prod decoy
inhibitors of NA syn(3)
quinolones
rifampins, rifamycins
metronidazole
mxn quinolones
inhibit NA syn
G+: inhibit dna gyrase
G-: inhibit topo 4
cidal
mxn rifampin/rifamycins
inhibits NA syn
inhibit DNA dependent RNA polymerase (transcription)
mxn metronidazole
inhibits NA syn
binds DNA
(blocks H2 syn)
also works against anaerobic organisms and parasites
charac of NA syn inhibitors
penetrate outer mbr G-
transported in
bind NA, enzyme, TF
resistance to NA syn inhibitors (2)
change target (DNA gyrase, topo)
decr uptake (change cell wall permeability)
antimetabolites (2)
sulfonamides
trimethoprim
-used in combination to prevent resistance and treat broad range organisms
mxn of sulfonamides
antimetabolite
compete with PABA (substrate for folic acid syn)
used in conjuction with trimethoprim
mxn of trimethoprim
antimetabolite
inhibit dihydrofolate reductase (syn THF)
resistance to antimetabolites (4)
form permeablity barrier
alter target (enzyme)
ability to take up exogenous folic acid
intrinsic resistance for org that use exogenous thymidine (ex: enterococci)
cytoplasmic mbr fxn inhibitors (3)
polymyxins
lipopeptides
bacitracin
mxn polymyxins
inhibits PM fxn
increase cell permeablity
mxn lipopeptides
inhibits PM fxn
trigger rapid depolarization -> lose mbr potential, prevents protein, DNA, RNA syn
mxn bacitracin
damange mbr (also prevents cell wall syn)
resistance to cytoplasmic mbr fxn inhibitors (3)
mutation of target
alter antibiotic
decrease uptake (G- with modified phospholipid bilayer, porins)