Stevens- Antibiotics and Resistance Flashcards
beta-lactams and vancomycin target what
cell wall
Fluoroquinolones and rifamycins target what
DNA/RNA synthesis
Trimethoprim
Sulfonamides
target what
Folate synthesis
Daptomycin targets what
cell membrane
Linezolid
Tetracyclines
Macrolides
Aminoglycosides
target what
Protein synthesis
Penicillins
Cephalosporins
Carbapenems
target what
PBPs (penicillin binding proteins)
target 50S ribosome (protein synthesis)
Macrolides
Lincomycins
target 30S ribosome (protein synthesis)
Aminoglycosides
Tetracyclines
target DNA gyrase or topoisomerase IV (DNA replication)
Quinolones
target paraaminobenzoic acid (folate inhibitor)
target dihydrofolate reductase (folate inhibitor)
sulfonamides
trimethoprim
____ is important for synthesizing DNA and RNA in bacteria
folate
major mechanisms of antibiotic resistance
- edit antibiotic
- reduce antibiotic uptake
- increase antibiotic efflux
- change/modify drug target
bacteria ___the antibiotic and prevent it from binding to target
edit the antibiotic
2 examples of editing the antibiotic
post-translational modification
destruction
bacteria reduce _______ by loss of porin
reduce antibiotic uptake
bacteria increase ______ that promotes loss of antibiotics from cell (in gram + and gram -)
increase antibiotic efflux
___ and ___ are needed to translate mRNA into bacterial peptides
50S and 30S ribosomes
bacteria can alter _____ to modify drug target
50S and 30S ribosome subunits
____ or ____ of bacterial ribosomes that inhibit antibiotics from binding
mutations or methylation
bacteria can change the type of _____ they have and make it insensitive and inhibit antibiotics from binding
PBP (penicillin binding protein)
bacteria have developed resistance mechanisms to these Ab’s by
increasing efflux pathways
bacteria have resistance mechanisms to these Ab’s by
changing folate pathway and protein synthesis and PBPs
bacteria have resistance mechanisms to these antibiotics by
modifying antibiotic targets
bacteria have resistance mechanisms to these antibiotics by
inactivating enzymes (ribosomal subunits and PBPs)