Antibiotic Resistance Mechansims Flashcards
Bacteriocidal antibiotic
Kills the bacteria
Bacteriostatic
Inhibits bacterial growth
Natural antibiotics
Secondary metabolic products from microbes
6 key strategies/targets of antibiotics
- Cell wall synthesis
- DNA replication
- RNA synthesis
- Protein synthesis
5. Folic acid synthesis - Membrane disruption
Transpeptidase
Cross links peptide chains of peptidoglycan cell wall using D-Ala D-Ala motif
Cell wall synthesis inhibitor
Penicillin
DNA gyrases
Reseal the bacterial DNA to begin DNA synthesis
DNA topoisomerases
Cut the bacteria to unwind supercoils
Fluoroquinolones
Bind to DNA gyrases, cause lethal DNA breaks
RNAP
Causes chain elongation in transcription
Rifamycin
Inhibits RNAP, stops RNA chain elongation
Tetracycline, clindamycin, chloramphenicol, neomycin, erythromycin
Inhibits protein synthesis
Folic acid synthesis
Synthesized de novo from PABA, needed for purine synthesis
Sulfanomides
Inhibit Folic acid synthesis
Daptomycin
Interrupts ion gradient of gram positive bacteria
Colistin
Membrane disruption of gram negative bacteria
How do bacteria resist the action of antibiotics? (5)
- Inactivating the antibiotic
- Modifying or replacing target
- Remove abx from cell 9multi-drug resistance)
- Prevent uptake of antibiotic
- Develop per sister populations (neither grow nor die during antibiotic exposure
Beta lactamase
Cleave beta lactam ring of penicillin
Vancomycin
Binds to D-Ala D-Ala to prevent transpeptidase activity
Vancomycin resistance
Replaces D-Ala D-ala with D-ala D-lactate, which vancomycin can’t bind to
2 types of effluent transporters
Single component or multi component
Prevention of antibiotic uptake (4)
- Decrease in OMP gene expression (gram -)
- Increase thickness of peptidoglycan (gram +)
- Capsule formation
- Biofil, production
Persister population
Not genetic mutants, metabolically inert “survive and advance”
