[W5-6] Antibiotics and AMR Flashcards
(40 cards)
What are antibiotics?
Low molecular weight compounds, often produced by microbes (e.g., Streptomyces), that kill or inhibit bacteria.
What’s the difference between antibiotics and antimicrobials?
Antibiotics = antibacterial; antimicrobials = act against bacteria, viruses, fungi, or protozoa.
What’s the difference between bacteriostatic and bactericidal?
Bacteriostatic: Inhibit growth.
Bactericidal: Kill bacteria.
What is a broad-spectrum antibiotic?
Active against many bacterial types; used before pathogen identification.
What is a narrow-spectrum antibiotic?
Targets specific bacteria; minimizes microbiome disruption.
What are common delivery routes for antibiotics?
Oral, intravenous, intranasal, topical.
List pharmacological and antimicrobial properties of a good antibiotic.
Antimicrobial:
* Selective toxicity
* Potent cidal activity
* Low resistance development
Pharmacological:
* Good tissue penetration
* Low toxicity
* Stable
* Various forms
* Low protein binding
What is intrinsic resistance?
Natural resistance due to structural features (e.g. Gram-negatives and β-lactams).
What is acquired resistance?
Resistance via mutation or horizontal gene transfer (HGT).
What are MIC and MBC?
MIC: Minimum inhibitory concentration.
MBC: Minimum bactericidal concentration.
Name 3 AMR testing methods.
Serial dilution (MIC/MBC), Etest, Disc diffusion assay.
What is the target of β-lactams?
Penicillin-binding proteins (PBPs) involved in peptidoglycan crosslinking.
What are two key resistance mechanisms to β-lactams?
β-lactamases (enzyme degradation), Altered PBPs (e.g. PBP2a in MRSA).
What are extended spectrum β-lactamases (ESBLs)?
Enzymes that hydrolyze a broad range of β-lactams, including cephalosporins.
How does clavulanic acid help β-lactam activity?
Inhibits β-lactamases; used in combo with amoxicillin (e.g. Co-amoxiclav).
What makes MRSA resistant to methicillin?
PBP2a has low affinity for β-lactams.
What infections is MRSA associated with?
Nosocomial infections, surgical wound infections, bloodstream infections.
How does vancomycin work?
Binds D-Ala-D-Ala on peptidoglycan precursors to inhibit crosslinking.
Why is vancomycin effective against MRSA?
Targets different site than β-lactams (not affected by β-lactamases or PBP2a).
Which antibiotics target the 30S subunit?
Tetracyclines: Block tRNA binding.
Aminoglycosides: Cause misreading of mRNA.
Which antibiotics target the 50S subunit?
Macrolides (e.g. erythromycin): Block translocation.
Chloramphenicol: Inhibits peptidyl transferase.
What are common tetracyclines?
Tetracycline, doxycycline, lymecycline.
What are major tetracycline resistance mechanisms?
Efflux pumps (most common), ribosome protection proteins, enzymatic inactivation.
What are side effects of aminoglycosides?
Nephrotoxicity and ototoxicity (hearing/balance loss).