Lecture 8: Antimicrobial Therapy and Resistance Flashcards
What are antibiotics, and how are they classified?
Definition: Chemical compounds that kill/inhibit bacteria (non-toxic to host).
Classification:
Natural (e.g., penicillin from Penicillium).
Semi-synthetic (e.g., ampicillin).
Synthetic (e.g., ciprofloxacin).
How do β-lactams work, and what are their clinical uses?
Mechanism: Inhibit transpeptidase (blocks peptidoglycan cross-linking) → cell lysis.
Uses: Pneumonia, STIs (e.g., gonorrhea), skin infections.
Limitation: Allergy risk (anaphylaxis).
Describe the mechanism and uses of quinolones.
Mechanism: Inhibit DNA gyrase/topoisomerase IV → DNA breaks.
Uses: UTIs, pneumonia, MDR infections.
Caution: Restricted in children (musculoskeletal toxicity).
How do macrolides function, and when are they prescribed?
Mechanism: Bind 50S ribosomal subunit (P site) → block protein synthesis (bacteriostatic).
Uses: Streptococcal infections, Chlamydia, Mycoplasma.
What is the action and toxicity of aminoglycosides?
Mechanism: Bind 30S subunit → misread mRNA → misfolded proteins → cell death.
Uses: Gram-negative infections (e.g., Pseudomonas), TB.
Toxicity: Nephro-/ototoxicity.
Explain tetracyclines’ mechanism and applications.
Mechanism: Block aminoacyl-tRNA binding to 30S ribosome (bacteriostatic).
Uses: Acne, Chlamydia, Lyme disease, anthrax.
Name 3 resistance mechanisms.
Enzymatic degradation (e.g., β-lactamases).
Target modification (e.g., altered ribosomes in macrolide resistance).
Efflux pumps (e.g., tetracyclines).
What is a major concern about antibiotic overuse?
MDR pathogens (e.g., MRSA, ESBL-producing E. coli) due to selective pressure.
Which antibiotic treats MRSA and why?
Vancomycin (inhibits cell wall synthesis; MRSA lacks PBP2a target for β-lactams).
Recall antibiotic classes by target:
Cell wall: β-Lactams, Vancomycin.
DNA: Quinolones.
Protein synthesis: Macrolides, Aminoglycosides, Tetracyclines.
