Lecture 7b Flashcards
(15 cards)
What Are Antibiotics?
Antibiotics are chemicals that kill or inhibit the growth of microorganisms, particularly bacteria.
They are selectively toxic, meaning they can harm bacteria without harming human cells.
Classifications of antibiotics
Antibiotics can be grouped by:
Chemical structure
Spectrum of activity (narrow vs broad)
Mode of action (what they target in the bacterial cell)
Bactericidal Antibiotics
Kills bacteria directly.
Irreversible damage.
Often inhibit cell wall synthesis.
Effective without needing the immune system.
Measured by Minimal Bactericidal Concentration (MBC): the lowest concentration that kills 99.99% of bacteria.
Examples: Beta-lactams
Bacteriostatic antibiotics
Stops bacteria from growing, does not kill them.
Action is reversible; bacteria can grow again if the drug is removed.
Inhibits DNA replication or protein synthesis.
Relies on the host immune system to clear the infection.
Measured by Minimal Inhibitory Concentration (MIC): the lowest drug concentration that prevents visible growth.
Examples: Tetracyclines, Chloramphenicol, Sulfonamides
Mechanisms of Antibiotic Action: Inhibition of Cell Wall Synthesis
Inhibition of Cell Wall Synthesis
e.g. Penicillins
Weakens the bacterial wall → cell bursts due to osmotic pressure.
Mechanisms of Antibiotic Action: Inhibition of Protein Synthesis
e.g. Tetracyclines, Aminoglycosides, Macrolides
Target ribosomes
Mechanisms of Antibiotic Action: Inhibition of Nucleic Acid Synthesis
e.g. Quinolones (DNA), Rifampin (RNA)
Prevents bacterial DNA or RNA replication.
Mechanisms of Antibiotic Action: Injury to Plasma Membrane
Disrupts membrane integrity → leakage of cell contents → death.
Mechanisms of Antibiotic Action: Inhibition of Metabolite Synthesis
e.g. Sulfonamides block folic acid synthesis, essential for DNA replication.
Penicillins (Beta-Lactams)
Mechanism: Binds to penicillin-binding proteins (PBPs) that form peptide crosslinks in peptidoglycan → weakens the bacterial cell wall → causes cell lysis (bursting).
Uses: Skin, soft tissue, chest infections, pneumonia, meningitis, staph infections.
Resistance: Many bacteria now make beta-lactamase enzymes that break the beta-lactam ring.
Side effects: Allergic reactions ranging from rashes to anaphylaxis.
Aminoglycosides (e.g., Gentamicin, Streptomycin)
Aminoglycosides (e.g., Gentamicin, Streptomycin)
Mechanism: Bind to the 30S ribosomal subunit → misreading of mRNA → defective proteins → cell death. Bactericidal.
Spectrum:
Mainly Gram-negative bacteria (E. coli, Klebsiella, Pseudomonas).
Weak against Gram-positives unless combined with beta-lactams.
Uses: UTIs, abdominal infections, endocarditis (with penicillin).
Side effects:
Ototoxicity: permanent hearing loss.
Nephrotoxicity: kidney damage.
Important: Only given via IV. Blood levels must be monitored
Tetracyclines (e.g., Tetracycline, Doxycycline)
Mechanism:
Binds to the 30S ribosomal subunit at the A-site.
Prevents tRNA binding, so protein synthesis halts.
Bacteriostatic.
Spectrum: Broad. Effective against many Gram-positives and some Gram-negatives.
Uses: Skin infections, chest infections, Lyme disease, Rickettsial diseases.
Mechanisms of Tetracycline Resistance
1. Efflux Pumps
Bacteria pump tetracycline out of the cell using energy.
Keeps drug concentration too low to be effective.
Genes encoding this pump are often on plasmids, making them easily spread.
Mechanisms of Tetracycline Resistance 2. Ribosomal Protection Proteins
e.g. Tet(M), Tet(O) and others
Bind to ribosomes and change their shape.
This prevents tetracycline from binding, without stopping protein synthesis.
Genes often found on plasmids or mobile DNA elements.
Mechanisms of Tetracycline Resistance: 3. Enzymatic Inactivation
Gene: tet(X)
Encodes a protein that chemically modifies tetracycline, inactivating it.
Requires oxygen and NADPH for the reaction.
