Antibiotics

Question 1

β-Lactam Antibiotics
Mechanism:

Answer 1

Inhibit transpeptidase (penicillin-binding proteins) by mimicking D-alanyl-D-alanine.

Prevent cross-linking of peptidoglycan in bacterial cell walls → cell lysis.

Irreversible competitive inhibition.

Question 2

β-Lactam Antibiotics Examples:

Answer 2

Penicillins (e.g., amoxicillin), cephalosporins (e.g., ceftriaxone), carbapenems.

Question 3

β-Lactam Antibiotics Spectrum:

Answer 3

Primarily Gram-positive (thick peptidoglycan), but some target Gram-negative.

Question 4

β-Lactam Antibiotics Key Points:

Answer 4

Bactericidal.
Resistance via β-lactamase enzymes (e.g., penicillinase).

Question 5

Quinolones
Mechanism:

Answer 5

Inhibit DNA gyrase (Gram-negative) and topoisomerase IV (Gram-positive).

Cause double-stranded DNA breaks → cell death.

Question 6

Quinolones
Examples:

Answer 6

Ciprofloxacin, moxifloxacin, levofloxacin.

Question 7

Quinolones Spectrum:

Answer 7

Broad-spectrum (Gram+ and Gram-).

Question 8

Quinolones Key Points:

Answer 8

Synthetic, bactericidal.

Used for UTIs, respiratory infections.

Resistance via mutations in gyrase/topoisomerase genes.
Quinolones Quash DNA replication.

Question 9

Macrolides Mechanism:

Answer 9

Bind reversibly to 50S ribosomal subunit (P site).

Block peptide chain elongation → bacteriostatic.

Question 10

Macrolides Examples:

Answer 10

Erythromycin, azithromycin, clarithromycin.

Question 11

Macrolides spectrum

Answer 11

Gram-positive (e.g., Staphylococcus, Streptococcus),
some Gram- negative (e.g., Mycoplasma).

Question 12

Macrolides key points:

Answer 12

Derived from Streptomyces erythraeus.

Used for respiratory infections, atypical pathogens.

Mnemonic: “Macrolides Muffle ribosomes.”

Question 13

Aminoglycosides Mechanism:

Answer 13

Bind 30S ribosomal subunit (A site) → misread mRNA → misfolded proteins.

Bactericidal (disrupt cell membrane via defective proteins).

Question 14

Aminoglycosides Examples:

Answer 14

Streptomycin, gentamicin, tobramycin.

Question 15

Aminoglycosides Spectrum:

Answer 15

Aerobic Gram-negative (e.g., E. coli, Pseudomonas).

Question 16

Aminoglycosides Key Points:

Answer 16

Require oxygen for uptake (ineffective against anaerobes).

Resistance via modifying enzymes (e.g., acetyltransferases).

Mnemonic: “Aminoglycosides Alter mRNA reading.”

Question 17

Tetracyclines
Mechanism:

Answer 17

Block 30S ribosomal subunit (A site) → prevent tRNA binding.

Bacteriostatic (stall protein synthesis).

Question 18

Tetracyclines Examples:

Answer 18

Tetracycline, doxycycline, minocycline.

Question 19

Tetracyclines spectrum:

Answer 19

Broad-spectrum (Gram+, Gram-, Chlamydia, Rickettsia).

Question 20

Tetracyclines key points :

Answer 20

Also inhibit matrix metalloproteinases (used in acne/rosacea).

Resistance via efflux pumps or ribosomal protection.

Mnemonic: “Tetracyclines Terminate tRNA attachment.”

Question 21

Global Antibiotic Usage
Key Stats:

Answer 21

β-lactams account for ~52% of global antibiotics (cephalosporins: 30%, penicillins: 7%).

Quinolones: 24% of manufactured antibiotics.

Question 22

Antibiotic Resistance (AMR)
Definition:

Answer 22

The ability of bacteria to survive treatment with antibiotics.

Multidrug-resistant (MDR): Resistance to ≥3 antibiotic classes.

Question 23

Key Causes of AMR:

Answer 23

Human misuse: Incomplete courses, over-prescription.

Non-therapeutic use: Agriculture (growth promoters), aquaculture, industrial biocides.

Lack of new antibiotics: Only 5 new classes since 1968.

Question 24

Mechanisms of Antibiotic Resistance

Answer 24

Enzymatic Destruction:
β-lactamases hydrolyze β-lactam antibiotics (e.g., penicillinase).

Target Alteration:
Modify penicillin-binding proteins (PBPs) to avoid β-lactam binding.

Efflux Pumps:
Actively pump antibiotics out (e.g., tetracycline resistance).

Reduced Permeability:
Alter porins to limit antibiotic entry (common in Gram-negative bacteria).

Metabolic Dormancy:
Enter a dormant state (persister cells) to avoid antibiotic action.

Example: MRSA alters PBPs to resist methicillin.

Question 25

β-Lactamases Function:

Answer 25

Hydrolyse the β-lactam ring in penicillin, cephalosporins, and carbapenems. Types: ESBLs (Extended-Spectrum β-Lactamases): Plasmid-encoded; confer resistance to most β-lactams except carbapenems. Carbapenemases: Break down carbapenems (e.g., Klebsiella pneumoniae).

Question 26

β-Lactam Antibiotics & Resistance Classes:

Answer 26

Penicillins: Narrow-spectrum (e.g., benzylpenicillin). Broad-spectrum (e.g., amoxicillin). Cephalosporins: 1st gen (cefalexin) → 4th gen (cefepime). Carbapenems: Last-resort drugs (e.g., meropenem).

Question 27

β-Lactam Antibiotics & Resistance

Answer 27

Resistance Mechanisms: β-lactamase production (e.g., E. coli ESBLs). Altered PBPs (e.g., MRSA). Mnemonic: "Penicillins, Cephalosporins, Carbapenems: PCC for Bacterial Walls."

Question 28

β-Lactamase Inhibitors

Answer 28

Function: Block β-lactamases to protect antibiotics (e.g., clavulanic acid inhibits penicillinase).

Question 29

β-Lactamase Inhibitors Examples:

Answer 29

Co-amoxiclav: Amoxicillin + clavulanic acid. Piperacillin-tazobactam: Targets hospital-acquired infections.

Question 30

β-Lactamase Inhibitors mechanism:

Answer 30

uicide inhibition: Irreversibly binds β-lactamases (clavulanic acid). Non-competitive inhibition: Tazobactam stabilizes antibiotics. Use: Treat UTIs, skin infections, and multidrug-resistant pathogens.