Q.30 Match the antibioticsinGroup Iwith the targets inGroup II.
Group I Group II
P. Sulfonamide 1. Peptidoglycan synthesis
Q. Quinolones 2. Peptide chain elongation
R. Erythromycin 3. Folic acid biosynthesis
S. Cephalosporin 4. Topoisomerase
(A) P-3, Q-4, R-1, S-2 (B) P-2, Q-4, R-3, S-1
(C) P-4, Q-1, R-2, S-3 (D) P-3, Q-4, R-2, S-1
Correct Answer: (D) P-3, Q-4, R-2, S-1. Sulfonamide inhibits folic acid biosynthesis, quinolones target topoisomerase, erythromycin blocks peptide chain elongation, and cephalosporin disrupts peptidoglycan synthesis.
Antibiotic Mechanisms Overview
Antibiotics selectively target bacterial processes absent or divergent in eukaryotes. Sulfonamides compete in folate pathways, quinolones unwind DNA, macrolides stall ribosomes, and β-lactams prevent cell wall cross-linking.
Correct Matching Explained
P. Sulfonamide → 3. Folic acid biosynthesis. Competitive inhibitor of dihydropteroate synthase, blocking para-aminobenzoic acid (PABA) incorporation into folate, essential for bacterial nucleotide synthesis.
Q. Quinolones → 4. Topoisomerase. Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV, preventing supercoil relaxation needed for replication and transcription.
R. Erythromycin → 2. Peptide chain elongation. Macrolide binds 50S ribosomal subunit at the peptidyl transferase center, inhibiting translocation during protein synthesis.
S. Cephalosporin → 1. Peptidoglycan synthesis. β-lactam ring mimics D-Ala-D-Ala, acylating penicillin-binding proteins (PBPs) to block transpeptidation in cell wall assembly.
Option Analysis
Option (A) P-3, Q-4, R-1, S-2 incorrectly assigns erythromycin to peptidoglycan (ribosome target) and cephalosporin to elongation (cell wall inhibitor).
Option (B) P-2, Q-4, R-3, S-1 mismatches sulfonamide to elongation (folate pathway) and erythromycin to folate (protein synthesis).
Option (C) P-4, Q-1, R-2, S-3 wrongly pairs sulfonamide with topoisomerase (PABA analog), quinolones to peptidoglycan (DNA enzymes), and cephalosporin to folate (PBP binder).
Clinical Microbiology Relevance
These targets underpin selective toxicity—folate inhibition starves nucleotide production, topoisomerase blockade halts replication, ribosomal stalling curbs virulence factors, and wall disruption triggers autolysis in growing cells.
