Fluoroquinolones: What is the primary bacterial target inhibited by this class?

Introduction / Context:
Fluoroquinolones are widely used bactericidal agents. Understanding the precise enzymatic target is essential to predict spectrum, tissue penetration utility, and resistance evolution.

Given Data / Assumptions:

• Fluoroquinolones affect bacterial DNA topology and replication.
• Different organisms rely on DNA gyrase vs topoisomerase IV to varying degrees.

Concept / Approach:
Fluoroquinolones stabilize DNA–enzyme cleavage complexes of DNA gyrase (gyrA/gyrB) and topoisomerase IV (parC/parE), preventing religation and blocking replication/segregation. In Gram-negatives, DNA gyrase is typically the primary target; in many Gram-positives, topoisomerase IV may be more critical, but “DNA gyrase” remains the canonical answer for this class.

Step-by-Step Solution:
Exclude RNA polymerase (rifamycins target this) and DNA polymerase (not the quinolone target). Exclude cell wall cross-linking enzymes (beta-lactam target) and ribosomal sites (aminoglycosides, tetracyclines, etc.). Select DNA gyrase as the prototypic target.

Verification / Alternative check:
Resistance mutations commonly appear in the quinolone resistance–determining regions (QRDR) of gyrA/gyrB and parC/parE, confirming the enzymatic targets.

Why Other Options Are Wrong:
They correspond to other drug classes and pathways, not fluoroquinolones.

Common Pitfalls:
Forgetting the topoisomerase IV contribution in Gram-positives; nevertheless, exams accept DNA gyrase as the best single answer.

Final Answer:
DNA gyrase.