How Do Antibiotics Work?

Antibiotics exploit fundamental differences between bacterial and human cells. Penicillin and its relatives (beta-lactams) block the enzymes that build bacterial cell walls — since human cells lack cell walls, these drugs are selectively toxic to bacteria. Tetracyclines and aminoglycosides bind to bacterial ribosomes (which differ structurally from human ribosomes), blocking protein synthesis. Fluoroquinolones (like ciprofloxacin) inhibit bacterial DNA gyrase, preventing DNA replication. Sulfonamides block a metabolic pathway for folic acid synthesis that bacteria need but humans obtain from food. The challenge is resistance: bacteria evolve rapidly through mutation and horizontal gene transfer, developing enzymes that destroy antibiotics (beta-lactamases), pumps that expel drugs from the cell, and altered target sites. Antibiotic-resistant infections kill an estimated 1.27 million people per year globally. The pipeline for new antibiotics has slowed dramatically since the 1980s — most major pharmaceutical companies have exited antibiotic research because the drugs are less profitable than treatments for chronic diseases.