Antibiotics target bacteria, not viruses or fungi. They achieve this by interfering with vital bacterial processes. Different antibiotics use different mechanisms.
Targeting Bacterial Cell Walls
Some antibiotics, like penicillin and vancomycin, disrupt bacterial cell wall synthesis. Bacteria need strong cell walls to survive; disrupting this construction leads to cell death. Penicillin blocks the enzyme responsible for cross-linking peptidoglycans, a key component of the cell wall. Vancomycin prevents the formation of peptidoglycans altogether.
Interfering with Protein Synthesis
Many antibiotics, including tetracycline and erythromycin, target bacterial ribosomes, the cellular machinery responsible for protein production. By binding to ribosomes, these antibiotics prevent the bacteria from producing the proteins they need for growth and survival. Tetracycline binds to the 30S ribosomal subunit, while erythromycin binds to the 50S subunit.
Inhibiting Nucleic Acid Synthesis
Other antibiotics, such as quinolones (like ciprofloxacin) and rifampin, interfere with bacterial DNA replication or RNA transcription. Quinolones block bacterial enzymes called topoisomerases, which are involved in DNA replication. Rifampin inhibits bacterial RNA polymerase, preventing the synthesis of messenger RNA and thus protein production.
Disrupting Metabolic Pathways
Some antibiotics, like sulfonamides and trimethoprim, disrupt specific metabolic pathways crucial for bacterial survival. Sulfonamides inhibit folic acid synthesis, a vital nutrient for bacterial growth. Trimethoprim blocks a later step in the same pathway. These antibiotics are often used in combination for synergistic effects.
Understanding these mechanisms helps explain why antibiotics are specific to bacteria and why resistance develops when bacteria adapt to circumvent antibiotic actions. This necessitates responsible antibiotic use to minimize resistance development.
