Chloramphenicol directly inhibits bacterial protein synthesis. It binds to the 50S ribosomal subunit, specifically the peptidyl transferase center. This binding prevents peptide bond formation, halting translation and effectively stopping bacterial growth. The drug’s action is bacteriostatic, meaning it slows bacterial growth rather than killing them directly, though at high concentrations it can exhibit bactericidal activity.
Gram-Positive and Gram-Negative Bacteria
Chloramphenicol’s spectrum of activity is broad. It’s effective against a wide range of both Gram-positive and Gram-negative bacteria. This includes organisms like Haemophilus influenzae, Salmonella species, Shigella species, and many others. However, resistance is a significant clinical concern, limiting its current use.
Limitations and Resistance
Resistance mechanisms vary, but often involve enzymatic inactivation of chloramphenicol via chloramphenicol acetyltransferase (CAT). This enzyme modifies the drug, rendering it ineffective. The emergence of resistant strains reduces the therapeutic potential of chloramphenicol. Therefore, susceptibility testing is crucial before treatment.
