Clinical meaning
Bacteria are classified by Gram stain: Gram-positive organisms (S. aureus, Streptococcus, Enterococcus) have a thick peptidoglycan cell wall that retains crystal violet stain, while Gram-negative organisms (E. coli, Pseudomonas, Klebsiella) have a thin peptidoglycan layer surrounded by an outer lipopolysaccharide (LPS) membrane that acts as an endotoxin. Antibiotics target essential bacterial processes: cell wall synthesis (beta-lactams, vancomycin), protein synthesis (aminoglycosides target 30S ribosome; macrolides, tetracyclines target 30S; chloramphenicol, clindamycin target 50S), DNA replication (fluoroquinolones inhibit DNA gyrase/topoisomerase IV), folic acid synthesis (sulfonamides, trimethoprim), and cell membrane integrity (daptomycin, polymyxins). Antimicrobial resistance develops through multiple mechanisms: enzymatic degradation (beta-lactamases including ESBLs and carbapenemases), target modification (altered PBPs in MRSA, ribosomal methylation), efflux pumps (pump antibiotic out of the cell), porin mutations (reduced drug entry in Gram-negatives), and biofilm formation. Resistance genes spread horizontally between bacteria via plasmids, transposons, and transformation. Multidrug-resistant organisms (MDROs) including MRSA, VRE, ESBL-producing Enterobacteriaceae, and CRE (carbapenem-resistant Enterobacteriaceae) represent critical public health threats. Antibiotic stewardship—using the right drug, right dose, right duration for the right indication—is essential to slow resistance development.