What is the table of available antibiotics and their mechanisms of action?

Comprehensive Table of Available Antibiotics and Their Mechanisms of Action

Antibiotics are categorized by their mechanism of action into four primary groups: inhibitors of bacterial cell wall synthesis, inhibitors of protein synthesis, inhibitors of nucleic acid metabolism, and membrane-active agents. 1

Major Antibiotic Classes by Mechanism of Action

Antibiotic Class	Mechanism of Action	Representative Agents	Primary Clinical Use
β-Lactams (Penicillins)	Inhibit cell wall synthesis by binding to penicillin-binding proteins (PBPs), causing autolysis [2]	Amoxicillin, Ampicillin, Amoxicillin-clavulanate	First-line for streptococcal infections, community-acquired pneumonia [3]
β-Lactams (Cephalosporins)	Inhibit cell wall synthesis via PBP binding; generations vary in spectrum [2]	Cefazolin (1st gen), Cefuroxime (2nd gen), Ceftriaxone (3rd gen)	Skin/soft tissue infections, pneumonia [3]
Carbapenems	Inhibit cell wall synthesis; highly stable against β-lactamases [4]	Meropenem, Imipenem, Ertapenem	Reserved for multidrug-resistant infections [2]
Monobactams	Inhibit cell wall synthesis; resistant to most β-lactamases [4]	Aztreonam	Gram-negative infections in penicillin-allergic patients [4]
Fluoroquinolones	Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV, blocking DNA replication [5]	Ciprofloxacin, Levofloxacin, Moxifloxacin	Respiratory infections, complicated UTIs [3]
Macrolides/Azalides	Bind to 23S rRNA of 50S ribosomal subunit, blocking protein synthesis [6]	Erythromycin, Azithromycin, Clarithromycin	Community-acquired pneumonia, atypical pathogens [3]
Tetracyclines	Inhibit bacterial protein synthesis at 30S ribosomal subunit [2]	Doxycycline, Tetracycline	COPD exacerbations, atypical infections [3]
Aminoglycosides	Inhibit protein synthesis by binding to 30S ribosomal subunit [1]	Gentamicin, Tobramycin, Amikacin	Serious gram-negative infections, synergy with β-lactams [7]
Lincosamides	Inhibit protein synthesis at 50S ribosomal subunit [2]	Clindamycin	Anaerobic infections, MRSA skin infections [3]
Sulfonamides/Trimethoprim	Inhibit folic acid synthesis pathway [2]	Trimethoprim-sulfamethoxazole (TMP-SMX)	UTIs, MRSA infections [3]
Glycopeptides	Inhibit cell wall synthesis by binding D-alanyl-D-alanine terminus [7]	Vancomycin, Teicoplanin	MRSA infections, C. difficile (oral vancomycin) [7]

WHO AWaRe Classification Framework

The World Health Organization categorizes antibiotics into three stewardship groups to guide appropriate use and preserve effectiveness 2:

Access Group Antibiotics

• Definition: First- or second-choice empiric options for common infections; should be widely available, affordable, and quality-assured 2
• Examples: Amoxicillin, amoxicillin-clavulanate, doxycycline, cefalexin, cefazolin 3
• Clinical Priority: These agents have lower resistance potential and favorable safety profiles 2

Watch Group Antibiotics

• Definition: Higher resistance potential and toxicity concerns; require stewardship monitoring 2
• Examples: Fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin), 3rd/4th generation cephalosporins, carbapenems 2
• Critical Consideration: These are on the WHO List of Critically Important Antimicrobials and should be used only for specific indications 2

Reserve Group Antibiotics

• Definition: Last-resort options for multidrug-resistant organisms when all other alternatives have failed 2
• Examples: Colistin, tigecycline, certain newer β-lactam/β-lactamase inhibitor combinations 2
• Stewardship Imperative: Must be protected through rigorous monitoring and reporting programs 2

Detailed Mechanism Considerations

β-Lactam Antibiotics: Cell Wall Synthesis Inhibition

• Penicillins achieve bactericidal activity through PBP binding, with amoxicillin being the most active oral β-lactam against streptococci due to superior bioavailability 2
• High-dose amoxicillin (4 g/day adults; 90 mg/kg/day children) overcomes relative penicillin resistance in S. pneumoniae through linear dose-absorption kinetics 2
• Cephalosporins have inherently lower activity against pneumococci than amoxicillin, with baseline MICs fourfold higher, and absorption limitations prevent dose escalation 2
• β-lactamase inhibitors (clavulanate) preserve amoxicillin activity against β-lactamase-producing organisms without affecting intrinsic anti-pneumococcal activity 2

Fluoroquinolones: DNA Synthesis Inhibition

• Ciprofloxacin inhibits both DNA gyrase and topoisomerase IV, enzymes essential for bacterial DNA replication, transcription, repair, and recombination 5
• Mechanism uniqueness: No cross-resistance with β-lactams, cephalosporins, aminoglycosides, macrolides, or tetracyclines 5
• Resistance development: Occurs slowly through multiple-step mutations in vitro 5
• Pediatric caution: Fluoroquinolones should be used cautiously in children due to potential effects on weight-bearing joints 3

Macrolides: Protein Synthesis Inhibition

• Azithromycin binds to 23S rRNA of the 50S ribosomal subunit, blocking transpeptidation/translocation and preventing 50S subunit assembly 6
• Unique pharmacokinetics: Concentrates in phagocytes and fibroblasts with intracellular:extracellular ratios >30:1 after one hour 6
• Resistance mechanism: Most commonly through 23S rRNA modification at positions A2058 and A2059, conferring cross-resistance to lincosamides and streptogramins B 6

Clinical Pitfalls and Stewardship Considerations

• Local resistance patterns must guide empiric therapy selection, as susceptibility varies geographically 3
• Shorter courses (5 days) are recommended for common infections like pneumonia and COPD exacerbations, with extension based on clinical response rather than default longer durations 3
• Drug interactions are critical: ciprofloxacin decreases theophylline clearance by 30-50%, and azithromycin causes QTc prolongation when combined with chloroquine 5, 6
• β-lactam selection should prioritize amoxicillin over cephalosporins for pneumococcal coverage due to superior intrinsic activity and dose-escalation capability 2
• Watch group antibiotics (fluoroquinolones, carbapenems) should be reserved for specific indications where Access group agents are inadequate, not used as routine first-line therapy 2