Anti-infectives · Medicine Class
Selective toxicity — targeting bacterial cell wall, ribosome, DNA replication, or metabolic pathways absent or sufficiently different in human cells
Antibiotics exploit the biological differences between bacterial and human cells to selectively inhibit or kill bacteria. Major mechanisms: cell wall synthesis inhibition (beta-lactams — penicillins, cephalosporins, carbapenems — bind penicillin-binding proteins that cross-link bacterial peptidoglycan; glycopeptides — vancomycin, teicoplanin — bind D-Ala-D-Ala peptidoglycan precursors); protein synthesis inhibition (aminoglycosides and tetracyclines bind the 30S ribosomal subunit; macrolides, chloramphenicol, lincosamides bind the 50S subunit); DNA/RNA synthesis disruption (fluoroquinolones inhibit bacterial topoisomerases II and IV; rifampin inhibits bacterial RNA polymerase); cell membrane disruption (polymyxins, daptomycin); and metabolic pathway inhibition (sulfonamides, trimethoprim inhibit folate synthesis absent in human cells that can use dietary folate).
Amoxicillin-Clavulanate (Augmentin)
Broad-spectrum aminopenicillin + beta-lactamase inhibitor. Most commonly prescribed oral antibiotic. Community respiratory, UTI, skin infections. GI side effects common.
Azithromycin (Zithromax)
Macrolide. Community pneumonia, STIs (chlamydia), pertussis. Short 3-5 day courses due to prolonged tissue levels. QTc prolongation risk. Growing resistance.
Ciprofloxacin (Cipro)
Fluoroquinolone. UTIs, respiratory, GI infections. Black box: tendinopathy, neuropathy. FDA guidance: reserve for infections with no alternatives.
Trimethoprim-Sulfamethoxazole (Bactrim)
Sulfonamide + DHFR inhibitor. UTIs, MRSA skin infections, PCP prophylaxis. Avoid in sulfa allergy, renal impairment, pregnancy near term.
Doxycycline (Vibramycin)
Tetracycline. Excellent spectrum including atypicals, Lyme, rickettsial diseases, acne. Avoid in children under 8. Photosensitivity. Take with plenty of water — esophageal ulceration risk.
Vancomycin (Vancocin)
Glycopeptide. MRSA, serious gram-positive infections. IV for systemic infection; oral for C. diff. Nephrotoxicity and ototoxicity — AUC-based monitoring now preferred over trough-based.
Metronidazole (Flagyl)
Nitroimidazole. Anaerobic bacteria and protozoa. C. diff (being replaced by vancomycin/fidaxomicin), pelvic inflammatory disease, Helicobacter pylori, giardia. Disulfiram-like reaction with alcohol.
Warfarin — many antibiotics (especially fluoroquinolones, metronidazole, azithromycin) markedly increase INR; rifampin dramatically reduces warfarin levels
Oral contraceptives — rifampin (a CYP3A4 inducer) reduces OCP effectiveness significantly; other antibiotics have minimal effect on OCPs despite historical concerns
QTc-prolonging drugs — additive risk with macrolides and fluoroquinolones
Antacids and dairy — bind fluoroquinolones and tetracyclines, drastically reducing absorption; take 2 hours apart
Probenecid — reduces renal penicillin secretion, increasing penicillin levels (historically used therapeutically)
For most standard antibiotic courses (7-10 days for UTI, 5 days for Z-pak, 10 days for strep throat), completing the prescribed course is important to eradicate the infection and reduce the risk of selecting for resistant bacteria. However, the evidence base for specific antibiotic durations has been revised — shorter courses are now standard for many infections (3 days for uncomplicated UTI, 5-7 days for community-acquired pneumonia, 24-hour prophylaxis after surgery). Never stop antibiotics early for tuberculosis — incomplete TB treatment is the primary driver of multidrug-resistant TB.
Antibiotic resistance occurs when bacteria evolve mechanisms to survive antibiotic exposure: producing enzymes that inactivate antibiotics (beta-lactamases, including extended-spectrum beta-lactamases [ESBLs] and carbapenemases); modifying drug targets; developing efflux pumps that remove antibiotics from the cell; or reducing permeability. Resistance genes can be transferred between bacteria via plasmids, accelerating the spread of resistance. The WHO designates antibiotic resistance as one of the greatest threats to global health. Carbapenem-resistant organisms, MRSA, and drug-resistant tuberculosis represent treatment crises. Antimicrobial stewardship — prescribing antibiotics only when needed, for the shortest effective duration, with the narrowest necessary spectrum — is the primary strategy to preserve antibiotic effectiveness.