Chapter 35  ·  Module 8

Chloramphenicol and Oxazolidinones

50S ribosomal inhibition — two drug classes, distinct mechanisms, contrasting toxicity profiles

Abbreviations: MRSA = methicillin-resistant Staphylococcus aureus  |  VRE = vancomycin-resistant Enterococcus  |  MAO = monoamine oxidase  |  CNS = central nervous system

Chloramphenicol

Mechanism & Spectrum

Chloramphenicol

Mechanism
  • Binds 23S rRNA at peptidyl transferase center on 50S subunit
  • Blocks peptide bond formation — halts elongation
  • Bacteriostatic (bactericidal vs. H. influenzae, N. meningitidis, S. pneumoniae)
Spectrum
  • Gram-positive, Gram-negative, anaerobes, rickettsiae
  • Active vs. Salmonella typhi, Bacteroides fragilis
  • No reliable activity vs. MRSA or Pseudomonas aeruginosa

Pharmacokinetics

Key Properties

CNS Penetration
  • CSF: 30–50% of plasma even without meningitis
  • Rises toward plasma levels with meningeal inflammation
  • Best CNS penetration among protein synthesis inhibitors
Metabolism
  • Hepatic glucuronidation → inactive glucuronide
  • Immature in neonates → accumulation → gray baby syndrome
  • Reduce dose in hepatic impairment; monitor serum levels

Toxicity

Two Bone Marrow Toxicities

Reversible Suppression
  • Dose-dependent; plasma levels >25 mcg/mL
  • All cell lines; fully reversible on stopping
  • Prevented by monitoring
Aplastic Anemia (Idiosyncratic)
  • Unrelated to dose or plasma level
  • ~1 in 30,000 courses; onset weeks–months after exposure
  • Irreversible; mortality >50% without transplant
  • Cannot be predicted or prevented by monitoring

Drug Interactions & Clinical Role

CYP Inhibition & Indications

Drug Interactions
  • Inhibits CYP2C19 (major), CYP2C9, CYP3A4
  • ↑ phenytoin levels → toxicity
  • ↑ warfarin effect → bleeding risk
Modern Systemic Use
  • Meningitis: severe beta-lactam allergy
  • Brain abscess (CNS penetration + anaerobic coverage)
  • Typhoid: multidrug-resistant S. typhi
  • Topical: bacterial conjunctivitis (safe)

Oxazolidinones: Linezolid and Tedizolid

Mechanism & Spectrum

Oxazolidinones

Mechanism — Unique
  • Block 70S initiation complex assembly (pre-elongation)
  • Bind 23S rRNA on 50S; prevent 30S + 50S joining
  • No cross-resistance with macrolides, lincosamides, or chloramphenicol
Spectrum (Gram-positive only)
  • MRSA, vancomycin-resistant S. aureus, VRE
  • Penicillin-resistant S. pneumoniae, streptococci
  • Linezolid: also active vs. Mycobacterium tuberculosis
  • No Gram-negative activity

Pharmacokinetics

Linezolid vs. Tedizolid

Linezolid
  • ~100% oral bioavailability — IV = oral, complete interchangeability
  • Non-CYP metabolism → no CYP-based drug interactions
  • No dose adjustment for renal impairment
  • Dosing: twice daily
Tedizolid (Prodrug)
  • Converted by plasma phosphatases to active form
  • Half-life ~12 h → once-daily dosing
  • 4–8× more potent than linezolid (lower daily dose)
  • Less myelosuppression than linezolid

Linezolid Adverse Effects and Resistance

Adverse Effects

Mitochondrial Inhibition + MAO Inhibition

Myelosuppression (reversible)
  • Thrombocytopenia most common (appears after ~2 weeks)
  • Fully reversible on stopping; monitor CBC weekly if >2 weeks
  • Tedizolid: significantly less myelosuppression
Serotonin Syndrome
  • Linezolid = reversible nonselective MAO inhibitor
  • Avoid with SSRIs, SNRIs, TCAs, meperidine, tramadol
  • Triad: mental status changes + autonomic instability + neuromuscular signs
Neuropathy (prolonged courses)
  • Peripheral: stocking-glove paresthesias — may be irreversible
  • Optic: visual loss, color vision loss — may be permanent
  • Monitor monthly if course >4 weeks

Clinical Niche & Resistance

Indications and Resistance

Use Linezolid For
  • MRSA pneumonia (superior to vancomycin — ZEPHYR trial)
  • MRSA skin/soft tissue infections
  • VRE infections
  • MRSA osteomyelitis (oral step-down advantage)
Do NOT Use For
  • MRSA bacteremia or endocarditis — bacteriostatic; use vancomycin or daptomycin
Resistance
  • 23S rRNA point mutations (reduced drug binding)
  • cfr gene: rRNA methyltransferase → cross-resistance with chloramphenicol
  • Tedizolid active vs. single-mutation isolates; inactive vs. cfr-positive

Key Distinction

Both chloramphenicol and linezolid inhibit mitochondrial protein synthesis, producing reversible bone marrow suppression. Chloramphenicol also causes aplastic anemia — an idiosyncratic, unpredictable, dose-independent reaction that linezolid does not. Linezolid also inhibits MAO, creating serotonin syndrome risk that chloramphenicol does not share.