Mechanism and Evolution of Antibiotic Resistance

Antibiotics target essential cellular functions but bacteria can become resistant by acquiring either exogenous resistance genes or chromosomal mutations. Resistance mutations typically occur in genes encoding essential functions; these mutations are therefore generally detrimental in the absence of drugs. However, bacteria can reduce this handicap by acquiring additional mutations, known as compensatory mutations. Genetic interactions (epistasis) either with the background or between resistances (in multiresistant bacteria) dramatically affect the fitness cost of antibiotic resistance and its compensation, therefore shaping dissemination of antibiotic resistance mutations.

  • Enzymatic degradation of antibacterial drugs
  • Alteration of bacterial proteins
  • Changes in membrane permeability to antibiotics
  • Exogenous resistance genes
  • Chromosomal mutations
  • Epistasis

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