Inhibition of protein synthesis: Antibiotics that inhibit protein synthesis work because of the fact that the bacterial ribosome and the eukaryotic ribosome differ structurally.  Consequently, there are some chemicals that can inhibit bacterial translation but not eukaryote translation.

It has to be said that the mitochondrial ribosome is very similar to the eubacteria ribosome. Thus antibiotics that inhibit protein synthesis are potentially toxic to humans (note: there are also other damaging effects).

Preventing protein synthesis does not necessarily kill the bacteria, it prevents growth. commonly these antibiotics are referred to as bacteriostatics.

Examples include: chloramphenicol,  erythromycin,  gentamycin, neomycin, streptomycin and tetracycline.

Mechanisms of Resistance

30S Ribosome site

Aminoglycosides: Irreversibly bind 30S ribosomal proteins (bactericidal)

Resistance occurs when there is:

  • a mutation of ribosomal binding site
  • decreased uptake
  • enzymatic modification of antibiotic

Tetracyclines: Block tRNA binding to 30S ribosome-mRNA complex (b-static)

Resistance occurs when there is:

  • decreased penetration
  • an active efflux of antibiotic out of cell
  • protection of 30S ribosome

50S Ribosome site

Chloramphenicol: Binds peptidyl transferase component of 50S ribosome, blocking peptide elongation (bacteriostatic)

Resistance occurs when there is:

  • a plasmid-encoded chloramphenicol transferase
  • an altered outer membrane (chromosomal mutations)

Macrolides: Reversibly bind 50S ribosome, block peptide elongation (b-static)

Resistance occurs when there is:

  • methylation of 23S ribosomal RNA subunit
  • enzymatic cleavage (erythromycin esterase)
  • an active efflux

Clindamycin: Binds 50S ribosome, blocks peptide elongation; Inhibits peptidyl transferase by interfering with binding of amino acid-acyl-tRNA complex

Resistance occurs when there is methylation of 23S ribosomal RNA subunit

Back to ‘mechanisms of antibiotic action and resistance mechanisms’