Multiantibiotic resistance caused by active drug extrusion in Pseudomonas aeruginosa and other gram-negative bacteria

Microbiologia. 1997 Sep;13(3):273-84.


All living organisms have been exposed to noxious compounds throughout their long evolutionary history and those surviving have evolved to fabricate devices that detoxicate and extrude these life threatening substances. It is likely, therefore, that all viable organisms, from bacteria to mammals, are equipped with active extrusion machinery. When bacteria are attacked by antibiotics, they use these tactics to combat the drugs and to develop resistance. Drugs extrusion machinery in Gram-negative bacteria is complex, consisting of the inner membrane transporter which acts as an energy-dependent extrusion pump; a binding protein which presumably connect both membranes; and the outer membrane exit channel. The extrusion pump assemblies are often encoded by chromosomal genes and might be expressed by mutation(s) or induced in the presence of drug(s).

Publication types

  • Review

MeSH terms

  • Anti-Bacterial Agents / metabolism*
  • Anti-Bacterial Agents / pharmacology
  • Bacterial Proteins / genetics
  • Bacterial Proteins / physiology
  • Biological Transport, Active
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology
  • Drug Resistance, Microbial / physiology*
  • Drug Resistance, Multiple / physiology*
  • Genes, Bacterial
  • Gram-Negative Bacteria / drug effects*
  • Gram-Negative Bacteria / physiology
  • Membrane Proteins / physiology
  • Models, Biological
  • Operon
  • Pseudomonas aeruginosa / drug effects*
  • Pseudomonas aeruginosa / genetics
  • Pseudomonas aeruginosa / physiology
  • Repressor Proteins / genetics
  • Repressor Proteins / physiology
  • Transcription Factors*


  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Carrier Proteins
  • DNA-Binding Proteins
  • Membrane Proteins
  • NfxB protein, Pseudomonas aeruginosa
  • Repressor Proteins
  • Transcription Factors