Multiple mechanisms of antimicrobial resistance in Pseudomonas aeruginosa: our worst nightmare?
Pseudomonas aeruginosa carries multiresistance plasmids less often than does Klebsiella pneumoniae, develops mutational resistance to cephalosporins less readily than Enterobacter species, and has less inherent resistance than Stenotrophomonas maltophilia. What nevertheless makes P. aeruginosa uniquely problematic is a combination of the following: the species' inherent resistance to many drug classes; its ability to acquire resistance, via mutations, to all relevant treatments; its high and increasing rates of resistance locally; and its frequent role in serious infections. A few isolates of P. aeruginosa are resistant to all reliable antibiotics, and this problem seems likely to grow with the emergence of integrins that carry gene cassettes encoding both carbapenemases and amikacin acetyltransferases.
Livermore
David M
DM
Antibiotic Resistance Monitoring and Reference Laboratory, Central Public Health Laboratory, Colindale, London, United Kingdom. DLivermore@phls.nhs.uk
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002463:Cell Membrane Permeability / Q000235:genetics; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D018432:Drug Resistance, Multiple / Q000235:genetics; D005787:Gene Frequency; D006801:Humans; D016023:Integrins / Q000235:genetics; D008826:Microbial Sensitivity Tests; D005810:Multigene Family; D009154:Mutation; D011550:Pseudomonas aeruginosa / Q000187:drug effects / Q000235:genetics* / Q000502:physiology
D000900:Anti-Bacterial Agents; D016023:Integrins