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Multiple Mechanisms of Antimicrobial Resistance in Pseudomonas aeruginosa: Our Worst Nightmare?
Author(s) -
D. M. Livermore
Publication year - 2002
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1086/338782
Subject(s) - pseudomonas aeruginosa , microbiology and biotechnology , stenotrophomonas maltophilia , klebsiella pneumoniae , antibiotic resistance , amikacin , drug resistance , medicine , biology , antibiotics , gene , bacteria , genetics , escherichia coli
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.

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