Carbapenem-resistance mechanisms are a challenge in the treatment of
Pseudomonas aeruginosa infections. We investigated changes in
P. aeruginosa carbapenem-resistance determinants over a time
period of eight years after the emergence of São Paulo metallo-β-lactamase in a
university hospital in Rio de Janeiro, Brazil. Patients admitted to the intensive
care unit (ICU) were screened for P. aeruginosa colonisation and
followed for the occurrence of infections from April 2007 to April 2008. The ICU
environment was also sampled. Isolates were typed using random amplified polymorphic
DNA, pulsed-field gel electrophoresis and multilocus sequence typing. Antimicrobial
susceptibility was determined by disk diffusion and E-test, production of
carbapenemases by a modified-CarbaNP test and presence of carbapenemase-encoding
genes by polymerase chain reaction. Non-carbapenemase resistance mechanisms studied
included efflux and AmpC overexpression by PAβN and cloxacillin susceptibility
enhancement, respectively, as well as oprD mutations. From 472
P. aeruginosa clinical isolates (93 patients) and 17 isolates
from the ICU environment, high genotypic diversity and several international clones
were observed; one environment isolate belonged to the blaSPM-1
P. aeruginosa epidemic genotype. Among isolates from infections,
10 (29%) were carbapenem resistant: none produced carbapenemases, three exhibited all
non-carbapenemase mechanisms studied, six presented a combination of two mechanisms,
and one exclusively displayed oprD mutations. Carbapenem-resistant
P. aeruginosa displayed a polyclonal profile after the SPM-1
epidemic genotype declined. This phenomenon is connected with
blaSPM-1 P. aeruginosa replaced by other
carbapenem-resistant pathogens.
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