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Mechanisms of carbapenem resistance in endemic Pseudomonas aeruginosa isolates after an SPM-1 metallo-β-lactamase producing strain subsided in an intensive care unit of a teaching hospital in Brazil
Cacci, Luciana Camila; Chuster, Stephanie Gomes; Martins, Natacha; Carmo, Pâmella Rodrigues do; Girão, Valéria Brígido de Carvalho; Nouér, Simone Aranha; Freitas, Wania Vasconcelos de; Matos, Juliana Arruda de; Magalhães, Ana Cristina de Gouveia; Ferreira, Adriana Lúcia Pires; Picão, Renata Cristina & Moreira, Beatriz Meurer
Abstract
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.
Keywords
P. aeruginosa; SPM-1; intensive care unit; multilocus sequence typing
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