Memorias do Instituto Oswaldo Cruz ()

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

  • Luciana Camila Cacci,
  • Stephanie Gomes Chuster,
  • Natacha Martins,
  • Pâmella Rodrigues do Carmo,
  • Valéria Brígido de Carvalho Girão,
  • Simone Aranha Nouér,
  • Wania Vasconcelos de Freitas,
  • Juliana Arruda de Matos,
  • Ana Cristina de Gouveia Magalhães,
  • Adriana Lúcia Pires Ferreira,
  • Renata Cristina Picão,
  • Beatriz Meurer Moreira

DOI
https://doi.org/10.1590/0074-02760160116
Journal volume & issue
Vol. 111, no. 9
pp. 551 – 558

Abstract

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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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