Recent years have seen a concerning increase in the number of carbapenem-resistant Pseudomonas aeruginosa strains. P aeruginosa is one of the most dangerous factors causing nosocomial infections, and immunosuppressed patients constitute a special risk group. The purpose of our study was to conduct a molecular analysis of 22 clinical isolates of carbapenem-resistant P aeruginosa obtained between 2008 and 2011.Metallo-beta-lactamase (MBL) phenotype tests were conducted. A polymerase chain reaction technique was used to detect VIM, IMP, NDM, and GIM carbapenemase-encoding genes. The minimum inhibitory concentrations were determined for imipenem, meropenem, and doripenem. Molecular typing was conducted with the use of restriction fragment length polymorphism/pulsed-field gel electrophoresis (RFLP-PFGE).Of the 22 strains initially resistant to at least one carbapenem, we selected 18 that exhibited the MBL phenotype. Of those 18, we identified 15 strains expressing VIM carbapenemase-encoding genes. None of the other evaluated genes were detected. VIM-positive isolates exhibited higher levels of resistance than the other ones. The RFLP technique revealed 10 different PFGE types and 6 epidemic foci. Identical strains were isolated over the period of up to 3 years.The reason for resistance to carbapenems in the majority (68%) of P aeruginosa strains isolated at the evaluated hospital was the presence of VIM carbapenemase. It is safe to say that the VIM carbapenemase is responsible for a higher level of resistance than unidentified mechanisms. Carbapenem-resistant strains of P aeruginosa spread clonally within individual wards and are likely to be of hospital origin.