VIM-2-producing multidrug-resistant Pseudomonas aeruginosa ST175 clone, Spain.

Members of the bacterial genus Pseudomonas, especially P. aeruginosa, are among the major nosocomial pathogens because of their ubiquitous nature and ability to colonize and survive in hospital reservoirs and because of their role in causing infections in immunocompromised and critically ill patients (1). P. aeruginosa shows a high level of intrinsic resistance to antimicrobial drugs and an ability to become even more drug resistant. These characteristics are caused by selective pressure of mutations in chromosomal genes that lead to ampC hyperexpression, repression or inactivation of oprD, and overexpression of efflux pumps (2). In addition, P. aeruginosa is able to acquire other drug-resistance determinants by horizontal transfer of mobile genetic elements coding for class B carbapenemases (also called metallo-β-lactamases [MBLs]), which hydrolyze all β-lactams except aztreonam (3). Because they can be disseminated horizontally through transfer of resistance determinants, MBLs have become a serious concern in hospitals worldwide over the past decade. Such acquired MBLs include the IMP and VIM types SPM-1, GIM-1, SIM-1, AIM-1, KHM-1, NDM-1, and SID-1 (4,5). MBL genes are normally encoded in class 1 integrons along with other resistance determinants, such as the aminoglycoside-modifying enzymes. The integrons are frequently located in plasmids or transposons, the dissemination of which contributes to the global spread of this resistance mechanism (6,7). The versatility and ability of P. aeruginosa to combine different resistance mechanisms has led to emergence of strains that are resistant to multiple antimicrobial drugs, which severely limits therapeutic options for treating infections (8,9). Interim definitions defining multidrug-resistant (MDR), extensively drug-resistant (XDR), and pandrug-resistant bacteria, including P. aeruginosa, have been recently reported (10). Although the prevalence of P. aeruginosa strains producing carbapenemases in Spain was considered low (0.4% of carbapenem-resistant isolates) (11) compared with prevalence in other countries in Europe, such as Italy (12.6% of carbapenem-resistant isolates) (12), detection of these isolates is no longer sporadic (13,14). Recent evidence from multicenter studies indicates an ≈10-fold increase in prevalence of these isolates in the past 5 years (15). During 2007 and 2008, a polyclonal outbreak of VIM-2–producing P. aeruginosa was detected in a hospital in Spain. At the same time, another outbreak in the hematology department of a hospital in Spain was caused by a P. aeruginosa ST235 clone, which produced GES-1 and GES-5, 2 extended-spectrum β-lactamases (16). We have observed a sharp increase in infections with drug-resistant P. aeruginosa that produces carbapenemase. Thus, we conducted a study to determine the clinical and molecular epidemiologic characteristics of drug-resistant P. aeruginosa isolates detected at a major hospital during 2007–2010.