The global spread of carbapenem-resistant Klebsiella pneumoniae (CR-Kp) has been largely associated with sequence type 258 (ST258) and its related variants (clonal group 258 [CG258]). Here we describe the molecular epidemiology of CR-Kp from five tertiary care hospitals in Medellín, the second largest city in Colombia. All CR-Kp-infected patients admitted from June 2012 to June 2014 were included (n ‫؍‬ 193). Patients' clinical information was obtained from medical records. Carbapenemase KPC, VIM, IMP, NDM, and OXA-48 genes were detected by PCR. A CG258-tonB79 cluster-specific real-time PCR (targeting the multilocus sequence type [MLST] tonB79 allele), pulsed-field gel electrophoresis (PFGE), and MLST analysis were performed for typing. Remarkably, 62.2% (n ‫؍‬ 120) of isolates were from STs unrelated to CG258 (non-CG258). KPC-3 predominated in CG258 isolates (86.3%), while KPC-2 prevailed in non-CG258 isolates (75.5%) (P < 0.001). Multidrug resistance (MDR) frequency was significantly higher in CG258 strains (91.4% versus 56.1%; P < 0.001). ST512 (a single-locus variant of ST258) is the main ST in CG258 (96.3%), and isolates in this group showed closely related pulsotype and similar resistance gene profiles, suggesting the clonal spread of this strain. In contrast, high heterogeneity of STs (34/54), including eight novel STs, was found in non-CG258 isolates. Among non-CG258 isolates, ST14 (13.3%; n ‫؍‬ 16) and ST307 (14.2%; n ‫؍‬ 17) were the most frequent, and they showed distinct molecular and clinical characteristics in comparison to CG258 isolates. Our results suggest that the dissemination of carbapenem resistance in Medellín is due to heterogeneous K. pneumoniae clones, likely the result of horizontal transmission of KPC in different unrelated lineages, further highlighting the challenge in CR-Kp infection control and the need for a multifocal intervention. Carbapenem-resistant Klebsiella pneumoniae (CR-Kp) is currently one of the most important pathogens causing health care-associated infections, which typically occur in patients with prolonged hospital stay and previous antibiotic exposure (1-3). The most common mechanism of carbapenem resistance in K. pneumoniae is the production of carbapenemases, among which K. pneumoniae carbapenemase (KPC) is by far the most relevant and prevalent (4, 5).Since the initial identification of KPC in 1996 in North Carolina (6), KPC-producing strains have spread worldwide, causing major hospital outbreaks in North America, Europe, Asia, and Latin America (2, 7, 8) and leading to a reduction of therapeutic options that has resulted in high mortality and morbidity rates and increasing length of hospital stay and associated costs (2, 4, 5, 9). The global spread of KPC-producing Klebsiella pneumoniae (KPC-Kp) has been linked mostly to one genetic lineage, the multilocus sequence type 258 (ST258) and its related variants, i.e., clonal group 258 (CG258) (1, 10, 11). Members of CG258 include ST258, its single-locus variants (SLVs) (e.g., ST11, ST512, ST340, and ST437), and the...

g Carbapenem-resistant Pseudomonas aeruginosa has become a serious health threat worldwide due to the limited options available for its treatment. Understanding its epidemiology contributes to the control of antibiotic resistance. The aim of this study was to describe the clinical and molecular characteristics of infections caused by carbapenem-resistant P. aeruginosa isolates in five tertiary-care hospitals in Medellín, Colombia. A cross-sectional study was conducted in five tertiary-care hospitals from June 2012 to March 2014. All hospitalized patients infected by carbapenem-resistant P. aeruginosa were included. Clinical information was obtained from medical records. Molecular analyses included PCR for detection of bla VIM , bla IMP , bla NDM , bla OXA-48 , and bla KPC genes plus pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) for molecular typing. A total of 235 patients were enrolled: 91.1% of them were adults (n ‫؍‬ 214), 88.1% (n ‫؍‬ 207) had prior antibiotic use, and 14.9% (n ‫؍‬ 35) had urinary tract infections. The bla VIM-2 and bla KPC-2 genes were detected in 13.6% (n ‫؍‬ 32) and 11.5% (n ‫؍‬ 27), respectively, of all isolates. Two isolates harbored both genes simultaneously. For KPC-producing isolates, PFGE revealed closely related strains within each hospital, and sequence types (STs) ST362 and ST235 and two new STs were found by MLST. With PFGE, VIM-producing isolates appeared highly diverse, and MLST revealed ST111 in four hospitals and five new STs. These results show that KPC-producing P. aeruginosa is currently disseminating rapidly and occurring at a frequency similar to that of VIM-producing P. aeruginosa isolates (approximately 1:1 ratio) in Medellín, Colombia. Diverse genetic backgrounds among resistant strains suggest an excessive antibiotic pressure resulting in the selection of resistant strains.

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