Laura J Rojas1,2, George M Weinstock3, Elsa De La Cadena4,5, Lorena Diaz5,6, Rafael Rios5, Blake M Hanson3, Joseph S Brown3, Purva Vats3, Daniel S Phillips3, Hoan Nguyen3, Kristine M Hujer7,2, Adriana Correa4, Mark D Adams3, Federico Perez7,8,2, Erica Sodergren3, Apurva Narechania9, Paul J Planet10,11,12, Maria V Villegas4,5, Robert A Bonomo7,1,13,14,15,8,2,16, Cesar A Arias5,6,17,9. 1. Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, Ohio. 2. Education and Clinical Center, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Ohio. 3. The Jackson Laboratory for Genomic Medicine, Farmington, Connecticut. 4. Bacterial Resistance and Hospital Epidemiology Unit, International Center for Medical Research and Training (CIDEIM), Cali, Colombia. 5. Molecular Genetics and Antimicrobial Resistance Unit - International Center for Microbial Genomics Universidad El Bosque, Bogotá, Colombia. 6. Center for Antimicrobial Resistance and Microbial Genomics, Division of Infectious Diseases, University of Texas McGovern Medical School at Houston Houston, Texas. 7. Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio. 8. Research Service, Medical Service, and Geriatric Research. 9. Center for Infectious Diseases, UTHealth School of Public Health, Houston, Texas. 10. Sackler Institute for Comparative Genomics, American Museum of Natural History, New York, New York. 11. Perelman School of Medicine, University of Pennsylvania, Philadelphia. 12. Pediatric Infectious Disease Division, Children's Hospital of Philadelphia, Pennsylvania. 13. Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, Ohio. 14. Department of Pharmacology, Case Western Reserve University School of Medicine, Cleveland, Ohio. 15. Department of Proteomics and Bioinformatics, Case Western Reserve University School of Medicine, Cleveland, Ohio. 16. Case Western Reserve University -Cleveland VAMC Center for Antimicrobial Resistance and Epidemiology, Ohio. 17. Department of Microbiology and Molecular Genetics, University of Texas Medical School at Houston Houston, Texas.
Abstract
Background: Carbapenem resistance is a critical healthcare challenge worldwide. Particularly concerning is the widespread dissemination of Klebsiella pneumoniae carbapenemase (KPC). Klebsiella pneumoniae harboring blaKPC (KPC-Kpn) is endemic in many areas including the United States, where the epidemic was primarily mediated by the clonal dissemination of Kpn ST258. We postulated that the spread of blaKPC in other regions occurs by different and more complex mechanisms. To test this, we investigated the evolution and dynamics of spread of KPC-Kpn in Colombia, where KPC became rapidly endemic after emerging in 2005. Methods: We sequenced the genomes of 133 clinical isolates recovered from 24 tertiary care hospitals located in 10 cities throughout Colombia, between 2002 (before the emergence of KPC-Kpn) and 2014. Phylogenetic reconstructions and evolutionary mapping were performed to determine temporal and genetic associations between the isolates. Results: Our results indicate that the start of the epidemic was driven by horizontal dissemination of mobile genetic elements carrying blaKPC-2, followed by the introduction and subsequent spread of clonal group 258 (CG258) isolates containing blaKPC-3. Conclusions: The combination of 2 evolutionary mechanisms of KPC-Kpn within a challenged health system of a developing country created the "perfect storm" for sustained endemicity of these multidrug-resistant organisms in Colombia.
Background: Carbapenem resistance is a critical healthcare challenge worldwide. Particularly concerning is the widespread dissemination of Klebsiella pneumoniae carbapenemase (KPC). Klebsiella pneumoniae harboring blaKPC (KPC-Kpn) is endemic in many areas including the United States, where the epidemic was primarily mediated by the clonal dissemination of Kpn ST258. We postulated that the spread of blaKPC in other regions occurs by different and more complex mechanisms. To test this, we investigated the evolution and dynamics of spread of KPC-Kpn in Colombia, where KPC became rapidly endemic after emerging in 2005. Methods: We sequenced the genomes of 133 clinical isolates recovered from 24 tertiary care hospitals located in 10 cities throughout Colombia, between 2002 (before the emergence of KPC-Kpn) and 2014. Phylogenetic reconstructions and evolutionary mapping were performed to determine temporal and genetic associations between the isolates. Results: Our results indicate that the start of the epidemic was driven by horizontal dissemination of mobile genetic elements carrying blaKPC-2, followed by the introduction and subsequent spread of clonal group 258 (CG258) isolates containing blaKPC-3. Conclusions: The combination of 2 evolutionary mechanisms of KPC-Kpn within a challenged health system of a developing country created the "perfect storm" for sustained endemicity of these multidrug-resistant organisms in Colombia.
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