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Comparative analysis of the complete genome of KPC-2-producing Klebsiella pneumoniae Kp13 reveals remarkable genome plasticity and a wide repertoire of virulence and resistance mechanisms

Pablo Ivan Pereira Ramos1, Renata Christina Picão2, Luiz Gonzaga Paula de Almeida1, Nicholas Costa B Lima1, Raquel Girardello4, Ana Carolina P Vivan5, Danilo E Xavier4, Fernando G Barcellos3, Marsileni Pelisson5, Eliana C Vespero5, Claudine Médigue6, Ana Tereza Ribeiro de Vasconcelos1*, Ana Cristina Gales4* and Marisa Fabiana Nicolás1*

Author Affiliations

1 Laboratório Nacional de Computação Científica, Petrópolis, Rio de Janeiro, Brazil

2 Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

3 Departamento de Biologia Geral, Universidade Estadual de Londrina, Paraná, Brazil

4 Disciplina de Infectologia, Universidade Federal de São Paulo, São Paulo, Brazil

5 Departamento de Patologia Clínica, Análises Clínicas e Toxicologia, Universidade Estadual de Londrina, Paraná, Brazil

6 Laboratoire d’Analyse Bio-informatique en Génomique et Métabolisme CNRS-UMR 8030, Commissariat à l’Energie Atomique (CEA), Institut de Génomique, Genoscope, Evry, France

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BMC Genomics 2014, 15:54  doi:10.1186/1471-2164-15-54

Published: 22 January 2014



Klebsiella pneumoniae is an important opportunistic pathogen associated with nosocomial and community-acquired infections. A wide repertoire of virulence and antimicrobial resistance genes is present in K. pneumoniae genomes, which can constitute extra challenges in the treatment of infections caused by some strains. K. pneumoniae Kp13 is a multidrug-resistant strain responsible for causing a large nosocomial outbreak in a teaching hospital located in Southern Brazil. Kp13 produces K. pneumoniae carbapenemase (KPC-2) but is unrelated to isolates belonging to ST 258 and ST 11, the main clusters associated with the worldwide dissemination of KPC-producing K. pneumoniae. In this report, we perform a genomic comparison between Kp13 and each of the following three K. pneumoniae genomes: MGH 78578, NTUH-K2044 and 342.


We have completely determined the genome of K. pneumoniae Kp13, which comprises one chromosome (5.3 Mbp) and six plasmids (0.43 Mbp). Several virulence and resistance determinants were identified in strain Kp13. Specifically, we detected genes coding for six beta-lactamases (SHV-12, OXA-9, TEM-1, CTX-M-2, SHV-110 and KPC-2), eight adhesin-related gene clusters, including regions coding for types 1 (fim) and 3 (mrk) fimbrial adhesins. The rmtG plasmidial 16S rRNA methyltransferase gene was also detected, as well as efflux pumps belonging to five different families. Mutations upstream the OmpK35 porin-encoding gene were evidenced, possibly affecting its expression. SNPs analysis relative to the compared strains revealed 141 mutations falling within CDSs related to drug resistance which could also influence the Kp13 lifestyle. Finally, the genetic apparatus for synthesis of the yersiniabactin siderophore was identified within a plasticity region. Chromosomal architectural analysis allowed for the detection of 13 regions of difference in Kp13 relative to the compared strains.


Our results indicate that the plasticity occurring at many hierarchical levels (from whole genomic segments to individual nucleotide bases) may play a role on the lifestyle of K. pneumoniae Kp13 and underlie the importance of whole-genome sequencing to study bacterial pathogens. The general chromosomal structure was somewhat conserved among the compared bacteria, and recombination events with consequent gain/loss of genomic segments appears to be driving the evolution of these strains.

Carbapenemase; Comparative genomics; Enterobacteriaceae; Gram-negative; Nosocomial pathogens; Pathogenic bacteria; SNPs