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Title: Genetic Diversity of KPC-Producing Escherichia coli, Klebsiella oxytoca, Serratia marcescens, and Citrobacter freundii Isolates from Argentina
Authors: De Belder, Denise 
Lucero, Celeste 
Rapoport, Melina J. 
Rosato, Adriana 
Faccone, Diego 
Petroni, Alejandro 
Pasteran, Fernando 
Albornoz, Ezequiel 
Corso, Alejandra 
Gomez, Sonia A. 
Keywords: Enterobacteriaceae;Resistencia a Medicamentos;Antiinfecciosos;Genética Microbiana
Issue Date: Sep-2018
Journal: Microbial drug resistance (Larchmont, N.Y.) 
The predominance of Klebsiella pneumoniae carbapenemase (KPC)-producing K. pneumoniae was caused by the spread of ST258 clone. In Latin America, KPC was reported in 2006, with the isolation of genetically unrelated K. pneumoniae in Colombia. Since then, the expansion of blaKPC in either K. pneumoniae ST258 or other Enterobacteriaceae (ETB) species was increasingly reported. In this study, we characterized 89 KPC-producing Escherichia coli, Klebsiella oxytoca, Serratia marcescens, and Citrobacter freundii that were received between 2010 and 2014. The results revealed that all isolates harbored blaKPC-2. Moreover, the dissemination of KPC by non-K. pneumoniae was mainly caused by the dispersion of ETB mostly genetically unrelated. E. coli is a community pathogen that may serve as the vehicle for the spread of KPC into community settings. Recently, KPC was detected in E. coli ST131, an international epidemic and multidrug-resistant clone. We found that 5/29 KPC-producing E. coli belonged to ST131 and four were blaCTXM-15 producers. The detection of blaKPC in ST131 should be closely monitored to prevent further dissemination. The blaKPC is generally located within Tn4401 transposon capable of mobilization through transposition found in plasmids in ST258. Less is known about the diversity of blaKPC genetic elements that disseminate horizontally among other species of ETB. We found that 16/29 E. coli and 2/18 S. marcescens harbored blaKPC-2 in Tn4401a. In 71 isolates, blaKPC-2 was located amidst diverse Tn3-derived genetic elements bearing non-Tn4401 structure. Further studies on the plasmids that encode blaKPC-2 in these clinical isolates may provide additional insight into its transmission mechanisms.
DOI: 10.1089/mdr.2017.0213
Appears in Collections:Publicaciones INEI

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