When carbapenem-hydrolyzing beta-lactamase Kpc meets Escherichia coli ST131 in France.

Service de Bactériologie-Virologie, Hôpital de Bicêtre, Assistance Publique/Hôpitaux de Paris, Faculté de Médecine Paris-Sud, Université Paris XI, 94275 Le Kremlin-Bicêtre, France.
Antimicrobial Agents and Chemotherapy (Impact Factor: 4.57). 07/2011; 55(10):4933-4. DOI: 10.1128/AAC.00719-11
Source: PubMed

ABSTRACT Carbapenem-resistance in E. coli isolates even though rare, can be attributed to outer-membrane protein deficiency coupled with plasmid-mediated ESBLs or class C ß-lactamases (2, 10, 11) or to carbapenemases.…

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    ABSTRACT: Twenty-two KPC-2-producing Escherichia coli isolates were obtained from three hospitals in Hangzhou, China, from 2007 to 2011. One isolate, with OmpC porin deficiency, exhibited high-level carbapenem resistance. Pulsed-field gel electrophoresis showed that few isolates were indistinguishable or closely related. Multilocus sequence typing indicated that sequence type 131 (ST131) was the predominant type (9 isolates, 40.9%), followed by ST648 (5 isolates), ST405 (2 isolates), ST38 (2 isolates), and 4 single STs, ST69, ST2003, ST2179, and ST744. Phylogenetic analysis indicated that 9 group B2 isolates belonged to ST131, and 5 of 11 group D isolates belonged to ST648. Only one group B1 isolate and one group A isolate were identified. A representative plasmid (pE1) was partially sequenced, and a 7,788-bp DNA fragment encoding Tn3 transposase, Tn3 resolvase, ISKpn8 transposase, KPC-2, and ISKpn6-like transposase was obtained. The blaKPC-2-surrounding sequence was amplified by a series of primers. The PCR results showed that 13 isolates were consistent with the genetic environment in pE1. It is the first report of rapid emergence of KPC-2-producing E. coli ST131 in China. The blaKPC-2 gene of most isolates was located on a similar genetic structure.
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    ABSTRACT: Pathogenic Escherichia coli cause a wide variety of intestinal and extraintestinal infections. The widespread geographic clonal dissemination of intestinal pathogenic E. coli, such as E. coli O157:H7, is well recognized and its mode of spread is most often attributed to contaminated food products. On the other hand, the clonal dissemination of extraintestinal pathogenic E. coli (ExPEC) strains is also recognized, but the mechanism of their spread is not well explained. Here, we describe major pandemic clonal lineages of ExPEC based on multilocus sequence typing (MLST) and discuss possible reasons for their global dissemination. These lineages include ST131, ST393, ST69, ST95, and ST73, which are all associated with community-onset as well as healthcare-associated infections, in particular, urinary tract infections (UTI) and blood stream infections (BSI). As with many other types of drug-resistant Gram negative and Gram positive bacterial infections, drug-resistant ExPEC infections are recognized to be caused by a limited set of clonal lineages. However, reported observations made about these major pandemic lineages suggest that the resistance phenotype is not necessarily the determinant of their clonal dissemination. Epidemiologic factors as well as their intrinsic biologic “fitness” are likely to contribute. An important public health and clinical concern is that pandemicity itself may be a determinant of progressive drug resistance acquisition by clonal lineages. New research is urgently needed to better understand the epidemiologic and biologic causes of ExPEC pandemicity.This article is protected by copyright. All rights reserved.
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    ABSTRACT: Escherichia coli ST131 has emerged as a global epidemic, multidrug-resistant clone of E. coli causing extra-intestinal infections. It is now highly prevalent among fluoroquinolone-resistant and CTX-M ESBL-producing E. coli isolates worldwide. Humans are likely the primary reservoir of ST131. Factors associated with its acquisition include residence in long-term care facilities and recent receipt of antimicrobial agents. E. coli ST131 causes a wide array of infections ranging from cystitis to life-threatening sepsis. Fluoroquinolones and trimethoprim-sulfamethoxazole are no longer adequate options for empiric therapy when E. coli ST131 is suspected from risk factors and local epidemiology. Expanded-spectrum cephalosporins, piperacillin-tazobactam and carbapenems are options to treat serious non-ESBL-producing E. coli ST131 infections, while carbapenems are indicated for ESBL-producing infections. There is a growing interest in reevaluating oral agents including fosfomycin and pivmecillinam for less serious infections such as uncomplicated cystitis.
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