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An analysis was made about the evolution of resistance to 3rd generation cephalosporins, imipenem, and other antibiotics in invasive isolates of Klebsiella pneumoniae (K. pneumoniae) according to the Spanish EARS-Net database (2010-2014).Forty-two hospitals from 16 Autonomous Communities with an approximate population coverage of 33% participated.A total 7,140 pneumoniae corresponding to the same number of patients were studied. Overall resistance percentages (I+R) were: cefotaxime 15.8%, ceftazidime 13.7%, imipenem 1.7%, ciprofloxacin 20.1%, tobramycin 14.1%, gentamicin 10.4%, and amikacin 1.9%. Resistance to 3rd generation cephalosporins increased from 9.8% (2010) to 19% (2014); to ciprofloxacin from 15.4% (2010) to 19.6% (2014); to gentamicin from 6.2% (2010) to 10.3% (2014) and to tobramycin from 7.1% (2010) to 14.2% (2014) (p.001 in all cases). Combined resistance to 3rd generation cephalosporins, ciprofloxacin, and aminoglycosides increased from 3.3% (2010) to 9.7% (2014) (p.001). Resistance to imipenem also increased from 0.27% (2010) to 3.46% (2014) (p.001). A total of 121 isolates were resistant to imipenem, of which 104 (86%) produced carbapenemases: 74 OXA-48, 14 VIM, 9 KPC (6 KPC-2 and 3 KPC-3), 6 IMP, and 1 GES.Over the 5 year period (2010-2014), resistance to 3rd generation cephalosporins in invasive K. pneumoniae in Spain has doubled. The combined resistance to 3rd generation cephalosporins, ciprofloxacin, and aminoglycosides has tripled, and imipenem resistance has increased almost 13 times, mostly due to the spread of carbapenemase-producing isolates.

Resumen Introduccion Se analizo la evolucion de la resistencia a cefalosporinas de 3.a generacion, imipenem y otros antibioticos en aislamientos invasivos de Klebsiella pneumoniae (K. pneumoniae) segun resultados de EARS-Net entre 2010 y 2014 en Espana. Metodos Participaron 42 hospitales de 16 Comunidades Autonomas, con una cobertura poblacional aproximada del 33%. Resultados Se aislaron 7.140 cepas de K. pneumoniae de un mismo numero de pacientes. Las resistencias globales (I + R) fueron: cefotaxima 15,8%, ceftazidima 13,7%, imipenem 1,7%, ciprofloxacina 20,1%, tobramicina 14,1%, gentamicina 10,4% y amikacina 1,9%. La resistencia a cefalosporinas de 3.a generacion aumento desde el 9,8% (2010) al 19% (2014); la de ciprofloxacina desde el 15,4% (2010) al 19,6% (2014); la de gentamicina desde el 6,2% (2010) al 10,3% (2014) y la de tobramicina desde el 7,1% (2010) al 14,2% (2014) (p Conclusiones En un periodo de 5 anos (2010-2014), la resistencia a cefalosporinas de 3.a generacion en K. pneumoniae invasivas en Espana se ha duplicado; la resistencia combinada a cefalosporinas de 3.a generacion, ciprofloxacina y aminoglucosidos se ha triplicado; la resistencia a imipenem ha aumentado casi 13 veces, principalmente por la diseminacion de aislados productores de carbapenemasas.

Objectives We analysed the microbiological traits and population structure of KPC-producing Enterobacteriaceae isolates collected in Spain between 2012 and 2014. We also performed a comparative WGS analysis of the three major KPC-producing Klebsiella pneumoniae clones detected. Methods Carbapenemase and ESBL genes were sequenced. The Institut Pasteur MLST scheme was used. WGS data were used to construct phylogenetic trees, to identify the determinants of resistance and to de novo assemble the genome of one representative isolate of each of the three major K. pneumoniae clones. Results Of the 2443 carbapenemase-producing Enterobacteriaceae isolates identified during the study period, 111 (4.5%) produced KPC. Of these, 81 (73.0%) were K. pneumoniae and 13 (11.7%) were Enterobacter cloacae. Three major epidemic clones of K. pneumoniae were identified: ST11/KPC-2, ST101/KPC-2 and ST512/KPC-3. ST11/KPC-2 differed from ST101/KPC-2 and ST512/KPC-3 by 27 819 and 6924 SNPs, respectively. ST101/KPC-2 differed from ST512/KPC-3 by 28 345 SNPs. Nine acquired resistance genes were found in ST11/KPC-2, 11 in ST512/KPC-3 and 13 in ST101/KPC-2. ST101/KPC-2 had the highest number of virulence genes (20). An 11 bp deletion at the end of the mgrB sequence was the cause of colistin resistance in ST512/KPC-3. Conclusions KPC-producing Enterobacteriaceae are increasing in Spain. Most KPC-producing K. pneumoniae isolates belonged to only five clones: ST11 and ST512 caused interregional spread, ST101 caused regional spread and ST1961 and ST678 produced independent hospital outbreaks. ST101/KPC-2 had the highest number of resistance and virulence genes. ST101/KPC-2 and ST512/KPC-3 were recently implicated in the spread of KPC in Italy.

OBJECTIVES The objective of this study was to analyse the microbiological traits and the population structure of carbapenemase-producing (CP) Escherichia coli isolates collected in Spain between 2012 and 2014. METHODS Two-hundred-and-thirty-nine E. coli isolates non-susceptible to carbapenems were studied. The carbapenemase genes and the phylogenetic groups were characterized using PCR. MLST was carried out using the typing schemes of the University of Warwick and the Institut Pasteur. The diversity of the population structure was estimated by calculating a simple diversity index (SDI). RESULTS One-hundred-and-twenty-one isolates (50.6%) produced carbapenemases, of which 87 (71.9%) were OXA-48, 27 (22.3%) were VIM-1, 4 (3.3%) were KPC-2, 2 (1.7%) were NDM and 1 (0.8%) was IMP-22; 4 isolates were collected in 2012, 40 in 2013 and 77 in 2014. Ertapenem was more sensitive than imipenem or meropenem for screening for OXA-48-producing E. coli. Using the Warwick typing scheme, 59 different STs were identified, the most prevalent being ST131 (16.5%). The population diversity was higher among VIM-1-producing isolates (SDI = 81.5%) than among OXA-48-producing isolates (SDI = 44.8%). The Pasteur scheme had a higher discrimination capability (SDI = 55.4%) than the Warwick scheme (SDI = 48.8%). CONCLUSIONS A progressive increase in the prevalence of CP E. coli was observed, mainly due to the dissemination of OXA-48 producers. The most sensitive method for detecting decreased susceptibility of CP E. coli to carbapenems was disc diffusion with ertapenem using the EUCAST screening cut-offs. The spread of CP E. coli was due to a polyclonal population. The Pasteur scheme showed the highest discrimination power. Surveillance is crucial for the early detection of CP E. coli.

Resumen Introduccion Descripcion clinica y epidemiologica de un brote en una unidad de cuidados intensivos (UCI) causado por Enterobacter cloacae complex multirresistente productor de una β-lactamasa de espectro extendido (BLEE) tipo CTX-M-9. Metodos Se realizo un estudio retrospectivo de las caracteristicas clinicas y epidemiologicas del brote causado por E. cloacae complex. La identificacion y estudio de sensibilidad de las cepas fueron realizados mediante el sistema semiautomatico BD Phoenix™, y la caracterizacion de la BLEE, por PCR y secuenciacion. La tipificacion molecular se realizo mediante electroforesis en gel de campo pulsado (PFGE). Resultados Durante febrero de 2014, 6 pacientes (50% mujeres; media de edad: 61,5 anos; rango de edad: 44-76 anos) ingresados en la UCI del Complejo Hospitalario de Pontevedra (CHOP) presentaron aislamientos de E. cloacae complex resistente a cefalosporinas de amplio espectro. Tres pacientes desarrollaron infeccion; uno presento bacteriemia primaria y shock septico, y 2 neumonia asociada a ventilacion mecanica. En los 3 casos restantes los aislamientos de E. cloacae complex se consideraron colonizacion. El analisis fenotipico y genotipico revelo que todos los aislados presentaban el mismo perfil por PFGE y que portaban la misma BLEE del tipo CTX-M-9. El brote se controlo mediante la mejora de las medidas universales y el aislamiento de contacto de los pacientes infectados y/o colonizados. Conclusion Se describe desde un punto de vista clinico y epidemiologico un brote de E. cloacae complex portador de CTX-M-9 en una UCI.

We report the epidemiological impact of carbapenemase-producing Enterobacteriaceae (CPE) in Spain in 2012. Of the 237 carbapenemases detected, 163 were from the OXA-48 group, 60 were from VIM-1, 8 were from KPC-2, 5 were from IMP, and 1 was from NDM-1. Interhospital spread of carbapenemase-producing Klebsiella pneumoniae was due to a limited number of multilocus sequence types (MLST) and carbapenemase types, including ST15-VIM-1, ST11-OXA-48, ST405-OXA-48, ST101-KPC-2, and ST11-VIM-1. The number of CPE cases in Spain has increased sharply in recent years, due mainly to the emergence of OXA-48. This study was supported by the Antibiotic Resistance Surveillance Program of the Spanish Centro Nacional de Microbiología of the Instituto de Salud Carlos III. Verónica Bautista was supported by the Ministerio de Economía y Competitividad, Instituto de Salud Carlos III, cofinanced by the European Development Regional Fund “A way to achieve Europe” ERDF, Spanish Network for the Research in Infectious Diseases (REIPI RD12/0015). Sí

Summary Background Healthcare-associated infections caused by Klebsiella pneumoniae isolates are increasing and few effective antibiotics are currently available to treat patients. Aim To assess the epidemiology, molecular basis, clinical features, and outcomes in the acquisition and dissemination of OXA-48-producing K. pneumoniae (OXA48KP) in a tertiary Spanish hospital between October 2013 and December 2015. Methods Clinical, demographic, and microbiological data of patients with OXA48KP in clinical samples were collected from medical records. Carbapenemase genes were detected by polymerase chain reaction. Genetic relationships were determined by pulsed-field gel electrophoresis and multi-locus sequence typing. Findings In all, 116 episodes of OXA48KP in clinical samples were identified. The most frequent types of infection were urinary tract ( N = 43, 42%), secondary bloodstream ( N = 18, 17%), and surgical site infection ( N = 17, 17%). More than one-quarter (28%) of infected patients died in hospital. Among infected patients ( N = 90, 78%), infections were mainly classified as hospital-acquired ( N = 70, 88%). A high number of OXA48KP isolates showed multidrug resistance, with highest susceptibility to colistin (86%), gentamicin (69%) and amikacin (59%). Most (87%) isolates were included in a main cluster. Seven ( N = 8, 88%) isolates showed an identical allelic profile, associated with ST15. Only the isolate from cluster P8 was associated with ST29. The results confirm high dissemination of OXA48KP in our hospital due to the main clone ST15. OXA48KP infection was associated with a high mortality and was mainly hospital-acquired. Conclusion This study highlights the importance of active surveillance programmes, especially those focusing on hospital readmissions in order to control the spread of carbapenemase-producing Enterobacteriaceae.

Little information is available about pediatric infections caused by extended-spectrum-β-lactamase (ESBL)-producing Escherichia coli . We characterized an outbreak caused by a CTX-M-14-producing E. coli isolate in a neonatal intensive care unit (NICU) and studied other infections caused by ESBL-producing E. coli in non-NICU pediatric units. All children ≤4 years old who were infected or colonized by ESBL-producing E. coli isolates between January 2009 and September 2010 were included. Molecular epidemiology was studied by phylogroup analysis, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing. Antibiotic resistance genes were analyzed by PCR and sequencing. Plasmids were studied by PFGE with S1 nuclease digestion and by incompatibility group analysis using a PCR-based replicon-typing scheme. Of the ESBL-producing E. coli isolates colonizing or infecting the 30 newborns, identical PFGE results were observed for 21 (70%) isolates, which were classified as CTX-M-14-producing E. coli of ST23 phylogroup A. bla CTX-M-14a was linked to IS Ecp1 and was carried on an ∼80-bp IncK plasmid. A smaller ongoing outbreak due to SHV-12-producing ST131 E. coli was also identified in the same NICU. Fifteen additional infections with ESBL-producing E. coli were identified in non-NICU pediatric units, but none was caused by the CTX-M-14-producing E. coli epidemic clone. Overall, CTX-M-14 (71.1%), CTX-M-15 (13.3%), and SHV-12 (13.3%) were the most important ESBLs causing pediatric infections in this study. Infections of newborns with CTX-M-14-producing E. coli were caused by both clonal and nonclonal isolates.

Clinical and epidemiological description of an outbreak in an intensive care unit (ICU) caused by a strain of multidrug-resistant Enterobacter cloacae complex carrying a CTX-M-9-type extended-spectrum β-lactamase (ESBL).A retrospective study of the clinical and epidemiological features of the outbreak caused by E.cloacae complex was performed. Identifying and studying the sensitivity of the strains were performed using the semi-automated system BD Phoenix™, and the characterisation of ESBL using PCR and sequencing. Molecular typing was performed by pulsed-field gel electrophoresis (PFGE).During February 2014, 6 patients (50% women; mean age: 61.5 years; age range: 44-76 years) admitted to the ICU of the Hospital of Pontevedra (CHOP) presented resistant E.cloacae complex isolates to extended-spectrum cephalosporins. Three patients developed infection; one had primary bacteraemia and septic shock, and 2 with ventilator-associated pneumonia. In the remaining three cases E.cloacae complex isolates were considered as colonisation. Phenotypic and genotypic analysis revealed that all isolates had the same PFGE profile and carried the same CTX-M-9 ESBL. The outbreak was controlled by improving universal precautions and contact isolation of patients infected and/or colonized.The clinical and epidemiological features of an outbreak in an ICU caused by E.cloacae complex carrying CTX-M-9 are described.

Several isolates of four different carbapenemase-producing Enterobacteriaceae species were recovered from a patient hospitalized for 4 months in a teaching hospital in Madrid. These species comprised seven Klebsiella pneumoniae belonging to ST15, four Escherichia coli belonging to ST2531, two Serratia marcescens and one Citrobacter freundii. This patient was the index case of a small outbreak of four patients infected and/or colonized by carbapenemase-producing K. pneumoniae. Molecular results identified the blaOXA-48 gene in all Enterobacteriaceae isolates from the index case and in all isolates from the other three patients, suggesting intra- and interpatient dissemination. Our results highlight the great ability of OXA-48 carbapenemase to spread among different enterobacterial species by both clonal and nonclonal dissemination.

Newborns are rarely infected by extended-spectrum β-lactamase (ESBL)-producing members of the Enterobacteriaceae. In a neonatal intensive care unit, 14 newborns were infected or colonized by CTX-M-15-producing Enterobacter cloacae. All seven infected patients had underlying medical conditions, and five of them were treated successfully with meropenem, whilst one untreated patient died. Paediatric infections caused by multidrug-resistant ESBL-producing Enterobacter cloacae constitute a critical clinical and epidemiological issue.

We describe a clinical case of an abdominal abscess due to NDM-1-producing Klebsiella pneumoniae in a 35-year-old Spanish patient after hospitalization in India for perforated appendicitis and peritonitis. The strain belonged to the MLST type 231 and had multiple additional antibiotic resistance genes such as bla(CTX-M-15), armA methylase, aac(6')-Ib-cr, dfrA12, sul1 and qnrB and lack of porin genes ompK35 and ompK36. The patient was cured after abscess drainage.

We study the epidemiology, molecular basis, clinical risk factors, and outcome involved in the clonal dissemination of VIM-1-producing Klebsiella pneumoniae isolates in the hospital setting. All patients infected/colonized by carbapenem-nonsusceptible K. pneumoniae (CNSKP) in 2009 were included. Molecular epidemiology was studied by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). Antibiotic resistance genes were analyzed by PCR and sequencing. Plasmids were studied by PFGE with S1 nuclease digestion and for incompatibility group by a PCR-based replicon typing scheme. Risk factors associated with CNSKP colonization/infection were assessed by an observational case-control study. All 55 patients studied were infected ( n = 28) or colonized ( n = 27) by VIM-1-producing K. pneumoniae . All but one acquired isolates of a single clone (PFGE cluster 1 [C1], sequence type 15 [ST15]), while another clone (PFGE C2, ST340) was detected in four patients. C1 isolates also produced the new extended-spectrum β-lactamase SHV-134. bla VIM-1 was carried in a class 1 integron and an untypeable plasmid of ∼50 bp. The number of days that the patient received mechanical ventilation, the use of parenteral nutrition, previous treatment with linezolid, and treatment with extended-spectrum cephalosporins for more than 7 days were detected to be independent risk factors for CNSKP acquisition. The VIM-1-producing K. pneumoniae ST15 clone has a high capacity to spread among intensive care unit patients with severe underlying conditions. A high rate of associated mortality and great difficulty in controlling the spread of this clone, without permanent behavioral changes in the personnel, were observed.