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[PMID]:28152085
[Au] Autor:Tang Y; Shen P; Liang W; Jin J; Jiang X
[Ad] Endereço:Department of Laboratory Medicine, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
[Ti] Título:A putative multi-replicon plasmid co-harboring beta-lactamase genes blaKPC-2, blaCTX-M-14 and blaTEM-1 and trimethoprim resistance gene dfrA25 from a Klebsiella pneumoniae sequence type (ST) 11 strain in China.
[So] Source:PLoS One;12(2):e0171339, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The global emergence of Klebsiella pneumoniae carbapenemase (KPC)-producing Klebsiella pneumoniae poses a major public health threat requiring immediate and aggressive action. Some older generation antibiotics, such as trimethoprim, serve as alternatives for treatment of infections. Here, we determined the complete nucleotide sequence of plasmid pHS091147, which co-harbored the carbapenemase (blaKPC-2) and trimethoprim resistance genes (dfrA25) from a Klebsiella pneumoniae sequence type (ST) 11 clone recovered in Shanghai, China. pHS091147 had three replication genes, several plasmid-stability genes and an intact type IV secretion system gene cluster. Besides blaKPC-2 and dfrA25, pHS091147 carried several other resistance genes, including ß-lactamase genes blaTEM-1 and blaCTX-M-14, sulphonamide resistance gene sul1, a quinolone resistance gene remnant (ΔqnrB2), and virulence associated gene iroN. Notably, the multidrug-resistance region was a chimeric structure composed of three subregions, which shared strong sequence homology with several plasmids previously assigned in Genbank. To our knowledge, this is the first report of the co-localization of blaKPC-2 and dfrA25 on a novel putative multi-replicon plasmid in a Klebsiella pneumoniae ST11 clone.
[Mh] Termos MeSH primário: Infecções por Klebsiella/tratamento farmacológico
Klebsiella pneumoniae/genética
Plasmídeos/genética
Resistência a Trimetoprima/genética
Trimetoprima/farmacologia
Resistência beta-Lactâmica/genética
[Mh] Termos MeSH secundário: China/epidemiologia
Farmacorresistência Bacteriana Múltipla/genética
Seres Humanos
Infecções por Klebsiella/epidemiologia
Infecções por Klebsiella/microbiologia
Klebsiella pneumoniae/efeitos dos fármacos
Testes de Sensibilidade Microbiana
Tipagem de Sequências Multilocus
Filogenia
Replicon/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
AN164J8Y0X (Trimethoprim)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171339


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[PMID]:28039273
[Au] Autor:Moran RA; Anantham S; Holt KE; Hall RM
[Ad] Endereço:School of Life and Environmental Sciences, The University of Sydney, NSW 2006, Australia.
[Ti] Título:Prediction of antibiotic resistance from antibiotic resistance genes detected in antibiotic-resistant commensal Escherichia coli using PCR or WGS.
[So] Source:J Antimicrob Chemother;72(3):700-704, 2017 Mar 01.
[Is] ISSN:1460-2091
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives: To assess the effectiveness of bioinformatic detection of resistance genes in whole-genome sequences in correctly predicting resistance phenotypes. Methods: Genomes of a collection of well-characterized commensal Escherichia coli were sequenced using Illumina HiSeq technology and assembled with SPAdes. Antibiotic resistance genes identified by PCR, SRST2 analysis of reads and ResFinder analysis of SPAdes assemblies were compared with known resistance phenotypes. Results: Generally, the antibiotic resistance genes detected using bioinformatic methods were concordant, but only ARG-ANNOT included sat2 . However, the presence or absence of genes was not always predictive of the phenotype. In one strain, trimethoprim resistance was due to a known mutation in the chromosomal folA gene. In cases where the copy number was low, the aadA5 gene downstream of dfrA17 did not confer streptomycin or spectinomycin resistance. Resistance genes were found in the genomes that were not detected previously by PCRs targeting a limited gene set and gene cassettes in class 1 or class 2 integrons. In one isolate, the aadA1 gene cassette in the estX - aadA1 cassettes pair was outside an integron context and was not expressed. The qnrS1 gene, conferring reduced susceptibility to fluoroquinolones, and the bla CMY-2 gene, encoding an ESBL, were each detected in a single isolate and mphA (macrolide resistance) was present in six isolates surrounded by IS 26 and IS 6100 . Conclusions: WGS analysis detected more genes than PCR. Some were not expressed, causing inconsistencies with the experimentally determined phenotype. An unpredicted chromosomal folA mutation causing trimethoprim resistance was found.
[Mh] Termos MeSH primário: DNA Bacteriano/genética
Farmacorresistência Bacteriana
Escherichia coli/efeitos dos fármacos
Escherichia coli/genética
Genoma Bacteriano
Simbiose
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Biologia Computacional/métodos
Farmacorresistência Bacteriana/genética
Escherichia coli/isolamento & purificação
Infecções por Escherichia coli/microbiologia
Genes Bacterianos
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Testes de Sensibilidade Microbiana
Fenótipo
Reação em Cadeia da Polimerase/métodos
Espectinomicina/farmacologia
Estreptomicina/farmacologia
Resistência a Trimetoprima/genética
beta-Lactamases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (DNA, Bacterial); 93AKI1U6QF (Spectinomycin); EC 3.5.2.- (beta-lactamase CMY-2); EC 3.5.2.6 (beta-Lactamases); Y45QSO73OB (Streptomycin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1093/jac/dkw511


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[PMID]:27489797
[Au] Autor:Miranda A; Ávila B; Díaz P; Rivas L; Bravo K; Astudillo J; Bueno C; Ulloa MT; Hermosilla G; Del Canto F; Salazar JC; Toro CS
[Ad] Endereço:Programa de Microbiología y Micología, Facultad de Medicina, Instituto de Ciencias Biomédicas, Universidad de Chile Santiago, Chile.
[Ti] Título:Emergence of Plasmid-Borne dfrA14 Trimethoprim Resistance Gene in Shigella sonnei.
[So] Source:Front Cell Infect Microbiol;6:77, 2016.
[Is] ISSN:2235-2988
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The most common mechanism of trimethoprim (TMP)-resistance is the acquisition of dihydrofolate reductase enzyme resistant to this drug. Previous molecular characterization of TMP-genes resistance in Chilean isolates of Shigella sonnei searching for dfrA1 and dfrA8, showed solely the presence of dfrA8 (formerly dhfrIIIc). However, these genetic markers were absent in S. sonnei strains further isolated during an outbreak in 2009. To identify the TMP-resistance gene in these strains, a genomic DNA library from a TMP-resistant (TMP(R)) S. sonnei representative strain for the outbreak was used to clone, select and identify a TMP-resistance marker. The TMP(R) clone was sequenced by primer walking, identifying the presence of the dfrA14 gene in the sul2-strA'-dfrA14-'strA-strB gene arrangement, harbored in a native 6779-bp plasmid. The same plasmid was isolated by transforming with a ~4.2 MDa plasmid extracted from several TMP(R) S. sonnei strains into Escherichia coli. This plasmid, named pABC-3, was present only in dfrA14-positive strains and was homologous to a previously described pCERC-1, but different due to the absence of an 11-bp repetitive unit. The distribution of dfrA1, dfrA8, and dfrA14 TMP-resistance genes was determined in 126 TMP(R) S. sonnei isolates. Most of the strains (96%) carried only one of the three TMP-resistance genes assessed. Thus, all strains obtained during the 2009-outbreak harbored only dfrA14, whereas, dfrA8 was the most abundant gene marker before outbreak and, after the outbreak dfrA1 seems have appeared in circulating strains. According to PFGE, dfrA14-positive strains were clustered in a genetically related group including some dfrA1- and dfrA8-positive strains; meanwhile other genetic group included most of the dfrA8-positive strains. This distribution also correlated with the isolation period, showing a dynamics of trimethoprim genetic markers prevalent in Chilean S. sonnei strains. To our knowledge, dfrA14 gene associated to a small non-conjugative plasmid was detected for the first time in Shigella. Apparently, the strain causing the outbreak must have been introduced, changing drastically the genetic distribution of trimethoprim resistance in Chilean S. sonnei strains.
[Mh] Termos MeSH primário: Genes Bacterianos
Plasmídeos
Shigella sonnei/efeitos dos fármacos
Shigella sonnei/genética
Tetra-Hidrofolato Desidrogenase/genética
Resistência a Trimetoprima
[Mh] Termos MeSH secundário: Chile/epidemiologia
Clonagem Molecular
Surtos de Doenças
Disenteria Bacilar/epidemiologia
Disenteria Bacilar/microbiologia
Ordem dos Genes
Transferência Genética Horizontal
Seres Humanos
Análise de Sequência de DNA
Shigella sonnei/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.5.1.3 (Tetrahydrofolate Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160805
[St] Status:MEDLINE
[do] DOI:10.3389/fcimb.2016.00077


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[PMID]:26391012
[Au] Autor:Sedgwick P
[Ad] Endereço:Institute for Medical and Biomedical Education, St George's, University of London, London, UK p.sedgwick@sgul.ac.uk.
[Ti] Título:Understanding the ecological fallacy.
[So] Source:BMJ;351:h4773, 2015 Sep 21.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Antibacterianos/administração & dosagem
Medicina Geral
Padrões de Prática Médica/estatística & dados numéricos
Resistência a Trimetoprima/efeitos dos fármacos
Trimetoprima/administração & dosagem
[Mh] Termos MeSH secundário: Viés
Estudos Transversais
Seres Humanos
Escócia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); AN164J8Y0X (Trimethoprim)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150923
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.h4773


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[PMID]:26344335
[Au] Autor:Nurjadi D; Schäfer J; Friedrich-Jänicke B; Mueller A; Neumayr A; Calvo-Cano A; Goorhuis A; Molhoek N; Lagler H; Kantele A; Van Genderen PJ; Gascon J; Grobusch MP; Caumes E; Hatz C; Fleck R; Mockenhaupt FP; Zanger P
[Ad] Endereço:Department of Infectious Diseases, Medical Microbiology and Hygiene, Heidelberg University Hospital, Heidelberg, Germany. Electronic address: dennis.nurjadi@uni-heidelberg.de.
[Ti] Título:Predominance of dfrG as determinant of trimethoprim resistance in imported Staphylococcus aureus.
[So] Source:Clin Microbiol Infect;21(12):1095.e5-9, 2015 Dec.
[Is] ISSN:1469-0691
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To investigate the global occurrence of trimethoprim-sulfamethoxazole resistance and the genetic mechanisms of trimethoprim resistance, we analysed Staphylococcus aureus from travel-associated skin and soft-tissue infections treated at 13 travel clinics in Europe. Thirty-eight per cent (75/196) were trimethoprim-resistant and 21% (41/196) were resistant to trimethoprim-sulfamethoxazole. Among methicillin-resistant S. aureus, these proportions were 30% (7/23) and 17% (4/23), respectively. DfrG explained 92% (69/75) of all trimethoprim resistance in S. aureus. Travel to South Asia was associated with the highest risk of acquiring trimethoprim-sulfamethoxazole-resistant S. aureus. We conclude that globally dfrG is the predominant determinant of trimethoprim resistance in human S. aureus infection.
[Mh] Termos MeSH primário: Staphylococcus aureus/genética
Tetra-Hidrofolato Desidrogenase/genética
Resistência a Trimetoprima
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Europa (Continente)
Seres Humanos
Infecções dos Tecidos Moles/microbiologia
Infecções Estafilocócicas/microbiologia
Infecções Cutâneas Estafilocócicas/microbiologia
Staphylococcus aureus/classificação
Staphylococcus aureus/isolamento & purificação
Viagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); EC 1.5.1.3 (Tetrahydrofolate Dehydrogenase)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151127
[Lr] Data última revisão:
151127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150908
[St] Status:MEDLINE


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[PMID]:26107669
[Au] Autor:Yayan J; Ghebremedhin B; Rasche K
[Ad] Endereço:From the Department of Internal Medicine, Division of Pulmonary, Allergy, and Sleep Medicine, HELIOS Clinic Wuppertal, Witten/Herdecke University, Wuppertal (JY, KR); Institute for Medical Laboratory Diagnostics, Center for Clinical and Translational Research Wuppertal, Witten/Herdecke University, Witten (BG), Germany.
[Ti] Título:No Development of Imipenem Resistance in Pneumonia Caused by Escherichia coli.
[So] Source:Medicine (Baltimore);94(25):e1020, 2015 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Antibiotic resistance continues to rise due to the increased number of antibiotic prescriptions and is now a major threat to public health. In particular, there is an increase in antibiotic resistance to Escherichia coli according to the latest reports. TRIAL DESIGN: This article examines, retrospectively, antibiotic resistance in patients with community- and nosocomial-acquired pneumonia caused by E coli. METHODS: The data of all patients with community- and nosocomial-acquired pneumonia caused by E coli were collected from the hospital charts at the HELIOS Clinic, Witten/Herdecke University, Wuppertal, Germany, within the study period 2004 to 2014. An antibiogram was performed for the study patients with pneumonia caused by E coli. Antimicrobial susceptibility testing was performed for the different antibiotics that have been consistently used in the treatment of patients with pneumonia caused by E coli. All demographic, clinical, and laboratory data of all of the patients with pneumonia caused by E coli were collected from the patients' records. RESULTS: During the study period of January 1, 2004 to August 12, 2014, 135 patients were identified with community- and nosocomial-acquired pneumonia affected by E coli. These patients had a mean age of 72.5 ±â€Š11.6 (92 [68.1%, 95% CI 60.2%-76.0%] males and 43 [31.9%, 95% CI 24.0%-39.8%] females). E coli had a high resistance rate to ampicillin (60.7%), piperacillin (56.3%), ampicillin-sulbactam (44.4%), and co-trimoxazole (25.9%). No patients with pneumonia caused by E coli showed resistance to imipenem (P < 0.0001). CONCLUSION: E coli was resistant to many of the typically used antibiotics. No resistance was detected toward imipenem in patients with pneumonia caused by E coli.
[Mh] Termos MeSH primário: Resistência a Ampicilina
Escherichia coli/fisiologia
Imipenem/uso terapêutico
Pneumonia/microbiologia
Resistência a Trimetoprima
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Tempo de Internação
Masculino
Meia-Idade
Pneumonia/tratamento farmacológico
Melhoria de Qualidade
Estudos Retrospectivos
Falha de Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
71OTZ9ZE0A (Imipenem)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150625
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000001020


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[PMID]:25957382
[Au] Autor:Bossé JT; Li Y; Walker S; Atherton T; Fernandez Crespo R; Williamson SM; Rogers J; Chaudhuri RR; Weinert LA; Oshota O; Holden MT; Maskell DJ; Tucker AW; Wren BW; Rycroft AN; Langford PR; BRaDP1T Consortium
[Ad] Endereço:Section of Paediatrics, Department of Medicine, Imperial College London, St Mary's Campus, London W2 1PG, UK j.bosse@imperial.ac.uk.
[Ti] Título:Identification of dfrA14 in two distinct plasmids conferring trimethoprim resistance in Actinobacillus pleuropneumoniae.
[So] Source:J Antimicrob Chemother;70(8):2217-22, 2015 Aug.
[Is] ISSN:1460-2091
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The objective of this study was to determine the distribution and genetic basis of trimethoprim resistance in Actinobacillus pleuropneumoniae isolates from pigs in England. METHODS: Clinical isolates collected between 1998 and 2011 were tested for resistance to trimethoprim and sulphonamide. The genetic basis of trimethoprim resistance was determined by shotgun WGS analysis and the subsequent isolation and sequencing of plasmids. RESULTS: A total of 16 (out of 106) A. pleuropneumoniae isolates were resistant to both trimethoprim (MIC >32 mg/L) and sulfisoxazole (MIC ≥256 mg/L), and a further 32 were resistant only to sulfisoxazole (MIC ≥256 mg/L). Genome sequence data for the trimethoprim-resistant isolates revealed the presence of the dfrA14 dihydrofolate reductase gene. The distribution of plasmid sequences in multiple contigs suggested the presence of two distinct dfrA14-containing plasmids in different isolates, which was confirmed by plasmid isolation and sequencing. Both plasmids encoded mobilization genes, the sulphonamide resistance gene sul2, as well as dfrA14 inserted into strA, a streptomycin-resistance-associated gene, although the gene order differed between the two plasmids. One of the plasmids further encoded the strB streptomycin-resistance-associated gene. CONCLUSIONS: This is the first description of mobilizable plasmids conferring trimethoprim resistance in A. pleuropneumoniae and, to our knowledge, the first report of dfrA14 in any member of the Pasteurellaceae. The identification of dfrA14 conferring trimethoprim resistance in A. pleuropneumoniae isolates will facilitate PCR screens for resistance to this important antimicrobial.
[Mh] Termos MeSH primário: Infecções por Actinobacillus/veterinária
Actinobacillus pleuropneumoniae/efeitos dos fármacos
Plasmídeos
Doenças dos Suínos/microbiologia
Tetra-Hidrofolato Desidrogenase/genética
Resistência a Trimetoprima
[Mh] Termos MeSH secundário: Infecções por Actinobacillus/microbiologia
Actinobacillus pleuropneumoniae/enzimologia
Actinobacillus pleuropneumoniae/genética
Actinobacillus pleuropneumoniae/isolamento & purificação
Animais
Anti-Infecciosos/farmacologia
Inglaterra
Genoma Bacteriano
Testes de Sensibilidade Microbiana
Dados de Sequência Molecular
Análise de Sequência de DNA
Sulfisoxazol/farmacologia
Suínos
Trimetoprima/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Infective Agents); 740T4C525W (Sulfisoxazole); AN164J8Y0X (Trimethoprim); EC 1.5.1.3 (Tetrahydrofolate Dehydrogenase)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150510
[St] Status:MEDLINE
[do] DOI:10.1093/jac/dkv121


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[PMID]:25750990
[Au] Autor:Kumar A; Tiwary BK; Kachhap S; Nanda AK; Chakraborty R
[Ad] Endereço:OMICS Laboratory, Department of Biotechnology, University of North Bengal, Dist, Darjeeling, 734013, India; Lignocellulose Biotechnology Laboratory, Department of Microbiology, University of Delhi South Campus, 110021, New Delhi.
[Ti] Título:An Escherichia coli strain, PGB01, isolated from feral pigeon Faeces, thermally fit to survive in pigeon, shows high level resistance to trimethoprim.
[So] Source:PLoS One;10(3):e0119329, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, of the hundred Escherichia coli strains isolated from feral Pigeon faeces, eighty five strains were resistant to one or more antibiotics and fifteen sensitive to all the antibiotics tested. The only strain (among all antibiotic-resistant E. coli isolates) that possessed class 1 integron was PGB01. The dihydrofolate reductase gene of the said integron was cloned, sequenced and expressed in E. coli JM109. Since PGB01 was native to pigeon's gut, we have compared the growth of PGB01 at two different temperatures, 42°C (normal body temperature of pigeon) and 37°C (optimal growth temperature of E. coli; also the human body temperature), with E. coli K12. It was found that PGB01 grew better than the laboratory strain E. coli K12 at 37°C as well as at 42°C. In the thermal fitness assay, it was observed that the cells of PGB01 were better adapted to 42°C, resembling the average body temperature of pigeon. The strain PGB01 also sustained more microwave mediated thermal stress than E. coli K12 cells. The NMR spectra of the whole cells of PGB01 varied from E. coli K12 in several spectral peaks relating some metabolic adaptation to thermotolerance. On elevating the growth temperature from 37°C to 42°C, susceptibility to kanamycin (both strains were sensitive to it) of E. coli K12 was increased, but in case of PGB01 no change in susceptibility took place. We have also attempted to reveal the basis of trimethoprim resistance phenotype conferred by the dfrA7 gene homologue of PGB01. Molecular Dynamics (MD) simulation study of docked complexes, PGB01-DfrA7 and E. coli TMP-sensitive-Dfr with trimethoprim (TMP) showed loss of some of the hydrogen and hydrophobic interaction between TMP and mutated residues in PGB01-DfrA7-TMP complex compared to TMP-sensitive-Dfr-TMP complex. This loss of interaction entails decrease in affinity of TMP for PGB01-DfrA7 compared to TMP-sensitive-Dfr.
[Mh] Termos MeSH primário: Columbidae/microbiologia
Escherichia coli/isolamento & purificação
Fezes/microbiologia
Resistência a Trimetoprima
[Mh] Termos MeSH secundário: Animais
Escherichia coli/classificação
Escherichia coli/crescimento & desenvolvimento
Proteínas de Escherichia coli/química
Proteínas de Escherichia coli/genética
Integrons
Testes de Sensibilidade Microbiana
Temperatura Ambiente
Tetra-Hidrofolato Desidrogenase/química
Tetra-Hidrofolato Desidrogenase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Escherichia coli Proteins); EC 1.5.1.3 (Tetrahydrofolate Dehydrogenase)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150310
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0119329


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[PMID]:25348695
[Au] Autor:Shin HW; Lim J; Kim S; Kim J; Kwon GC; Koo SH
[Ad] Endereço:College of Medicine, Department of Laboratory Medicine, Chungnam National University, Daejeon 301-721, Republic of Korea.
[Ti] Título:Characterization of trimethoprim-sulfamethoxazole resistance genes and their relatedness to class 1 integron and insertion sequence common region in gram-negative bacilli.
[So] Source:J Microbiol Biotechnol;25(1):137-42, 2015 Jan.
[Is] ISSN:1738-8872
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Trimethoprim-sulfamethoxazole (TMP-SMX) has been used for the treatment of urinary tract infections, but increasing resistance to TMP-SMX has been reported. In this study, we analyzed TMP-SMX resistance genes and their relatedness with integrons and insertion sequence common regions (ISCRs) in uropathogenic gram-negative bacilli. Consecutive nonduplicate TMP-SMX nonsusceptible clinical isolates of E. coli, K. pneumoniae, Acinetobacter spp., and P. aeruginosa were collected from urine. The minimal inhibitory concentration was determined by Etest. TMP-SMX resistance genes (sul and dfr), integrons, and ISCRs were analyzed by PCR and sequencing. A total of 45 E. coli (37.8%), 15 K. pneumoniae (18.5%), 12 Acinetobacter spp. (70.6%), and 9 Pseudomonas aeruginosa (30.0%) isolates were found to be resistant to TMP-SMX. Their MICs were all over 640. In E. coli and K. pneumoniae, sul1 and dfr genes were highly prevalent in relation with integron1. The sul3 gene was detected in E. coli. However, in P. aeruginosa and Acinetobacter spp., only sul1 was prevalent in relation with class 1 integron; however, dfr was not detected and sul2 was less prevalent than in Enterobacteriaceae. ISCR1 and/or ISCR2 were detected in E. coli, K. pneumoniae, and Acinetobacter spp. but the relatedness with TMP-SMX resistance genes was not prominent. ISCR14 was detected in six isolates of E. coli. In conclusion, resistance mechanisms for TMP-SMX were different between Enterobacteriaceae and glucose non-fermenting gram-negative bacilli. Class 1 integron was widely disseminated in uropathogenic gram-negative baciili, so the adoption of prudent use of antimicrobial agents and the establishment of a surveillance system are needed.
[Mh] Termos MeSH primário: Elementos de DNA Transponíveis
Farmacorresistência Bacteriana Múltipla/genética
Bactérias Gram-Negativas/efeitos dos fármacos
Bactérias Gram-Negativas/genética
Integrons
Resistência a Trimetoprima/genética
Combinação Trimetoprima e Sulfametoxazol/farmacologia
[Mh] Termos MeSH secundário: Acinetobacter/genética
Acinetobacter/isolamento & purificação
Escherichia coli/genética
Escherichia coli/isolamento & purificação
Infecções por Bactérias Gram-Negativas/microbiologia
Seres Humanos
Klebsiella pneumoniae/genética
Klebsiella pneumoniae/isolamento & purificação
Testes de Sensibilidade Microbiana
Reação em Cadeia da Polimerase
Pseudomonas aeruginosa/genética
Pseudomonas aeruginosa/isolamento & purificação
Análise de Sequência de DNA
Urina/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA Transposable Elements); 8064-90-2 (Trimethoprim, Sulfamethoxazole Drug Combination)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141029
[St] Status:MEDLINE


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[PMID]:25288083
[Au] Autor:Lamb KM; Lombardo MN; Alverson J; Priestley ND; Wright DL; Anderson AC
[Ad] Endereço:Department of Pharmaceutical Sciences, University of Connecticut, Storrs, Connecticut, USA.
[Ti] Título:Crystal structures of Klebsiella pneumoniae dihydrofolate reductase bound to propargyl-linked antifolates reveal features for potency and selectivity.
[So] Source:Antimicrob Agents Chemother;58(12):7484-91, 2014 Dec.
[Is] ISSN:1098-6596
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Resistance to the antibacterial antifolate trimethoprim (TMP) is increasing in members of the family Enterobacteriaceae, driving the design of next-generation antifolates effective against these Gram-negative pathogens. The propargyl-linked antifolates are potent inhibitors of dihydrofolate reductases (DHFR) from several TMP-sensitive and -resistant species, including Klebsiella pneumoniae. Recently, we have determined that these antifolates inhibit the growth of strains of K. pneumoniae, some with MIC values of 1 µg/ml. In order to further the design of potent and selective antifolates against members of the Enterobacteriaceae, we determined the first crystal structures of K. pneumoniae DHFR bound to two of the propargyl-linked antifolates. These structures highlight that interactions with Leu 28, Ile 50, Ile 94, and Leu 54 are necessary for potency; comparison with structures of human DHFR bound to the same inhibitors reveal differences in residues (N64E, P61G, F31L, and V115I) and loop conformations (residues 49 to 53) that may be exploited for selectivity.
[Mh] Termos MeSH primário: Antibacterianos/química
Proteínas de Bactérias/química
Antagonistas do Ácido Fólico/química
Klebsiella pneumoniae/química
Tetra-Hidrofolato Desidrogenase/química
Trimetoprima/química
[Mh] Termos MeSH secundário: Proteínas de Bactérias/antagonistas & inibidores
Proteínas de Bactérias/genética
Cristalografia por Raios X
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Klebsiella pneumoniae/enzimologia
Simulação de Acoplamento Molecular
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Relação Estrutura-Atividade
Tetra-Hidrofolato Desidrogenase/genética
Resistência a Trimetoprima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Folic Acid Antagonists); 0 (Recombinant Proteins); AN164J8Y0X (Trimethoprim); EC 1.5.1.3 (Tetrahydrofolate Dehydrogenase)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141008
[St] Status:MEDLINE
[do] DOI:10.1128/AAC.03555-14



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