oru.sePublications
Change search
Link to record
Permanent link

Direct link
BETA
Persson, Katarina
Publications (10 of 27) Show all publications
Lindblad, A., Persson, K. & Demirel, I. (2019). IL-1RA is part of the inflammasome-regulated immune response in bladder epithelial cells and influences colonization of uropathogenic E. coli. Cytokine, 123, Article ID 154772.
Open this publication in new window or tab >>IL-1RA is part of the inflammasome-regulated immune response in bladder epithelial cells and influences colonization of uropathogenic E. coli
2019 (English)In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 123, article id 154772Article in journal (Refereed) Epub ahead of print
Abstract [en]

The NLRP3 inflammasome, IL-1β release and pyroptosis (cell lysis) have recently been proposed to be essential for the progression of urinary tract infection (UTI) and elimination of intracellular bacterial niches. However, the effects of IL-1R antagonist (IL-1RA) on immune responses during UTI, except for its ability to disrupt IL-1β signalling, are not well understood. The aim of this study was to investigate the role of IL-1RA in UPEC colonization of bladder epithelial cells and the subsequent host inflammatory response. Human bladder epithelial cells (5637) and CRISPR/Cas9 generated NLRP3 and caspase-1 knockdown cells and IL-1RA knockout cells were stimulated with the UPEC isolate CFT073. The results showed that the UPEC virulence factor α-hemolysin is essential for IL-1RA release, and that the inflammasome-associated proteins caspase-1 and NLRP3 affect the release of IL-1RA. IL-1RA deficient cells showed a reduced adherence and invasion by CFT073 compared to wild-type cells, suggesting that IL-1RA may oppose mechanisms that protects against bacterial colonization. A targeted protein analysis of inflammation-related proteins showed that the basal expression of 23 proteins and the UPEC-induced expression of 10 proteins were significantly altered in IL-1RA deficient bladder epithelial cells compared to Cas9 control cells. This suggests that IL-1RA has a broad effect on the inflammatory response in bladder epithelial cells.

Place, publisher, year, edition, pages
Academic Press, 2019
Keywords
IL-1 receptor antagonist, Inflammasome, NLRP3, Urinary tract infections, Uropathogenic Escherichia coli
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-75559 (URN)10.1016/j.cyto.2019.154772 (DOI)31299415 (PubMedID)
Available from: 2019-08-06 Created: 2019-08-06 Last updated: 2019-08-07Bibliographically approved
Eriksson, A. L., Böttiger, Y., Ekman, A., Reis, M., Persson, K., Pettersson Kymmer, U. & Wallerstedt, S. M. (2019). Läkemedelsarbete behöver vara integrerat i klinisk utbildning: Att göra många läkemedelsgenomgångar ökar trygghet och reflektion över patientens behandling, visar enkätstudie [Preparing for the licence to prescribe in medical school: a questionnaire study on medical students professional confidence in the art of prescribing].. Läkartidningen, 116, Article ID FHCT.
Open this publication in new window or tab >>Läkemedelsarbete behöver vara integrerat i klinisk utbildning: Att göra många läkemedelsgenomgångar ökar trygghet och reflektion över patientens behandling, visar enkätstudie [Preparing for the licence to prescribe in medical school: a questionnaire study on medical students professional confidence in the art of prescribing].
Show others...
2019 (Swedish)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 116, article id FHCTArticle in journal (Refereed) Published
Abstract [sv]

Att behandla med läkemedel är en kärnuppgift för läkare; grundutbildningen behöver ge studenterna förutsättningar att klara detta.

Enkätresultat från fyra lärosäten visade att 45 procent av studenterna efter sin invärtesmedicinska placering kände sig trygga med att göra läkemedelsgenomgångar och 62 procent med att skriva läkemedelsberättelser.

Studenter som gör många läkemedelsgenomgångar/läkemedelsberättelser känner större trygghet och reflekterar mer över patientens behandling.

Klinisk handledning gör skillnad.

När kursplaner revideras vid införandet av en sexårig läkarutbildning, med förskrivningsrätt direkt efter examen, behöver klinisk träning i läkemedelsarbete inklusive handledning tydliggöras.

Abstract [en]

A prerequisite for rational use of medicines is adequate prescribing skills; drug treatment is a complex task requiring diagnostic competence combined with pharmacologic knowledge and patient communication skills. Acquiring professional confidence in the art of prescribing is essential during medical training. The results of this questionnaire study, conducted in four medical schools in Sweden after the course in internal medicine (252 respondents; response rate: 74%; median age: 24 years, 61% female), show that 45% and 62% were confident in performing medication reviews and writing medication summary reports, respectively, i.e. the basics of prescribing. The confidence increased by the number of reviews and reports performed, i.e. the extent of practice (correlation coefficients: 0.41 and 0.38, respectively, both p<0.0001), as did the extent of the students' reflection on important aspects of drug treatment such as adherence, adverse reactions, renal function, dosing, and drug interactions. In multivariate regression analyses, major predictors for confidence in performing medication reviews were extent of practice and extent of clinical supervision. The results suggest that these factors are keys to acquiring professional confidence in the art of prescribing.

Place, publisher, year, edition, pages
Läkartidningen Förlag AB, 2019
National Category
Other Medical Sciences not elsewhere specified
Identifiers
urn:nbn:se:oru:diva-75048 (URN)31192436 (PubMedID)
Available from: 2019-07-08 Created: 2019-07-08 Last updated: 2019-07-11Bibliographically approved
Demirel, I., Persson, A., Brauner, A., Särndahl, E., Kruse, R. & Persson, K. (2018). Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells. Frontiers in Cellular and Infection Microbiology, 8, Article ID 81.
Open this publication in new window or tab >>Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells
Show others...
2018 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 8, article id 81Article in journal (Refereed) Published
Abstract [en]

The NLRP3 inflammasome and IL-1 beta release have recently been suggested to be important for the progression of urinary tract infection (UTI). However, much is still unknown regarding the interaction of UPEC and the NLRP3 inflammasome. The purpose of this study was to elucidate what virulence factors uropathogenic Escherichia coil (UPEC) use to modulate NLRP3 inflammasome activation and subsequent IL-1 beta release and the role of NLRP3 for UPEC colonization of bladder epithelial cells. The bladder epithelial cell line 5637, CRISPR/Cas9 generated NLRP3, caspase-1 and mesotrypsin deficient cell lines and transformed primary bladder epithelial cells (HBLAK) were stimulated with UPEC isolates and the non-pathogenic MG1655 strain. We found that the UPEC strain CFT073, but not MG1655, induced an increased caspase-1 activity and IL-1 beta release from bladder epithelial cells. The increase was shown to be mediated by et-hemolysin activation of the NLRP3 inflammasome in an NE-kappa B-independent manner. The effect of-hemolysin on IL-1 beta release was biphasic, initially suppressive, later inductive. Furthermore, the phase-locked type-1-fimbrial ON variant of CFT073 inhibited caspase-1 activation and IL-1 beta release. In addition, the ability of CFT073 to adhere to and invade NLRP3 deficient cells was significantly reduced compare to wild-type cells. The reduced colonization of NLRP3-deficient cells was type-1 fimbriae dependent. In conclusion, we found that the NLRP3 inflammasome was important for type-1 fimbriae-dependent colonization of bladder epithelial cells and that both type-1 fimbriae and alpha-hemolysin can modulate the activity of the NLRP3 inflammasome.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
UPEC, NLRP3 inflammasome, IL-1 beta, alpha-hemolysin, type-1 fimbriae
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-66388 (URN)10.3389/fcimb.2018.00081 (DOI)000427407100001 ()2-s2.0-85043771169 (Scopus ID)
Note

Funding Agency:

Faculty of Medicine and Health at Örebro University 

Available from: 2018-04-09 Created: 2018-04-09 Last updated: 2018-08-20Bibliographically approved
Svensson, L., Poljakovic, M., Demirel, I., Sahlberg, C. & Persson, K. (2018). Host-Derived Nitric Oxide and Its Antibacterial Effects in the Urinary Tract. Advances in Microbial Physiology, 73, 1-62
Open this publication in new window or tab >>Host-Derived Nitric Oxide and Its Antibacterial Effects in the Urinary Tract
Show others...
2018 (English)In: Advances in Microbial Physiology, ISSN 0065-2911, E-ISSN 2162-5468, Vol. 73, p. 1-62Article, review/survey (Refereed) Published
Abstract [en]

Urinary tract infection (UTI) is one of the most common bacterial infections in humans, and the majority are caused by uropathogenic Escherichia coli (UPEC). The rising antibiotic resistance among UPEC and the frequent failure of antibiotics to effectively treat recurrent UTI and catheter-associated UTI motivate research on alternative ways of managing UTI. Abundant evidence indicates that the toxic radical nitric oxide (NO), formed by activation of the inducible nitric oxide synthase, plays an important role in host defence to bacterial infections, including UTI. The major source of NO production during UTI is from inflammatory cells, especially neutrophils, and from the uroepithelial cells that are known to orchestrate the innate immune response during UTI. NO and reactive nitrogen species have a wide range of antibacterial targets, including DNA, heme proteins, iron-sulfur clusters, and protein thiol groups. However, UPEC have acquired a variety of defence mechanisms for protection against NO, such as the NO-detoxifying enzyme flavohemoglobin and the NO-tolerant cytochrome bd-I respiratory oxidase. The cytotoxicity of NO-derived intermediates is nonspecific and may be detrimental to host cells, and a balanced NO production is crucial to maintain the tissue integrity of the urinary tract. In this review, we will give an overview of how NO production from host cells in the urinary tract is activated and regulated, the effect of NO on UPEC growth and colonization, and the ability of UPEC to protect themselves against NO. We also discuss the attempts that have been made to develop NO-based therapeutics for UTI treatment.

Place, publisher, year, edition, pages
Academic Press, 2018
Keywords
Antimicrobial factor, Flavohemoglobin, Inducible nitric oxide synthase, Nitric oxide, Nitrosative stress, Urinary bladder, Urinary tract infection, Uropathogenic E. coli
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-70674 (URN)10.1016/bs.ampbs.2018.05.001 (DOI)000452097400001 ()30262107 (PubMedID)2-s2.0-85048708739 (Scopus ID)
Available from: 2018-12-10 Created: 2018-12-10 Last updated: 2018-12-17Bibliographically approved
Bang, C. S., Demirel, I., Kruse, R. & Persson, K. (2017). Global gene expression profiling and antibiotic susceptibility after repeated exposure to the carbon monoxide-releasing molecule-2 (CORM-2) in multidrug-resistant ESBL-producing uropathogenic Escherichia coli. PLoS ONE, 12(6), Article ID e0178541.
Open this publication in new window or tab >>Global gene expression profiling and antibiotic susceptibility after repeated exposure to the carbon monoxide-releasing molecule-2 (CORM-2) in multidrug-resistant ESBL-producing uropathogenic Escherichia coli
2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 6, article id e0178541Article in journal (Refereed) Published
Abstract [en]

Treatment of urinary tract infections is today a challenge due to the increasing prevalence of multidrug-resistant ESBL-producing uropathogenic Escherichia coli (UPEC). There is an urgent need for new treatment strategies for multidrug-resistant UPEC and preferably with targets that have low potential for development of resistance. Carbon monoxide-releasing molecules (CORMs) are novel and potent antibacterial agents. The present study examines the transcriptomic targets of CORM-2 in a multidrug-resistant ESBL-producing UPEC isolate in response to a single exposure to CORM-2 and after repeated exposure to CORM-2. The bacterial viability and minimal inhibitory concentration (MIC) were also examined after repeated exposure to CORM-2. Microarray analysis revealed that a wide range of processes were affected by CORM-2, including a general trend of down-regulation in energy metabolism and biosynthesis pathways and up-regulation of the SOS response and DNA repair. Several genes involved in virulence (ibpB), antibiotic resistance (marAB, mdtABC) and biofilm formation (bhsA, yfgF) were up-regulated, while some genes involved in virulence (kpsC, fepCEG, entABE), antibiotic resistance (evgA) and biofilm formation (artIP) were down-regulated. Repeated exposure to CORM-2 did not alter the gene expression patterns, the growth inhibitory response to CORM-2 or the MIC values for CORM-2, cefotaxime, ciprofloxacin and trimethoprim. This study identifies several enriched gene ontologies, modified pathways and single genes that are targeted by CORM-2 in a multidrug-resistant UPEC isolate. Repeated exposure to CORM-2 did not change the gene expression patterns or fold changes and the susceptibility to CORM-2 remained after repeated exposure.

Place, publisher, year, edition, pages
Public Library of Science, 2017
National Category
Microbiology
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-58779 (URN)10.1371/journal.pone.0178541 (DOI)000402880700036 ()28591134 (PubMedID)2-s2.0-85020463890 (Scopus ID)
Note

Funding Agencies:

Faculty of Medicine and Health at Örebro University  

Nyckelfonden at Örebro University Hospital 

Available from: 2017-07-26 Created: 2017-07-26 Last updated: 2017-11-29Bibliographically approved
Demirel, I., Rangel, I., Petersson, U., Persson, K. & Kruse, R. (2017). Transcriptional Alterations of Virulence-Associated Genes in Extended Spectrum Beta-Lactamase (ESBL)-Producing Uropathogenic Escherichia coli during Morphologic Transitions Induced by Ineffective Antibiotics. Frontiers in Microbiology, 8, Article ID 1058.
Open this publication in new window or tab >>Transcriptional Alterations of Virulence-Associated Genes in Extended Spectrum Beta-Lactamase (ESBL)-Producing Uropathogenic Escherichia coli during Morphologic Transitions Induced by Ineffective Antibiotics
Show others...
2017 (English)In: Frontiers in Microbiology, ISSN 1664-302X, E-ISSN 1664-302X, Vol. 8, article id 1058Article in journal (Refereed) Published
Abstract [en]

It is known that an ineffective antibiotic treatment can induce morphological shifts in uropathogenic Escherichia coli (UPEC) but the virulence properties during these shifts remain to be studied. The present study examines changes in global gene expression patterns and in virulence factor-associated genes in an extended spectrum beta-lactamase (ESBL)-producing UPEC (ESBL019) during the morphologic transitions induced by an ineffective antibiotic and in the presence of human primary bladder epithelial cells. Microarray results showed that the different morphological states of ESBL019 had significant transcriptional alterations of a large number of genes (Transition; 7%, Filamentation; 32%, and Reverted 19% of the entities on the array). All three morphological states of ESBL019 were associated with a decreased energy metabolism, altered iron acquisition systems and altered adhesion expression. In addition, genes associated with LPS synthesis and bacterial motility was also altered in all the morphological states. Furthermore, the transition state induced a significantly higher release of TNF-alpha from bladder epithelial cells compared to all other morphologies, while the reverted state was unable to induce INF-alpha release. Our findings show that the morphological shifts induced by ineffective antibiotics are associated with significant transcriptional virulence alterations in ESBL-producing UPEC, which may affect survival and persistence in the urinary tract.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2017
Keywords
filamentation, extended-spectrum beta-lactamase, uropathogenic Escherichia coli, ineffective antibiotics, morphological plasticity
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-58778 (URN)10.3389/fmicb.2017.01058 (DOI)000403139300001 ()28659883 (PubMedID)2-s2.0-85020493714 (Scopus ID)
Funder
Swedish Society of Medicine
Note

Funding Agencies:

Research Committee of Örebro County Council, Nyckelfonden

Faculty of Medicine and Health at Örebro University

Available from: 2017-07-26 Created: 2017-07-26 Last updated: 2018-02-05Bibliographically approved
Vumma, R., Bang, C. S., Kruse, R., Johansson, K. & Persson, K. (2016). Antibacterial effects of nitric oxide on uropathogenic Escherichia coli during bladder epithelial cell colonization-a comparison with nitrofurantoin. Journal of antibiotics (Tokyo. 1968), 69(3), 183-186
Open this publication in new window or tab >>Antibacterial effects of nitric oxide on uropathogenic Escherichia coli during bladder epithelial cell colonization-a comparison with nitrofurantoin
Show others...
2016 (English)In: Journal of antibiotics (Tokyo. 1968), ISSN 0021-8820, E-ISSN 1881-1469, Vol. 69, no 3, p. 183-186Article in journal (Refereed) Published
Place, publisher, year, edition, pages
Japan Antibiotics Research Association, 2016
National Category
Immunology in the medical area Pharmacology and Toxicology
Research subject
Immunology
Identifiers
urn:nbn:se:oru:diva-49933 (URN)10.1038/ja.2015.112 (DOI)000373096800011 ()26531685 (PubMedID)
Note

Funding Agencies:

Swedish Council for Working Life and Social Research (FAS)

Nyckelfonden at Örebro University Hospital

Faculty of Medicine and Health at Örebro University

Available from: 2016-04-26 Created: 2016-04-26 Last updated: 2018-01-10Bibliographically approved
Sahlberg Bang, C., Kruse, R., Johansson, K. & Persson, K. (2016). Carbon monoxide releasing molecule-2 (CORM-2) inhibits growth of multidrug-resistant uropathogenic Escherichia coli in biofilm and following host cell colonization. BMC Microbiology, 16(1), Article ID 64.
Open this publication in new window or tab >>Carbon monoxide releasing molecule-2 (CORM-2) inhibits growth of multidrug-resistant uropathogenic Escherichia coli in biofilm and following host cell colonization
2016 (English)In: BMC Microbiology, ISSN 1471-2180, E-ISSN 1471-2180, Vol. 16, no 1, article id 64Article in journal (Other academic) Published
Abstract [en]

Increased resistance to antimicrobial agents is a characteristic of many bacteria growing in biofilms on for example indwelling urinary catheters or in intracellular bacterial reservoirs. Biofilm-related infections caused by multidrug-resistant bacteria, such as extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae, are a major challenge. The aim of this study was to investigate if a carbon monoxide-releasing molecule (CORM-2) has antibacterial effects against ESBL-producing uropathogenic E. coli (UPEC) in the biofilm mode of growth and following colonization of host bladder epithelial cells.

Results

The effect of CORM-2 was examined on bacteria grown within an established biofilm (biofilm formed for 24 h on plastic surface) by a live/dead viability staining assay. CORM-2 (500 μM) exposure for 24 h killed approximately 60 % of the ESBL-producing UPEC isolate. A non-ESBL-producing UPEC isolate and the E. coli K-12 strain TG1 were also sensitive to CORM-2 exposure when grown in biofilms. The antibacterial effect of CORM-2 on planktonic bacteria was reduced and delayed in the stationary growth phase compared to the exponential growth phase. In human bladder epithelial cell colonization experiments, CORM-2 exposure for 4 h significantly reduced the bacterial counts of an ESBL-producing UPEC isolate.

Conclusion

This study shows that CORM-2 has antibacterial properties against multidrug-resistant UPEC under biofilm-like conditions and following host cell colonization, which motivate further studies of its therapeutic potential.

Place, publisher, year, edition, pages
BioMed Central, 2016
National Category
Other Basic Medicine Microbiology
Identifiers
urn:nbn:se:oru:diva-49071 (URN)10.1186/s12866-016-0678-7 (DOI)000374282400001 ()27067266 (PubMedID)2-s2.0-84964033699 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare
Note

Funding Agencies:

Faculty of Medicine and Health at Orebro University 

 Nyckelfonden at Orebro University Hospital 

Available from: 2016-03-10 Created: 2016-03-10 Last updated: 2018-07-10Bibliographically approved
Demirel, I., Kruse, R., Önnberg, A. & Persson, K. (2015). Ceftibuten-induced filamentation of extended spectrum beta lactamase (ESBL)-producing uropathogenic Escherichia coli alters host cell responses during an in vitro infection. Microbial Pathogenesis, 78, 52-62
Open this publication in new window or tab >>Ceftibuten-induced filamentation of extended spectrum beta lactamase (ESBL)-producing uropathogenic Escherichia coli alters host cell responses during an in vitro infection
2015 (English)In: Microbial Pathogenesis, ISSN 0882-4010, E-ISSN 1096-1208, Vol. 78, p. 52-62Article in journal (Refereed) Published
Abstract [en]

Inadequate and delayed antibiotic treatment of extended spectrum beta-lactamase (ESBL)-producing isolates have been associated with increased mortality of affected patients. The purpose of this study was to compare the host response of human renal epithelial cells and polymorphonuclear leucocyte (PMN) cells when infected by ESBL-producing uropathogenic Escherichia coli (UPEC) isolates in the presence or absence of ineffective antibiotics.

The renal epithelial cell line A498 and PMN cells were stimulated with ESBL-producing UPEC isolates in the presence or absence of three different antibiotics (trimetoprim, ceftibuten and ciprofloxacin). Host cell responses were evaluated as release of cytokines (IL-6, IL-8), reactive oxygen species (ROS), ATP and endotoxins. Bacterial morphology and PMN phagocytosis were evaluated by microscopy.

In the presence of ceftibuten, 2 out of 3 examined ESBL-isolates changed their morphology into a filamentous form. The presence of ceftibuten enhanced IL-6, IL-8 and ROS-production from host cells, but only from cells stimulated by the filamentous isolates. The bacterial supernatant and not the filamentous bacteria per se was responsible for the increased release of IL-6, IL-8 and ROS. Increased endotoxin and ATP levels were found in the bacterial supernatants from filamentous isolates. Apyrase decreased IL-6 secretion from A498 cells and polymyxin B abolished the increased ROS-production from PMN cells. PMN were able to inhibit the bacterial growth of some ESBL-isolates in the presence of ceftibuten.

In conclusion, antibiotic-induced filamentation of ESBL-producing UPEC isolates and the associated release of ATP and endotoxins can alter the host cell response in the urinary tract.

Place, publisher, year, edition, pages
Elsevier, 2015
Keywords
Urinary tract infections; Polymorphonucleated leukocytes; Uropathogenic Escherichia coli; Extended spectrum beta-lactamases; Filamentous bacteria
National Category
Clinical Laboratory Medicine
Identifiers
urn:nbn:se:oru:diva-39257 (URN)10.1016/j.micpath.2014.11.015 (DOI)000348248400008 ()25433242 (PubMedID)2-s2.0-84913601578 (Scopus ID)
Note

Funding Agencies:

Swedish Council for Working Life and Social Research 65X-12601-11

Nyckelfonden at Örebro University Hospital

Faculty of Medicine and Health at Örebro University

Available from: 2014-12-02 Created: 2014-12-02 Last updated: 2017-12-05Bibliographically approved
Önnberg, A., Söderquist, B., Persson, K. & Mölling, P. (2014). Characterization of CTX-M-producing Escherichia coli by repetitive sequence-based PCR and real-time PCR-based replicon typing of CTX-M-15 plasmids. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 122(11), 1136-1143
Open this publication in new window or tab >>Characterization of CTX-M-producing Escherichia coli by repetitive sequence-based PCR and real-time PCR-based replicon typing of CTX-M-15 plasmids
2014 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, no 11, p. 1136-1143Article in journal (Refereed) Published
Abstract [en]

The emergence of extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae is a major global concern. CTX-M is the dominating ESBL type worldwide, and CTX-M-15 is the most widespread CTX-M type. The dissemination of CTX-M appears to be in part due to global spread of the Escherichia coli clone O25b-ST131. However, the gene-encoding CTX-M is mainly located on mobile genetic elements, such as plasmids, that also promote the horizontal dissemination of the CTX-M genes. In this study, 152 CTX-M-producing E. coli isolated in 1999-2008 in Örebro County, Sweden, were typed using a commercial repetitive sequence-based PCR (the DiversiLab system), and the prevalence of ST131 was investigated by pabB PCR. Real-time PCR-based plasmid replicon typing was performed on 82 CTX-M-15-producing E. coli isolates. In general, the CTX-M-producing E. coli population was genetically diverse; however, ST131 was highly prevalent (27%), and the dominating clone in our area. The blaCTX -M-15 gene was mainly located on IncF plasmids (69%), but a relatively high proportion of IncI1 plasmids (29%) were also detected among E. coli with diverse rep-PCR patterns, indicating that horizontal transmission of IncI1 plasmids carrying blaCTX -M-15 may have occurred between different E. coli strains.

Place, publisher, year, edition, pages
Malden, USA: John Wiley & Sons, 2014
Keywords
Escherichia coli, ESBL, ST131, plasmid
National Category
Medical and Health Sciences Microbiology
Research subject
Medicine
Identifiers
urn:nbn:se:oru:diva-35271 (URN)10.1111/apm.12270 (DOI)000344383200011 ()24735173 (PubMedID)2-s2.0-84922019604 (Scopus ID)
Note

Funding Agencies:

Research Committee of the County Council of Örebro 

Nyckelfonden at Örebro University Hospital

Available from: 2014-06-09 Created: 2014-06-09 Last updated: 2018-06-07Bibliographically approved
Organisations

Search in DiVA

Show all publications