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  • 1.
    Björkqvist, Olle
    et al.
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Rangel, Ignacio
    Örebro University, School of Medical Sciences.
    Serrander, Lena
    Division of Clinical Microbiology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Magnusson, Cecilia
    Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden; Department of Infectious Diseases, Region Jönköping County, Jönköping, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Faculty of Medicine and Health, Department of Laboratory Medicine, National Reference Laboratory for Clostridioides Difficile, Clinical Microbiology.
    Bergman-Jungeström, Malin
    Division of Clinical Microbiology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Faecalibacterium prausnitzii increases following fecal microbiota transplantation in recurrent Clostridioides difficile infection2021In: PLOS ONE, E-ISSN 1932-6203, Vol. 16, no 4, article id e0249861Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Fecal microbiota transplantation (FMT) is a highly effective treatment for Clostridioides difficile infection (CDI). However, the fecal transplant's causal components translating into clearance of the CDI are yet to be identified. The commensal bacteria Faecalibacterium prausnitzii may be of great interest in this context, since it is one of the most common species of the healthy gut microbiota and produces metabolites with anti-inflammatory properties. Although there is mounting evidence that F. prausnitzii is an important regulator of intestinal homeostasis, data about its role in CDI and FMT are relatively scarce.

    METHODS: Stool samples from patients with recurrent CDI were collected to investigate the relative abundance of F. prausnitzii before and after FMT. Twenty-one patients provided fecal samples before the FMT procedure, at 2 weeks post-FMT, and at 2-4 months post-FMT. The relative abundance of F. prausnitzii was determined using quantitative polymerase chain reaction.

    RESULTS: The abundance of F. prausnitzii was elevated in samples (N = 9) from donors compared to pre-FMT samples (N = 15) from patients (adjusted P<0.001). No significant difference in the abundance of F. prausnitzii between responders (N = 11) and non-responders (N = 4) was found before FMT (P = 0.85). In patients with CDI, the abundance of F. prausnitzii significantly increased in the 2 weeks post-FMT samples (N = 14) compared to the pre-FMT samples (N = 15, adjusted P<0.001). The increase persisted 2-4 months post-FMT (N = 15) compared to pre-FMT samples (N = 15) (adjusted P<0.001).

    CONCLUSIONS: FMT increases the relative abundance of F. prausnitzii in patients with recurrent CDI, and this microbial shift remains several months later. The baseline abundance of F. prausnitzii in donors or recipients was not associated with future treatment response, although a true predictive capacity cannot be excluded because of the limited sample size. Further studies are needed to discern whether F. prausnitzii plays an active role in the resolution of CDI.

  • 2.
    Gili, Nasser J.
    et al.
    Department of Ophthalmology, Örebro University Hospital, Örebro, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine.
    Törnquist, Eva
    Department of Laboratory Medicine, Örebro University Hospital, Örebro, Sweden.
    Crafoord, Sven
    Department of Ophthalmology, Örebro University Hospital, Örebro, Sweden.
    Bäckman, Anders
    Örebro University, School of Medical Sciences. Department of Clinical Research Laboratory.
    Preoperative preparation of eye with chlorhexidine solution significantly reduces bacterial load prior to 23-gauge vitrectomy in Swedish health care2018In: BMC Ophthalmology, E-ISSN 1471-2415, Vol. 18, article id 167Article in journal (Refereed)
    Abstract [en]

    Background: Bacteria in the conjunctiva present a potential risk of vitreous cavity infection during 23-gauge pars plana vitrectomy (PPV). Current preoperative procedures used in Sweden include irrigation with chlorhexidine solution (CHX) 0.05% only and no iodine solutions. We evaluated the bacterial diversity and load before and after this single antibacterial measure.

    Methods: In a prospective, consecutive cohort we investigated bacterial growth in samples from 40 eyes in 39 consecutive individuals subjected to vitrectomy. A conjunctival specimen was collected from each preoperative patient before and after irrigating of eye with CHX, 0.05% solution. Iodine was not used during any part of the surgery. One drop of chloramphenicol was administered prior to surgery. Samples from vitreous cavity were collected at the beginning and end of vitrectomy. All conjunctival specimens were cultured for different species and quantified using colony forming units (CFU).

    Results: There was a significant 82% reduction in the total number of CFUs for all bacteria in all eyes (P < 0.0001), and 90% reduction for coagulase negative staphylococci (CoNS) alone (P = 0.0002). The number of eyes with positive bacterial growth in conjunctival samples decreased from 33 to 18 after irrigation with CHX (P = 0.0023). The most common bacteria prior to surgery were CoNS (70%), Propionibacterium acnes (55%) and Corynebacterium species (36%). No case of post-vitrectomy endophthalmitis was reported during mean follow-up time, which was 4.6 +/- 2.3 (range; 1.5 to 9) months.

    Conclusions: Patients undergoing PPV harbored bacteria in conjunctiva capable of causing post-vitrectomy endophthalmitis. Preoperative preparation with CHX significantly reduced the bacterial load in the conjunctival samples subsequently leading to very low inoculation rates in recovered vitreous samples. Thus, CHX used as a single disinfectant agent might be an effective preoperative procedure for eye surgery in Sweden. This is a relatively small study but the results could be a reference for other intraocular surgeries.

  • 3.
    Gunnarsson, Lars-Gunnar
    et al.
    Örebro University, School of Medical Sciences.
    Julin, Per
    Karolinska institutet, Stockholm; Neurologiska rehabiliteringskliniken, Stora Sköndal, Sköndal.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences.
    Inflammation, långvarig trötthet och värk: uppdatering av kunskapsläget2020In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 117, article id 20008Article, review/survey (Refereed)
  • 4.
    Johansson, Karin
    et al.
    Department of Laboratory Medicine, Molecular Diagnostics, Örebro University Hospital, Örebro, Sweden.
    Karlsson, Hanna
    Department of Laboratory Medicine, Molecular Diagnostics, Örebro University Hospital, Örebro, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Clostridium difficile infection diagnostics: evaluation of the C. DIFF Quik Chek Complete assay, a rapid enzyme immunoassay for detection of toxigenic C. difficile in clinical stool samples2016In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 124, no 11, p. 1016-1020Article in journal (Refereed)
    Abstract [en]

    Diagnostic testing for Clostridium difficile infection (CDI) has, in recent years, seen the introduction of rapid dual-EIA (enzyme immunoassay) tests combining species-specific glutamate dehydrogenase (GDH) with toxin A/B. In a prospective study, we compared the C. DIFF Quik Chek Complete test to a combination of selective culture (SC) and loop-mediated isothermal amplification (LAMP) of the toxin A gene. Of 419 specimens, 68 were positive in SC including 62 positive in LAMP (14.7%). The combined EIA yielded 82 GDH positives of which 47 were confirmed toxin A/B positive (11%) corresponding to a sensitivity and specificity of 94% for GDH EIA compared to SC and for toxin A/B EIA a sensitivity of 71% and a specificity of 99% compared to LAMP. Twenty different PCR ribotypes were evenly distributed except for UK 081 where only 25% were toxin A/B positive compared to LAMP. We propose a primary use of a combined GDH toxin A/B EIA permitting a sensitive 1-h result of 379 of 419 (90%, all negatives plus GDH and toxin EIA positives) referred specimens. The remaining 10% being GDH positive should be tested for toxin A/B gene on the same day and positive results left to a final decision by the physician.

  • 5.
    Kumar, Nitin
    et al.
    Host-Microbiota Interactions Laboratory, Wellcome Sanger Institute, Hinxton, UK.
    Browne, Hilary P.
    Host-Microbiota Interactions Laboratory, Wellcome Sanger Institute, Hinxton, UK.
    Viciani, Elisa
    Host-Microbiota Interactions Laboratory, Wellcome Sanger Institute, Hinxton, UK.
    Forster, Samuel C.
    Host-Microbiota Interactions Laboratory, Wellcome Sanger Institute, Hinxton, UK; Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia; Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia.
    Clare, Simon
    Wellcome Sanger Institute, Hinxton, UK.
    Harcourt, Katherine
    Wellcome Sanger Institute, Hinxton, UK.
    Stares, Mark D.
    Host-Microbiota Interactions Laboratory, Wellcome Sanger Institute, Hinxton, UK.
    Dougan, Gordon
    Wellcome Sanger Institute, Hinxton, UK.
    Fairley, Derek J.
    Belfast Health and Social Care Trust, Belfast, Northern, Ireland.
    Roberts, Paul
    University of Liverpool, Liverpool, UK.
    Pirmohamed, Munir
    University of Liverpool, Liverpool, UK.
    Clokie, Martha R. J.
    Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK.
    Jensen, Mie Birgitte Frid
    Department of Clinical Microbiology, Slagelse Hospital, Slagelse, Denmark.
    Hargreaves, Katherine R.
    Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK.
    Ip, Margaret
    Department of Microbiology, Chinese University of Hong Kong, Shatin, Hong Kong.
    Wieler, Lothar H.
    Institute of Microbiology and Epizootics, Department of Veterinary Medicine, Freie Universität Berlin, Berlin, Germany; Robert Koch Institute, Berlin, Germany.
    Seyboldt, Christian
    Institute of Bacterial Infections and Zoonoses, Federal Research Institute for Animal Health (Friedrich-Loeffler-Institut), Jena, Germany.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, Örebro University Hospital Örebro, Örebro, Sweden.
    Riley, Thomas V.
    Department of Microbiology, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Nedlands, Western Australia, Australia; School of Pathology & Laboratory Medicine, The University of Western Australia, Nedlands, Western Australia, Australia.
    Kuijper, Ed J.
    Section Experimental Bacteriology, Department of Medical Microbiology, Leiden University Medical Center, Leiden, Netherlands.
    Wren, Brendan W.
    Department of Pathogen Molecular Biology, London School of Hygiene and Tropical Medicine, University of London, London, UK.
    Lawley, Trevor D.
    Host-Microbiota Interactions Laboratory, Wellcome Sanger Institute, Hinxton, UK.
    Adaptation of host transmission cycle during Clostridium difficile speciation2019In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 51, no 9, p. 1315-1320Article in journal (Refereed)
    Abstract [en]

    Bacterial speciation is a fundamental evolutionary process characterized by diverging genotypic and phenotypic properties. However, the selective forces that affect genetic adaptations and how they relate to the biological changes that underpin the formation of a new bacterial species remain poorly understood. Here, we show that the spore-forming, healthcare-associated enteropathogen Clostridium difficile is actively undergoing speciation. Through large-scale genomic analysis of 906 strains, we demonstrate that the ongoing speciation process is linked to positive selection on core genes in the newly forming species that are involved in sporulation and the metabolism of simple dietary sugars. Functional validation shows that the new C. difficile produces spores that are more resistant and have increased sporulation and host colonization capacity when glucose or fructose is available for metabolism. Thus, we report the formation of an emerging C. difficile species, selected for metabolizing simple dietary sugars and producing high levels of resistant spores, that is adapted for healthcare-mediated transmission.

  • 6.
    Kättström, Magdalena
    et al.
    Örebro University, School of Medical Sciences. Section of Hematology, Department of Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Uggla, Bertil
    Örebro University, School of Medical Sciences. Section of Hematology, Department of Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Tina, Elisabet
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Clinical Research Laboratory, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Kimby, Eva
    Unit of Hematology, Department of Medicine, Karolinska Institute, Stockholm, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, Clinical Microbiology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Athlin, Simon
    Örebro University, School of Medical Sciences.
    Improved plasmablast response after repeated pneumococcal revaccinations following primary immunization with 13-valent pneumococcal conjugate vaccine or 23-valent pneumococcal polysaccharide vaccine in patients with chronic lymphocytic leukemia2023In: Vaccine, ISSN 0264-410X, E-ISSN 1873-2518, Vol. 41, no 9, p. 3128-3136Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Patients with chronic lymphocytic leukemia (CLL) show an immune dysfunction with increased risk of infections and poor response to vaccination. Streptococcus pneumoniae is a common cause of morbidity and mortality in CLL patients. In a previous randomized clinical trial, we found a superior immune response in CLL patients receiving conjugated pneumococcal vaccine compared to non-conjugated vaccine. The response to revaccination in CLL patients is scarcely studied. In this study, early humoral response to repeated revaccinations with pneumococcal vaccines was evaluated, by determination of B cell subsets and plasmablast dynamics in peripheral blood.

    METHOD: CLL patients (n = 14) and immunocompetent controls (n = 31) were revaccinated with a 13-valent pneumococcal conjugate vaccine (PCV13) after previous primary immunization (3-6 years ago) with PCV13 or a 23-valent pneumococcal polysaccharide vaccine (PPSV23). Eight weeks after the first revaccination, all CLL patients received a second revaccination with PCV13 or PPSV23. B cell subsets including plasmablasts were analyzed in peripheral blood by flow cytometry, before and after the first and the second revaccination.

    RESULTS: None of the CLL patients, but all controls, had detectable plasmablasts at baseline (p < 0.001). After the first revaccination with PCV13, the plasmablast proportions did not increase in CLL patients (p = 0.13), while increases were seen in controls (p < 0.001). However, after a second revaccination with PCV13 or PPSV23, plasmablasts increased compared to baseline also in CLL patients (p < 0.01). If no response was evident after first revaccination, only a second revaccination with PCV13 increased plasmablasts in contrast to PPSV23 revaccination. Patients with hypogammaglobulinemia and ongoing/previous CLL specific treatment responded poorly, also to a second revaccination.

    CONCLUSION: In CLL patients, pneumococcal revaccination induced minor early plasmablast response compared to controls, but the response improved using a strategy of repeated doses with of conjugated T cell dependent pneumococcal vaccine.

  • 7.
    König, Julia
    et al.
    Örebro University, School of Medical Sciences.
    Siebenhaar, A.
    Hamburg, Germany.
    Högenauer, C.
    Graz, Austria.
    Arkkila, P.
    Helsinki, Finland.
    Nieuwdorp, M.
    Amsterdam, The Netherlands; Gothenburg, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences.
    Ponsioen, C. Y.
    Amsterdam, The Netherlands.
    Rosien, U.
    Hamburg, Germany.
    Rossen, N. G.
    Amsterdam, The Netherlands.
    Satokari, R.
    Helsinki, Finland.
    Stallmach, A.
    Jena, Germany.
    de Vos, W.
    Helsinki, Finland; Wageningen, The Netherlands.
    Keller, J.
    Hamburg, Germany.
    Brummer, Robert Jan
    Örebro University, School of Medical Sciences.
    Consensus report: Faecal microbiota transfer - clinical applications and procedures2017In: Alimentary Pharmacology and Therapeutics, ISSN 0269-2813, E-ISSN 1365-2036, Vol. 45, no 2, p. 222-239Article, review/survey (Refereed)
    Abstract [en]

    Background: Faecal microbiota transplantation or transfer (FMT) aims at replacing or reinforcing the gut microbiota of a patient with the microbiota from a healthy donor. Not many controlled or randomised studies have been published evaluating the use of FMT for other diseases than Clostridium difficile infection, making it difficult for clinicians to decide on a suitable indication.

    Aim: To provide an expert consensus on current clinical indications, applications and methodological aspects of FMT.

    Methods: Well-acknowledged experts from various countries in Europe have contributed to this article. After literature review, consensus has been achieved by repetitive circulation of the statements and the full manuscript among all authors with intermittent adaptation to comments (using a modified Delphi process). Levels of evidence and agreement were rated according to the GRADE system. Consensus was defined a priori as agreement by at least 75% of the authors.

    Results: Key recommendations include the use of FMT in recurrent C. difficile infection characterised by at least two previous standard treatments without persistent cure, as well as its consideration in severe and severe-complicated C. difficile infection as an alternative to total colectomy in case of early failure of antimicrobial therapy. FMT in inflammatory bowel diseases (IBD), irritable bowel syndrome (IBS) and metabolic syndrome should only be performed in research settings.

    Conclusions: Faecal microbiota transplantation or transfer is a promising treatment for a variety of diseases in which the intestinal microbiota is disturbed. For indications other than C. difficile infection, more evidence is needed before more concrete recommendations can be made.

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  • 8.
    Magnusson, Cecilia
    et al.
    Department of Infectious Diseases, Region Jönköping County, Jönköping and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Mernelius, Sara
    Laboratory Medicine, Region Jönköping County, Jönköping and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Bengnér, Malin
    Office for control of Communicable Diseases, Region Jönköping County, Jönköping, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Faculty of Medicine and Health, Department of Laboratory Medicine, National Reference Laboratory for Clostridioides difficile, Clinical Microbiology.
    Serrander, Lena
    Department of Clinical and Experimental Medicine, Division of Clinical Microbiology, Faculty of Health Sciences, Linköping University, Sweden.
    Forshell, Sophie
    Department of Infectious Diseases, Region Jönköping County, Jönköping and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
    Matussek, Andreas
    Laboratory Medicine, Region Jönköping County, Jönköping and Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden; Division of Laboratory Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Division of Laboratory Medicine, Oslo University Hospital, Oslo, Norway .
    Characterization of a Clostridioides difficile outbreak caused by PCR ribotype 046, associated with increased mortality2022In: Emerging Microbes & Infections, E-ISSN 2222-1751, Vol. 11, no 1, p. 850-859Article in journal (Refereed)
    Abstract [en]

    This study describe a large nosocomial outbreak of Clostridioides difficile infections (CDI) dominated by ribotype (RT) 046 in a Swedish hospital. The aim of the present study was to examine the pathogenicity of this RT, explore epidemiological links by whole genome sequencing (WGS) and evaluate different interventions implemented to stop the outbreak. Clinical isolates (n= 366) collected during and after the outbreak were ribotyped and 246 isolates were subjected to WGS. Medical records of patients infected with the seven most common RTs were evaluated. RT046 was spread effectively throughout the hospital and was the most common among the 44 different RTs found (114/366 isolates). Infection with RT046 was associated with higher mortality compared to other strains (20.2% to 7.8%), although there were no differences in concomitant disease, age or antibiotic treatment. In order to control the outbreak, a number of measures were successfully implemented.

  • 9.
    Norén, Torbjörn
    Örebro University, Department of Clinical Medicine.
    Clostridium difficile: epidemiology and antibiotic resistance2006Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Clostridium difficile is a spore-forming toxin-producing intestinal bacterium abundant in soils and waters. This pathogen relies on increased growth by a disturbed intestinal microflora and the production of two cytotoxins, toxin A and toxin B, which may cause anything from mild self-limiting C. difficile associated diarrhea (CDAD) to severe and fatal pseudomembranous colitis (PMC). Typically CDAD following antibiotic therapy is due either to overgrowth of endogenous C. difficile or through spores transmitted from the environment. The hospital setting provides frequent antibiotic use and the source of numerous infective spores from CDAD patients, the environment or nursing staff. Today we experience a 10-fold increase of incidence in the US and Canada (1991-2003) apparently due to a current epidemic C. difficile strain (NAP1/027). Current incidence from Canada is estimated to 156/100 000 compared to 50/100 000 in Sweden 1995.

    In the following thesis, investigations of CDAD in Örebro County in central Sweden resulted in the discovery an epidemic nosocomial C. difficile strain (SE17, serogroup C), found to be clindamycin-resistant. The majority of the isolates carried a gene (ermB) related to this resitance. We found an overall incidence during 1999-2000 of 97/100 000 or, if including recurrent episodes, 135/100 000 i.e. more than 100% increase since 1995. The incidence among hospitalized individuals was 1300-fold that in the community and 78% of episodes were classified as hospital-associated. This reflects a 37-fold difference in antibiotic consumption, as well as the predominance of the resistant SE17 hospital-associated strain (22% of hospital isolates compared to 6% of community isolates, p=0.008). Only 10% of the recurrent cases were found to be reinfections indicating that CDAD is mainly caused by endogenous strains and not by hospital transmission.

    Recent reports on failure of standard metronidazole therapy urge for alternative treatment agents and fusidic acid has been proven as effective in the treatment of CDAD. We could verify this, but in both treatment groups we found that persistence of C. difficile isolates post-treatment related to an increased risk of recurrent CDAD compared to the patients who were culture negative at follow-up (p=0.03). Most importantly, 55% of patients with follow-up isolates and who had been treated with fusidic acid, the strains had developed fusidic acid resistance. The corresponding pre-treatment identity of isolate genotype indicated selection of mutants. Relating to the known fusA resistance mechanism in Staphylococcus aureus we used the published sequence for this gene in Clostridium perfringens and found homologous fusA in the sequence of the referent strain C. difficile 630. Comparing fusA of the resistant mutants with the initial wild-type isolates, we identified novel mutations in fusA as the genetic key to fusidic acid resistance in C. difficile.

    List of papers
    1. Clindamycin resistant strains of Clostridium difficile isolated from cases of C. difficile associated diarrhea (CDAD) in a hospital in Sweden
    Open this publication in new window or tab >>Clindamycin resistant strains of Clostridium difficile isolated from cases of C. difficile associated diarrhea (CDAD) in a hospital in Sweden
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    2002 (English)In: Diagnostic microbiology and infectious disease, ISSN 0732-8893, E-ISSN 1879-0070, Vol. 42, no 2, p. 149-151Article in journal (Refereed) Published
    Abstract [en]

    Fifty three strains of C. difficile recovered from the stools of 13 patients with clinical C. difficile associated diarrhea (CDAD) were analyzed for the presence of the ermB gene, for toxigenicity and fingerprinting profile by PCR based assays. Forty five percent of the isolates were resistant to clindamycin and positive for the ermB gene. All clindamycin resistant isolates were ermB positive and belonged to the same fingerprinting group, suggesting clonal spread. These preliminary results suggest that clindamycin resistant isolates may be common etiologic agents of CDAD in Sweden.

    National Category
    Medical and Health Sciences
    Research subject
    Medicine
    Identifiers
    urn:nbn:se:oru:diva-3198 (URN)10.1016/S0732-8893(01)00337-6 (DOI)
    Available from: 2006-11-23 Created: 2006-11-23 Last updated: 2017-12-14Bibliographically approved
    2. Molecular epidemiology of hospital-associated and community-acquired Clostridium difficile infection in a Swedish county
    Open this publication in new window or tab >>Molecular epidemiology of hospital-associated and community-acquired Clostridium difficile infection in a Swedish county
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    2004 (English)In: Journal of Clinical Microbiology, ISSN 0095-1137, E-ISSN 1098-660X, Vol. 42, no 8, p. 3635-3643Article in journal (Refereed) Published
    Abstract [en]

    All episodes of Clostridium difficile associated diarrhea (CDAD) diagnosed in a defined population of 274,000 including one tertiary and two primary hospitals and their catchment areas were studied during 12 months. The annual CDAD incidence in the county was 97 primary episodes per 100,000, and 78% of all episodes were classified as hospital associated with a mean incidence of 5.3 (range, 1.4 to 6.5) primary episodes per 1,000 admissions. The incidence among hospitalized individuals was 1,300-fold higher than that in the community (33,700 versus 25 primary episodes per 100,000 persons per year), reflecting a 37-fold difference in antibiotic consumption (477 versus 13 defined daily doses [DDD]/1,000 persons/day) and other risk factors. Three tertiary hospital wards with the highest incidence (13 to 36 per 1,000) had CDAD patients of high age (median age of 80 years versus 70 years for other wards, P < 0.001), long hospital stay (up to 25 days versus 4 days), or a high antibiotic consumption rate (up to 2,427 versus 421 DDD/1,000 bed days). PCR ribotyping of C. difficile isolates available from 330 of 372 CDAD episodes indicated nosocomial acquisition of the strain in 17 to 27% of hospital-associated cases, depending on the time interval between index and secondary cases allowed (2 months or up to 12 months), and only 10% of recurrences were due to a new strain of C. difficile (apparent reinfection). In other words, most primary and recurring episodes were apparently caused by the patient's endogenous strain rather than by one of hospital origin. Typing also indicated that a majority of C. difficile strains belonged to international serotypes, and the distribution of types was similar within and outside hospitals and in primary and relapsing CDAD. However, type SE17 was an exception, comprising 22% of hospital isolates compared to 6% of community isolates (P = 0.008) and causing many minor clusters and a silent nosocomial outbreak including 36 to 44% of the CDAD episodes in the three high-incidence wards.

    National Category
    Medical and Health Sciences
    Research subject
    Medicine
    Identifiers
    urn:nbn:se:oru:diva-15678 (URN)10.1128/jcm.42.8.3635-3643.2004 (DOI)000223286500038 ()
    Available from: 2011-05-24 Created: 2011-05-24 Last updated: 2017-12-11Bibliographically approved
    3. Frequent emergence of resistance in Clostridium difficile during treatment of C-difficile-associated diarrhea with Fusidic acid
    Open this publication in new window or tab >>Frequent emergence of resistance in Clostridium difficile during treatment of C-difficile-associated diarrhea with Fusidic acid
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    2006 (English)In: Antimicrobial Agents and Chemotherapy, ISSN 0066-4804, E-ISSN 1098-6596, Vol. 50, no 9, p. 3028-3032Article in journal (Refereed) Published
    Abstract [en]

    Samples from patients with Clostridium difficile-associated diarrhea (CDAD) that were randomized to fusidic acid (n = 59) or metronidazole (n = 55) therapy for 7 days were cultured for Clostridium difficile in feces on days 1, 8 to 13, and 35 to 40. Of the patients who were culture positive only before treatment, 77% (36/47) were permanently cured (no treatment failure and no clinical recurrence), compared to 54% (22/41) of those with persistence of C. difficile at one or both follow-ups (P = 0.03). A similar association between bacterial persistence and a worse outcome of therapy was seen in both treatment groups. Resistance to fusidic acid was found in 1 of 88 pretherapy isolates available, plus in at least 1 subsequent isolate from 55% (11/20) of patients who remained culture-positive after fusidic acid therapy. In 10 of these 11 patients, the resistant follow-up isolate(s) belonged to the same PCR ribotype as the susceptible day 1 isolate, confirming frequent emergence of resistance to fusidic acid during treatment. Despite this, 5 of these 11 patients were permanently cured with fusidic acid, relative to 5 of 9 patients with susceptible C. difficile at follow-up (P = 1.0). None of the 36 PCR ribotypes of C. difficile identified was associated with any particular clinical outcome or emergence of fusidic acid resistance. In conclusion, culture positivity for C. difficile was common after both fusidic acid and metronidazole therapy and was associated with treatment failure or recurrence of CDAD. Development of resistance in C. difficile was frequent in patients given fusidic acid, but it was without apparent negative impact on therapeutic efficacy in the actual CDAD episode.

    National Category
    Medical and Health Sciences
    Research subject
    Medicine
    Identifiers
    urn:nbn:se:oru:diva-15679 (URN)10.1128/AAC.00019-06 (DOI)000240297000019 ()
    Available from: 2011-05-24 Created: 2011-05-24 Last updated: 2017-12-11Bibliographically approved
    4. Nucleotide polymorphisms in fusA associated with post-therapy fusidic acid resistance in Clostridium difficile
    Open this publication in new window or tab >>Nucleotide polymorphisms in fusA associated with post-therapy fusidic acid resistance in Clostridium difficile
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    (English)Manuscript (preprint) (Other academic)
    National Category
    Medical and Health Sciences
    Research subject
    Medicine
    Identifiers
    urn:nbn:se:oru:diva-15681 (URN)
    Available from: 2011-05-24 Created: 2011-05-24 Last updated: 2017-10-17Bibliographically approved
  • 10.
    Norén, Torbjörn
    et al.
    Örebro University, School of Medicine, Örebro University, Sweden. Department of Laboratory Medicine, Microbiology, Örebro University Hospital, Örebro, Sweden.
    Johansson, Karin
    Department of Laboratory Medicine, Microbiology, Örebro University Hospital, Örebro, Sweden.
    Unemo, Magnus
    Department of Laboratory Medicine, Microbiology, Örebro University Hospital, Örebro, Sweden.
    Clostridium difficile PCR ribotype 046 is common among neonatal pigs and humans in Sweden2014In: Clinical Microbiology and Infection, ISSN 1198-743X, E-ISSN 1469-0691, Vol. 20, no 1, p. O2-O6Article in journal (Refereed)
    Abstract [en]

    Clostridium difficile PCR ribotype 046 was found in 67% of neonatal piglets (45/67) sampled from three separate pig-breeding farms in Sweden. Sows from the same farms were tested and 50% were colonized in faeces and 30% were colonized on skin. An environmental source was suggested because identical PCR ribotypes were isolated from faeces as well as externally. Human C.difficile infection outbreaks in southern Sweden by the identical PCR ribotype 046 indicate its zoonotic potential.

  • 11.
    Norén, Torbjörn
    et al.
    Örebro University, Department of Clinical Medicine.
    Tang-Feldman, Yayarayma
    Cohen, Stuart H.
    Silva Jr, Joseph
    Olcén, Per
    Clindamycin resistant strains of Clostridium difficile isolated from cases of C. difficile associated diarrhea (CDAD) in a hospital in Sweden2002In: Diagnostic microbiology and infectious disease, ISSN 0732-8893, E-ISSN 1879-0070, Vol. 42, no 2, p. 149-151Article in journal (Refereed)
    Abstract [en]

    Fifty three strains of C. difficile recovered from the stools of 13 patients with clinical C. difficile associated diarrhea (CDAD) were analyzed for the presence of the ermB gene, for toxigenicity and fingerprinting profile by PCR based assays. Forty five percent of the isolates were resistant to clindamycin and positive for the ermB gene. All clindamycin resistant isolates were ermB positive and belonged to the same fingerprinting group, suggesting clonal spread. These preliminary results suggest that clindamycin resistant isolates may be common etiologic agents of CDAD in Sweden.

  • 12.
    Norén, Torbjörn
    et al.
    Örebro University Hospital. Örebro University, School of Medical Sciences. Dept Lab Med, Örebro University Hospital, Örebro, Sweden.
    Unemo, Magnus
    Örebro University Hospital. Dept Lab Med, Örebro University Hospital, Örebro, Sweden.
    Magnusson, Cecilia
    Dept Infect Control, Ryhov Cty Hosp, Jönköping, Sweden; Dept Infect Dis, Ryhov Cty Hosp, Jönköping, Sweden.
    Eiserman, Maud
    Ryhov Cty Hosp, Jönköping, Sweden.
    Matussek, Andreas
    Div Med Serv, Dept Lab Med, Ryhov Cty Hosp, Jönköping, Sweden.
    Evaluation of the rapid loop-mediated isothermal amplification assay Illumigene for diagnosis of Clostridium difficile in an outbreak situation2014In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, no 2, p. 155-160Article in journal (Refereed)
    Abstract [en]

    An outbreak of Clostridium difficile infection (CDI) at Hoglandet Hospital Eksjo in southern Sweden in 2011 was mainly due to a multidrug-resistant PCR ribotype 046 (30% of all samples). Diagnostics used routinely was the Vidas CDAB assay, but to control the outbreak the rapid loop-mediated isothermal amplification (LAMP) assay Illumigene was introduced and both techniques were compared to Toxigenic culture (TC) prospectively. The LAMP assay had a superior sensitivity, that is, 98% compared to 79% for the Vidas CDAB assay. Most importantly, the mean turn-around-time from collecting sample to result was reduced from 59h to 2h enabling early isolation of patients and effective hygiene precautions. This may potentially decrease the morbidity and nosocomial transmissions of C. difficile.

  • 13.
    Norén, Torbjörn
    et al.
    Örebro University, Department of Clinical Medicine.
    Wullt, M.
    Åkerlund, Thomas
    Bäck, Erik
    Örebro University, Department of Clinical Medicine.
    Odenholt, I.
    Burman, L. G.
    Frequent emergence of resistance in Clostridium difficile during treatment of C-difficile-associated diarrhea with Fusidic acid2006In: Antimicrobial Agents and Chemotherapy, ISSN 0066-4804, E-ISSN 1098-6596, Vol. 50, no 9, p. 3028-3032Article in journal (Refereed)
    Abstract [en]

    Samples from patients with Clostridium difficile-associated diarrhea (CDAD) that were randomized to fusidic acid (n = 59) or metronidazole (n = 55) therapy for 7 days were cultured for Clostridium difficile in feces on days 1, 8 to 13, and 35 to 40. Of the patients who were culture positive only before treatment, 77% (36/47) were permanently cured (no treatment failure and no clinical recurrence), compared to 54% (22/41) of those with persistence of C. difficile at one or both follow-ups (P = 0.03). A similar association between bacterial persistence and a worse outcome of therapy was seen in both treatment groups. Resistance to fusidic acid was found in 1 of 88 pretherapy isolates available, plus in at least 1 subsequent isolate from 55% (11/20) of patients who remained culture-positive after fusidic acid therapy. In 10 of these 11 patients, the resistant follow-up isolate(s) belonged to the same PCR ribotype as the susceptible day 1 isolate, confirming frequent emergence of resistance to fusidic acid during treatment. Despite this, 5 of these 11 patients were permanently cured with fusidic acid, relative to 5 of 9 patients with susceptible C. difficile at follow-up (P = 1.0). None of the 36 PCR ribotypes of C. difficile identified was associated with any particular clinical outcome or emergence of fusidic acid resistance. In conclusion, culture positivity for C. difficile was common after both fusidic acid and metronidazole therapy and was associated with treatment failure or recurrence of CDAD. Development of resistance in C. difficile was frequent in patients given fusidic acid, but it was without apparent negative impact on therapeutic efficacy in the actual CDAD episode.

  • 14.
    Norén, Torbjörn
    et al.
    Örebro University, Department of Clinical Medicine.
    Åkerlund, T.
    Bäck, Erik
    Örebro University, Department of Clinical Medicine.
    Sjöberg, L.
    Persson, I.
    Alriksson, I.
    Burman, L. G.
    Molecular epidemiology of hospital-associated and community-acquired Clostridium difficile infection in a Swedish county2004In: Journal of Clinical Microbiology, ISSN 0095-1137, E-ISSN 1098-660X, Vol. 42, no 8, p. 3635-3643Article in journal (Refereed)
    Abstract [en]

    All episodes of Clostridium difficile associated diarrhea (CDAD) diagnosed in a defined population of 274,000 including one tertiary and two primary hospitals and their catchment areas were studied during 12 months. The annual CDAD incidence in the county was 97 primary episodes per 100,000, and 78% of all episodes were classified as hospital associated with a mean incidence of 5.3 (range, 1.4 to 6.5) primary episodes per 1,000 admissions. The incidence among hospitalized individuals was 1,300-fold higher than that in the community (33,700 versus 25 primary episodes per 100,000 persons per year), reflecting a 37-fold difference in antibiotic consumption (477 versus 13 defined daily doses [DDD]/1,000 persons/day) and other risk factors. Three tertiary hospital wards with the highest incidence (13 to 36 per 1,000) had CDAD patients of high age (median age of 80 years versus 70 years for other wards, P < 0.001), long hospital stay (up to 25 days versus 4 days), or a high antibiotic consumption rate (up to 2,427 versus 421 DDD/1,000 bed days). PCR ribotyping of C. difficile isolates available from 330 of 372 CDAD episodes indicated nosocomial acquisition of the strain in 17 to 27% of hospital-associated cases, depending on the time interval between index and secondary cases allowed (2 months or up to 12 months), and only 10% of recurrences were due to a new strain of C. difficile (apparent reinfection). In other words, most primary and recurring episodes were apparently caused by the patient's endogenous strain rather than by one of hospital origin. Typing also indicated that a majority of C. difficile strains belonged to international serotypes, and the distribution of types was similar within and outside hospitals and in primary and relapsing CDAD. However, type SE17 was an exception, comprising 22% of hospital isolates compared to 6% of community isolates (P = 0.008) and causing many minor clusters and a silent nosocomial outbreak including 36 to 44% of the CDAD episodes in the three high-incidence wards.

  • 15.
    Norén, Torbjörn
    et al.
    Örebro University, School of Health and Medical Sciences.
    Åkerlund, T.
    Wullt, M.
    Burman, L. G.
    Unemo, M.
    Mutations in fusA associated with posttherapy fusidic acid resistance in Clostridium difficile2007In: Antimicrobial Agents and Chemotherapy, ISSN 0066-4804, E-ISSN 1098-6596, Vol. 51, no 5, p. 1840-1843Article in journal (Refereed)
    Abstract [en]

    In silico, we identified fusA (2,067 bp) in Clostridium difficile 630. Sequencing of fusA in posttherapy fusidic acid-resistant C. difficile isolates from 12 patients with C. difficile-associated diarrhea (CDAD) identified fusA mutations, one or two nonsynonymous substitutions, or in one case a deletion of one codon associated with resistance. Five of these mutations have previously been described in fusA of fusidic acid-resistant Staphylococcus aureus, but seven were novel fusA mutations. Fusidic acid monotherapy for CDAD seemed to rapidly select conserved resistant mutants.

  • 16.
    Norén, Torbjörn
    et al.
    Örebro University, Department of Clinical Medicine.
    Åkerlund, T.
    Wullt, M.
    Burman, L. G.
    Unemo, M.
    Nucleotide polymorphisms in fusA associated with post-therapy fusidic acid resistance in Clostridium difficileManuscript (preprint) (Other academic)
  • 17.
    Rizzardi, Kristina
    et al.
    Public Health Agency of Sweden, Solna, Sweden .
    Norén, Torbjörn
    Örebro University, School of Medical Sciences.
    Aspevall, Olov
    Public Health Agency of Sweden, Solna, Sweden .
    Mäkitalo, Barbro
    Public Health Agency of Sweden, Solna, Sweden .
    Toepfer, Michael
    Unilabs Clinical Microbiology, Skövde, Sweden.
    Johansson, Åsa
    Växjö Hospital, Växjö, Sweden.
    Åkerlund, Thomas
    Public Health Agency of Sweden, Solna, Sweden .
    National Surveillance for Clostridioides difficile Infection, Sweden, 2009-20162018In: Emerging Infectious Diseases, ISSN 1080-6040, E-ISSN 1080-6059, Vol. 24, no 9, p. 1617-1625Article in journal (Refereed)
    Abstract [en]

    We report results from a national surveillance program for Clostridioides difficile infection (CDI) in Sweden, where CDI incidence decreased by 22% and the proportion of multidrug-resistant isolates decreased by 80% during 2012-2016. Variation in incidence between counties also diminished during this period, which might be attributable to implementation of nucleic acid amplification testing as the primary diagnostic tool for most laboratories. In contrast to other studies, our study did not indicate increased CDI incidence attributable the introduction of nucleic acid amplification testing. Our results also suggest that successful implementation of hygiene measures is the major cause of the observed incidence decrease. Despite substantial reductions in CDI incidence and prevalence of multidrug-resistant isolates, Sweden still has one of the highest CDI incidence levels in Europe. This finding is unexpected and warrants further investigation, given that Sweden has among the lowest levels of antimicrobial drug use.

  • 18.
    Rizzardi, Kristina
    et al.
    Department of Microbiology, Public Health Agency of Sweden, Solna, Sweden.
    Åkerlund, Thomas
    Department of Microbiology, Public Health Agency of Sweden, Solna, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences.
    Matussek, Andreas
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska University Hospital, Huddinge, Sweden; Karolinska University Laboratory, Solna, Stockholm, Sweden; Department of Laboratory Medicine, Jönköping, Jönköping County, Sweden.
    Impact of ribotype on Clostridioides difficile diagnostics2020In: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 39, no 5, p. 847-853Article in journal (Refereed)
    Abstract [en]

    This study investigates the performance of diagnostic methods for detection of Clostridioides difficile infection in Sweden, including impact of PCR ribotype on diagnostic performance. Between 2011 and 2016, a total of 17,878 stool samples from 26 laboratories were tested by either well-type enzyme immunoassays (EIAs), membrane bound EIAs, cell cytotoxicity neutralization assay (CTA), or nucleic acid amplification tests (NAATs) and subsequently cultured for C. difficile. Roughly half of the samples (9454/17878) were subjected to diagnostic testing both on the fecal sample and on the 1323 isolated C. difficile strains. All C. difficile isolates were typed by PCR ribotyping, and the isolates were classified as toxigenic or non-toxigenic based on the empirical knowledge of the association between toxin-positivity and ribotype. The overall sensitivity, specificity, and positive and negative predictive values were highest for NAATs and membrane EIAs. Ribotype-specific sensitivity varied greatly between methods and ribotypes. All methods had 100% sensitivity against ribotype 027 and 013. For other types, the sensitivity ranged from 33 to 85% in fecal samples and from 78 to 100% on isolates. For the most prevalent ribotypes (014, 020, and 001), the sensitivity varied between 38 and 100% in the fecal samples, with the lowest sensitivity observed for well-type EIAs and CTA. The large variation in diagnostic sensitivity implies that type distribution significantly affects the outcome when evaluating diagnostic performance. Furthermore, performing comparative studies of diagnostic tests in settings with high prevalence of ribotype 027 will overestimate the general performance of diagnostic tests.

  • 19.
    Rosdahl, Anja
    et al.
    Örebro University, School of Medical Sciences. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Hellgren, F.
    Department of Medicine Solna, Karolinska institutet and Karolinska University Hospital, Stockholm, Sweden; Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Smolander, J.
    Department of Renal Medicine, Danderyd Hospital, Stockholm, Sweden.
    Wopenka, U.
    Department of Renal Medicine, Örebro University Hospital, Örebro, Sweden.
    Loré, K.
    Department of Medicine Solna, Karolinska institutet and Karolinska University Hospital, Stockholm, Sweden. Center for Molecular Medicine, Karolinska Institutet..
    Askling H., H.
    Academic Specialist Center, Stockholm County Healthcare Area, Region Stockholm, Sweden; Division of Infectious Diseases, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Cellular and humoral response to SARS-CoV-2 vaccine BNT162b2 in 2 adults with Chronic Kidney Disease stage 4 and 5Manuscript (preprint) (Other academic)
  • 20.
    Rosdahl, Anja
    et al.
    Örebro University, School of Medical Sciences. Dept. of Infectious Diseases, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Herzog, Christian
    Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland .
    Frösner, Gert
    Institute of Virology, Technical University of Munich / Helmholtz Zentrum München, Munich, Germany.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Dept. of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Rombo, Lars
    Centre for Clinical Research, Sörmland, Uppsala University, Eskilstuna, Sweden.
    Askling, Helena H.
    Dept. of Medicine Solna, Unit for Infectious Diseases, Karolinska Institutet, Stockholm, Sweden; Dept. of Communicable Diseases Control and Prevention, Eskilstuna, Sweden.
    An extra priming dose of hepatitis A vaccine to adult patients with rheumatoid arthritis and drug induced immunosuppression: A prospective, open-label, multi-center study2018In: Travel Medicine and Infectious Disease, ISSN 1477-8939, E-ISSN 1873-0442, Vol. 21, p. 43-50Article in journal (Refereed)
    Abstract [en]

    Background: Previous studies have indicated that a pre-travel single dose of hepatitis A vaccine is not sufficient as protection against hepatitis A in immunocompromised travelers. We evaluated if an extra dose of hepatitis A vaccine given shortly prior to traveling ensures seroconversion.

    Method: Patients with rheumatoid arthritis (n = 69, median age = 55 years) treated with Tumor Necrosis Factor inhibitor(TNFi) and/or Methotrexate (MTX) were immunized with two doses of hepatitis A vaccine, either as double dose or four weeks apart, followed by a booster dose at six months. Furthermore, 48 healthy individuals, median age = 60 years were immunized with two doses, six months apart. Anti-hepatitis A antibodies were measured at 0, 1, 2, 6, 7 and 12 months.

    Results: Two months after the initial vaccination, 84% of the RA patients had protective antibodies, compared to 85% of the healthy individuals. There was no significant difference between the two vaccine schedules. At twelve months, 99% of RA patients and 100% of healthy individuals had seroprotective antibodies.

    Conclusion: An extra priming dos of hepatitis A vaccine prior to traveling offered an acceptable protection in individuals treated with TNFi and/or MTX. This constitutes an attractive pre-travel solution to this vulnerable group of patients.

  • 21.
    Rosdahl, Anja
    et al.
    Örebro University, School of Medical Sciences. Dept. of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Herzog, Christian
    Swiss Tropical and Public Health Institute, Basel, Switzerland; University of Basel, Basel, Switzerland.
    Frösner, Gert
    Institute of Virology, Technical University of Munich / Helmholtz Zentrum München, Munich, Germany.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Dept. of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Rombo, Lars
    Centre for Clinical Research, Sörmland, Uppsala University, Eskilstuna, Sweden.
    Askling, Helena H.
    Karolinska Institutet, Dept. of Medicine/Solna, Unit for Infectious Diseases, Stockholm, Sweden; Dept. of Communicable Diseases Control and Prevention, Sörmland, Eskilstuna, Sweden.
    Corrigendum to " An extra priming dose of hepatitis A vaccine to adult patients with rheumatoid arthritis and drug induced immunosuppression - A prospective, open-label, multi-center study" [Trav. Med. Infect. Dis. 21, January-February 2018, 43-50]2019In: Travel Medicine and Infectious Disease, ISSN 1477-8939, E-ISSN 1873-0442, Vol. 27, p. 115-115Article in journal (Refereed)
  • 22.
    Sjöberg, Maria
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Eriksson, Mats
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital. Centre for Health Care Sciences, Örebro University Hospital, Örebro, Sweden.
    Andersson, Josefin
    Department of Laboratory Medicine, Microbiology, Örebro University Hospital, Örebro, Sweden.
    Norén, Torbjörn
    Örebro University Hospital. Department of Laboratory Medicine, Microbiology, Örebro University Hospital, Örebro, Sweden.
    Transmission of Clostridium difficile spores in isolation room environments and through hospital beds2014In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 122, no 9, p. 800-803Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to determine the dissemination of Clostridium difficile (CD) spores in a hospital setting where the potassium monopersulfate-based disinfectant VirkonTM was used for cleaning. In the initial part of the study, we sampled 16 areas of frequent patient contact in 10 patient rooms where a patient with CD infection (CDI) had been accommodated. In the second part of the study, we obtained samples from 10 patient beds after discharge of CDI patients, both before and after the beds were cleaned. In the first part, CDspores were isolated in only 30% of the rooms. In the second part, which focused on transmission to hospital beds, C. difficile was found in four of 10 beds either before or after cleaning. In conclusion, in both parts of the study, we demonstrated a moderate spread of CD spores to the environment despite routine cleaning procedures involving VirkonTM. 

  • 23.
    Stenberg, Reidun
    et al.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of University Research Centre, Örebro University Faculty of Medicine and Health, Örebro, Sweden; Child Rehabilitation Centre, Halltorp, Örebro, Sweden Halltorp, Örebro, Sweden.
    Brummer, Robert Jan
    Örebro University, School of Medical Sciences.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, National Reference Laboratory for Clostridioides difficile, Clinical Microbiology.
    Faecal transplantation in a 2-year-old child with therapy-resistant Clostridiodes difficile infection2022In: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 111, no 8, p. 1628-1629Article in journal (Refereed)
  • 24.
    Säll, Olof
    et al.
    Örebro University, School of Medical Sciences. Faculty of Medicine and Health, Department of Infectious Diseases, Örebro University, Örebro, Sweden.
    Johansson, Karin
    Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden; , Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Norén, Torbjörn
    Örebro University, School of Medicine, Örebro University, Sweden. Department of Laboratory Medicine, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden; , Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Low colonization rates of Clostridium difficile among patients and healthcare workers at Örebro University Hospital in Sweden2015In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 123, no 3, p. 240-244Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to investigate the rate of asymptomatic colonization rate of Clostridium difficile among both healthcare workers (HCWs) and patients in a hospital ward in Sweden. In a prospective observational study, asymptomatic HCWs (n=22) (22/60; 37%) attending patients in an infectious disease ward in Sweden participated and were screened once for C. difficile. At the same time, 58 consecutive patients (58/227; 26%) admitted to the same ward were screened for C. difficile, first at admission and thereafter two times weekly. Fecal samples were obtained by rectal swabs and cultured anaerobically using both cycloserine-cefoxitin-fructose agar and enrichment (Cooked Meat broth). All samples were also tested by loop-mediated isothermal amplification and isolates were tested for the presence of toxin A or B by enzyme immunoassay. None of the analyzed fecal samples from HCWs contained C. difficile. Among the patients during a 2-month observational period, three of the 58 patients (5.2%) were culture positive regarding C. difficile on admission and one additional patient became asymptomatically colonized with C. difficile during the hospital stay. Thus, the colonization rates were 0% (0/22) (95% confidence interval (CI): 0-15.4%) among HCWs and 5.2% (3/58) (95% CI: 1.1-14.4%) among patients at admission. As the HCWs were screened only once, we have not studied transient colonization. In conclusion, with observed low colonization rates, we find no support that HCWs would be an important source for C. difficile transmission.

  • 25.
    Tschudin-Sutter, S.
    et al.
    Division of Infectious Diseases and Hospital Epidemiology, University Hospital Basel, University Basel, Basel, Switzerland.
    Kuijper, E. J.
    Department of Medical Microbiology, Centre for Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands.
    Durovic, A.
    Division of Infectious Diseases and Hospital Epidemiology, University Hospital Basel, University Basel, Basel, Switzerland.
    Vehreschild, M. J. G. T.
    Department I of Internal Medicine, University Hospital of Cologne, Cologne, Germany; German Centre for Infection Research (DZIF), Partner Site Bonn-Cologne, Germany.
    Barbut, F.
    National Reference Laboratory for Clostridium difficile, Paris, France.
    Eckert, C.
    National Reference Laboratory for Clostridium difficile, Paris, France.
    Fitzpatrick, F.
    Departments of Clinical Microbiology, Royal College of Surgeons in Ireland and Beaumont Hospital, Ireland.
    Hell, M.
    Department of Medical Microbiology and Infection Control, Academic Teaching Laboratories-Medilab OG, Paracelsus Medizinische Privatuniversität (PMU), Salzburg, Austria.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, Clinical Microbiology.
    O'Driscoll, J.
    Department of Medical Microbiology, Stoke Mandeville Hospital, Aylesbury, UK.
    Coia, J.
    Scottish Microbiology Reference Laboratories, Glasgow, UK.
    Gastmeier, P.
    Institute of Hygiene and Environmental Medicine, Charité, Universitätsmedizin Berlin, Berlin, Germany.
    von Müller, L.
    Institute for Medical Microbiology and Hygiene, University of Saarland Medical Center, State Laboratory of Saarland, Consiliary Laboratory for Clostridium difficile, Homburg/Saar, Germany.
    Wilcox, M. H.
    Department of Microbiology, Leeds Teaching Hospitals, Leeds, UK; University of Leeds, Leeds, UK.
    Widmer, A. F.
    Division of Infectious Diseases and Hospital Epidemiology, University Hospital Basel, University Basel, Basel, Switzerland.
    Guidance document for prevention of Clostridium difficile infection in acute healthcare settings2018In: Clinical Microbiology and Infection, ISSN 1198-743X, E-ISSN 1469-0691, Vol. 24, no 10, p. 1051-1054, article id S1198-743X(18)30195-2Article, review/survey (Refereed)
    Abstract [en]

    SCOPE: Clostridium difficile infection (CDI) is the most important infective cause of healthcare-associated diarrhoea in high income countries and one of the most important healthcare-associated pathogens in both Europe and the United States. It is associated with high morbidity and mortality resulting in both societal and financial burden. A significant proportion of this burden is potentially preventable by a combination of targeted infection prevention and control measures and antimicrobial stewardship. The aim of this guidance document is to provide an update on recommendations for prevention of CDI in acute care settings to provide guidance to those responsible for institutional infection prevention and control programmes.

    METHODS: An expert group was set up by the European society of clinical microbiology and infectious diseases (ESCMID) Study Group for C. difficile (ESGCD), which performed a systematic review of the literature on prevention of CDI in adults hospitalized in acute care settings and derived respective recommendations according to the GRADE approach. Recommendations are stratified for both outbreak and endemic settings.

    QUESTIONS ADDRESSED BY THE GUIDELINE AND RECOMMENDATIONS: This guidance document provides thirty-six statements on strategies to prevent CDI in acute care settings, including 18 strong recommendations. No recommendation was provided for three questions.

  • 26.
    van Prehn, Joffrey
    et al.
    Department of Medical Microbiology, Centre for Infectious Diseases, Leiden University Medical Center, Leiden, the Netherlands.
    Reigadas, Elena
    Department of Clinical Microbiology and Infectious Diseases, Hospital General Universitario Gregorio Marañón, Madrid, Spain.
    Vogelzang, Erik H.
    Department of Medical Microbiology and Infection Control, Amsterdam University Medical Center, Location VUmc, Amsterdam, the Netherlands.
    Bouza, Emilio
    Department of Clinical Microbiology and Infectious Diseases, Hospital General Universitario Gregorio Marañón, Madrid, Spain.
    Hristea, Adriana
    University of Medicine and Pharmacy Carol Davila, National Institute for Infectious Diseases Prof Dr Matei Bals, Romania.
    Guery, Benoit
    Infectious Diseases Specialist, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
    Krutova, Marcela
    Department of Medical Microbiology, Charles University in Prague and Motol University Hospital, Czech Republic.
    Norén, Torbjörn
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine, National Reference Laboratory for Clostridioides difficile, Clinical Microbiology, Örebro University Hospital, Örebro, Sweden.
    Allerberger, Franz
    Austrian Agency for Health and Food Safety (AGES), Vienna, Austria.
    Coia, John E.
    Department of Clinical Microbiology, Hospital South West Jutland and Department of Regional Health Research IRS, University of Southern Denmark, Esbjerg, Denmark.
    Goorhuis, Abraham
    Department of Infectious Diseases, Amsterdam University Medical Centers, Academic Medical Center, Amsterdam, the Netherlands.
    van Rossen, Tessel M.
    Department of Medical Microbiology and Infection Control, Amsterdam University Medical Center, Location VUmc, Amsterdam, the Netherlands.
    Ooijevaar, Rogier E.
    Department of Gastroenterology, Amsterdam University Medical Center, Location VUmc, Amsterdam, the Netherlands.
    Burns, Karen
    Departments of Clinical Microbiology, Beaumont Hospital & Royal College of Surgeons in Ireland, Dublin, Ireland.
    Olesen, Bente R. Scharvik
    Department of Medical Microbiology, Herlev, Denmark.
    Tschudin-Sutter, Sarah
    Department of Infectious Diseases and Infection Control, University Hospital Basel, University Basel, Universitatsspital, Basel, Switzerland.
    Wilcox, Mark H.
    Department of Microbiology, Old Medical, School Leeds General Infirmary, Leeds Teaching Hospitals & University of Leeds, Leeds, United Kingdom.
    Vehreschild, Maria J. G. T.
    German Centre for Infection Research (DZIF), Partner Site Bonn-Cologne, Cologne, Germany; Department of Internal Medicine, Infectious Diseases, University Hospital Frankfurt, Goethe University Frankfurt, Frankfurt am Main, Germany.
    Fitzpatrick, Fidelma
    Department of Clinical Microbiology, Beaumont Hospital, Dublin, Ireland; Department of Clinical Microbiology, Royal College of Surgeons in Ireland, Dublin, Ireland.
    Kuijper, Ed J.
    Department of Medical Microbiology, Centre for Infectious Diseases, Leiden University Medical Center, Leiden, the Netherlands; National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands.
    European Society of Clinical Microbiology and Infectious Diseases: 2021 update on the treatment guidance document for Clostridioides difficile infection in adults2021In: Clinical Microbiology and Infection, ISSN 1198-743X, E-ISSN 1469-0691, Vol. 27, no Suppl. 2, p. S1-S21Article, review/survey (Refereed)
    Abstract [en]

    Scope: In 2009, the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) published the first treatment guidance document for Clostridioides difficile infection (CDI). This document was updated in 2014. The growing literature on CDI antimicrobial treatment and novel treatment approaches, such as faecal microbiota transplantation (FMT) and toxin-binding monoclonal antibodies, prompted the ESCMID study group on C. difficile (ESGCD) to update the 2014 treatment guidance document for CDI in adults.

    Methods and questions: Key questions on CDI treatment were formulated by the guideline committee and included: What is the best treatment for initial, severe, severe-complicated, refractory, recurrent and multiple recurrent CDI? What is the best treatment when no oral therapy is possible? Can prognostic factors identify patients at risk for severe and recurrent CDI and is there a place for CDI prophylaxis? Outcome measures for treatment strategy were: clinical cure, recurrence and sustained cure. For studies on surgical interventions and severe-complicated CDI the outcome was mortality. Appraisal of available literature and drafting of recommendations was performed by the guideline drafting group. The total body of evidence for the recommendations on CDI treatment consists of the literature described in the previous guidelines, supplemented with a systematic literature search on randomized clinical trials and observational studies from 2012 and onwards. The Grades of Recommendation Assessment, Development and Evaluation (GRADE) system was used to grade the strength of our recommendations and the quality of the evidence. The guideline committee was invited to comment on the recommendations. The guideline draft was sent to external experts and a patients' representative for review. Full ESCMID endorsement was obtained after a public consultation procedure.

    Recommendations: Important changes compared with previous guideline include but are not limited to: metronidazole is no longer recommended for treatment of CDI when fidaxomicin or vancomycin are available, fidaxomicin is the preferred agent for treatment of initial CDI and the first recurrence of CDI when available and feasible, FMT or bezlotoxumab in addition to standard of care antibiotics (SoC) are preferred for treatment of a second or further recurrence of CDI, bezlotoxumab in addition to SoC is recommended for the first recurrence of CDI when fidaxomicinwas used to manage the initial CDI episode, and bezlotoxumab is considered as an ancillary treatment to vancomycin for a CDI episode with high risk of recurrence when fidaxomicin is not available. Contrary to the previous guideline, in the current guideline emphasis is placed on risk for recurrence as a factor that determines treatment strategy for the individual patient, rather than the disease severity.

  • 27. Åkerlund, Thomas
    et al.
    Persson, Ingela
    Unemo, Magnus
    Örebro University, School of Health and Medical Sciences.
    Norén, Torbjörn
    Svenungsson, Bo
    Wullt, Marlene
    Burman, Lars G.
    Increased sporulation rate of epidemic Clostridium difficile Type 027/NAP12008In: Journal of Clinical Microbiology, ISSN 0095-1137, E-ISSN 1098-660X, Vol. 46, no 4, p. 1530-1533Article in journal (Refereed)
    Abstract [en]

    Clostridium difficile PCR ribotype 027 comprised 0.2% of a collection of Swedish isolates in 1997-2001 (3 of 1,325 isolates). These isolates had lower moxifloxacin MICs than the epidemic type 027 isolates, but they had the same tcdC sequence and toxin yield. Type 027 produced 3- to 13-fold more toxin than did major Swedish types. One epidemic strain (027/NAP1a) sporulated more than did other type 027 isolates, a feature that should contribute to its survival and spread. 

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