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  • 1.
    Ammerlaan, H S M
    et al.
    University of Medical Centre Utrecht, Netherlands.
    Harbarth, S
    Geneva University Hospital and Medical Sch, Switzerland.
    Buiting, A G M
    John Radcliffe Hospital, England.
    Crook, D W
    Amphia Hospital, Netherlands.
    Fitzpatrick, F
    Beaumont Hospital, Ireland.
    Hanberger, Håkan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Infektionskliniken i Östergötland.
    Herwaldt, L A
    University of Iowa, IA USA.
    van Keulen, P H J
    Amphia Hospital, Netherlands.
    Kluytmans, J A J W
    St Elizabeth Hospital, Netherlands.
    Kola, A
    Charite University of Medical Berlin, Germany.
    Kuchenbecker, R S
    University of Federal Rio Grande do Sul, Brazil.
    Lingaas, E
    University of Oslo, Norway.
    Meessen, N
    University of Medical Centre Groningen, Netherlands.
    Morris-Downes, M -m.
    Beaumont Hospital, Ireland.
    Pottinger, J M.
    University of Iowa Hospital and Clin, IA USA.
    Rohner, P
    Geneva University Hospital and Medical Sch, Switzerland.
    dos Santos, R P.
    University of Federal Rio Grande do Sul, Brazil.
    Seifert, H
    University of Cologne, Germany.
    Wisplinghoff, H
    University of Cologne, Germany.
    Ziesing, S
    Hannover Medical Sch, Germany.
    Walker, A S.
    John Radcliffe Hospital, England.
    Bonten, M J M.
    University of Medical Centre Utrecht, Netherlands.
    Secular Trends in Nosocomial Bloodstream Infections: Antibiotic-Resistant Bacteria Increase the Total Burden of Infection2013Ingår i: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, Vol. 56, nr 6, s. 798-805Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. It is unknown whether rising incidence rates of nosocomial bloodstream infections (BSIs) caused by antibiotic-resistant bacteria (ARB) replace antibiotic-susceptible bacteria (ASB), leaving the total BSI rate unaffected.

    Methods. We investigated temporal trends in annual incidence densities (events per 100 000 patient-days) of nosocomial BSIs caused by methicillin-resistant Staphylococcus aureus (MRSA), ARB other than MRSA, and ASB in 7 ARB-endemic and 7 ARB-nonendemic hospitals between 1998 and 2007.

    Results. 33 130 nosocomial BSIs (14% caused by ARB) yielded 36 679 microorganisms. From 1998 to 2007, the MRSA incidence density increased from 0.2 to 0.7 (annual increase, 22%) in ARB-nonendemic hospitals, and from 3.1 to 11.7 (annual increase, 10%) in ARB-endemic hospitals (P = .2), increasing the incidence density difference between ARB-endemic and ARB-nonendemic hospitals from 2.9 to 11.0. The non-MRSA ARB incidence density increased from 2.8 to 4.1 (annual increase, 5%) in ARB-nonendemic hospitals, and from 1.5 to 17.4 (annual increase, 22%) in ARB-endemic hospitals (P < .001), changing the incidence density difference from −1.3 to 13.3. Trends in ASB incidence densities were similar in both groups (P = .7). With annual increases of 3.8% and 5.4% of all nosocomial BSIs in ARB-nonendemic and ARB-endemic hospitals, respectively (P < .001), the overall incidence density difference of 3.8 increased to 24.4.

    Conclusions.  Increased nosocomial BSI rates due to ARB occur in addition to infections caused by ASB, increasing the total burden of disease. Hospitals with high ARB infection rates in 2005 had an excess burden of BSI of 20.6 per 100 000 patient-days in a 10-year period, mainly caused by infections with ARB.

  • 2. Darenberg, J
    et al.
    Ihendyane, N
    Sjölin, J
    Aufwerber, E
    Haidl, S
    Follin, Per
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Östergötlands Läns Landsting, Medicincentrum, Infektionskliniken i Östergötland.
    Andersson, J
    Norrby-Teglund, A
    Streptlg Study, Group
    Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: A European randomized, double-blind, placebo-controlled trial2003Ingår i: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, Vol. 37, nr 3, s. 333-340Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The efficacy and safety of high-dose intravenous polyspecific immunoglobulin G (IVIG) as adjunctive therapy in streptococcal toxic shock syndrome (STSS) were evaluated in a multicenter, randomized, double-blind, placebo-controlled trial. The trial was prematurely terminated because of slow patient recruitment, and results were obtained from 21 enrolled patients (10 IVIG recipients and 11 placebo recipients). The primary end point was mortality at 28 days, and a 3.6-fold higher mortality rate was found in the placebo group. A significant decrease in the sepsis-related organ failure assessment score at days 2 (P = .02) and 3 (P = .04) was noted in the IVIG group. Furthermore, a significant increase in plasma neutralizing activity against superantigens expressed by autologous isolates was noted in the IVIG group after treatment (P = .03). Although statistical significance was not reached in the primary end point, the trial provides further support for IVIG as an efficacious adjunctive therapy in STSS.

  • 3.
    Davies Forsman, Lina
    et al.
    Karolinska Inst, Sweden; Karolinska Univ Hosp Solna, Sweden.
    Jonsson, Jerker
    Karolinska Inst, Sweden; Publ Hlth Agcy Sweden, Sweden.
    Wagrell, Charlotta
    Karolinska Inst, Sweden.
    Werngren, Jim
    Publ Hlth Agcy Sweden, Sweden.
    Mansjo, Mikael
    Publ Hlth Agcy Sweden, Sweden.
    Wijkander, Maria
    Publ Hlth Agcy Sweden, Sweden.
    Groenheit, Ramona
    Publ Hlth Agcy Sweden, Sweden.
    Hammar, Ulf
    Karolinska Inst, Sweden.
    Giske, Christian G.
    Karolinska Inst, Sweden; Karolinska Univ Hosp, Sweden.
    Schön, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi, infektion och inflammation. Linköpings universitet, Medicinska fakulteten. Kalmar Cty Hosp, Sweden.
    Bruchfeld, Judith
    Karolinska Inst, Sweden; Karolinska Univ Hosp Solna, Sweden.
    Minimum Inhibitory Concentrations of Fluoroquinolones and Pyrazinamide Susceptibility Correlate to Clinical Improvement in Multidrug-resistant Tuberculosis Patients: A Nationwide Swedish Cohort Study Over 2 Decades2019Ingår i: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, Vol. 69, nr 8, s. 1394-1402Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. Minimum inhibitory concentration (MIC) testing, unlike routine drug susceptibility testing (DST) at a single critical concentration, quantifies drug resistance. The association of MICs and treatment outcome in multidrug-resistant (MDR)-tuberculosis patients is unclear. Therefore, we correlated MICs of first- and second-line tuberculosis drugs with time to sputum culture conversion (tSCC) and treatment outcome in MDR-tuberculosis patients. Methods. Clinical and demographic data of MDR-tuberculosis patients in Sweden, including DST results, were retrieved from medical records from 1992 to 2014. MIC determinations were performed retrospectively for the stored individual Mycobacterium tuberculosis (Mtb) isolates using broth microdilution in Middlebrook 7H9. We fitted Cox proportional hazard models correlating MICs, DST results, and clinical variables to tSCC and treatment outcome. Results. Successful treatment outcome was observed in 83.5% (132/158) of MDR-tuberculosis patients. Increasing MICs of fluoroquinolones, diabetes, and age amp;gt;40 years were significantly associated with unsuccessful treatment outcome. Patients treated with pyrazinamide (PZA) had a significantly shorter tSCC compared to patients who were not (median difference, 27 days). Conclusions. Increasing MICs of fluoroquinolones were correlated with unsuccessful treatment outcome in MDR-tuberculosis patients. Further studies, including MIC testing and clinical outcome data to define clinical Mtb breakpoints, are warranted. PZA treatment was associated with shorter tSCC, highlighting the importance of PZA DST.

  • 4.
    Deshpande, Devyani
    et al.
    Baylor Univ, TX USA.
    Alffenaar, Jan-Willem C.
    Univ Groningen, Netherlands.
    Koser, Claudio U.
    Univ Cambridge, England.
    Dheda, Keertan
    Univ Cape Town, South Africa.
    Chapagain, Moti L.
    Baylor Univ, TX USA.
    Simbar, Noviana
    Univ Groningen, Netherlands.
    Schön, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Sturkenboom, Marieke G. G.
    Univ Groningen, Netherlands.
    McIlleron, Helen
    Univ Cape Town, South Africa.
    Lee, Pooi S.
    Baylor Univ, TX USA.
    Koeuth, Thearith
    Baylor Univ, TX USA.
    Mpagama, Stellah G.
    Kibongoto Infect Dis Hosp, Tanzania.
    Banu, Sayera
    Int Ctr Diarrhoeal Dis Res, Bangladesh.
    Foongladda, Suporn
    Mahidol Univ, Thailand.
    Ogarkov, Oleg
    Sci Ctr Family Hlth and Human Reprod Problem, Russia.
    Pholwat, Suporn
    Univ Virginia, VA USA.
    Houpt, Eric R.
    Univ Virginia, VA USA.
    Heysell, Scott K.
    Univ Virginia, VA USA.
    Gumbo, Tawanda
    Baylor Univ, TX USA.
    D-Cycloserine Pharmacokinetics/Pharmacodynamics, Susceptibility, and Dosing Implications in Multidrug-resistant Tuberculosis: A Faustian Deal2018Ingår i: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, Vol. 67, s. S308-S316Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. D-cycloserine is used to treat multidrug-resistant tuberculosis. Its efficacy, contribution in combination therapy, and best clinical dose are unclear, also data on the D-cycloserine minimum inhibitory concentration (MIC) distributions is scant. Methods. We performed a systematic search to identify pharmacokinetic and pharmacodynamic studies performed with D-cycloserine. We then performed a combined exposure-effect and dose fractionation study of D-cycloserine in the hollow fiber system model of tuberculosis (HFS-TB). In parallel, we identified D-cycloserine MICs in 415 clinical Mycobacterium tuberculosis (Mtb) isolates from patients. We utilized these results, including intracavitary concentrations, to identify the clinical dose that would be able to achieve or exceed target exposures in 10 000 patients using Monte Carlo experiments (MCEs). Results. There were no published D-cycloserine pharmacokinetics/pharmacodynamics studies identified. Therefore, we performed new HFS-TB experiments. Cyloserine killed 6.3 log(10) colony-forming units (CFU)/mL extracellular bacilli over 28 days. Efficacy was driven by the percentage of time concentration persisted above MIC (% T-MIC), with 1.0 log(10) CFU/mL kill achieved by % T-MIC = 30% (target exposure). The tentative epidemiological cutoff value with the Sensititre MYCOTB assay was 64 mg/L. In MCEs, 750 mg twice daily achieved target exposure in lung cavities of 92% of patients whereas 500 mg twice daily achieved target exposure in 85% of patients with meningitis. The proposed MCE-derived clinical susceptibility breakpoint at the proposed doses was 64 mg/L. Conclusions. Cycloserine is cidal against Mtb. The susceptibility breakpoint is 64 mg/L. However, the doses likely to achieve the cidality in patients are high, and could be neurotoxic.

  • 5.
    Nordgren, Johan
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Hälsouniversitetet.
    Sharma, Sumit
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Hälsouniversitetet.
    Bucardo, Filemon
    University of Leon, Nicaragua.
    Nasir, Waqas
    University of Gothenburg, Sweden.
    Gunaydin, Gokce
    Karolinska Institute, Sweden.
    Ouermi, Djeneba
    University of Ouagadougou, Burkina Faso.
    Nitiema, Leon W.
    University of Ouagadougou, Burkina Faso.
    Becker-Dreps, Sylvia
    University of N Carolina, NC USA.
    Simpore, Jacques
    University of Ouagadougou, Burkina Faso.
    Hammarstrom, Lennart
    Karolinska Institute, Sweden.
    Larson, Goran
    University of Gothenburg, Sweden.
    Svensson, Lennart
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Hälsouniversitetet.
    Both Lewis and Secretor Status Mediate Susceptibility to Rotavirus Infections in a Rotavirus Genotype-Dependent Manner2014Ingår i: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, Vol. 59, nr 11, s. 1567-1573Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background. The live oral rotavirus (RV) vaccines have shown a reduced efficacy in Africa. Recent in vitro studies have shown binding of the RV surface protein (VP4) to histo-blood group antigens (HBGAs) in an RV genotype-dependent manner, suggesting them to be putative receptors for RV. The diversity of HBGA phenotypes in different ethnic populations, combined with prevalence/absence of specific RV genotypes, led us to hypothesize whether the genetic variations in HBGAs in a population limit susceptibility to certain RV genotypes, plausibly leading to reduced vaccine efficacy. Methods. Association between HBGAs status and susceptibility to RV P genotypes was investigated in children in Burkina Faso and Nicaragua. In total, 242 children with diarrhea in Burkina Faso and Nicaragua were investigated, 93 of whom were RV positive. Results. In Burkina Faso, the P[8] RV strains (n = 27) infected only Lewis-and secretor-positive children (27/27; P less than .0001), but no Lewis-negative children. In contrast, the P[6] strains (n = 27) infected predominantly Lewis-negative children (n = 18; P less than.0001) but also Lewis-positive children, irrespective of their secretor status. The results from Nicaragua confirmed that all P[8]-infected children (n = 22) were secretor Lewis positive. Conclusions. As VP4 of genotype P[8] is a component of current RV vaccines, our finding that Lewis-negative children are resistant to P[8] strains provides a plausible explanation for the reduced vaccine efficacy in populations with a high percentage of Lewis-negative individuals, such as in Africa. Furthermore, our findings provide a plausible explanation as to why P[6] RV strains are more common in Africa.

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