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Epidemiology of invasive group A streptococcal infections in Norway 2010-2014: A retrospective cohort study.

https://arctichealth.org/en/permalink/ahliterature280238
Source
Eur J Clin Microbiol Infect Dis. 2016 Oct;35(10):1639-48
Publication Type
Article
Date
Oct-2016
Author
U. Naseer
M. Steinbakk
H. Blystad
D A Caugant
Source
Eur J Clin Microbiol Infect Dis. 2016 Oct;35(10):1639-48
Date
Oct-2016
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Anti-Bacterial Agents - pharmacology
Antigens, Bacterial - genetics
Bacterial Outer Membrane Proteins - genetics
Carrier Proteins - genetics
Child
Child, Preschool
Cluster analysis
Drug Resistance, Bacterial
Female
Genetic Variation
Genotype
Humans
Incidence
Infant
Infant, Newborn
Male
Middle Aged
Multilocus Sequence Typing
Norway - epidemiology
Retrospective Studies
Streptococcal Infections - epidemiology
Streptococcus pyogenes - classification - genetics - isolation & purification
Young Adult
Abstract
Streptococcus pyogenes or group A streptococcus (GAS) causes mild to severe infections in humans. GAS genotype emm1 is the leading cause of invasive disease worldwide. In the Nordic countries emm28 has been the dominant type since the 1980s. Recently, a resurgence of genotype emm1 was reported from Sweden. Here we present the epidemiology of invasive GAS (iGAS) infections and their association with emm-types in Norway from 2010-2014. We retrospectively collected surveillance data on antimicrobial susceptibility, multilocus sequence type and emm-type, and linked them with demographic and clinical manifestation data to calculate age and sex distributions, major emm- and sequence types and prevalence ratios (PR) on associations between emm-types and clinical manifestations. We analysed 756 iGAS cases and corresponding isolates, with overall incidence of 3.0 per 100000, median age of 59 years (range, 0-102), and male 56 %. Most frequent clinical manifestation was sepsis (49 %) followed by necrotizing fasciitis (9 %). Fifty-two different emm-types and 67 sequence types were identified, distributed into five evolutionary clusters. The most prevalent genotype was emm1 (ST28) in all years (range, 20-33 %) followed by 15 % emm28 in 2014. All isolates were susceptible to penicillin, 15 % resistant to tetracycline and
PubMed ID
27311458 View in PubMed
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Large IncHI2-plasmids encode extended-spectrum ß-lactamases (ESBLs) in Enterobacter spp. bloodstream isolates, and support ESBL-transfer to Escherichia coli.

https://arctichealth.org/en/permalink/ahliterature112772
Source
Clin Microbiol Infect. 2013 Nov;19(11):E516-8
Publication Type
Article
Date
Nov-2013
Author
E. Nilsen
B C Haldorsen
A. Sundsfjord
G S Simonsen
A. Ingebretsen
U. Naseer
O. Samuelsen
Author Affiliation
Reference Centre for Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway; Laboratory of Medical Microbiology, Molde Hospital, Molde, Norway.
Source
Clin Microbiol Infect. 2013 Nov;19(11):E516-8
Date
Nov-2013
Language
English
Publication Type
Article
Keywords
Bacteremia - epidemiology - microbiology
Conjugation, Genetic
Drug Resistance, Multiple
Enterobacter - enzymology - genetics - isolation & purification
Enterobacteriaceae Infections - epidemiology - microbiology
Escherichia coli - genetics
Gene Transfer, Horizontal
Humans
Norway - epidemiology
Plasmids - analysis
beta-Lactamases - genetics
Abstract
We investigated the prevalence of extended-spectrum ß-lactamases (ESBLs) in Enterobacter spp. bloodstream isolates from 19 hospital laboratories in Norway during 2011. A total of 62/230 (27%) isolates were resistant to third-generation cephalosporins and four (1.7%) were ESBL-positive; blaCTX -M-15 (n = 3) and blaSHV -12 (n = 1). This is comparable to the prevalence of ESBLs in clinical isolates of Escherichia coli and Klebsiella pneumoniae in Norway during the same period. All ESBL-positive isolates were multidrug resistant (MDR) and harboured plasmid-mediated quinolone resistance. Three isolates supported transfer of large IncHI2-plasmids harbouring ESBL- and MDR-encoding genes to E. coli recipients by in vitro conjugation.
PubMed ID
23800169 View in PubMed
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Sporadic occurrence of CMY-2-producing multidrug-resistant Escherichia coli of ST-complexes 38 and 448, and ST131 in Norway.

https://arctichealth.org/en/permalink/ahliterature150120
Source
Clin Microbiol Infect. 2010 Feb;16(2):171-8
Publication Type
Article
Date
Feb-2010
Author
U. Naseer
B. Haldorsen
G S Simonsen
A. Sundsfjord
Author Affiliation
Reference Centre for Detection of Antimicrobial Resistance (K-res), Department of Microbiology and Infection Control, University Hospital of North-Norway, Tromsø, Norway. Umaer.Naseer@uit.no
Source
Clin Microbiol Infect. 2010 Feb;16(2):171-8
Date
Feb-2010
Language
English
Publication Type
Article
Keywords
Anti-Bacterial Agents - pharmacology
Bacterial Typing Techniques
Cluster analysis
DNA Fingerprinting
DNA, Bacterial - chemistry - genetics
Drug Resistance, Multiple, Bacterial
Electrophoresis, Gel, Pulsed-Field
Escherichia coli - drug effects - enzymology - isolation & purification
Escherichia coli Infections - microbiology
Escherichia coli Proteins - biosynthesis - genetics
Genotype
Humans
Microbial Sensitivity Tests - methods
Molecular Epidemiology
Norway
Plasmids - analysis
Polymerase Chain Reaction
Sequence Analysis, DNA
beta-Lactamases - biosynthesis - genetics
Abstract
Clinical isolates of Escherichia coli with reduced susceptibility to oxyimino-cephalosporins and not susceptible to clavulanic acid synergy (n = 402), collected from Norwegian diagnostic laboratories in 2003-2007, were examined for the presence of plasmid-mediated AmpC beta-lactamases (PABLs). Antimicrobial susceptibility testing was performed for beta-lactam and non-beta-lactam antibiotics using Etest and Vitek2, respectively. The AmpC phenotype was confirmed using the boronic acid test. PABL-producing isolates were detected using ampC multiplex-PCR and examined by bla(AmpC) sequencing, characterization of the bla(AmpC) genetic environment, phylogenetic grouping, XbaI- pulsed-field gel electrophoresis (PFGE), multi-locus sequence typed (MLST), plasmid profiling and PCR-based replicon typing. For the PABL-positive isolates (n = 38), carrying bla(CMY-2) (n = 35), bla(CMY-7) (n = 1) and bla(DHA-1) (n = 2), from out- (n = 23) and in-patients (n = 15), moderate-high MICs of beta-lactams, except cefepime and carbapenems, were determined. All isolates were resistant to trimethoprim-sulphamethoxazole. Multidrug resistance was detected in 58% of the isolates. The genes bla(CMY-2) and bla(CMY-7) were linked to ISEcp1 upstream in 32 cases and in one case, respectively, and bla(DHA-1) was linked to qacEDelta1sul1 upstream and downstream in one case. Twenty isolates were of phylogenetic groups B2 or D. Thirty-three XbaI-PFGE types, including three clusters, were observed. Twenty-five sequence types (ST) were identified, of which ST complexes (STC) 38 (n = 7), STC 448 (n = 5) and ST131 (n = 4) were dominant. Plasmid profiling revealed 1-4 plasmids (50-250 kb) per isolate and 11 different replicons in 37/38 isolates; bla(CMY-2) was carried on transferable multiple-replicon plasmids, predominantly of Inc groups I1 (n = 12), FII (n = 10) and A/C (n = 7). Chromosomal integration was observed for bla(CMY-2) in ten strains. CMY-2 is the dominant PABL type in Norway and is associated with ISEcp1 and transferable, multiple-replicon IncI1, IncA/C, or IncFII plasmids in nationwide strains of STC 448, STC 38 and ST131.
PubMed ID
19548922 View in PubMed
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Virulence factors of Shiga toxin-producing Escherichia coli and the risk of developing haemolytic uraemic syndrome in Norway, 1992-2013.

https://arctichealth.org/en/permalink/ahliterature292718
Source
Eur J Clin Microbiol Infect Dis. 2017 Sep; 36(9):1613-1620
Publication Type
Historical Article
Journal Article
Date
Sep-2017
Author
U Naseer
I Løbersli
M Hindrum
T Bruvik
L T Brandal
Author Affiliation
Domain for Environmental Health and Infectious Disease Control, Norwegian Institute of Public Health, P.O. Box 4404 Nydalen, 0403, Oslo, Norway. mohammed.umaer.naseer@fhi.no.
Source
Eur J Clin Microbiol Infect Dis. 2017 Sep; 36(9):1613-1620
Date
Sep-2017
Language
English
Publication Type
Historical Article
Journal Article
Keywords
Adhesins, Bacterial - genetics
Escherichia coli Proteins - genetics
Hemolytic-Uremic Syndrome - epidemiology - history - microbiology
History, 20th Century
History, 21st Century
Humans
Norway - epidemiology
Odds Ratio
Risk assessment
Shiga Toxin - genetics
Shiga-Toxigenic Escherichia coli - classification - genetics - pathogenicity
Virulence - genetics
Virulence Factors - genetics
Abstract
Shiga toxin-producing Escherichia coli (STEC) may cause haemolytic uraemic syndrome (HUS). Age =5 years and presence of stx2a and eae are risk factors for the development of HUS. In this study, we investigated STEC isolates for the presence of adhesins, toxins and molecular risk assessment (MRA) factors to identify virulence genes associated with HUS development. We included non-duplicate isolates from all STEC infections (n = 340, HUS = 32) reported to the Norwegian National Reference Laboratory (NRL) for Enteropathogenic Bacteria from 1992 to 2013. The most common STEC were O157:H7/H- (34%) and O103:H2 (14%). We retrospectively screened the isolates by three multiplex polymerase chain reactions (PCRs) for adhesins (n = 11), toxins (n = 5) and MRA (n = 15). We calculated odds ratios (ORs) and adjusted odds ratios (aORs) for associations with HUS development. On average, isolates were positive for 15 virulence genes (range: 1-24); two toxins (range: 0-4), five adhesins (range: 0-8) and eight MRA genes (range: 0-13). The gene combinations were clustered within serotypes. Isolates from HUS cases were positive for eae and IpfA O26, and negative for saa, eibG, astA, cnf, subA and pic. We identified 11 virulence genes with a significant association to HUS development. Multivariable analyses adjusted for age group and Shiga toxin identified nleH1-2 [aOR 8.4, 95% confidence interval (CI); 2.18-32.3] as an independent risk factor for the development of HUS from an STEC infection. This study demonstrated that the non-LEE effector protein nleH1-2 may be an important predictor for elevated risk of developing HUS from STEC infections. We recommend the NRL for Enteropathogenic Bacteria to consider including nleH1-2 screening as part of routine STEC surveillance.
Notes
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PubMed ID
28391537 View in PubMed
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