ORCID Profile
0000-0002-3728-2270
Current Organisations
UiT Norges arktiske universitet
,
Universitetssykehuset Nord-Norge
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Publisher: Cold Spring Harbor Laboratory
Date: 19-07-2021
DOI: 10.1101/2021.07.16.452602
Abstract: We have used the nationwide Norwegian surveillance program on resistant microbes in humans (NORM) to address longitudinal changes in the population structure K. pneumoniae isolates during 2001-15, encompassing the emergence and spread of ESBL-producing Enterobacterales (ESBL-E) in Norway. Among blood (n= 6124) and urinary tract (n=5496) surveillance isolates from 2001-15, we used Illumina technology to whole genome sequence 201 ESBL-producing isolates from blood (n=130) and urine (n=71), and 667 non-ESBL isolates from blood. Complete genomes for four isolates were resolved with Oxford Nanopore sequencing. In a highly erse collection , Klebsiella variicola ssp . variicola caused a quarter of Klebsiella pneumoniae species complex bacteraemias. ESBL-production was limited to K. pneumoniae sensu stricto (98.5 %). A erse ESBL population of 57 clonal groups (CGs) were dominated by multidrug resistant CG307 (17%), CG15 (12%), CG70 (6%), CG258 (5%) and CG45 (5%) carrying bla CTX-M-15 . Yersiniabactin was significantly more common in ESBL-positive (37.8%) compared to non-ESBL K. pneumoniae sensu stricto isolates (12.7%), indicating convergence of virulence and resistance determinants Moreover, we found a significant lower prevalence of yersinabactin (3.0 %, 37.8 % and 17.3 %), IncFIB (58.7 %, 87.9 % and 79.4 %) and IncFII plasmid replicons (40.5 %, 82.8 % and 54.2%) in K. variicola ssp. variicola compared to ESBL- and non-ESBL K. pneumoniae sensu stricto , respectively. The increase in Norwegian KpSC ESBLs during 2010-15 was driven by bla CTX-M-15 carrying CG307 and CG15. K. variicola ssp. variicola was a frequent cause of invasive KpSC infection, but rarely carried ESBL.
Publisher: Informa UK Limited
Date: 2021
Publisher: Microbiology Society
Date: 18-05-2023
Abstract: Klebsiella pneumoniae sequence type (ST) 17 is a global problem clone that causes multidrug-resistant (MDR) hospital infections worldwide. In 2008–2009, an outbreak of MDR ST17 occurred at a neonatal intensive care unit (NICU) in Stavanger, Norway. Fifty-seven children were colonized. We observed intestinal persistence of ST17 in all of the children for up to two years after hospital discharge. Here, we investigated the within–host evolution of ST17 in 45 of those children during long-term colonization and compared the outbreak with 254 global strains. Ninety-two outbreak-related isolates were whole-genome sequenced. They had capsule locus KL25, O locus O5 and carried yersiniabactin. During within–host colonization ST17 remained stable with few single nucleotide polymorphisms, no acquisition of antimicrobial resistance (AMR) or virulence determinants, and persistent carriage of a bla CTX-M-15 -encoding IncFII(K) IncFIB(K) plasmid (pKp2177_1). The global collection included ST17 from 1993 to 2020 from 34 countries, that were from human infection (41.3%), colonization (39.3%) and respiratory specimens (7.3%), from animals (9.3%), and from the environment (2.7%). We estimate that ST17 emerged mid-to-late 19th century (1859, 95 % HPD 1763–1939) and ersified through recombinations of the K and O loci to form several sublineages, with various AMR genes, virulence loci and plasmids. There was limited evidence of persistence of AMR genes in any of these lineages. A globally disseminated sublineage with KL25/O5 accounted for 52.7 % of the genomes. It included a monophyletic subclade that emerged in the mid-1980s, which comprised the Stavanger NICU outbreak and 10 genomes from three other countries, which all carried pKp2177_1. The plasmid was also observed in a KL155/OL101 subclade from the 2000s. Three clonal expansions of ST17 were identified all were healthcare-associated and carried either yersiniabactin and/or pKp2177_1. To conclude, ST17 is globally disseminated and associated with opportunistic hospital-acquired infections. It contributes to the burden of global MDR infections, but many erse lineages persist without acquired AMR. We hypothesize that non-human sources and human colonization may play a crucial role for severe infections in vulnerable patients, such as preterm neonates.
Publisher: Informa UK Limited
Date: 31-08-2022
Publisher: Cold Spring Harbor Laboratory
Date: 08-02-2021
DOI: 10.1101/2021.02.06.21251253
Abstract: Klebsiella pneumoniae is a leading public health threat due to its increasing prevalence of antibiotic resistance. Gastrointestinal carriage of K. pneumoniae is a risk factor for subsequent infections in hospitalised patients. We determined risk factors for gastrointestinal carriage and the genomic population structure of K. pneumoniae colonising humans in a representative s le of a general population. 2,975 in iduals (54% women) ≥40y participating in the population-based Tromsø Study 7 (2015-2016) were included. Faecal s les were screened for K. pneumoniae which were characterised using whole-genome sequencing. Risk factors for carriage were analysed using data from the Norwegian Prescription Database and questionnaires, using multivariable logistic regression. Prevalence of K. pneumoniae gastrointestinal carriage was 16·3% (95% CI 15·0-17·7%) with no gender difference. Risk factors associated with carriage included age ≥60y, travel to Greece or Asia past 12 months (adjusted odds ratio 1·49, 95% CI 1·11-2·00), Crohn’s disease/ulcerative colitis (2·26, 1·20-4·27), use of protein pump inhibitors (1·62, 1·18-2·22) and non-steroidal anti-inflammatory drugs past six months (1·38, 1·04-1·84), and antibiotic use last month (1·73, 1·05-2·86). Prevalence was higher among those having used combinations of drug classes and decreased over time with respect to preceding antibiotic use. The K. pneumoniae population was erse with 300 sequence types among 484 isolates distributed across four phylogroups. Among the isolates, 5·2% and 11·6% harboured acquired resistance and virulence factors, respectively. Identification of risk factors for gastrointestinal carriage in a representative s le of a general population allows for identification of in iduals that may have a higher risk of extraintestinal infection during hospitalisation. The erse population structure of K. pneumoniae carriage isolates reflects the ecologically adaptive capacity of the bacterium, and the low antibacterial consumption probably contributes to the low prevalence of resistance in clinical isolates in Norway.
Publisher: Elsevier BV
Date: 07-2023
Publisher: Cold Spring Harbor Laboratory
Date: 11-2022
DOI: 10.1101/2022.11.01.514664
Abstract: Klebsiella pneumoniae sequence type (ST) 17 is a global problem clone that causes multidrug-resistant (MDR) hospital infections worldwide. In 2008-2009, an outbreak of MDR ST17 occurred at a neonatal intensive care unit (NICU) in Stavanger, Norway. Fifty-seven children were colonised. We observed intestinal persistence of ST17 in all of the children for up to two years after hospital discharge. Here, we investigated the within-host evolution of ST17 in 45 of those children during long-term colonisation and compared the outbreak with 254 global strains. Ninety-two outbreak-related isolates were whole-genome sequenced. They had capsule locus KL25, O locus O5 and carried yersiniabactin. During within-host colonisation ST17 remained stable with few single nucleotide polymorphisms, no acquisition of antimicrobial resistance (AMR) or virulence determinants, and persistent carriage of a bla CTX-M-15 -encoding IncFII(K) IncFIB(K) plasmid (pKp2177_1). The global collection included ST17 from 1993-2020 from 34 countries, that were from human infection (41.3%), colonisation (39.3%) and respiratory specimens (7.3%), from animals (9.3%), and from the environment (2.7%). We estimate that ST17 emerged mid-to-late 19th century (1859, 95% HPD 1763-1939) and ersified through recombinations of the K and O loci to form several sublineages, with various AMR genes, virulence loci and plasmids. There was limited evidence of persistence of AMR genes in any of these lineages. A globally disseminated sublineage with KL25/O5 accounted for 52.7% of the genomes. It included a monophyletic subclade that emerged in the mid-1980s, which comprised the Stavanger NICU outbreak and 10 genomes from three other countries, which all carried pKp2177_1. The plasmid was also observed in a KL155/OL101 subclade from the 2000s. Three clonal expansions of ST17 were identified, all were healthcare-associated and carried either yersiniabactin and/or pKp2177_1. To conclude, ST17 is globally disseminated and associated with opportunistic hospital-acquired infections. It contributes to the burden of global MDR infections, but many erse lineages persist without acquired AMR. We hypothesise that non-human sources and human colonisation may play a crucial role for severe infections in vulnerable patients, such as preterm neonates. Klebsiella pneumoniae is an opportunistic pathogen that frequently causes hospital-associated multidrug-resistant (MDR) infections. Infections with K. pneumoniae strains that are resistant to third generation cephalosporins and/or carbapenems are considered a major public health threat, as there are limited treatment options available. Some MDR K. pneumoniae clones, including ST307 and ST258, are global problem clones because they disproportionately contribute to the burden of MDR infections and are common causes of such infections and/or outbreaks in hospitals around the world. Here we describe another such clone, ST17, which caused an MDR outbreak in our neonatal intensive care unit, affecting 57 children. We found that this clone underwent minor within-host evolution during two years of long-term gastrointestinal colonisation after hospital discharge. We then investigated the evolutionary history of ST17 globally, as it had not previously been studied. When we compared ST17 isolates from around the world with the isolates from our hospital, we discovered that whilst ST17 with antimicrobial resistance has contributed to outbreaks in other neonatal care units, it also frequently causes infections or colonises humans and non-human sources without any antimicrobial resistance. The genome sequences generated in this study have been deposited at the European Nucleotide Archive under BioProject PRJEB36392. The BioS le accession numbers and associated metadata for the genomes are available in Table S1. The completed annotated genome assembly of Kp2177 is available in GenBank under accession numbers CP075591 (chromosome), CP075592 (pKp2177_1), CP075593 (pKp2177_2) and CP075594 (pKp2177_3). The global dataset of 300 ST17 genomes is available for interactive viewing in Microreact at roject/kpst17 .
Publisher: Oxford University Press (OUP)
Date: 18-10-2008
DOI: 10.1093/JAC/DKN444
No related grants have been discovered for Arnfinn Sundsfjord.