scholarly journals Evolutionary origins of the emergent ST796 clone of vancomycin resistantEnterococcus faecium

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e2916 ◽  
Author(s):  
Andrew H. Buultjens ◽  
Margaret M.C. Lam ◽  
Susan Ballard ◽  
Ian R. Monk ◽  
Andrew A. Mahony ◽  
...  

From early 2012, a novel clone of vancomycin resistantEnterococcus faecium(assigned the multi locus sequence type ST796) was simultaneously isolated from geographically separate hospitals in south eastern Australia and New Zealand. Here we describe the complete genome sequence of Ef_aus0233, a representative ST796E. faeciumisolate. We used PacBio single molecule real-time sequencing to establish a high quality, fully assembled genome comprising a circular chromosome of 2,888,087 bp and five plasmids. Comparison of Ef_aus0233 to otherE. faeciumgenomes shows Ef_aus0233 is a member of the epidemic hospital-adapted lineage and has evolved from an ST555-like ancestral progenitor by the accumulation or modification of five mosaic plasmids and five putative prophage, acquisition of two cryptic genomic islands, accrued chromosomal single nucleotide polymorphisms and a 80 kb region of recombination, also gaining Tn1549and Tn916, transposons conferring resistance to vancomycin and tetracycline respectively. The genomic dissection of this new clone presented here underscores the propensity of the hospitalE. faeciumlineage to change, presumably in response to the specific conditions of hospital and healthcare environments.

2016 ◽  
Author(s):  
Andrew H Buultjens ◽  
Margaret M C Lam ◽  
Susan Ballard ◽  
Ian R Monk ◽  
Andrew A Mahony ◽  
...  

From early 2012, a novel clone of vancomycin resistant Enterococcus faecium (assigned the multi locus sequence type ST796) was simultaneously isolated from geographically separate hospitals in south eastern Australia and New Zealand. Here we describe the complete genome sequence of Ef_aus0233, a representative ST796 E. faecium isolate. We used PacBio single molecule real-time sequencing to establish a high quality, fully assembled genome comprising a circular chromosome of 2,888,087 bp and five plasmids. Comparison of Ef_aus0233 to other E. faecium genomes shows Ef_aus0233 is a member of the epidemic hospital-adapted lineage and has evolved from an ST555-like ancestral progenitor by the accumulation or modification of five mosaic plasmids and five putative prophage, acquisition of two cryptic genomic islands, accrued chromosomal single nucleotide polymorphisms and a 80kb region of recombination, also gaining Tn1549 and Tn916, transposons conferring resistance to vancomycin and tetracycline respectively. The genomic dissection of this new clone presented here underscores the propensity of the hospital E. faecium lineage to change, presumably in response to the specialized conditions of hospital and healthcare environments.


2016 ◽  
Author(s):  
Andrew H Buultjens ◽  
Margaret M C Lam ◽  
Susan Ballard ◽  
Ian R Monk ◽  
Andrew A Mahony ◽  
...  

From early 2012, a novel clone of vancomycin resistant Enterococcus faecium (assigned the multi locus sequence type ST796) was simultaneously isolated from geographically separate hospitals in south eastern Australia and New Zealand. Here we describe the complete genome sequence of Ef_aus0233, a representative ST796 E. faecium isolate. We used PacBio single molecule real-time sequencing to establish a high quality, fully assembled genome comprising a circular chromosome of 2,888,087 bp and five plasmids. Comparison of Ef_aus0233 to other E. faecium genomes shows Ef_aus0233 is a member of the epidemic hospital-adapted lineage and has evolved from an ST555-like ancestral progenitor by the accumulation or modification of five mosaic plasmids and five putative prophage, acquisition of two cryptic genomic islands, accrued chromosomal single nucleotide polymorphisms and a 80kb region of recombination, also gaining Tn1549 and Tn916, transposons conferring resistance to vancomycin and tetracycline respectively. The genomic dissection of this new clone presented here underscores the propensity of the hospital E. faecium lineage to change, presumably in response to the specialized conditions of hospital and healthcare environments.


2019 ◽  
Author(s):  
Ana Paula Barbosa do Nascimento ◽  
Fernando Medeiros Filho ◽  
Hério Sousa ◽  
Hermes Senger ◽  
Rodolpho Mattos Albano ◽  
...  

AbstractPseudomonas aeruginosa is one of the most common pathogens related to healthcare-associated infections. The Brazilian isolate, named CCBH4851, is a multidrug-resistant clone belonging to the sequence type 277. The antimicrobial resistance mechanisms of the CCBH4851 strain are associated with the presence of blaSPM-1 gene, encoding a metallo-beta-lactamase, in addition to other exogenously acquired genes. Whole-genome sequencing studies focusing on emerging pathogens are essential to identify physiological key aspects that may lead to the exposure of new targets for therapy. This study was designed to characterize the genome of Pseudomonas aeruginosa CCBH4851 through the detection of genomic features and genome comparison with other Pseudomonas aeruginosa strains. The CCBH4851 closed genome showed features that were consistent with data reported for the specie. However, comparative genomics revealed the absence of genes important for pathogenesis. On the other hand, CCBH4851 genome contained acquired genomic islands that carry additional virulence and antimicrobial resistance-related genes. The presence of single nucleotide polymorphisms in the core genome, mainly those located in resistance-associated genes, suggests that these mutations could influence the multidrug-resistant behavior of CCBH4851. Overall, the characterization of Pseudomonas aeruginosa CCBH4851 complete genome revealed several features that could directly impact the profile of virulence and antibiotic resistance of this pathogen in infectious outbreaks.


2017 ◽  
Vol 4 (4) ◽  
pp. 170053 ◽  
Author(s):  
Lauren C. White ◽  
Jeremy J. Austin

Today, the Tasmanian devil ( Sarcophilus harrisii ) is found only on the island of Tasmania, despite once being widespread across mainland Australia. While the devil is thought to have become extinct on the mainland approximately 3000 years ago, three specimens were collected in Victoria (south-eastern Australia) between 1912 and 1991, raising the possibility that a relict mainland population survived in the area. Alternatively, these devils may have escaped captivity or were deliberately released after being transported from Tasmania, a practice that has been strictly controlled since the onset of devil facial tumour disease in the early 1990s. Such quarantine regimes are important to protect disease-free, ‘insurance populations’ in zoos on the mainland. To test whether the three Victorian devils were members of a relict mainland population or had been recently transported from Tasmania we identified seven single nucleotide polymorphisms (SNPs) in the mitochondrial genome that can distinguish between Tasmanian and ancient mainland populations. The three Victorian devil specimens have the same seven SNPs diagnostic of modern Tasmanian devils, confirming that they were most likely transported from Tasmania and do not represent a remnant population of mainland devils.


2017 ◽  
Vol 55 (3) ◽  
pp. 931-941 ◽  
Author(s):  
Yi Chen ◽  
Yan Luo ◽  
James Pettengill ◽  
Ruth Timme ◽  
David Melka ◽  
...  

ABSTRACT Three multistate outbreaks between 2014 and 2016, involving case patients in and outside the United States, were linked to stone fruit, caramel apples, and packaged leafy green salad contaminated with Listeria monocytogenes singleton sequence type 382 (ST382), a serotype IVb-v1 clone with limited genomic divergence. Isolates from these outbreaks and other ST382 isolates not associated with these outbreaks were analyzed by whole-genome sequencing (WGS) analysis. The primary differences among ST382 strains were single nucleotide polymorphisms (SNPs). WGS analysis differentiated ST382 from a clonal complex 1 outbreak strain co-contaminating the caramel apples. WGS clustered food, environmental, and clinical isolates within each outbreak, and also differentiated among the three outbreak strains and epidemiologically unrelated ST382 isolates, which were indistinguishable by pulsed-field gel electrophoresis. ST382 appeared to be an emerging clone that began to diverge from its ancestor approximately 32 years before 2016. We estimated that there was 1.29 nucleotide substitution per genome (2.94 Mbp) per year for this clone.


2017 ◽  
Vol 29 (2) ◽  
pp. 462-476 ◽  
Author(s):  
Maarten M. Brandt ◽  
Claartje A. Meddens ◽  
Laura Louzao-Martinez ◽  
Noortje A.M. van den Dungen ◽  
Nico R. Lansu ◽  
...  

Genome-wide association studies (GWASs) have identified many genetic risk factors for CKD. However, linking common variants to genes that are causal for CKD etiology remains challenging. By adapting self-transcribing active regulatory region sequencing, we evaluated the effect of genetic variation on DNA regulatory elements (DREs). Variants in linkage with the CKD-associated single-nucleotide polymorphism rs11959928 were shown to affect DRE function, illustrating that genes regulated by DREs colocalizing with CKD-associated variation can be dysregulated and therefore, considered as CKD candidate genes. To identify target genes of these DREs, we used circular chromosome conformation capture (4C) sequencing on glomerular endothelial cells and renal tubular epithelial cells. Our 4C analyses revealed interactions of CKD-associated susceptibility regions with the transcriptional start sites of 304 target genes. Overlap with multiple databases confirmed that many of these target genes are involved in kidney homeostasis. Expression quantitative trait loci analysis revealed that mRNA levels of many target genes are genotype dependent. Pathway analyses showed that target genes were enriched in processes crucial for renal function, identifying dysregulated geranylgeranyl diphosphate biosynthesis as a potential disease mechanism. Overall, our data annotated multiple genes to previously reported CKD-associated single-nucleotide polymorphisms and provided evidence for interaction between these loci and target genes. This pipeline provides a novel technique for hypothesis generation and complements classic GWAS interpretation. Future studies are required to specify the implications of our dataset and further reveal the complex roles that common variants have in complex diseases, such as CKD.


2015 ◽  
Vol 11 (7) ◽  
pp. 20150303 ◽  
Author(s):  
L. Y. Rutledge ◽  
S. Devillard ◽  
J. Q. Boone ◽  
P. A. Hohenlohe ◽  
B. N. White

Top predators are disappearing worldwide, significantly changing ecosystems that depend on top-down regulation. Conflict with humans remains the primary roadblock for large carnivore conservation, but for the eastern wolf ( Canis lycaon ), disagreement over its evolutionary origins presents a significant barrier to conservation in Canada and has impeded protection for grey wolves ( Canis lupus ) in the USA. Here, we use 127 235 single-nucleotide polymorphisms (SNPs) identified from restriction-site associated DNA sequencing (RAD-seq) of wolves and coyotes, in combination with genomic simulations, to test hypotheses of hybrid origins of Canis types in eastern North America. A principal components analysis revealed no evidence to support eastern wolves, or any other Canis type, as the product of grey wolf × western coyote hybridization. In contrast, simulations that included eastern wolves as a distinct taxon clarified the hybrid origins of Great Lakes-boreal wolves and eastern coyotes. Our results support the eastern wolf as a distinct genomic cluster in North America and help resolve hybrid origins of Great Lakes wolves and eastern coyotes. The data provide timely information that will shed new light on the debate over wolf conservation in eastern North America.


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