scholarly journals Whole-Genome Sequence Variation among Multiple Isolates of Pseudomonas aeruginosa

2003 ◽  
Vol 185 (4) ◽  
pp. 1316-1325 ◽  
Author(s):  
David H. Spencer ◽  
Arnold Kas ◽  
Eric E. Smith ◽  
Christopher K. Raymond ◽  
Elizabeth H. Sims ◽  
...  

ABSTRACT Whole-genome shotgun sequencing was used to study the sequence variation of three Pseudomonas aeruginosa isolates, two from clonal infections of cystic fibrosis patients and one from an aquatic environment, relative to the genomic sequence of reference strain PAO1. The majority of the PAO1 genome is represented in these strains; however, at least three prominent islands of PAO1-specific sequence are apparent. Conversely, ∼10% of the sequencing reads derived from each isolate fail to align with the PAO1 backbone. While average sequence variation among all strains is roughly 0.5%, regions of pronounced differences were evident in whole-genome scans of nucleotide diversity. We analyzed two such divergent loci, the pyoverdine and O-antigen biosynthesis regions, by complete resequencing. A thorough analysis of isolates collected over time from one of the cystic fibrosis patients revealed independent mutations resulting in the loss of O-antigen synthesis alternating with a mucoid phenotype. Overall, we conclude that most of the PAO1 genome represents a core P. aeruginosa backbone sequence while the strains addressed in this study possess additional genetic material that accounts for at least 10% of their genomes. Approximately half of these additional sequences are novel.

2019 ◽  
Vol 8 (40) ◽  
Author(s):  
Sofia B. Mohamed ◽  
Sumaya Kambal ◽  
Abdalla Munir ◽  
Nusiba I. Abdalla ◽  
Ahmed Hamad ◽  
...  

Pseudomonas aeruginosa is a common nosocomial pathogen often associated with a high mortality rate in vulnerable populations. Here, we describe the genomic sequence of a pan-resistant, high-risk clone of P. aeruginosa sequence type 111 (ST111) isolated from a hospital patient in Sudan.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Syed A. K. Shifat Ahmed ◽  
Michelle Rudden ◽  
Sabrina M. Elias ◽  
Thomas J. Smyth ◽  
Roger Marchant ◽  
...  

AbstractPseudomonas aeruginosa uses quorum sensing (QS) to modulate the expression of several virulence factors that enable it to establish severe infections. The QS system in P. aeruginosa is complex, intricate and is dominated by two main N-acyl-homoserine lactone circuits, LasRI and RhlRI. These two QS systems work in a hierarchical fashion with LasRI at the top, directly regulating RhlRI. Together these QS circuits regulate several virulence associated genes, metabolites, and enzymes in P. aeruginosa. Paradoxically, LasR mutants are frequently isolated from chronic P. aeruginosa infections, typically among cystic fibrosis (CF) patients. This suggests P. aeruginosa can undergo significant evolutionary pathoadaptation to persist in long term chronic infections. In contrast, mutations in the RhlRI system are less common. Here, we have isolated a clinical strain of P. aeruginosa from a CF patient that has deleted the transcriptional regulator RhlR entirely. Whole genome sequencing shows the rhlR locus is deleted in PA80 alongside a few non-synonymous mutations in virulence factors including protease lasA and rhamnolipid rhlA, rhlB, rhlC. Importantly we did not observe any mutations in the LasRI QS system. PA80 does not appear to have an accumulation of mutations typically associated with several hallmark pathoadaptive genes (i.e., mexT, mucA, algR, rpoN, exsS, ampR). Whole genome comparisons show that P. aeruginosa strain PA80 is closely related to the hypervirulent Liverpool epidemic strain (LES) LESB58. PA80 also contains several genomic islands (GI’s) encoding virulence and/or resistance determinants homologous to LESB58. To further understand the effect of these mutations in PA80 QS regulatory and virulence associated genes, we compared transcriptional expression of genes and phenotypic effects with isogenic mutants in the genetic reference strain PAO1. In PAO1, we show that deletion of rhlR has a much more significant impact on the expression of a wide range of virulence associated factors rather than deletion of lasR. In PA80, no QS regulatory genes were expressed, which we attribute to the inactivation of the RhlRI QS system by deletion of rhlR and mutation of rhlI. This study demonstrates that inactivation of the LasRI system does not impact RhlRI regulated virulence factors. PA80 has bypassed the common pathoadaptive mutations observed in LasR by targeting the RhlRI system. This suggests that RhlRI is a significant target for the long-term persistence of P. aeruginosa in chronic CF patients. This raises important questions in targeting QS systems for therapeutic interventions.


2016 ◽  
Vol 4 (4) ◽  
Author(s):  
Fatemeh Sanjar ◽  
S. L. Rajasekhar Karna ◽  
Tsute Chen ◽  
Ping Chen ◽  
Johnathan J. Abercrombie ◽  
...  

We report here the complete genome sequence ofPseudomonas aeruginosastrain BAMCPA07-48, isolated from a combat injury wound. The closed genome sequence of this isolate is a valuable resource for pathogenome characterization ofP. aeruginosaassociated with wounds, which will aid in the development of a higher-resolution phylogenomic framework for molecular-guided pathogen-surveillance.


2019 ◽  
Vol 14 (16) ◽  
pp. 1357-1367
Author(s):  
Jumamurat R Bayjanov ◽  
Miquel B Ekkelenkamp ◽  
Malbert RC Rogers ◽  
Rafael Cantón ◽  
Barry J Benaissa-Trouw ◽  
...  

Aim: Genetic characterization of Pandoraea strains recovered from cystic fibrosis patients. Materials & methods: The whole-genome sequence of 12 Pandoraea strains was determined using Illumina technology. The position of the strains within the genus Pandoraea was analyzed using selected partial gene sequences, core genome multi-locus sequence typing and average nucleotide identity analysis. Furthermore, the sequences were annotated. Results: The results show that some strains previously identified as Pandoraea pnomenusa, Pandoraea sputorum, Pandoraea oxalativorans and Pandoraea pulmonicola belong to novel species. The strains did not harbor acquired antibiotic resistance genes but encoded an OXA-type ß-lactamase. Conclusion: The taxonomy of the genus Pandoraea needs to be revised.


PLoS ONE ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. e0210929
Author(s):  
Laura J. Sherrard ◽  
Anna S. Tai ◽  
Bryan A. Wee ◽  
Kay A. Ramsay ◽  
Timothy J. Kidd ◽  
...  

2019 ◽  
Vol 8 (17) ◽  
Author(s):  
Sidra Irum ◽  
Robert F. Potter ◽  
Rubina Kamran ◽  
Zeeshan Mustafa ◽  
Meghan A. Wallace ◽  
...  

We performed Illumina whole-genome sequencing on a carbapenem-resistant Pseudomonas aeruginosa strain isolated from a cystic fibrosis patient with chronic airway colonization. The draft genome comprises 6,770,411 bp, including the carbapenemase bla NDM-1 and the extended-spectrum beta-lactamase bla PME-1.


2018 ◽  
Vol 7 (10) ◽  
Author(s):  
Julien Crovadore ◽  
Damien Grizard ◽  
Romain Chablais ◽  
Bastien Cochard ◽  
Philippe Blanc ◽  
...  

We report here the draft genome sequence of strain 4014 of Pseudomonas aeruginosa, a common human pathogen, isolated from soil in France. This sequence predicts resistance to multiple antibiotics, including vancomycin.


mSphere ◽  
2018 ◽  
Vol 3 (2) ◽  
Author(s):  
Xuan Qin ◽  
Chuan Zhou ◽  
Danielle M. Zerr ◽  
Amanda Adler ◽  
Amin Addetia ◽  
...  

ABSTRACTClinical isolates ofPseudomonas aeruginosafrom patients with cystic fibrosis (CF) are known to differ from those associated with non-CF hosts by colony morphology, drug susceptibility patterns, and genomic hypermutability.Pseudomonas aeruginosaisolates from CF patients have long been recognized for their overall reduced rate of antimicrobial susceptibility, but their intraclonal MIC heterogeneity has long been overlooked. Using two distinct cohorts of clinical strains (n= 224 from 56 CF patients,n= 130 from 68 non-CF patients) isolated in 2013, we demonstrated profound Etest MIC heterogeneity in CFP. aeruginosaisolates in comparison to non-CFP. aeruginosaisolates. On the basis of whole-genome sequencing of 19 CFP. aeruginosaisolates from 9 patients with heterogeneous MICs, the core genome phylogenetic tree confirmed the within-patient CFP. aeruginosaclonal lineage along with considerable coding sequence variability. No extrachromosomal DNA elements or previously characterized antibiotic resistance mutations could account for the wide divergence in antimicrobial MICs betweenP. aeruginosacoisolates, though many heterogeneous mutations in efflux and porin genes and their regulators were present. A unique OprD sequence was conserved among the majority of isolates of CFP. aeruginosaanalyzed, suggesting a pseudomonal response to selective pressure that is common to the isolates. Genomic sequence data also suggested that CF pseudomonal hypermutability was not entirely due to mutations inmutL,mutS, anduvr. We conclude that the net effect of hundreds of adaptive mutations, both shared between clonally related isolate pairs and unshared, accounts for their highly heterogeneous MIC variances. We hypothesize that this heterogeneity is indicative of the pseudomonal syntrophic-like lifestyle under conditions of being “locked” inside a host focal airway environment for prolonged periods.IMPORTANCEPatients with cystic fibrosis endure “chronic focal infections” with a variety of microorganisms. One microorganism,Pseudomonas aeruginosa, adapts to the host and develops resistance to a wide range of antimicrobials. Interestingly, as the infection progresses, multiple isogenic strains ofP. aeruginosaemerge and coexist within the airways of these patients. Despite a common parental origin, the multiple strains ofP. aeruginosadevelop vastly different susceptibility patterns to actively used antimicrobial agents—a phenomenon we define as “heterogeneous MICs.” By sequencing pairs ofP. aeruginosaisolates displaying heterogeneous MICs, we observed widespread isogenic gene lesions in drug transporters, DNA mismatch repair machinery, and many other structural or cellular functions. Coupled with the heterogeneous MICs, these genetic lesions demonstrated a symbiotic response to host selection and suggested evolution of a multicellular syntrophic bacterial lifestyle. Current laboratory standard interpretive criteria do not address the emergence of heterogeneous growth and susceptibilitiesin vitrowith treatment implications.


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