Literature DB >> 26823594

Genome Sequence of Highly Virulent Pseudomonas aeruginosa Strain VA-134, Isolated from a Burn Patient.

Christine L Miller1, Tsute Chen2, Ping Chen1, Kai P Leung3.   

Abstract

Infection with Pseudomonas aeruginosa leads to impairment of healing and many deaths in severe burn patients. The phenotypic diversity of P. aeruginosa strains makes it difficult to define a therapeutic strategy. Here we report the genome sequence of a highly virulent strain of P. aeruginosa, VA-134, isolated from a burn patient.
Copyright © 2016 Miller et al.

Entities:  

Year:  2016        PMID: 26823594      PMCID: PMC4732347          DOI: 10.1128/genomeA.01662-15

Source DB:  PubMed          Journal:  Genome Announc


GENOME ANNOUNCEMENT

Pseudomonas aeruginosa is a Gram-negative bacterium and common burn wound pathogen (1–4). Factors leading to poor outcomes from burn patients include the invasive nature and virulence of the P. aeruginosa infecting strain and burn severity such as increased depth and coverage. P. aeruginosa’s virulence can be attributed to its metabolic versatility, adherence to and biofilm formation on the host, and the ability to evade and combat the host’s immune response (5). P. aeruginosa secretes toxic compounds and degradative enzymes (e.g., hemolysins, leukocidins, elastase, LasA protease, phospholipase C, exotoxin A, exoenzyme S, rhamnolipid, hydrogen cyanide [HCN], and pyocyanin) that contribute to pathogenesis (6, 7). The intrinsic and acquired biocide-resistance of P. aeruginosa strain VA-134 further hinder many treatment processes (8). Studies using third-degree burn models in rats and burn wounds covering 20% (9, 10) or 30% (11) of the surface area, showed that P. aeruginosa strain VA-134, originally isolated from the urine of a burn victim, was the most virulent compared to strains isolated from other burn patients. Burned animals infected with VA-134 had the highest rates of mortality (9–11). Additionally, VA-134 demonstrated the greatest invasive potential leading to septicemia (9–11) and was less susceptible to phagocytosis and killing by granulocytes compared to other strains (11). To determine the mechanisms underlying the highly virulent nature of the VA-134 isolate, the genome was sequenced. De novo genomic sequencing service was provided by BGI Tech Solutions Co., Ltd. (Cambridge, MA, USA) using a hybrid sequencing approach on two sequencing platforms—the Illumina HiSeq 4000 and PacBio RS II systems This approach generated a high-quality close-circular final assembly of 6,400,418-bp in size. The sequence was annotated by the NCBI Prokaryotic Genomes Automatic Annotation Pipeline (PGAP) (12), which generated the following: 5,854 genes, 5,725 coding sequences (CDS), 52 pseudogenes, 3 clustered regularly interspaced short palindromic repeat (CRISPR) arrays, 12 rRNAs, 64 tRNAs, and 1 noncoding RNA (nc-RNA). Bacterial culture is available from author K.P.L.

Nucleotide sequence accession number.

This genome sequence was deposited in GenBank under the accession number CP013245.
  12 in total

1.  Common pathogens in burn wound and changes in their drug sensitivity.

Authors:  Ezzatollah Rezaei; Hosain Safari; Mahbobe Naderinasab; Hassan Aliakbarian
Journal:  Burns       Date:  2011-03-08       Impact factor: 2.744

2.  Persistence of a multidrug-resistant Pseudomonas aeruginosa clone in an intensive care burn unit.

Authors:  P R Hsueh; L J Teng; P C Yang; Y C Chen; S W Ho; K T Luh
Journal:  J Clin Microbiol       Date:  1998-05       Impact factor: 5.948

3.  Control of experimental and clinical burn wounds sepsis by topical application of sulfamylon compounds.

Authors:  R B Lindberg; J A Moncrief; A D Mason
Journal:  Ann N Y Acad Sci       Date:  1968-08-14       Impact factor: 5.691

4.  Correlation between pseudomonas burn wound infection and granulocyte antibacterial activity.

Authors:  D D McEuen; P Blair; V E Delbene; K Eurenius
Journal:  Infect Immun       Date:  1976-05       Impact factor: 3.441

5.  The time-related changes of antimicrobial resistance patterns and predominant bacterial profiles of burn wounds and body flora of burned patients.

Authors:  Ulku Altoparlak; Serpil Erol; Mufide N Akcay; Fehmi Celebi; Ayten Kadanali
Journal:  Burns       Date:  2004-11       Impact factor: 2.744

6.  Distribution, organization, and ecology of bacteria in chronic wounds.

Authors:  Klaus Kirketerp-Møller; Peter Ø Jensen; Mustafa Fazli; Kit G Madsen; Jette Pedersen; Claus Moser; Tim Tolker-Nielsen; Niels Høiby; Michael Givskov; Thomas Bjarnsholt
Journal:  J Clin Microbiol       Date:  2008-05-28       Impact factor: 5.948

7.  Burn sepsis: bacterial interference with Pseudomonas aeruginosa.

Authors:  S M Levenson; D K Gruber; C Gruber; A Watford; E Seifter
Journal:  J Trauma       Date:  1981-05

8.  Pseudomonas infections in the thermally injured patient.

Authors:  Edward E Tredget; Heather A Shankowsky; Robert Rennie; Robert E Burrell; Sarvesh Logsetty
Journal:  Burns       Date:  2004-02       Impact factor: 2.744

Review 9.  Global regulatory pathways and cross-talk control pseudomonas aeruginosa environmental lifestyle and virulence phenotype.

Authors:  Kimberly A Coggan; Matthew C Wolfgang
Journal:  Curr Issues Mol Biol       Date:  2012-02-22       Impact factor: 2.081

10.  Survey of bacterial diversity in chronic wounds using pyrosequencing, DGGE, and full ribosome shotgun sequencing.

Authors:  Scot E Dowd; Yan Sun; Patrick R Secor; Daniel D Rhoads; Benjamin M Wolcott; Garth A James; Randall D Wolcott
Journal:  BMC Microbiol       Date:  2008-03-06       Impact factor: 3.605

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