Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016 Jan 28;11(1):e0147478.
doi: 10.1371/journal.pone.0147478. eCollection 2016.

Specific Gene Loci of Clinical Pseudomonas putida Isolates

Affiliations

Specific Gene Loci of Clinical Pseudomonas putida Isolates

Lázaro Molina et al. PLoS One. .

Abstract

Pseudomonas putida are ubiquitous inhabitants of soils and clinical isolates of this species have been seldom described. Clinical isolates show significant variability in their ability to cause damage to hosts because some of them are able to modulate the host's immune response. In the current study, comparisons between the genomes of different clinical and environmental strains of P. putida were done to identify genetic clusters shared by clinical isolates that are not present in environmental isolates. We show that in clinical strains specific genes are mostly present on transposons, and that this set of genes exhibit high identity with genes found in pathogens and opportunistic pathogens. The set of genes prevalent in P. putida clinical isolates, and absent in environmental isolates, are related with survival under oxidative stress conditions, resistance against biocides, amino acid metabolism and toxin/antitoxin (TA) systems. This set of functions have influence in colonization and survival within human tissues, since they avoid host immune response or enhance stress resistance. An in depth bioinformatic analysis was also carried out to identify genetic clusters that are exclusive to each of the clinical isolates and that correlate with phenotypical differences between them, a secretion system type III-like was found in one of these clinical strains, a determinant of pathogenicity in Gram-negative bacteria.

PubMed Disclaimer

Conflict of interest statement

Competing Interests: Amalia Roca is employed by Bio-Iliberis R&D. There are no patents, products in development or marketed products to declare. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials, as detailed online in the guide for authors.

Figures

Fig 1
Fig 1. Phenotypical array characterization of clinical strains.
Graphics show the growth of the studied P. putida clinical strains and KT2440 in the presence of heavy metals (A); oxidative and other stressors (B); DNA intermediates as the only nitrogen source (C); amino acids (D) or fatty acid (E) as the only carbon source; and cysteine (cys) as the only sulfur (S), nitrogen (N), carbon (C) or carbon+nitrogen source (C+N). Blue bars, HB13667; red bars, H8234; green bars, HB3267 and white bars, KT2440. Error bars indicate standard deviation from three experimental repetitions. In parentheses concentration of stressor used, if concentration is not indicated means this was 5 mM. HB4184 was not included in this study because it forms lumps and thick biofilms in these culture conditions.
Fig 2
Fig 2. Genetic modules in clusters XVII and XVIII of H8234.
Lines represent the length of the modules. Represented in white, genes that have the highest identity with other Pseudomonas environmental strains. In red, genes that do not have homology with any other strain or have homology only with pathogens, opportunistic pathogens or clinic isolates of P. putida. In black, genes involved in transposition events. dh means dehydrogenase, red means oxidoreductase.

Similar articles

Cited by

References

    1. Klevens RM, Edwards JR, Richards CL, Horan TC, Gaynes RP, Pollock DA, et al. Estimating Health Care-Associated Infections and Deaths in U.S. Hospitals, 2002. Public Health Reports 2007;122:160–166. - PMC - PubMed
    1. Di Bonito M, Caiazzo S, Iannazzone M, Miccichè V, De Marco G, De Robertis E, et al. Prognostic differences between VAP from Acinetobacter baumanii and VAP from other microorganisms. Transl Med UniSa. 2012;3:15–21. - PMC - PubMed
    1. Micek ST, Wunderink RG, Kollef MH, Chen C, Rello J, Chastre J, et al. An international multicenter retrospective study of Pseudomonas aeruginosa nosocomial pneumonia: impact of multidrug resistance. Crit Care. 2015;19:219 10.1186/s13054-015-0926-5 - DOI - PMC - PubMed
    1. Ottosen J, Evans H. Pneumonia: challenges in the definition, diagnosis, and management of disease. Surg Clin North Am. 2014;94:1305–1317. 10.1016/j.suc.2014.09.001 - DOI - PubMed
    1. Iacovelli V, Gaziev G, Topazio L, Bove P, Vespasiani G, Finazzi Agrò E. Nosocomial urinary tract infections: A review. Urologia. 2014;81:222–227. 10.5301/uro.5000092 - DOI - PubMed

Publication types