Comparative Genomic Analysis of Multidrug-Resistant Pseudomonas aeruginosa Clinical Isolates VRFPA06 and VRFPA08 with VRFPA07

Murugan, Nandagopal; Malathi, Jambulingam; Vetrivel, Umashankar; Madhavan, H. N.

doi:10.1128/genomea.00140-14

Cited by 16 publications

(17 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We designed primers for the selected genes found to be most prevalent among clinical studies as well as our own observation from NGS based study and other reports [12–21]. Multiplex PCR Primer designed against drug resistance gene include Group‐1; (ESBL‐MBL) blaTem, blaOXA, blaCTX‐M‐15, blaVim) Group‐2, (blaGes, blaVeb and DIM and AmpC) Efflux pump genes‐ Group‐3 (MexA,B‐oprM); Group‐4 (MexC,D‐oprJ); Group‐5 (Mex X,Y‐oprN) Group‐6 (oprD, nfxB, MexR) primers were purchased from Eurofins Genomics India Pvt Ltd, Bangalore, India.…”

Section: Methodsmentioning

confidence: 99%

“…From our experience, emergence of culture negative intraocular specimens is steadily increasing, which leads to unwanted avoidable blindness. Hence, the current study designed to target most common betalactamase and efflux pump genes among P aeruginosa reported in literature and our own study experiences [3–5,12–17]. In addition, the current study will assess the coexistence of ESBL, MBL and efflux pump genes among P. aeruginosa isolates obtained from variety of clinical specimens (ocular tissues, blood, urine, pus and etc) using multiplex PCR and the same were compared with Phenotypic methods [18].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Application of six multiplex PCR's among 200 clinical isolates of Pseudomonas aeruginosa for the detection of 20 drug resistance encoding genes

Murugan

Malathi

Therese

et al. 2017

The Kaohsiung J of Med Scie

Self Cite

View full text Add to dashboard Cite

Pseudomonas aeruginosa (P. aeruginosa) is a menacing opportunistic, nosocomial pathogen; become a growing concern as conventional antimicrobial therapy is now futile against it. Multi‐drug resistant P. aeruginosa (MDRPA) has distinctive resistance mechanisms such as production of β‐lactamases, repression of porin genes and over‐expression of efflux pumps. The focus of this study is to standardize and application of multiplex PCR (mPCR) to detect the presence of betalactamase genes encoding blaTem, blaOXA, blaCTX‐M‐15, blaVim, blaGes, blaVeb, blaDIM, AmpC and Efflux pump genes encoding Mex A,B‐oprM, Mex C,D‐oprJ, Mex X,Y‐oprN, oprD, nfxB, MexR. A total of 200 clinical isolates of P. aeruginosa were tested for the presence of the above mentioned genes genotypically through mPCR and characterized by phenotypic methods for ESBL and MBL production. Out of 200 isolates, 163 (81.5%) nfxB regulator gene, 102 (51%) MexA, 96 (48%) MexC, 93 (46.5%) MexB, 86 (43%) MexD, 81 (40.5%) OprM, 74 (37%) OprJ, 72 (36%) OprD and MexR, 53 (26.5%) Mex X and OprN, 49 (24.5%) MexY gene. Betalactamase genes 145 (72.5%) blaTem, 67 (33.5%) blaOXA, 35 (17.5%) blaVim, 25(12.50%), 23 (11.50%) blaVeb, 21 (11.5%) blaGes, 14 (7%) Ctx‐m and 10 (5%) AmpC and 5 (2.5%) blaDim‐1 gene were tested positive by mPCR. Phenotypically 38 (19%) and 29 (14.5%) out of 200 tested positive for ESBL and MBL production. Application of this mPCR on clinical specimens is fast, accurate, specific and low‐cost reliable tool for the screening, where culture negative Eubacterial PCR positive cases for an early molecular detection of drug resistance mechanism assisting the clinician to treat the disease with appropriate antibiotic selection.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Application of six multiplex PCR's among 200 clinical isolates of Pseudomonas aeruginosa for the detection of 20 drug resistance encoding genes

Murugan

Malathi

Therese

et al. 2017

The Kaohsiung J of Med Scie

Self Cite

View full text Add to dashboard Cite

show abstract

“…Inspection of the fully sequenced trpE-trpG genomic regions of 91 P. aeruginosa strains showed a quite similar number of 'mono-tailocin' strains, pyocinogenic for either R (29) or F (31), as compared to 'duo-tailocin' strains, pyocinogenic for both R and F (30). A fourth type of trpE-trpG intergenic organization is found in the multidrug-resistant blood isolate VRFPA06, in which a 30.3-kb DNA sequence with several coding regions of unknown function is positioned between the end of a pyocin R2 cluster and the trpG gene (Murugan et al, 2014). The presence of a bacteriophage P4-like integrase gene flanking the R-pyocin lysis cassette genes suggests a mobile nature for this inserted DNA region (Kung et al, 2010).…”

Section: Genomic Backbones Of Pseudomonad Tailocinsmentioning

confidence: 99%

Ribosomally encoded antibacterial proteins and peptides fromPseudomonas

2014

View full text Add to dashboard Cite

Members of the Pseudomonas genus produce diverse secondary metabolites affecting other bacteria, fungi or predating nematodes and protozoa but are also equipped with the capacity to secrete different types of ribosomally encoded toxic peptides and proteins, ranging from small microcins to large tailocins. Studies with the human pathogen Pseudomonas aeruginosa have revealed that effector proteins of type VI secretion systems are part of the antibacterial armamentarium deployed by pseudomonads. A novel class of antibacterial proteins with structural similarity to plant lectins was discovered by studying antagonism among plant-associated Pseudomonas strains. A genomic perspective on pseudomonad bacteriocinogeny shows that the modular architecture of S pyocins of P. aeruginosa is retained in a large diversified group of bacteriocins, most of which target DNA or RNA. Similar modularity is present in as yet poorly characterized Rhs (recombination hot spot) proteins and CDI (contact-dependent inhibition) proteins. Well-delimited domains for receptor recognition or cytotoxicity enable the design of chimeric toxins with novel functionalities, which has been applied successfully for S and R pyocins. Little is known regarding how these antibacterials are released and ultimately reach their targets. Other remaining issues concern the identification of environmental triggers activating these systems and assessment of their ecological impact in niches populated by pseudomonads.

show abstract

“…Their pigmentation is due to homogentisic acid, which accumulates due to the inactivation of the gene hmgA (pa2009 in P. aeruginosa strain PAO1), which encodes homogentisate-1,2-dioxygenase (Rodriguez-Rojas et al, 2009). Although the inactivation of hmgA may occur in clinical strains by large chromosomal deletion that included hmgA Le et al, 2014), other authors have described single point mutations in this gene (Murugan et al, 2014;Tielen et al, 2014). First, we compared the genomes and phenotypes of a collection of clinical pyomelaninproducing mutants with those of their wild-type parents.…”

Section: Introductionmentioning

confidence: 99%

Pyomelanin‐producing Pseudomonas aeruginosa selected during chronic infections have a large chromosomal deletion which confers resistance to pyocins

Hocquet

Petitjean

Rohmer

et al. 2016

Environmental Microbiology

View full text Add to dashboard Cite

Summary When bacterial lineages make the transition from free-living to permanent association with hosts, they can undergo massive gene losses, for which the selective forces within host tissues are unknown. We identified here melanogenic clinical isolates of Pseudomonas aeruginosa with large chromosomal deletions (66 to 270 kbp) and characterized them to investigate how they were selected. When compared with their wild-type parents, melanogenic mutants (i) exhibited a lower fitness in growth conditions found in human tissues, such as hyperosmolarity and presence of aminoglycoside antibiotics, (ii) narrowed their metabolic spectrum with a growth disadvantage with particular carbon sources, including aromatic amino acids and acyclic terpenes, suggesting a reduction of metabolic flexibility. Despite an impaired fitness in rich media, melanogenic mutants can inhibit their wild-type parents and compete with them in coculture. Surprisingly, melanogenic mutants became highly resistant to two intraspecific toxins, the S-pyocins AP41 and S1. Our results suggest that pyocins produced within a population of infecting P. aeruginosa may have selected for bacterial mutants that underwent massive gene losses and that were adapted to the life in diverse bacterial communities in the human host. Intraspecific interactions may therefore be an important factor driving the continuing evolution of pathogens during host infections.

show abstract

Comparative Genomic Analysis of Multidrug-Resistant Pseudomonas aeruginosa Clinical Isolates VRFPA06 and VRFPA08 with VRFPA07

Cited by 16 publications

References 4 publications

Application of six multiplex PCR's among 200 clinical isolates of Pseudomonas aeruginosa for the detection of 20 drug resistance encoding genes

Application of six multiplex PCR's among 200 clinical isolates of Pseudomonas aeruginosa for the detection of 20 drug resistance encoding genes

Ribosomally encoded antibacterial proteins and peptides fromPseudomonas

Pyomelanin‐producing Pseudomonas aeruginosa selected during chronic infections have a large chromosomal deletion which confers resistance to pyocins

Contact Info

Product

Resources

About