Diversity of virulence genes in multidrug resistant Pseudomonas aeruginosa isolated from burn wound infections

Haghi, Fakhri; Zeighami, Habib; Monazami, Arefeh; Toutouchi, Farnaz; Nazaralian, Shima; Naderi, Ghazal

doi:10.1016/j.micpath.2017.12.052

Cited by 41 publications

(30 citation statements)

References 17 publications

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“…Some genes, normally encode and participate in the virulence factors are, toxA, exoS, exoY, exoU, oprL, oprI, lasA, lasB, oprD, plcH, plcN and nan1 etc. (9).…”

Section: Introductionmentioning

confidence: 99%

Prevalence of some virulence genes and antibiotic susceptibility pattern of Pseudomonas aeruginosa isolated from different clinical specimens

Chand¹,

Khanal²,

Panta³

et al. 2020

Preprint

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Background: Pseudomonas aeruginosa is an opportunistic human pathogen and are reported to cause acute and chronic infectious diseases. Due to its high ability to acquire resistance to many antibiotics, it has become a global public health threat. It consists of some virulence genes that may lead to its pathogenicity. The main objective of this cross-sectional study was to detect the virulence genes and antibiotic susceptibility pattern of P. aeruginosa isolated from clinical specimens collected from governmental hospital of Nepal.Methods: A total of 7898 clinical specimens were analyzed for the period of six months from November 2018 to April 2019. The specimens were cultured on Nutrient agar, Blood agar, MacConkey agar, Chocolate agar, Cysteine-Lactose, Electrolyte Deficient agar plates and were incubated at 37°C for 24 hours. All the isolates were identified by standard biochemical tests and further confirmed by growth on Cetrimide agar plate. The antibiotic susceptibility testing was performed by modified Kirby-Bauer disc diffusion method following CLSI guideline. Multiplex-PCR was done to detect the virulence genes oprL and toxA. Statistical analysis was carried out using IBM SPSS Statistic ver. 25 and the p-value was calculated at significance level (0.05%) by using Chi square.Results: Out of these specimens investigated, 87 isolates were tentatively identified to be P. aeruginosa in which 20 (22.98 %) were found to be multidrug resistant. Comparatively, most of the P. aeruginosa were isolated from outpatients 63 (72.41 %) than inpatients 24 (27.58 %), from male 56 (64.36 %) than female 31 (35.63 %) and in age group 60-79 years (41.37 %). AST result showed the highest resistance of 100% with cefixime whereas susceptibilities of 83.9% and 81.6% with polymixin B and tobramycin were noticed respectively. The PCR results showed that all P. aeruginosa isolates carried oprL 87 (100%) and 83 (95.4 %) isolates showed toxA genes. Conclusion: The studies revealed that almost all P. aeruginosa harbors both oprL and toxA genes.

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“…Some genes, normally encode and participate in the virulence factors are, toxA, exoS, exoY, exoU, oprL, oprI, lasA, lasB, oprD, plcH, plcN and nan1 etc. (9).…”

Section: Introductionmentioning

confidence: 99%

Prevalence of some virulence genes and antibiotic susceptibility pattern of Pseudomonas aeruginosa isolated from different clinical specimens

Chand¹,

Khanal²,

Panta³

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Upon delivery, the effector proteins interact with specific eukaryotic cofactors and become potent enzymes that hijack cellular processes (5)(6)(7). ExoY, one of the most prevalent T3SS effectors of P. aeruginosa (8,9), generates cGMP and cAMP upon interaction with its specific cofactor, F-actin (10). The binding of ExoY to F-actin stabilizes actin filaments and alters their turnover (10).…”

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confidence: 99%

The extreme C terminus of the Pseudomonas aeruginosa effector ExoY is crucial for binding to its eukaryotic activator, F-actin

Belyy

Santecchia²,

Renault

et al. 2018

Journal of Biological Chemistry

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Edited by Velia M. FowlerBacterial nucleotidyl cyclase toxins are potent virulence factors that upon entry into eukaryotic cells are stimulated by endogenous cofactors to catalyze the production of large amounts of 35-cyclic nucleoside monophosphates. The activity of the effector ExoY from Pseudomonas aeruginosa is stimulated by the filamentous form of actin (F-actin). Utilizing yeast phenotype analysis, site-directed mutagenesis, functional biochemical assays, and confocal microscopy, we demonstrate that the last nine amino acids of the C terminus of ExoY are crucial for the interaction with F-actin and, consequently, for ExoY's enzymatic activity in vitro and toxicity in a yeast model. We observed that isolated C-terminal sequences of P. aeruginosa ExoY that had been fused to a carrier protein bind to F-actin and that synthetic peptides corresponding to the extreme ExoY C terminus inhibit ExoY enzymatic activity in vitro and compete with the full-length enzyme for F-actin binding. Interestingly, we noted that various P. aeruginosa isolates of the PA14 family, including highly virulent strains, harbor ExoY variants with a mutation altering the C terminus of this effector. We found that these naturally occurring ExoY variants display drastically reduced enzymatic activity and toxicity. Our findings shed light on the molecular basis of the ExoY-F-actin interaction, revealing that the extreme C terminus of ExoY is critical for binding to F-actin in target cells and that some P. aeruginosa isolates carry C-terminally mutated, low-activity ExoY variants.

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“…One can hypothesize that this loss could be somehow compensated by newly acquired genes since CCBH4851 has a chromosome approximately 600 kb larger than PAO1. However, these alterations are common among MDR strains (29,30) , and to have a network comprising these features could impact dynamics simulations designed to assess MDR bacteria behaviors based on P. aeruginosa CCBH4851 GRN. Overall, the reconstruction included additional regulators, target genes, and new interactions Table 2.…”

Section: Discussionmentioning

confidence: 99%

Gene regulatory network inference and analysis of multidrug-resistant Pseudomonas aeruginosa

Filho

Nascimento

Santos

et al. 2019

Preprint

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Background -Healthcare-associated infections caused by bacteria such as Pseudomonas aeruginosa are a major public health problem worldwide.Gene regulatory networks computationally represent interactions among regulatory genes and their targets, an important approach to understand bacterial behavior and to provide novel ways of overcoming scientific challenges, including the identification of potential therapeutic targets and the development of new drugs. Objectives -Our goal in this manuscript is to present a reconstruction of multidrug-resistant P. aeruginosa gene regulatory network and to analyze its topological properties. Methods -The methodology was based on gene orthology inference by the reciprocal best hit method. We used the genome of P. aeruginosa CCBH4851 as the basis of the reconstruction process. This multidrug-resistant strain is representative of an endemic outbreak in Brazilian territory belonging to ST277. Findings -As the main finding, we obtained a network with a larger number of regulatory genes, target genes and interactions compared to previous work. Topological analysis results are accordant to the complex network representation of biological processes. Main conclusions -The network properties are consistent with P. aeruginosa biological features. To the best of our knowledge, the P. aeruginosa gene regulatory network presented here is the most complete version available to date. Pseudomonas aeruginosa | gene regulatory network | multidrug resistanceCorrespondence: ana.pbn@gmail.com

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Diversity of virulence genes in multidrug resistant Pseudomonas aeruginosa isolated from burn wound infections

Cited by 41 publications

References 17 publications

Prevalence of some virulence genes and antibiotic susceptibility pattern of Pseudomonas aeruginosa isolated from different clinical specimens

Prevalence of some virulence genes and antibiotic susceptibility pattern of Pseudomonas aeruginosa isolated from different clinical specimens

The extreme C terminus of the Pseudomonas aeruginosa effector ExoY is crucial for binding to its eukaryotic activator, F-actin

Gene regulatory network inference and analysis of multidrug-resistant Pseudomonas aeruginosa

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