Molecular characterization of lpxACD and pmrA/B two-component regulatory system in the colistin resistance Acinetobacter baumannii clinical isolates

Gene Reports ◽  
2020 ◽  
Vol 21 ◽  
pp. 100952
Author(s):  
Mohammad Reza Kandehkar Ghahraman ◽  
Hossein Hosseini-Nave ◽  
Omid Azizi ◽  
Mohammad Reza Shakibaie ◽  
Hamid Reza Mollaie ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Molecular Characterization ◽  
Regulatory System ◽  
Clinical Isolates ◽  
Colistin Resistance ◽  
Two Component

scholarly journals Phenotypic and molecular characterization of Acinetobacter baumannii clinical isolates in Saudi Arabia

2020 ◽  
Vol 13 (2) ◽  
pp. 327
Author(s):  
R Bawazeer ◽  
M Algoribi ◽  
T Abujamel ◽  
L Okdah ◽  
M Alzayer ◽  
...  
Keyword(s):  
Saudi Arabia ◽  
Acinetobacter Baumannii ◽  
Molecular Characterization ◽  
Clinical Isolates

scholarly journals Molecular Characterization of Integrons in Epidemiologically Unrelated Clinical Isolates of Acinetobacter baumannii from Italian Hospitals Reveals a Limited Diversity of Gene Cassette Arrays

2002 ◽  
Vol 46 (11) ◽  
pp. 3665-3668 ◽  
Author(s):  
Francesca Gombac ◽  
Maria Letizia Riccio ◽  
Gian Maria Rossolini ◽  
Cristina Lagatolla ◽  
Enrico Tonin ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Acinetobacter Baumannii ◽  
Molecular Characterization ◽  
Horizontal Transfer ◽  
Gene Cassette ◽  
Clinical Isolates

ABSTRACT Integron carriage by 36 epidemiologically unrelated Acinetobacter baumannii isolates collected over an 11-year period from patients in six different Italian hospitals was investigated. Sixteen type 1 integron-positive isolates (44%) were found, 13 of which carried the same array of cassettes, i.e., aacC1, orfX, orfX′, and aadA1a. As ribotype analysis of the isolates demonstrated a notable genetic diversity, horizontal transfer of the entire integron structure or ancient acquisition was hypothesized.

scholarly journals Globally Expanding Carbapenemase Finally Appears in Spain: Nosocomial Outbreak of Acinetobacter baumannii Producing Plasmid-Encoded OXA-23 in Barcelona, Spain

2013 ◽  
Vol 57 (10) ◽  
pp. 5155-5157 ◽  
Author(s):  
Noraida Mosqueda ◽  
Paula Espinal ◽  
Clara Cosgaya ◽  
Sergio Viota ◽  
Virginia Plasensia ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Molecular Characterization ◽  
Multidrug Resistant ◽  
Sequence Type ◽  
Clinical Isolates ◽  
Nosocomial Outbreak ◽  
Content Type ◽  
Hospital Outbreak

ABSTRACTResistance ofAcinetobacter baumanniiclinical isolates to carbapenems is on the rise worldwide mainly in association with the production of OXA-23. Until recently, however, OXA-23 was absent in Spain. In this work, we report the molecular characterization of a hospital outbreak of OXA-23-producingA. baumanniiin Barcelona caused by a multidrug-resistant (MDR) clone belonging to international clone IC-II/sequence type ST85 between October 2010 and May 2011.blaOXA-23was carried in a plasmid of 90 kb and located within the composite transposon Tn2006.

scholarly journals RND-Type Efflux Pumps in Multidrug-Resistant Clinical Isolates of Acinetobacter baumannii: Major Role for AdeABC Overexpression and AdeRS Mutations

2013 ◽  
Vol 57 (7) ◽  
pp. 2989-2995 ◽  
Author(s):  
Eun-Jeong Yoon ◽  
Patrice Courvalin ◽  
Catherine Grillot-Courvalin
Keyword(s):  
Acinetobacter Baumannii ◽  
Efflux Pump ◽  
Regulatory System ◽  
Multidrug Resistant ◽  
Clinical Isolates ◽  
Clinical Settings ◽  
Two Component System ◽  
Content Type ◽  
High Incidence ◽  
Two Component

ABSTRACTIncreased expression of chromosomal genes for resistance-nodulation-cell division (RND)-type efflux systems plays a major role in the multidrug resistance (MDR) ofAcinetobacter baumannii. However, the relative contributions of the three most prevalent pumps, AdeABC, AdeFGH, and AdeIJK, have not been evaluated in clinical settings. We have screened 14 MDR clinical isolates shown to be distinct on the basis of multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE) for the presence and overexpression of the three Ade efflux systems and analyzed the sequences of the regulators AdeRS, a two-component system, for AdeABC and AdeL, a LysR-type regulator, for AdeFGH. GeneadeBwas detected in 13 of 14 isolates, andadeGand the intrinsicadeJgene were detected in all strains. Significant overexpression ofadeBwas observed in 10 strains, whereas only 7 had moderately increased levels of expression of AdeFGH, and none overexpressed AdeIJK. Thirteen strains had reduced susceptibility to tigecycline, but there was no correlation between tigecycline MICs and the levels of AdeABC expression, suggesting the presence of other mechanisms for tigecycline resistance. No mutations were found in the highly conserved LysR regulator of the nine strains expressing AdeFGH. In contrast, functional mutations were found in conserved domains of AdeRS in all the strains that overexpressed AdeABC with two mutational hot spots, one in AdeS near histidine 149 suggesting convergent evolution and the other in the DNA binding domain of AdeR compatible with horizontal gene transfer. This report outlines the high incidence of AdeABC efflux pump overexpression in MDRA. baumanniias a result of a variety of single mutations in the corresponding two-component regulatory system.

scholarly journals Phosphoethanolamine Modification of Lipid A in Colistin-Resistant Variants of Acinetobacter baumannii Mediated by the pmrAB Two-Component Regulatory System

2011 ◽  
Vol 55 (7) ◽  
pp. 3370-3379 ◽  
Author(s):  
Alejandro Beceiro ◽  
Enrique Llobet ◽  
Jesús Aranda ◽  
José Antonio Bengoechea ◽  
Michel Doumith ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Clinical Isolate ◽  
Lipid A ◽  
Gene Knockout ◽  
Regulatory System ◽  
Clinical Isolates ◽  
Strain Atcc ◽  
Colistin Resistance ◽  
Content Type ◽  
Knockout Mutants

ABSTRACTColistin resistance is rare inAcinetobacter baumannii, and little is known about its mechanism. We investigated the role of PmrCAB in this trait, using (i) resistant and susceptible clinical strains, (ii) laboratory-selected mutants of the type strain ATCC 19606 and of the clinical isolate ABRIM, and (iii) a susceptible/resistant pair of isogenic clinical isolates, Ab15/133 and Ab15/132, isolated from the same patient.pmrABsequences in all the colistin-susceptible isolates were identical to reference sequences, whereas resistant clinical isolates harbored one or two amino acid replacements variously located in PmrB. Single substitutions in PmrB were also found in resistant mutants of strains ATCC 19606 and ABRIM and in the resistant clinical isolate Ab15/132. No mutations in PmrA or PmrC were found. Reverse transcriptase (RT)-PCR identified increased expression ofpmrA(4- to 13-fold),pmrB(2- to 7-fold), andpmrC(1- to 3-fold) in resistant versus susceptible organisms. Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry showed the addition of phosphoethanolamine to the hepta-acylated form of lipid A in the resistant variants and in strain ATCC 19606 grown under low-Mg2+induction conditions.pmrBgene knockout mutants of the colistin-resistant ATCC 19606 derivative showed >100-fold increased susceptibility to colistin and 5-fold decreased expression ofpmrC; they also lacked the addition of phosphoethanolamine to lipid A. We conclude that the development of a moderate level of colistin resistance inA. baumanniirequires distinct genetic events, including (i) at least one point mutation inpmrB, (ii) upregulation ofpmrAB, and (iii) expression ofpmrC, which lead to addition of phosphoethanolamine to lipid A.

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