Transferable Acinetobacter baumannii plasmid pDETAB2 encodes OXA-58 and NDM-1 and represents a new class of antibiotic resistance plasmids

2021 ◽  
Author(s):  
Haiyang Liu ◽  
Robert A Moran ◽  
Ying Chen ◽  
Emma L Doughty ◽  
Xiaoting Hua ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Resistance Genes ◽  
Antibiotic Resistance Genes ◽  
Care Patient ◽  
Mercury Resistance ◽  
Acinetobacter Species ◽  
New Class ◽  
Oxford Nanopore ◽  
Resistance Plasmids

Abstract Objectives To characterize a blaOXA-58- and blaNDM-1-containing MDR plasmid from a rare Acinetobacter baumannii lineage and compare it with related plasmids to explore the distribution and evolution of a new plasmid group. Methods A. baumannii DETAB-P2 was isolated from a rectal swab of an intensive care patient. Antibiotic susceptibility was determined using broth microdilution. DETAB-P2 was mated with A. baumannii ATCC 17978 and putative transconjugants were characterized by S1/PFGE and Southern hybridization. WGS was performed on the Illumina and Oxford Nanopore platforms. MLST was performed with the Pasteur and Oxford schemes. Antibiotic resistance genes were identified with ABRicate. Plasmid sequence annotation was performed manually. Complete plasmids in GenBank with the same rep gene were used for comparative analyses. Results A. baumannii DETAB-P2 was ST138 by the Pasteur scheme and a novel Oxford type, ST2209. It transferred blaOXA-58 and blaNDM-1 to ATCC 17978 in the 100 072 bp plasmid pDETAB2 that also carried bleMBL, sul2, aacC2d, tet(39), msr(E)-mph(E) and putative mercury resistance and RND efflux system determinants. pDETAB2 represents a new plasmid type, GR34, and contained 16 pdif sites and several novel dif modules. Only a 10 kbp core sequence is shared amongst pDETAB2 and 18 further GR34 plasmids in GenBank, with diverse accessory regions comprised of various dif modules. Conclusions GR34 plasmids are found in several Acinetobacter species from diverse environments. They display considerable variation in accessory content owing to the presence of pdif sites and an array of dif modules, some of which contain antibiotic resistance genes.

Acquisition of a genomic resistance island (AbGRI5) from global clone 2 through homologous recombination in a clinical Acinetobacter baumannii isolate

2020 ◽  
Vol 76 (1) ◽  
pp. 65-69
Author(s):  
Xiaoting Hua ◽  
Robert A Moran ◽  
Qingye Xu ◽  
Jintao He ◽  
Youhong Fang ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Resistance Genes ◽  
Antibiotic Resistance Genes ◽  
Whole Genome Sequence ◽  
Oxford Nanopore ◽  
History Of ◽  
Agar Dilution ◽  
Resistance Island ◽  
New Location

Abstract Objectives To reconstruct the evolutionary history of the clinical Acinetobacter baumannii XH1056, which lacks the Oxford scheme allele gdhB. Methods Susceptibility testing was performed using broth microdilution and agar dilution. The whole-genome sequence of XH1056 was determined using the Illumina and Oxford Nanopore platforms. MLST was performed using the Pasteur scheme and the Oxford scheme. Antibiotic resistance genes were identified using ABRicate. Results XH1056 was resistant to all antibiotics tested, apart from colistin, tigecycline and eravacycline. MLST using the Pasteur scheme assigned XH1056 to ST256. However, XH1056 could not be typed with the Oxford MLST scheme as gdhB is not present. Comparative analyses revealed that XH1056 contains a 52 933 bp region acquired from a global clone 2 (GC2) isolate, but is otherwise closely related to the ST23 A. baumannii XH858. The acquired region in XH1056 also contains a 34 932 bp resistance island that resembles AbGRI3 and contains the armA, msrE-mphE, sul1, blaPER-1, aadA1, cmlA1, aadA2, blaCARB-2 and ere(B) resistance genes. Comparison of the XH1056 chromosome to that of GC2 isolate XH859 revealed that the island in XH1056 is in the same chromosomal region as that in XH859. As this island is not in the standard AbGRI3 position, it was named AbGRI5. Conclusions XH1056 is a hybrid isolate generated by the acquisition of a chromosomal segment from a GC2 isolate that contains a resistance island in a new location—AbGRI5. As well as generating ST256, it appears likely that a single recombination event is also responsible for the acquisition of AbGRI5 and its associated antibiotic resistance genes.

Mercury resistance (mer) operons in enterobacteria

2002 ◽  
Vol 30 (4) ◽  
pp. 719-722 ◽  
Author(s):  
J. L. Hobman ◽  
A. M. M. Essa ◽  
N. L. Brown
Keyword(s):  
Antibiotic Resistance ◽  
Resistance Genes ◽  
Antibiotic Resistance Genes ◽  
Mercury Resistance ◽  
Genetic Elements ◽  
Mercuric Ion

Mercury resistance is found in many genera of bacteria. Common amongst enterobacteria are transposons related to Tn21, which is both mercuric ion- and streptomycin-/spectinomycin-and sulphonamide-resistant. Other Tn21-related transposons often have different antibiotic resistances compared with Tn21, but share many non-antibiotic-resistance genes with it. In this article we discuss possible mechanisms for the evolution of Tn21 and related genetic elements.

scholarly journals Using WGS to identify antibiotic resistance genes and predict antimicrobial resistance phenotypes in MDR Acinetobacter baumannii in Tanzania

2019 ◽  
Vol 74 (6) ◽  
pp. 1484-1493 ◽  
Author(s):  
Happiness H Kumburu ◽  
Tolbert Sonda ◽  
Marco van Zwetselaar ◽  
Pimlapas Leekitcharoenphon ◽  
Oksana Lukjancenko ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Antimicrobial Resistance ◽  
Acinetobacter Baumannii ◽  
Resistance Genes ◽  
Antibiotic Resistance Genes

scholarly journals Enterococcus faecalisCRISPR-Cas is a robust barrier to conjugative antibiotic resistance dissemination in the murine intestine

2018 ◽  
Author(s):  
Valerie J. Price ◽  
Sara W. McBride ◽  
Karthik Hullahalli ◽  
Anushila Chatterjee ◽  
Breck A. Duerkop ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Enterococcus Faecalis ◽  
Resistance Genes ◽  
Antibiotic Resistance Genes ◽  
Conjugative Plasmids ◽  
Resistance Plasmids ◽  
The Impact ◽  
Mammalian Intestine

AbstractCRISPR-Cas systems are barriers to horizontal gene transfer (HGT) in bacteria. Little is known about CRISPR-Cas interactions with conjugative plasmids, and studies investigating CRISPR-Cas/plasmid interactions inin vivomodels relevant to infectious disease are lacking. These are significant gaps in knowledge because conjugative plasmids disseminate antibiotic resistance genes among pathogensin vivo, and it is essential to identify strategies to reduce the spread of these elements. We use enterococci as models to understand the interactions of CRISPR-Cas with conjugative plasmids.Enterococcus faecalisis a native colonizer of the mammalian intestine and harbors pheromone-responsive plasmids (PRPs). PRPs mediate inter- and intraspecies transfer of antibiotic resistance genes. We assessedE. faecalisCRISPR-Cas anti-PRP activity in the mouse intestine and under varyingin vitroconditions. We observed striking differences in CRISPR-Cas efficiencyin vitroversusin vivo. With few exceptions, CRISPR-Cas blocked intestinal PRP dissemination, whilein vitro, the PRP frequently escaped CRISPR-Cas defense. Our results further the understanding of CRISPR-Cas biology by demonstrating that standardin vitroexperiments do not adequately model thein vivoanti-plasmid activity of CRISPR-Cas. Additionally, our work identifies several variables that impact the apparentin vitroanti-plasmid activity of CRISPR-Cas, including planktonic versus biofilm settings, different donor/recipient ratios, production of a plasmid-encoded bacteriocin, and the time point at which matings are sampled. Our results are clinically significant because they demonstrate that barriers to HGT encoded by normal human microbiota can have significant impacts onin vivoantibiotic resistance dissemination.ImportanceCRISPR-Cas is a type of immune system encoded by bacteria that is hypothesized to be a natural impediment to the spread of antibiotic resistance genes. In this study, we directly assessed the impact of CRISPR-Cas on antibiotic resistance dissemination in the mammalian intestine and under varyingin vitroconditions. We observed a robust effect of CRISPR-Cas onin vivobut notin vitrodissemination of antibiotic resistance plasmids in the native mammalian intestinal colonizerEnterococcus faecalis. We conclude that standard laboratory experiments currently do not appropriately model thein vivoconditions where antibiotic resistance dissemination occurs betweenE. faecalisstrains. Moreover, our results demonstrate that CRISPR-Cas encoded by native members of the mammalian intestinal microbiota can block the spread of antibiotic resistance plasmids.

scholarly journals PixR, a Novel Activator of Conjugative Transfer of IncX4 Resistance Plasmids, Mitigates the Fitness Cost of mcr-1 Carriage in Escherichia coli

mBio ◽  
2022 ◽  
Author(s):  
Lingxian Yi ◽  
Romain Durand ◽  
Frédéric Grenier ◽  
Jun Yang ◽  
Kaiyang Yu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Antibiotic Resistance ◽  
Resistance Genes ◽  
Molecular Mechanisms ◽  
Antibiotic Resistance Genes ◽  
Fitness Cost ◽  
Conjugative Transfer ◽  
Resistance Plasmids

The spread of clinically relevant antibiotic resistance genes is often linked to the dissemination of epidemic plasmids. However, the underlying molecular mechanisms contributing to the successful spread of epidemic plasmids remain unclear.

Case report: Detection of aadB and tet (39) on the plasmid of Acinetobacter baumannii TN81 in Vietnam through next-generation sequencing and bioinformatics analysis

2021 ◽  
Vol 31 (4) ◽  
pp. 51-60
Author(s):  
Vu Nhi Ha ◽  
Kieu Chi Thanh ◽  
Nguyen Thai Son ◽  
Dao Van Thang ◽  
Tran Huy Hoang
Keyword(s):  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Resistance Genes ◽  
De Novo Assembly ◽  
De Novo ◽  
Antibiotic Resistance Genes ◽  
Common Mechanism ◽  
Genes Encoding ◽  
Short Read Sequence ◽  
Genome Shotgun Sequence

Acinetobacter baumannii (A. baumannii) is currently ranked as the frst concern for the development of new antibiotics due to its capacity of resistance to all available families of antibiotics. The most common mechanism of antibiotic resistance development in A. baumannii is through the acquisition of mobile genetic elements such as plasmid, transposon and integrons carrying resistance genes. A. baumannii strain TN81 was isolated from sputum specimen of a 45-year-old man at Thanh Nhan Hospital (Hanoi, Vietnam) and confrmed to be a multidrug resistance strain with high minimum inhibitory concentration value of 8/9 type of antibiotics, especially colistin. De novo assembly of the whole genome shotgun sequence of strain TN81 yielded an estimated genome size of 3,739,193 bp with 593 contigs and N50 is 9,126 bp. MLST analysis showed that TN81 belongs to ST164, which was frst reported as genome assembly in Vietnam. Resistance genes identifcation through database found that TN81 contained 12 genes encoding for antibiotic resistance. Notably, we performed de novo assembly of plasmid through short read sequence and identifed two potential plasmid-encoded antibiotic resistance genes (ant(2’’)-Ia / aadB and tet (39), which were reported for the first time as in ST164 group. This study aimed to investigate the plasmid-containing antibiotic resistance genes from a nosocomial isolate of Acinetobacter baumannii. Conclusively, all of these results would be crucial information on antibiotic resistance in A. baumannii in Vietnam.

scholarly journals Effect of frameshift mutagen acriflavine on control of resistance genes in Acinetobacter baumannii

2011 ◽  
Vol 60 (2) ◽  
pp. 211-215 ◽  
Author(s):  
B. S. Lopes ◽  
A. Hamouda ◽  
J. Findlay ◽  
S. G. B. Amyes
Keyword(s):  
Gene Expression ◽  
Antibiotic Resistance ◽  
Acinetobacter Baumannii ◽  
Resistance Genes ◽  
Outer Membrane Proteins ◽  
Antibiotic Resistance Gene ◽  
Antibiotic Resistance Genes ◽  
Multidrug Resistant ◽  
The Body

Acinetobacter baumannii is a Gram-negative pathogenic bacterium that often exhibits a multidrug-resistant phenotype causing infections at various sites of the body and increasingly leading to septicaemic shock. This study evaluated the role of acriflavine, a frameshift mutagen, on the movement of insertion sequence ISAba1 in clinical isolates of A. baumannii, with the focus on changes in expression levels of the bla ADC and bla OXA-51-like genes. Resistance profiles were assessed with consideration of ISAba1 acting as a promoter upstream of the bla ADC or bla OXA-51-like gene. ISAba1 movement was observed in the acriflavine mutants Ab153M and Ab1225M. Ab153M exhibited an increase in the MIC values of carbapenems and ceftazidime, with ISAba1 gained upstream of the bla ADC and bla OXA-51-like genes, correlating with an increase in gene expression. Reduced expression of the 17, 23 and 25 kDa outer-membrane proteins (OMPs) was also observed in Ab153M. There was a significant decrease in MIC values of carbapenems with the loss of ISAba1 upstream of the bla ADC and bla OXA-51-like genes in strain Ab1225M, and a significant decrease in bla OXA-51-like gene expression and, to a lesser extent, in bla ADC expression. Ab1225M and a serially subcultured Ab1225 strain (Ab1225s) exhibited overexpression of the 17, 23, 25 and 27 kDa OMPs. There was a decrease in MIC values of the carbapenems and piperacillin/tazobactam but not of ceftazidime in Ab1225s, which had ISAba1 upstream of the bla ADC and bla OXA-51-like genes. A significant decrease in bla OXA-51-like expression was observed in Ab1225s, whereas the expression of bla ADC was similar to that in the Ab1225 parental strain. The attenuation in this strain may be due to overexpression of OMPs and it is clear that, even if ISAba1 is present upstream of an antibiotic resistance gene, it may not necessarily contribute towards the overexpression of antibiotic resistance genes (bla OXA-51-like in Ab1225s). Movement of the IS element within the A. baumannii chromosome may be an important regulatory mechanism employed by the bacterium under particular stress conditions, and the ability to upregulate the expression of antibiotic resistance genes is likely to be an important factor in the pathogenicity of this bacterium.

scholarly journals Is exposure to mercury a driving force for the carriage of antibiotic resistance genes?

2010 ◽  
Vol 59 (7) ◽  
pp. 804-807 ◽  
Author(s):  
David Skurnik ◽  
Raymond Ruimy ◽  
Derren Ready ◽  
Etienne Ruppe ◽  
Claire Bernède-Bauduin ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Resistance Gene ◽  
Resistance Genes ◽  
Driving Force ◽  
Antibiotic Resistance Gene ◽  
Antibiotic Resistance Genes ◽  
Mercury Exposure ◽  
Mercury Resistance ◽  
High Exposure ◽  
E Coli

The mercury resistance gene merA has often been found together with antibiotic resistance genes in human commensal Escherichia coli. To study this further, we analysed mercury resistance in collections of strains from various populations with different levels of mercury exposure and various levels of antibiotic resistance. The first population lived in France and had no known mercury exposure. The second lived in French Guyana and included a group of Wayampi Amerindians with a known high exposure to mercury. Carriage rates of mercury resistance were assessed by measuring the MIC and by detecting the merA gene. Mercury-resistant E. coli was found significantly more frequently in the populations that had the highest carriage rates of antibiotic-resistant E. coli and in parallel antibiotic resistance was higher in the population living in an environment with a high exposure to mercury, suggesting a possible co-selection. Exposure to mercury might be a specific driving force for the acquisition and maintenance of mobile antibiotic resistance gene carriage in the absence of antibiotic selective pressure.

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