Carbapenem and amikacin resistance on a large conjugative <i>Acinetobacter baumannii</i> plasmid

Nigro, Steven J.; Holt, Kathryn E.; Pickard, Derek; Hall, Ruth M.

doi:10.1093/jac/dku486

Cited by 34 publications

(22 citation statements)

References 9 publications

(16 reference statements)

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“…The second plasmid (pAB-MAL-2) was found to share high similarity and a common backbone with the recently described pAD46-3 and pA105-2 plasmids, recovered from an A. baumannii isolate collected in Australia in 2010 (Fig. 2) (22) and Sweden in 2013 (18), respectively. As shown in Fig.…”

Section: Discussionmentioning

confidence: 65%

“…2) (22). Since no antibiotic resistance genes are located on this plasmid, no transformant could be obtained.…”

Section: Resultsmentioning

confidence: 99%

“…Plasmid pD72-2 might itself be considered the progenitor of plasmid pD46-3, in which Tn2006 containing the bla OXA-23 gene has been inserted ( Fig. 2) (22). Sixty-one SNPs were identified between pAB-MAL-2 and pD72-2, suggesting an ancient acquisition of TnaphA6 by pAB-MAL-2.…”

Section: Discussionmentioning

confidence: 99%

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First Occurrence of OXA-72-Producing Acinetobacter baumannii in Serbia

Dortet

Bonnin

Bernabeu

et al. 2016

Antimicrob Agents Chemother

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e Here, we characterized the first OXA-72-producing Acinetobacter baumannii isolate (designated MAL) recovered from a urine sample from a Serbian patient. Antimicrobial susceptibility testing, plasmid analysis, and whole-genome sequencing (WGS) were performed to fully characterize the resistome of the A. baumannii MAL clinical isolate. The isolate was multidrug resistant and remained susceptible only to colistin and tigecycline. PCR analysis revealed the presence of the carbapenemase OXA-72, an OXA-40 variant. Extraction by the Kieser method revealed the presence of two plasmids, and one of these, a ca. 10-kb plasmid, harbored the bla OXA-72 gene. WGS revealed 206 contigs corresponding to a genome of 3.9 Mbp in size with a G؉C content of 38.8%. The isolate belonged to sequence type 492 and to worldwide clone II (WWCII). Naturally occurring ␤-lactamase-encoding genes (bla ADC-25 and bla OXA-66 ) were also identified. Aminoglycoside resistance genes encoding one aminoglycoside adenyltransferase (aadA2), three aminoglycoside phosphatases (strA, strB, aphA6), and one 16S RNA methylase (armA) conferring resistance to all aminoglycosides were identified. Resistance to fluoroquinolones was likely due to mutations in gyrA, parC, and parE. Of note, the resistome matched perfectly with the antibiotic susceptibility testing results.

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Section: Discussionmentioning

confidence: 65%

“…2) (22). Since no antibiotic resistance genes are located on this plasmid, no transformant could be obtained.…”

Section: Resultsmentioning

confidence: 99%

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First Occurrence of OXA-72-Producing Acinetobacter baumannii in Serbia

Dortet

Bonnin

Bernabeu

et al. 2016

Antimicrob Agents Chemother

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“…Consequently the MAR, XAR, and panresistant GC2 isolates seen in many countries today are all derived from a single cell that had acquired both AbGRI1 and AbGRI2. Current XAR GC2 isolates have usually retained resistance to at least some of the older antibiotics but have gained resistance to newer antibiotics, either through mutations or by acquisition of new genes in transposons that are located in plasmids or inserted into the chromosome (e.g., oxa23 or aphA6) (13,24,25). The AbGRI3 island carrying armA is also a later addition found only in some GC2 isolates (13,14).…”

Section: Discussionmentioning

confidence: 99%

Evolution of AbGRI2-0, the Progenitor of the AbGRI2 Resistance Island in Global Clone 2 of Acinetobacter baumannii

Blackwell

Nigro

Hall

2016

Antimicrob Agents Chemother

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A320, isolated in the Netherlands in 1982 and also known as RUH134, is the earliest available multiply antibiotic-resistant (MAR) Acinetobacter baumannii isolate belonging to global clone 2 (GC2) and is the reference strain for this clone. The draft genome sequence of A320 was used to investigate the original location and configuration of the IS26-bounded AbGRI2 resistance island found in current GC2 isolates. PCR mapping and sequencing were used to order contigs composing the resistance islands. A320 contains two IS26-bounded resistance islands, AbGRI2-0a and AbGRI2-0b, of 7.8 kb and 25.4 kb, respectively. Together they contain bla TEM , aacC1, aadA1, sul1, catA1, and aphA1b genes, which confer resistance to antibiotics used clinically in the 1970s, as well as an incomplete mercury resistance module. Tracking the continuity of the chromosome and the target site duplications revealed that the two resistance islands were originally together as AbGRI2-0, an island of 32.4 kb, and were subsequently separated via an IS26-mediated intramolecular inversion that reversed the orientation of 1.54 Mb of the chromosome and duplicated an IS26. A320 contains an ancestral form of AbGRI2, and the original insertion site of the AbGRI2 island was identified. Many of the AbGRI2 versions present in the completed GC2 genomes can be derived from it via the variant AbGRI2-1. IS26-mediated inversions have also played a part in forming AbGRI2-0, and, upon reversal, large regions of AbGRI2-0 are identical to parts of AbaR0, the ancestral version of the AbaR islands present in GC1 isolates. This indicates a common source.

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“…In many cases, intraspecies phenotypic variation can in part be attributed to the variable presence of mobile genetic elements, such as the presence of a Shiga-like toxin-encoding bacteriophage in the enterohemorrhagic Escherichia coli pathotype (3) or the presence of bla OXA-23 -bearing plasmids or transposons in carbapenem-resistant Acinetobacter baumannii isolates (4,5). An additional process that drives intraspecies phenotypic variation is the differential regulation of gene expression (6).…”

mentioning

confidence: 99%

RocA Is an Accessory Protein to the Virulence-Regulating CovRS Two-Component System in Group A Streptococcus

et al. 2017

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Regulating gene expression during infection is critical to the ability of pathogens to circumvent the immune response and cause disease. This is true for the group A Streptococcus (GAS), a pathogen that causes both invasive (e.g., necrotizing fasciitis) and noninvasive (e.g., pharyngitis) diseases. The control of virulence (CovRS) two-component system has a major role in regulating GAS virulence factor expression. The regulator of cov (RocA) protein, which is a predicted kinase, functions in an undetermined manner through CovRS to alter gene expression and reduce invasive disease virulence. Here, we show that the ectopic expression of a truncated RocA derivative, harboring the membrane-spanning domains but not the dimerization or HATPase domain, is sufficient to complement a rocA mutant strain. Coupled with a previous bioinformatic study, the data are consistent with RocA being a pseudokinase. RocA reduces the ability of serotype M1 GAS isolates to express capsule and to evade killing in human blood, phenotypes that are not observed for M3 or M18 GAS due to isolates of these serotypes naturally harboring mutant rocA alleles. In addition, we found that varying the RocA concentration attenuates the regulatory activity of Mg 2ϩ and the antimicrobial peptide LL-37, which positively and negatively regulate CovS function, respectively. Thus, we propose that RocA is an accessory protein to the CovRS system that influences the ability of GAS to modulate gene expression in response to host factors. A model of how RocA interacts with CovRS, and of the regulatory consequences of such activity, is presented.

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Carbapenem and amikacin resistance on a large conjugative Acinetobacter baumannii plasmid

Cited by 34 publications

References 9 publications

First Occurrence of OXA-72-Producing Acinetobacter baumannii in Serbia

First Occurrence of OXA-72-Producing Acinetobacter baumannii in Serbia

Evolution of AbGRI2-0, the Progenitor of the AbGRI2 Resistance Island in Global Clone 2 of Acinetobacter baumannii

RocA Is an Accessory Protein to the Virulence-Regulating CovRS Two-Component System in Group A Streptococcus

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