Genetic Environment and Transcription of
            <i>ampC</i>
            in an
            <i>Acinetobacter baumannii</i>
            Clinical Isolate

Segal, Heidi; Nelson, E. C.

doi:10.1128/aac.48.2.612-614.2004

Cited by 70 publications

(79 citation statements)

References 17 publications

(9 reference statements)

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“…As previously described, the bla OXA-23 gene was not embedded in a class 1 integron (9, 17, and data not shown). The genetic environment was similar to that of the prototype bla OXA-23 gene, with insertion sequence ISabaI inserted upstream of this gene, as revealed by PCR analysis (9,14,18).…”

mentioning

confidence: 95%

“…Similarly, the class A ␤-lactamase bla TEM gene and the chromosomal class C ␤-lactamase bla AMPC gene were sought by PCR (11,18). The presence of ISAbaI inserted upstream of a bla AMPC -␤-lactamase gene was sought by PCR as previously described (14,18). PCR products were purified using a QIAquick PCR purification kit (QIAGEN, Courtaboeuf, France) and sequenced on both strands with an automated sequencer (ABI 3100; Applied Biosystems, Foster City, Calif.).…”

mentioning

confidence: 99%

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Outbreak of Carbapenem-Resistant Acinetobacter baumannii Producing the Carbapenemase OXA-23 in a Tertiary Care Hospital of Papeete, French Polynesia

et al. 2005

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Carbapenem-resistantImipenem and meropenem are among the drugs of choice used to treat nosocomial infections due to multidrug-resistant Acinetobacter baumannii isolates. However, their efficacy is being increasingly compromised by the emergence of carbapenem-hydrolyzing ␤-lactamases of molecular Ambler class B (metalloenzymes) and D enzymes (oxacillinases) (1,2,3,12,17). Whereas the metalloenzymes are of IMP and VIM types, the carbapenem-hydrolyzing oxacillinases are members of three subgroups of enzymes: the OXA-23, OXA-24, and OXA-58 enzymes (2,5,9,15,16,17). Outbreaks of OXA-type carbapenemase-producing A. baumannii strains have been reported worldwide: OXA-24 in Madrid, Spain (4, 5); OXA-23 in Spain and in Curitiba, Brazil (2, 8); OXA-58 in Toulouse,

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confidence: 95%

mentioning

confidence: 99%

Outbreak of Carbapenem-Resistant Acinetobacter baumannii Producing the Carbapenemase OXA-23 in a Tertiary Care Hospital of Papeete, French Polynesia

et al. 2005

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“…However, unlike those of class A ESBLs, the activities of class C ␤-lactamases are not generally inhibited by clavulanic acid or tazobactam. Genes encoding class C ␤-lactamases are found on the chromosomes of many enteric bacteria and also are intrinsic to some nonfermenting gram-negative bacteria such as P. aeruginosa and Acinetobacter spp., where they may be silent and under tight transcriptional control (58,91). However, recently resistance to cephamycins and cephalosporins has been acquired by Klebsiella spp.…”

Section: Iscr1mentioning

confidence: 99%

IS CR Elements: Novel Gene-Capturing Systems of the 21st Century?

Toleman

Bennett

Walsh

2006

Microbiol Mol Biol Rev

512

481

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SUMMARY “Common regions” (CRs), such as Orf513, are being increasingly linked to mega-antibiotic-resistant regions. While their overall nucleotide sequences show little identity to other mobile elements, amino acid alignments indicate that they possess the key motifs of IS91-like elements, which have been linked to the mobility ent plasmids in pathogenic Escherichia coli. Further inspection reveals that they possess an IS91-like origin of replication and termination sites (terIS), and therefore CRs probably transpose via a rolling-circle replication mechanism. Accordingly, in this review we have renamed CRs as ISCRs to give a more accurate reflection of their functional properties. The genetic context surrounding ISCRs indicates that they can procure 5′ sequences via misreading of the cognate terIS, i.e., “unchecked transposition.” Clinically, the most worrying aspect of ISCRs is that they are increasingly being linked with more potent examples of resistance, i.e., metallo-β-lactamases in Pseudomonas aeruginosa and co-trimoxazole resistance in Stenotrophomonas maltophilia. Furthermore, if ISCR elements do move via “unchecked RC transposition,” as has been speculated for ISCR1, then this mechanism provides antibiotic resistance genes with a highly mobile genetic vehicle that could greatly exceed the effects of previously reported mobile genetic mechanisms. It has been hypothesized that bacteria will surprise us by extending their “genetic construction kit” to procure and evince additional DNA and, therefore, antibiotic resistance genes. It appears that ISCR elements have now firmly established themselves within that regimen.

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“…Genes coding for Ambler class B and D carbapenemases were sought by PCR with primers specific for the bla IMP (22), bla VIM (22), bla OXA-23 -like (8), bla OXA-26 -like (1), and bla and bla OXA-69 -like (20) genes. Similarly, the class A ␤-lactamase bla TEM gene (10), the bla OXA-20 gene (forward primer, 5Ј-GAT GGGACGGCGCTAAAAGA-3Ј; reverse primer, 5Ј-TACCCA ACCGACCCACCAAC-3Ј), the chromosomal class C ␤-lactamase bla AmpC gene, and the presence of ISAba1 inserted upstream of a bla AmpC ␤-lactamase gene were sought by PCR (21). Both strands of the PCR products were sequenced with an automated sequencer (ABI 3100; Applied Biosystems, Foster City, CA).…”

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confidence: 99%

Outbreak of Infection by Carbapenem-Resistant Acinetobacter baumannii Producing the Carbapenemase OXA-58 in Belgium

et al. 2006

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Carbapenem-resistant Acinetobacter baumannii isolates were obtained from 17 patients between September 2004 and August 2005 at the Academisch Ziekenhuis Vrije Universiteit Brussel, Brussels, Belgium. These multidrug-resistant isolates, which belonged to a single clone, remained susceptible to colistin and tigecycline only and produced the carbapenem-hydrolyzing oxacillinase OXA-58. This study highlights the importance of the intercountry spread of this ␤-lactamase-mediated resistance mechanism and its epidemic evolution.Imipenem and meropenem are among the drugs of choice for the treatment of nosocomial infections due to multidrugresistant (MDR) Acinetobacter baumannii (2). However, their efficacies are increasingly being compromised and carbapenem-resistant isolates are becoming widespread in several regions of the world (7, 16). A large variety of molecular mechanisms for resistance to carbapenems have been reported in A. baumannii, i.e., not only the acquisition of carbapenemhydrolyzing ␤-lactamases of molecular Ambler class B (metalloenzymes) and the acquisition of mostly class D enzymes (oxacillinases) (19, 24) but also rare mutations in genes coding for penicillin-binding proteins (9) and decreased outer membrane permeability (5). Whereas the class B enzymes found in A. baumannii are of the IMP and VIM types (24), the acquired carbapenem-hydrolyzing class D ␤-lactamases (CHDLs) are members of three subgroups of enzymes: the OXA-23, 18). OXA-58 shares less than 50% amino acid identity with the members of two other CHDL groups, which share 60% amino acid sequence identity. Recently, a fourth subgroup of OXA ␤-lactamases sharing less than 63% amino

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Genetic Environment and Transcription of ampC in an Acinetobacter baumannii Clinical Isolate

Cited by 70 publications

References 17 publications

Outbreak of Carbapenem-Resistant Acinetobacter baumannii Producing the Carbapenemase OXA-23 in a Tertiary Care Hospital of Papeete, French Polynesia

Outbreak of Carbapenem-Resistant Acinetobacter baumannii Producing the Carbapenemase OXA-23 in a Tertiary Care Hospital of Papeete, French Polynesia

IS CR Elements: Novel Gene-Capturing Systems of the 21st Century?

Outbreak of Infection by Carbapenem-Resistant Acinetobacter baumannii Producing the Carbapenemase OXA-58 in Belgium

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