Extended −10 Promoter in IS
 Aba
 -
 1
 Upstream of
 bla
 OXA-23
 from
 Acinetobacter baumannii

Segal, Heidi; Jacobson, Rachael; Garny, Seike; Bamford, Colleen; Elisha, B. Gay

doi:10.1128/aac.00594-07

Cited by 31 publications

(19 citation statements)

References 12 publications

(13 reference statements)

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“…When ISAba1 is located upstream of bla OXA genes, it tends to increase their expression to a level that confers resistance to the carbapenems. The location of ISAba1 25 bp upstream of bla OXA-23 provides a promoter sequence that drives transcription of the gene (80,81). Similarly, when ISAba1 is located 7 bp upstream of the bla OXA-51-like genes, it provides a promoter that can increase bla OXA-51-like gene expression levels by 50-fold (82).…”

Section: Isaba1mentioning

confidence: 99%

OXA β-Lactamases

2014

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SUMMARY The OXA β-lactamases were among the earliest β-lactamases detected; however, these molecular class D β-lactamases were originally relatively rare and always plasmid mediated. They had a substrate profile limited to the penicillins, but some became able to confer resistance to cephalosporins. From the 1980s onwards, isolates of Acinetobacter baumannii that were resistant to the carbapenems emerged, manifested by plasmid-encoded β-lactamases (OXA-23, OXA-40, and OXA-58) categorized as OXA enzymes because of their sequence similarity to earlier OXA β-lactamases. It was soon found that every A. baumannii strain possessed a chromosomally encoded OXA β-lactamase (OXA-51-like), some of which could confer resistance to carbapenems when the genetic environment around the gene promoted its expression. Similarly, Acinetobacter species closely related to A. baumannii also possessed their own chromosomally encoded OXA β-lactamases; some could be transferred to A. baumannii , and they formed the basis of transferable carbapenem resistance in this species. In some cases, the carbapenem-resistant OXA β-lactamases (OXA-48) have migrated into the Enterobacteriaceae and are becoming a significant cause of carbapenem resistance. The emergence of OXA enzymes that can confer resistance to carbapenems, particularly in A. baumannii , has transformed these β-lactamases from a minor hindrance into a major problem set to demote the clinical efficacy of the carbapenems.

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Section: Isaba1mentioning

confidence: 99%

OXA β-Lactamases

2014

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“…Therefore, CHDL-producing clinical isolates that have carbapenem MICs above the clinical breakpoints often possess additional resistance mechanisms, such as efflux, decreased permeability and/ or modification of PBPs [4,48]. In addition, as observed for bla AmpC and bla OXA-51-like , the insertion of ISAba1 upstream of some CHDLencoding genes has been reported to enhance their expression [49,50].…”

Section: Narrow-spectrum and Extended-spectrum Oxacillinasesmentioning

confidence: 99%

Multidrug-resistantPseudomonas aeruginosaandAcinetobacter baumannii: resistance mechanisms and implications for therapy

Zavascki¹,

Carvalhaes

Picão

et al. 2010

Expert Review of Anti-infective Therapy

278

195

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Pseudomonas aeruginosa and Acinetobacter baumannii are major nosocomial pathogens worldwide. Both are intrinsically resistant to many drugs and are able to become resistant to virtually any antimicrobial agent. An increasing prevalence of infections caused by multidrug-resistant (MDR) isolates has been reported in many countries. The resistance mechanisms of P. aeruginosa and A. baumannii include the production of beta-lactamases, efflux pumps, and target-site or outer membrane modifications. Resistance to multiple drugs is usually the result of the combination of different mechanisms in a single isolate or the action of a single potent resistance mechanism. There are many challenges in the treatment of MDR P. aeruginosa and A. baumannii, especially considering the absence of new antimicrobials in the drug-development pipeline. In this review, we present the major resistance mechanisms of P. aeruginosa and A. baumannii, and discuss how they can affect antimicrobial therapy, considering recent clinical, microbiological, pharmacokinetic and pharmacodynamic findings of the main drugs used to treat MDR isolates.

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“…They are divided into four subgroups according to their amino acid sequence identities as follows: bla OXA-23-like , bla OXA-24/40-like , bla OXA-58-like , and bla OXA-143 genes. In particular, bla OXA-23-like genes are widespread, 16 and these bla OXA-type genes are related to overexpression and dissemination due to insertion sequences at ISAba 19 and XerC/XerD 14 recombination sites, respectively. To date, few studies have investigated bla OXA-type genes in A. baumannii clinical isolates in Mexico.…”

Section: Introductionmentioning

confidence: 99%

Outbreak Caused bybla_OXA-72-ProducingAcinetobacter baumanniiST417 Detected in Clinical and Environmental Isolates

Tamayo-Legorreta

Turrubiartes-Martínez

Garza–Ramos

et al. 2016

Microbial Drug Resistance

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We characterized an outbreak of imipenem-resistant Acinetobacter baumannii with clinical and environmental isolates from a tertiary care hospital in San Luis Potosi, Mexico. During a 4-month period, a total of 32 nonrepetitive imipenem-resistant clinical isolates of A. baumannii were collected. All isolates were susceptible to colistin and tigecycline and resistant to cefepime, ceftazidime, ceftriaxone, imipenem, and meropenem. Genotyping by pulsed-field gel electrophoresis showed a major clone (A). Multilocus sequence type (MLST) analysis was performed, revealing sequence type (ST) 417 (ST417) and 208 (ST208). The bla IMP-, bla VIM-, bla GIM-, bla SIM-, bla NDM-type , and bla OXA-type (bla OXA-23-like , bla OXA-24-like , bla OXA-51-like , and bla OXA-58-like ) genes were screened and showed that the bla OXA-51-like and bla OXA-24-like genes were present in all isolates. Sequencing and southern hybridization were performed, confirming the presence of the bla OXA-72 gene and its plasmid-borne nature. In addition, the bla OXA-72 -XerC/XerD-like association was identified. These findings indicate that a clonal spread of bla OXA-72 -producing A. baumannii ST417 had occurred throughout the hospital. The ST417 corresponded with a previous ST described in the United States.

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Extended −10 Promoter in IS Aba - 1 Upstream of bla _OXA-23 from Acinetobacter baumannii

Cited by 31 publications

References 12 publications

OXA β-Lactamases

OXA β-Lactamases

Multidrug-resistantPseudomonas aeruginosaandAcinetobacter baumannii: resistance mechanisms and implications for therapy

Outbreak Caused bybla_OXA-72-ProducingAcinetobacter baumanniiST417 Detected in Clinical and Environmental Isolates

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Extended −10 Promoter in IS Aba - 1 Upstream of bla OXA-23 from Acinetobacter baumannii

Cited by 31 publications

References 12 publications

OXA β-Lactamases

OXA β-Lactamases

Multidrug-resistantPseudomonas aeruginosaandAcinetobacter baumannii: resistance mechanisms and implications for therapy

Outbreak Caused byblaOXA-72-ProducingAcinetobacter baumanniiST417 Detected in Clinical and Environmental Isolates

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Extended −10 Promoter in IS Aba - 1 Upstream of bla _OXA-23 from Acinetobacter baumannii

Outbreak Caused bybla_OXA-72-ProducingAcinetobacter baumanniiST417 Detected in Clinical and Environmental Isolates