Comparative Genomics Reveals a Well-Conserved Intrinsic Resistome in the Emerging Multidrug-Resistant Pathogen Cupriavidus gilardii
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Univ Arizona, Sch Anim & Comparat Biomed SciIssue Date
2019-10-02
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AMER SOC MICROBIOLOGYCitation
Ruiz C, McCarley A, Espejo ML, Cooper KK, Harmon DE. 2019. Comparative genomics reveals a well-conserved intrinsic resistome in the emerging multidrug-resistant pathogen Cupriavidus gilardii. mSphere 4:e00631-19. https://doi.org/10.1128/mSphere.00631-19.Journal
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Copyright © 2019 Ruiz et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
The Gram-negative bacterium Cupriavidus gilardii is an emerging multidrug-resistant pathogen found in many environments. However, little is known about this species or its antibiotic resistance mechanisms. We used biochemical tests, antibiotic susceptibility experiments, and whole-genome sequencing to characterize an environmental C. gilardii isolate. Like clinical isolates, this isolate was resistant to meropenem, gentamicin, and other antibiotics. Resistance to these antibiotics appeared to be related to the large number of intrinsic antibiotic resistance genes found in this isolate. As determined by comparative genomics, this resistome was also well conserved in the only two other C. gilardii strains sequenced to date. The intrinsic resistome of C. gilardii did not include the colistin resistance gene mcr-5, which was in a transposon present only in one strain. The intrinsic resistome of C. gilardii was comprised of (i) many multidrug efflux pumps, such as a homolog of the Pseudomonas aeruginosa MexAB-OprM pump that may be involved in resistance to meropenem, other β-lactams, and aminoglycosides; (ii) a novel β-lactamase (OXA-837) that decreases susceptibility to ampicillin but not to other β-lactams tested; (iii) a new aminoglycoside 3-N-acetyltransferase [AAC(3)-IVb, AacC10] that decreases susceptibility to gentamicin and tobramycin; and (iv) a novel partially conserved aminoglycoside 3"-adenylyltransferase [ANT(3")-Ib, AadA32] that decreases susceptibility to spectinomycin and streptomycin. These findings provide the first mechanistic insight into the intrinsic resistance of C. gilardii to multiple antibiotics and its ability to become resistant to an increasing number of drugs during therapy.IMPORTANCECupriavidus gilardii is a bacterium that is gaining increasing attention both as an infectious agent and because of its potential use in the detoxification of toxic compounds and other biotechnological applications. In recent years, however, there has been an increasing number of reported infections, some of them fatal, caused by C. gilardii These infections are hard to treat because this bacterium is naturally resistant to many antibiotics, including last-resort antibiotics, such as carbapenems. Moreover, this bacterium often becomes resistant to additional antibiotics during therapy. However, little is known about C. gilardii and its antibiotic resistance mechanisms. The significance of our research is in providing, for the first time, whole-genome information about the natural antibiotic resistance genes found in this bacterium and their conservation among different C. gilardii strains. This information may provide new insights into the appropriate use of antibiotics in combating infections caused by this emerging pathogen.Note
Open access journalISSN
2379-5042PubMed ID
31578249Version
Final published versionSponsors
California State University, Northridge; National Institutes of Health BUILD PODER programUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [5RL5GM118975-03]; California State University CSUPERB New Investigator grantsae974a485f413a2113503eed53cd6c53
10.1128/mSphere.00631-19
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Except where otherwise noted, this item's license is described as Copyright © 2019 Ruiz et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.
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