Genomic analysis of in vivo acquired resistance to colistin and rifampicin in Acinetobacter baumannii

With the dissemination of extremely drug resistant bacteria, colistin is now considered as the last-resort therapy for the treatment of infection caused by Gram-negative bacilli (including carbapenemase producers). Unfortunately, the increase use of colistin has resulted in the emergence of resistance as well. In A. baumannii, colistin resistance is mostly caused by the addition of phosphoethanolamine to the lipid A through the action of a phosphoethanolamine transferase chromosomally-encoded by the pmrC gene, which is regulated by the two-component system PmrA/PmrB. In A. baumannii clinical isolate the main resistance mechanism to colistin involves mutations in pmrA, pmrB or pmrC genes leading to the overexpression of pmrC. Although, rapid detection of resistance is one of the key issues to improve the treatment of infected patient, detection of colistin resistance in A. baumannii still relies on MIC determination through microdilution, which is time-consuming (16–24 h). Here, we evaluated the performance of a recently described MALDI-TOF-based assay, the MALDIxin test, which allows the rapid detection of colistin resistance-related modifications to lipid A (i.e phosphoethanolamine addition). This test accurately detected all colistin-resistant A. baumannii isolates in less than 15 minutes, directly on intact bacteria with a very limited sample preparation prior MALDI-TOF analysis.

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“… *Ab-R1 and Ab-S1 clinical isolates are isogenic 18 . **Ab-R8 (=AB CR17) and Ab-S7 (=AB CS01) are isogenic 19 .…”

Section: Resultsmentioning

confidence: 99%

Rapid detection of colistin resistance in Acinetobacter baumannii using MALDI-TOF-based lipidomics on intact bacteria

Dortet

Potron

Bonnin

et al. 2018

Sci Rep

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“…In MDR strains of P. aeruginosa, a series of plasmids (pS04 90, pBM41, p14057 A, and p14057 B) encoding carbapenemase resistance have been highlighted (Liu et al, 2018;Shi et al, 2018;van der Zee et al, 2018). Strains of A. baumannii show plasmid-encoded resistance to carbapenems (Cameranesi et al, 2018;Leungtongkam et al, 2018;Silva et al, 2018), aminoglycosides (armA) (Upadhyay et al, 2018), colistin (Jaidane et al, 2018), sulfonamides, or streptomycin (Hamidian et al, 2016). In addition, plasmids conferring resistance to various classes of antibiotics have been found in Staphylococcus spp.…”

Section: Plasmidsmentioning

confidence: 99%

“…In addition, plasmids conferring resistance to various classes of antibiotics have been found in Staphylococcus spp. (Mugnier et al, 2009;Ruiz-Martinez et al, 2011;Hamidian et al, 2016;Holmes et al, 2016;Liu et al, 2016Liu et al, , 2018Becker et al, 2018;Cameranesi et al, 2018;Fessler et al, 2018;Jaidane et al, 2018;Leungtongkam et al, 2018;Shi et al, 2018;Silva et al, 2018;Upadhyay et al, 2018;van der Zee et al, 2018). Resistance plasmids exhibit a high degree of plasticity, which is translated into an increased frequency of insertions, deletions, and changes in DNA (Kado, 2014).…”

Section: Plasmidsmentioning

confidence: 99%

Targeting Plasmids to Limit Acquisition and Transmission of Antimicrobial Resistance

et al. 2020

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Antimicrobial resistance (AMR) is a significant global threat to both public health and the environment. The emergence and expansion of AMR is sustained by the enormous diversity and mobility of antimicrobial resistance genes (ARGs). Different mechanisms of horizontal gene transfer (HGT), including conjugation, transduction, and transformation, have facilitated the accumulation and dissemination of ARGs in Gram-negative and Gram-positive bacteria. This has resulted in the development of multidrug resistance in some bacteria. The most clinically significant ARGs are usually located on different mobile genetic elements (MGEs) that can move intracellularly (between the bacterial chromosome and plasmids) or intercellularly (within the same species or between different species or genera). Resistance plasmids play a central role both in HGT and as support elements for other MGEs, in which ARGs are assembled by transposition and recombination mechanisms. Considering the crucial role of MGEs in the acquisition and transmission of ARGs, a potential strategy to control AMR is to eliminate MGEs. This review discusses current progress on the development of chemical and biological approaches for the elimination of ARG carriers.

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“…The impact of emergent resistance was evaluable in 28 cases; in 86% (24/28) emergent resistance was associated with persistent or recurrent infection [8,11,12,17,22,23,28,32,37,38,40,43,46] (Table 1), while in 14% (4/28) emergent resistance did not require any further treatment [13,19,27,43], possibly due to reduced virulence of the resistant strains [15,19,27].…”

Section: Does Emergent Resistance Explain Treatment Failure?mentioning

confidence: 99%

A Systematic Review of Implications, Mechanisms, and Stability of In Vivo Emergent Resistance to Colistin and Tigecycline in <em>Acinetobacter baumannii</em>

Karakonstantis

2020

Preprint

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The potential of A. baumannii for acquired resistance to last resort antibiotics (colistin and tigecycline) during treatment has important clinical implications, especially when dealing with patients failing to improve despite treatment with an active antimicrobial. However, the relevant literature remains scattered. Therefore, a systematic search was conducted in PubMed and Scopus. Several studies reported emergence of resistance to colistin or tigecycline during treatment, in most cases (86%) resulting in persistent or recurrent infections, especially in cases of emergent resistance without fitness cost. Lipopolysaccharide modification in the case of colistin and overexpression of efflux pumps in the case of tigecycline were the main mechanisms of resistance. Emergent colistin resistance is often associated with fitness cost resulting in re-emergence of the fitter and more virulent colistin susceptible strain after cessation of antibiotic pressure. Prospective studies are needed to determine the frequency of emergent resistance during treatment and its impact on patient outcomes.

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Genomic analysis of in vivo acquired resistance to colistin and rifampicin in Acinetobacter baumannii

Cited by 26 publications

References 16 publications

Rapid detection of colistin resistance in Acinetobacter baumannii using MALDI-TOF-based lipidomics on intact bacteria

Rapid detection of colistin resistance in Acinetobacter baumannii using MALDI-TOF-based lipidomics on intact bacteria

Targeting Plasmids to Limit Acquisition and Transmission of Antimicrobial Resistance

A Systematic Review of Implications, Mechanisms, and Stability of In Vivo Emergent Resistance to Colistin and Tigecycline in <em>Acinetobacter baumannii</em>

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