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Article

Colistin Resistance Onset Strategies and Genomic Mosaicism in Clinical Acinetobacter baumannii Lineages

1
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123 Catania, Italy
2
Department of Translational Research and New Technology in Medicine and Surgery, Azienda Ospedaliero-Universitaria Pisana, University of Pisa, 56126 Pisa, Italy
3
Bacteriology Unit of Azienda Ospedaliero-Universitaria Pisana, 56126 Pisa, Italy
*
Author to whom correspondence should be addressed.
Pathogens 2021, 10(11), 1516; https://doi.org/10.3390/pathogens10111516
Submission received: 20 October 2021 / Revised: 17 November 2021 / Accepted: 18 November 2021 / Published: 20 November 2021
(This article belongs to the Special Issue Current Status of Acinetobacter Infections)

Abstract

The treatment of multidrug-resistant Gram-negative infections is based on colistin. As result, COL-resistance (COL-R) can develop and spread. In Acinetobacter baumannii, a crucial step is to understand COL-R onset and stability, still far to be elucidated. COL-R phenotypic stability, onset modalities, and phylogenomics were investigated in a clinical A. baumannii sample showing a COL resistant (COLR) phenotype at first isolation. COL-R was confirmed by Minimum-Inhibitory-Concentrations as well as investigated by Resistance-Induction assays and Population-Analysis-Profiles (PAPs) to determine: (i) stability; (ii) inducibility; (iii) heteroresistance. Genomics was performed by Mi-Seq Whole-Genome-Sequencing, Phylogenesis, and Genomic Epidemiology by bioinformatics. COLRA. baumannii were subdivided as follows: (i) 3 A. baumannii with stable and high COL MICs defining the “homogeneous-resistant” onset phenotype; (ii) 6 A. baumannii with variable and lower COL MICs displaying a “COL-inducible” onset phenotype responsible for adaptive-resistance or a “subpopulation” onset phenotype responsible for COL-heteroresistance. COL-R stability and onset strategies were not uniquely linked to the amount of LPS and cell envelope charge. Phylogenomics categorized 3 lineages clustering stable and/or unstable COL-R phenotypes with increasing genomic complexity. Likewise, different nsSNP profiling in genes already associated with COL-R marked the stable and/or unstable COL-R phenotypes. Our investigation finds out that A. baumannii can range through unstable or stable COLR phenotypes emerging via different “onset strategies” within phylogenetic lineages displaying increasing genomic mosaicism.
Keywords: A. baumannii; colistin resistance stability; genomic mosaicism; phylogenetic lineages A. baumannii; colistin resistance stability; genomic mosaicism; phylogenetic lineages

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MDPI and ACS Style

Cafiso, V.; Stracquadanio, S.; Dovere, V.; Lo Verde, F.; Zega, A.; Pigola, G.; Barnini, S.; Ghelardi, E.; Stefani, S. Colistin Resistance Onset Strategies and Genomic Mosaicism in Clinical Acinetobacter baumannii Lineages. Pathogens 2021, 10, 1516. https://doi.org/10.3390/pathogens10111516

AMA Style

Cafiso V, Stracquadanio S, Dovere V, Lo Verde F, Zega A, Pigola G, Barnini S, Ghelardi E, Stefani S. Colistin Resistance Onset Strategies and Genomic Mosaicism in Clinical Acinetobacter baumannii Lineages. Pathogens. 2021; 10(11):1516. https://doi.org/10.3390/pathogens10111516

Chicago/Turabian Style

Cafiso, Viviana, Stefano Stracquadanio, Veronica Dovere, Flavia Lo Verde, Alessandra Zega, Giuseppe Pigola, Simona Barnini, Emilia Ghelardi, and Stefania Stefani. 2021. "Colistin Resistance Onset Strategies and Genomic Mosaicism in Clinical Acinetobacter baumannii Lineages" Pathogens 10, no. 11: 1516. https://doi.org/10.3390/pathogens10111516

APA Style

Cafiso, V., Stracquadanio, S., Dovere, V., Lo Verde, F., Zega, A., Pigola, G., Barnini, S., Ghelardi, E., & Stefani, S. (2021). Colistin Resistance Onset Strategies and Genomic Mosaicism in Clinical Acinetobacter baumannii Lineages. Pathogens, 10(11), 1516. https://doi.org/10.3390/pathogens10111516

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