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Review
. 2019 Oct;5(10):e000306.
doi: 10.1099/mgen.0.000306.

Emergence, molecular mechanisms and global spread of carbapenem-resistant Acinetobacter baumannii

Mohammad Hamidian  1 , Steven J Nigro  2
Affiliations
Review

Emergence, molecular mechanisms and global spread of carbapenem-resistant Acinetobacter baumannii

Mohammad Hamidian et al. Microb Genom. 2019 Oct.

Abstract

Acinetobacter baumannii is a nosocomial pathogen that has emerged as a global threat because of high levels of resistance to many antibiotics, particularly those considered to be last-resort antibiotics, such as carbapenems. Although alterations in the efflux pump and outer membrane proteins can cause carbapenem resistance, the main mechanism is the acquisition of carbapenem-hydrolyzing oxacillinase-encoding genes. Of these, oxa23 is by far the most widespread in most countries, while oxa24 and oxa58 appear to be dominant in specific regions. Historically, much of the global spread of carbapenem resistance has been due to the dissemination of two major clones, known as global clones 1 and 2, although new lineages are now common in some parts of the world. The analysis of all publicly available genome sequences performed here indicates that ST2, ST1, ST79 and ST25 account for over 71 % of all genomes sequenced to date, with ST2 by far the most dominant type and oxa23 the most widespread carbapenem resistance determinant globally, regardless of clonal type. Whilst this highlights the global spread of ST1 and ST2, and the dominance of oxa23 in both clones, it could also be a result of preferential selection of carbapenem-resistant strains, which mainly belong to the two major clones. Furthermore, ~70 % of the sequenced strains have been isolated from five countries, namely the USA, PR China, Australia, Thailand and Pakistan, with only a limited number from other countries. These genomes are a vital resource, but it is currently difficult to draw an accurate global picture of this important superbug, highlighting the need for more comprehensive genome sequence data and genomic analysis.

Keywords: AbaR4 and plasmid; Acinetobacter baumannii; GC1; GC2; Tn2006; Tn2008; Tn2009; carbapenem resistance; global clones; oxa23; oxa235; oxa24; oxa58.

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Conflict of interest statement

The authors declare that there are no conflicts of interest.

Figures

Fig. 1.
Fig. 1.
Distribution of carbapenem resistance genes and trend of A. baumannii genomes released. (a) Distribution of carbapenem resistance genes in the 15 most prevalent sequence types (STs; according to the Institut Pasteur MLST scheme). Numbers coloured turquoise indicate carbapenem resistance genes and black numbers show STs. SLV1 and SLV2 indicate single-locus variants of ST1 and ST2, respectively. All STs are based on the Institut Pasteur MLST scheme. (b) Geographical distribution of CRGs in A. baumannii genomes publicly available in the GenBank non-redundant and WGS databases (only countries with ≥1 CRG-containing genome are shown). Countries are shown on the y-axis and the numbers on x-axis indicate the number of CRGs. (c) Acinetobacter genomes released between 2008 and early April 2019. Black indicates total genome releases, red shows genomes with a carbapenem resistance gene and dark purple indicates genomes carrying the oxa23 gene. These figures were drawn using the ggplot2 package in R v3.5.2.
Fig. 2.
Fig. 2.
Geographical distribution of A. baumannii genomes released. Countries are colour coded according to the number of genomes available as of April 2019. Countries with no genome available are coloured grey. Pie charts indicate the distribution of STs in each country. Sequence types (STs) were determined according to the Institut Pasteur MLST scheme.
Fig. 3.
Fig. 3.
Structure of transposons carrying the oxa23 gene. (a) Genes and open reading frames are shown using arrows. Filled boxes are insertion sequences (ISs) with ISAba1 coloured green, ISAba33 coloured dark orange and ISAba2 coloured dark purple. Arrows inside the boxes indicate the direction of transposition gene expression. The oxa23 gene is shown in dark blue and open reading frames encoding hypothetical proteins are shown in white. (b) Vertical bars marked as IR indicate inverted repeats of AbaR4. (c) DRs indicates direct repeats. Arrows located in the central segments of Tn2006, Tn2008 and Tn6549, coloured grey, yellow and pink, respectively, indicate open reading frames that encode unrelated hypothetical proteins.
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