# Evolution of an extensively antibiotic resistant sublineage of lineage 1 of GC1 Acinetobacter baumannii

## TL;DR

This study traces the evolution of an antibiotic-resistant sublineage of Acinetobacter baumannii, showing how it gained resistance through genetic changes and spread globally.

## Contribution

The paper identifies specific genetic events, such as capsule locus switching and integrative element acquisition, that drove the evolution of antibiotic resistance in this bacterial sublineage.

## Key findings

- The MRSN56 sublineage evolved through insertions of resistance genes at specific chromosomal positions.
- The KL17 capsule type replaced KL1 and was associated with the acquisition of Aci-IE1 carrying blaNDM.
- Some KL17 isolates acquired additional resistance genes like blaPER, reducing susceptibility to newer antibiotics.

## Abstract

The multiply antibiotic-resistant lineage 1 of Acinetobacter baumannii global clone 1 (GC1) emerged in the 1970s, and subsequently more extensively resistant sublineages have emerged. Here, we examined the evolution of the extensively resistant MRSN56 sublineage and showed it is characterised by insertions carrying resistance genes at specific chromosomal positions. An evolved form of the sublineage carries KL17 replacing KL1 at the capsule locus and includes an additional integrative element Aci-IE1 carrying further resistance genes including blaNDM. Further members of the modified sublineage (isolated 2014–2021) identified among publicly available genomes were from several countries and appear to have replaced the original form (2007–2010). Some KL17 type isolates had acquired even more resistance genes including blaPER. The blaNDM and blaPER genes contribute to reduced susceptibility to cefiderocol and/or sulbactam/durlobactam. The phylogeny indicated that separation of the sublineage into KL1 and KL17 groups coincided with the KL switch and Aci-IE1 was acquired later.