OBJECTIVES: To reconstruct the evolutionary history of the clinical 
Acinetobacter baumannii XH1056, which lacks the Oxford scheme allele gdhB.
METHODS: Susceptibility testing was performed using broth microdilution and agar 
dilution. The whole-genome sequence of XH1056 was determined using the Illumina 
and Oxford Nanopore platforms. MLST was performed using the Pasteur scheme and 
the Oxford scheme. Antibiotic resistance genes were identified using ABRicate.
RESULTS: XH1056 was resistant to all antibiotics tested, apart from colistin, 
tigecycline and eravacycline. MLST using the Pasteur scheme assigned XH1056 to 
ST256. However, XH1056 could not be typed with the Oxford MLST scheme as gdhB is 
not present. Comparative analyses revealed that XH1056 contains a 52 933 bp 
region acquired from a global clone 2 (GC2) isolate, but is otherwise closely 
related to the ST23 A. baumannii XH858. The acquired region in XH1056 also 
contains a 34 932 bp resistance island that resembles AbGRI3 and contains the 
armA, msrE-mphE, sul1, blaPER-1, aadA1, cmlA1, aadA2, blaCARB-2 and ere(B) 
resistance genes. Comparison of the XH1056 chromosome to that of GC2 isolate 
XH859 revealed that the island in XH1056 is in the same chromosomal region as 
that in XH859. As this island is not in the standard AbGRI3 position, it was 
named AbGRI5.
CONCLUSIONS: XH1056 is a hybrid isolate generated by the acquisition of a 
chromosomal segment from a GC2 isolate that contains a resistance island in a 
new location-AbGRI5. As well as generating ST256, it appears likely that a 
single recombination event is also responsible for the acquisition of AbGRI5 and 
its associated antibiotic resistance genes.