Two carbapenem-resistant ST1:ST231:KL1:OCL1 Acinetobacter baumannii strains recovered in Tehran, Iran, carry AbaR31 in the chromosome and AbaR4 and Tn aphA6 in a RepAci6 plasmid

Masoumeh Douraghi; Parisa Aris; Joyce To; Garry S A Myers; Mohammad Hamidian

doi:10.1093/jacamr/dlab112

Two carbapenem-resistant ST1:ST231:KL1:OCL1 Acinetobacter baumannii strains recovered in Tehran, Iran, carry AbaR31 in the chromosome and AbaR4 and Tn aphA6 in a RepAci6 plasmid

JAC Antimicrob Resist. 2021 Aug 7;3(3):dlab112. doi: 10.1093/jacamr/dlab112. eCollection 2021 Sep.

Authors

Masoumeh Douraghi¹, Parisa Aris¹, Joyce To², Garry S A Myers², Mohammad Hamidian²

Affiliations

¹ Division of Microbiology, Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
² The iThree institute, University of Technology Sydney, Ultimo, NSW, Australia.

Abstract

Objectives: To analyse the context of genes conferring antibiotic resistance in two carbapenem-resistant Acinetobacter baumannii isolates recovered in Tehran, Iran.

Methods: The antibiotic resistance phenotype for 28 antibiotics was determined using disc diffusion. The whole genome sequences of ABH008 and ABS200 were determined using the Illumina HiSeq X Ten platform. Resistance genes were identified using ResFinder and multilocus sequence types were determined using the Oxford and Institut Pasteur schemes.

Results: Isolates ABH008 and ABS200, recovered in 2012 and 2013, respectively, in two different Tehran hospitals, belong to the common global clone 1 lineage, ST1_IP and ST231_OX. They are resistant to sulfamethoxazole, tetracycline, gentamicin, amikacin, third-generation cephalosporins and carbapenems. Despite being isolated in different hospitals, phylogenetic analysis indicated they are closely related. Consistent with this, both isolates carry catA1, sul1, aacC1 and aadA1 in a novel variant of the AbaR3-type resistance island, named AbaR31. Both isolates are resistant to amikacin and carbapenems owing to aphA6 and oxa23, respectively. The oxa23 gene is located in the AbaR4 resistance island, and aphA6 in TnaphA6, and both mobile elements are in an ∼90 kbp plasmid encoding the putative RepAci6 replication initiation protein. Resistance to third-generation cephalosporins is due to the acquisition by homologous recombination of a 5 kb DNA segment that contains ISAba1-ampC from a ST623 strain.

Conclusions: The resistance gene complements of ABH008 and ABS200 were found in AbaR31 and a plasmid that encodes RepAci6. The close genetic relationship of ABH008 and ABS200, despite each being recovered from different hospitals, indicates transmission between the two hospitals.