The absence of the Type VI Secretion System in the successful lineage of Acinetobacter baumannii ST19

Abstract

Acinetobacter baumannii is an opportunistic pathogen, often multi- to pandrug-resistant, including to last-resort antibiotics such as carbapenems. A. baumannii can acquire DNA through multiple mechanisms including natural competence and conjugation. An active Type VI Secretion System (T6SS), which kills nonkin bacteria and challenges and inhibits the conjugation. The acquisition of resistance genes has helped the spread of resistant clones of A. baumannii, such as those of Sequence Types (STPas), ST1, ST2, ST10, ST15, ST25, ST79 and ST85. While ST1 and ST2 were thoroughly studied, there are new emerging clones whose genetic background facilitating the rise is still unknown or poorly understood. The emergence of Acinetobacter baumannii ST19 first peaked in 2003, coinciding with the Iraq conflict and increased detection among U.S. military personnel. Its prevalence later surged in Georgia and Ukraine, around the onset of the conflict in Ukraine in 2022, associating it with regions affected by military activity. In this study, we have sequenced whole-genome three isolates of A. baumannii ST19 and compared them with further 156 A. baumannii ST19 genomes were obtained from public repositories. In total, 157/159 genomes revealed loss of T6SS locus, which was replaced in 56/157 genomes (35,7%) by {Delta}Tn9 carrying chloramphenicol and {Delta}Tn10 carrying tetracycline resistance genes, and formaldehyde and chlorite resistance genes. Surprisingly, the antibiotic resistance-encoding transposons likely originated from Enterobacteriaceae plasmids. The loss of a functional T6SS in A. baumannii ST19 may potentially facilitate horizontal gene transfer and promoting a cooperative or less competitive lifestyle providing a selective advantage at the population level.