The contribution of Acinetobacter baumannii A424 resistance island TnAbaR23 on fitness and virulence associated phenotypes

• Main Author: Sapkota, Nutan Prasai
• Other Authors: Rajakumar, Kumar
• Published: University of Leicester 2016
• Subjects: 616.9
• Online Access: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.682415

The Acinetobacter baumannii specific resistance islands called AbaR islands are foreign acquired resistance islands and are widely represented in the genome of multi-drug resistance [MDR] A. baumannii strains. The resistance genes and determinants within AbaR are found to contribute minimally towards the overall MDR phenotype of the host. Therefore, the maintenance of AbaR islands purely for the enhancement and development of antimicrobial resistance phenotype appears to be an inadequate explanation. This study investigates the contribution of AbaR island called TnAbaR23, in a MDR A. baumannii strain A424, towards the resistance and virulence phenotypes of the host. The TnAbaR23 deleted mutants were created by allelic exchange and the fitness and virulence of mutants was compared with their parent in a head-to-head competition assay and Galleria mellonella killing assay. During this study, spontaneous deletion of internal region of TnAbaR23 was observed in wild type A424 sub-population. In this study, the role of transposase gene tnpA in the spontaneous deletion within TnAbaR23 was also investigated. The spontaneous mutants of A424 were isolated and analysed for their antimicrobial resistance, fitness and virulence phenotypes. Although complete or partial deletion of TnAbaR23 had no effect on the growth of bacteria, the wild type appeared less fit in a head-to-head growth competition with TnAbaR23 deleted and spontaneous mutants. Except from the anticipated antibiotic susceptibility upon the deletion of TnAbaR23, the overall resistance phenotype in mutants remained unchanged. Intriguingly, the TnAbaR23 deleted and spontaneous mutants exhibited reduced virulence compared to their parent in a G. mellonella killing assay. Despite the associated cost, the maintenance of TnAbaR23 appears to be vital to exhibit enhanced virulence or pathogenesis in A. baumannii strain A424. It is therefore possible that A. baumannii AbaR islands positively contribute towards the development of traits that are vital for the survival of these bacteria.