Evading host defences: Genome sequence analysis of the environmental Acinetobacter baumannii NCIMB8209 strain indicates extensive insertion sequence-mediated genome remodelling with loss of exposed cell structures and defensive mechanisms

VIALE AM; SERAVALLE JL; DÍAZ MILOSLAVICH JI; REPIZO GD; ESPARIZ M.; SHUMAN HA

Frankfurt

Simposio; Acinetobacter 2019; 2019

Acinetobacter baumannii currently represents an important opportunistic pathogen of obscure reservoirsoutside the clinical setting. Here we traced the origins of the collection strain Acinetobacter sp.NCIMB8209 to an isolate first reported in 1944 in the U.S.A. NCIMB8209 was isolated from the enrichedmicrobiota responsible for the aerobic decomposition of guayule, a resinous desert shrub. Whole-genomesequencing analysis indicated the presence of a 3.9 Mb chromosome and a plasmid of 134 kb.Phylogenetic analysis based on core genes and a chromosomal bla OXA-51 -type gene confirmedNCIMB8209 affiliation to A. baumannii. The NCIMB8209 chromosome contains 7 genomic islands (GI)and 5 regions encompassing phage-related genes. Remarkably, 93 insertion sequences (IS) were foundin its genome, 15 of them correspond to novel mobile elements. No antimicrobial resistance islands wereidentified, agreeing with a general antimicrobial susceptibility phenotype including to folate synthesisinhibitors. In contrast to its companion, the environmental strain NCIMB8208/DSM30011 [1], NCIMB8209displayed low virulence in both the Galleria mellonella and Caenorhabditis elegans infection models.Moreover, this strain lacks GIs providing defences against biological aggressors such as Type 6 secretionsystems and corresponding toxin genes. NCIMB8209 harbours many genes linked to persistence andvirulence in pathogenic A. baumannii strains, but many of them encoding external structures areinterrupted by IS. Searching for catabolic genes and metabolic assays revealed several clusters involvedin the degradation of plant defence substances, pointing to alternative environmental niche(s) for thisspecies. These results suggest that the disruption in NCIMB8209 of exposed structures likely recognizedby host defences most probably resulted from the adaptation of this particular A. baumannii strain to aspecific environmental niche. Moreover, they also indicated that the reported genetic plasticity of A.baumannii represents an intrinsic characteristic of this species, having evolved prior to its adaptation tothe clinical environment.