Genome Of Multidrug Resistant Acinetobacter Baumannii And"Resistance Island"

Acinetobacter baumannii is an important opportunistic pathogen that has caused global outbreaks of nosocomial infection. The multidrug-resistant (MDR) A. baumannii strain MDR-ZJ06, belonging to European clone II, was widely spread in China. In this study, we complete the whole-genome sequence of this clinical important strain by high-throughput sequencing. The strain MDR-ZJ06 genome and plasmid sizes are approximately 4 million and 20,000 bp, and were predicted to encode 3,887 and 25 proteins, respectively. A 38.6-kb AbaR-type genomic resistance island (AbaR22) was identified in MDR-ZJ06. AbaR22 has a structure similar to those of the resistance islands found in A. baumannii strains AYE and AB0057, but it contained only a few antibiotic resistance genes. The region of resistant gene accumulation as previously described was not found in AbaR22. In the chromosome of the strain MDR-ZJ06, we identified the gene blaoxA-23 in a composite transposon (Tn2009). Tn2009 shared the backbone with other A. baumannii transponsons that harbor blaoxA-23, but it was bracketed by two ISAbal elements which were transcribed in the same orientation. MDR-ZJ06 also expressed the armA gene on its plasmid pZJ06, and this gene has the same genetic environment as the armA gene of the Enterobacteriaceae. These results suggest variability of resistance acquisition even in closely related A. baumannii strains.Through genomic comparison of 9 complete genome we identified a novel genomic island in A. baumannii, which we designated AbaGI. The GC content of the AbaGI region showed breaking points with adjacent regions, and meanwhile, a tRNA-Val gene is located at one end of this region, both of which are typical characteristics of a foreign genomic island. We tested AbaGI distribution in 39 clinical isolates. The antimicrobial-resistant profiles of these isolates were also measured. As a result, we found that AbaGI is preferentially located in strains that are resistant toβ-lactams, aminoglycesides and fluoroquinolones, suggesting this island may contribute to the resistance to these antibiotics. But the expression of these genes clone from AbaGI was failed. In future, the further study will be done to elucidate the AbaGI resistance mechanism.