Comparative genomics of environmental and clinical Stenotrophomonas maltophilia strains with different antibiotic resistance profiles.

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Comparative genomics of environmental and clinical Stenotrophomonas maltophilia strains with different antibiotic resistance profiles.

Genome Biol Evol. 2015 Aug 14;

Authors: Youenou B, Favre-Bonté S, Bodilis J, Brothier E, Dubost A, Muller D, Nazaret S

Abstract
Stenotrophomonas maltophilia, a ubiquitous Gram negative γ-proteobacterium, has emerged as an important opportunistic pathogen responsible for nosocomial infections. A major characteristic of clinical isolates is their high intrinsic or acquired antibiotic resistance level. The aim of this study was to decipher the genetic determinism of antibiotic resistance among strains from different origins (i.e. natural environment and clinical origin) showing various antibiotic resistance profiles. To this purpose we selected 3 strains isolated from soil collected in France or Burkina Faso that showed contrasting antibiotic resistance profiles. After whole genome sequencing, the phylogenetic relationships of these 3 strains and 11 strains with available genome sequences were determined. Results showed that a strain's phylogeny did not match their origin or antibiotic resistance profiles. Numerous antibiotic resistance coding genes and efflux pump operons were revealed by the genome analysis, with 57% of the identified genes not previously described. No major variation in the antibiotic resistance gene content was observed between strains irrespective of their origin and antibiotic resistance profiles. Although environmental strains generally carry as many MDR efflux pumps as clinical strains, the absence of RND pumps (i.e. SmeABC) previously described to be specific to S. maltophilia was revealed in two environmental strains (BurA1 and PierC1). Furthermore the genome analysis of the environmental MDR strain BurA1 showed the absence of SmeABC but the presence of another putative MDR RND efflux pump, named EbyCAB on a genomic island probably acquired via horizontal gene transfer.

PMID: 26276674 [PubMed - as supplied by publisher]