text: Tolerance to 5% NaCl in Löwenstein-Jensen medium, tolerance to 0.2% picrate in Sauton agar, and non-use of citrate as a sole carbon source are characteristics that distinguish M. abscessus from M. chelonae. M. abscessus and M. chelonae sequevar I share an identical sequence in the 54-510 region of 16S rRNA, though both species can be differentiated by their hsp65, ITS or rpoB gene sequences.
  Genetics
  A draft genome sequence of M. abscessus subsp. bolletii BDT was completed in 2012. Since then, a large number of strains from this subspecies have had their genomes sequenced, leading to a clarification of subspecies boundaries. In 1992, M. abscessus was first recognised as a distinct species. In 2006, this group was separated into three subspecies: M. a. abscessus, M. a. bolletii, and M. a. massiliense. In 2011, the latter two were briefly merged into a single subspecies, but were subsequently separated again following greater availability of genome sequence data, which showed the three subspecies formed genetically distinct groups. It has been proposed that M. bolletii and M. massiliense be reinstated as unique species.
  These distinct groups also correspond to important biological differences. Clinically important differences include differing susceptibilities to antibiotics. M. a. abscessus and M. a. bolletii carry a common antibiotic resistance gene, which confers resistance to macrolide antibiotics, while M. a. massiliense is thought to carry a nonfunctional copy, so is more susceptible to antibiotics and more easily treated.
  Pathogenesis
  M. abscessus can cause lung disease, skin infections, central nervous system infections, bacteremia, eye infections, and other, less common diseases.