LAUSR

Mycobacterium abscessus is the second most common nontuberculous mycobacterial lung disease pathogen and comprises three subspecies, abscessus, massiliense and bolletii. Subspecies identification is critical for disease management as subspecies abscessus and bolletii have an inducible macrolide resistance gene (erm(41)) that results in clinical macrolide resistance. In contrast subspecies massiliense does not have an active erm(41) gene and is therefore susceptible in vitro and clinically to macrolide-containing regimens. M. abscessus is also vulnerable to acquired mutational macrolide resistance. Macrolide resistance has such a profoundly negative impact on M. abscessus treatment response that preserving macrolide susceptibility with adequate companion drugs for macrolides is among the highest treatment priorities. After macrolides, amikacin is regarded as the next most important drug for M. abscessus treatment, although data validating that assertion are lacking. The considerations for preventing acquired macrolide resistance also apply to amikacin. Recent guidelines suggest treatment should be guided by in vitro susceptibilities but aside from macrolide and amikacin, no other antibiotics have a validated minimum inhibitory concentration for M. abscessus. Currently, phase therapy (intensive and continuation) is recommended for M. abscessus. This approach is successful with macrolide susceptible M. abscessus but not with macrolide resistant M. abscessus where even more aggressive therapy is not predictably successful. Newer drugs have become available with encouraging in vitro activity against M. abscessus, but in vivo validation of their superiority to current agents is not yet available. In the absence of unequivocally effective regimens, we offer suggestions for managing this treatment refractory organism.