Table 2.

Intrinsic drug resistance mechanisms in Mycobacterium avium and Mycobacterium abscessus^a

Agent	Target	M. avium (genes involved)	M. abscessus (genes involved)	Refs
Isoniazid	InhA	Presumably efflux pumps	Presumably efflux pumps	[73]
Rifampicin	RNA polymerase	NAb	Inactivation of drug (arrMab)	[188]
Ethambutol	Arabinosyl transferase	NAb	Polymorphisms in target gene embB	[79]
Pyrazinami de	PanD	Presumably due to active efflux of POAc	Presumably owing to active efflux of POAc	[189,190]
Aminoglyc osides	16S rRNA	NAb	Inactivation of drug [aac(2′), eis2 – whiB7]	[82,84,191]
Fluoroquin olones	DNA gyrase	Polymorphisms in target gene gyrA	Polymorphisms in target gene gyrA	[192]
β-lactams	Penicillin-binding protein	β-lactamase with mild activity Other unknown reasons	Inactivation of drug (blaMab)	[81]
Thiacetazo ne	FAS-II dehydratased	The target is not essential: redundant dehydratase present	The target is not essential: redundant dehydratase present	[193]
BTZ043	DprE1	Polymorphisms in target gene dprE1	Polymorphisms in target gene dprE1	[194,195]
BRD4592	Tryptophan synthase	NAb	Polymorphisms in target gene trpA	[196]
Macrolides	23S rRNA	Efflux pumps (MAV_1695, MAV_1406)	Modification of drug target [erm(41) – whiB7]	[78,80,84,191]

^aCell envelope, porins and efflux pumps are likely to be involved in intrinsic drug resistance to many antimicrobials and are thus not specified in the table unless roles have been experimentally proven or suggested.

^bNA: not applicable, the drug is active.

^cPOA: pyrazinoic acid, bioactive metabolite of pyrazinamide.

^dFAS-II: type II fatty acid synthase.