Table 2.

Phenotypic and Genotypic Antibiotic Susceptibility Profiles of Newly Isolated Strains

			Genotypic Resistance mutations
Name	Previously treated	Phenotypic resistance	rpoB	katG	PinhA	pncA	Other
NRC1	No	Susceptible	wt	wt	wt	wt
NRC2	No	Isoniazid (Low), streptomycin	wt	wt	c−15t	wt	gyrA/gyrB: wt
NRC3	Yes	Streptomycin	wt	wt	wt	wt	gyrA/gyrB: wt
NRC4	No	Susceptible	wt	wt	wt	wt
NRC5	No	Susceptible	wt	wt	wt	wt
NRC6	Unknown	Isoniazid (High), rifampicin, ethionamide, streptomycin, para-aminosalicylic acid	S450(531)L	S315T	wt	wt	ethA G124D ethR: wt gyrA/gyrB: wt rrs1400*: wt embB M306: wt
NRC7	No	Isoniazid (High), rifampicin, pyrazinamide, ethambutol, ethionamide, streptomycin, kanamycin, para-aminosalicylic acid	S450(531)L	S315T	wt	S104R	embB M306I ethA: G124D ethR: wt gyrA/gyrB: wt rrs1400*: wt

Genotypic antibiotic susceptibility was tested for first-line drugs isoniazid (katG, PinhA, promoter of inhA), rifampicin (rpoB), pyrazinamide (pncA) (Barrera et al. 2008; WHO 2014), by different PCRs and Sanger-sequencing as described previously (Brossier et al. 2017). When an isolate was resistant to any of these antituberculosis drugs, second-line drugs ethionamide (ethA, ethR); aminoglycosides (*, rrs region 1400, eis promoter), fluoroquinolones (gyrA/gyrB) and para-aminosalicylic acid were tested. Genotypic susceptibility is indicated as “wt” (wild-type), or the resulting amino acid (upper case), or base (lower case) changes. First letter depicts amino acid in reference sequence; second letter depicts detected amino acid/base; rpoB positions between brackets represent positions in older nomenclature system; Position is depicted as number in subscript. N.P., not performed.