We assessed for mutations in the inhA regulatory region of all the 44 INHR M. tuberculosis strains and found a substitution at position 15 upstream of the start codon in 13 (28.9%) isolates. The frequency of the occurrence of specific INH-resistance conferring mutations varied between geographical regions in the world [26]. A study in Equatorial Guinea reported the absence of mutation in the katG gene of M. tuberculosis

selleck inhibitor INH -resistant isolates [44]. The unique katG mutation observed in this study was the substitution of Serine to Threonine at codon 315. High proportion of Ser315katG mutations has been reported in Russia (76.9%) [26], in Morocco (68.6%) [45], in isolates of the LAM family in Cameroon [30] and also in Korea (49.1%) [46]. In INHR strains, neither insertions nor complete deletions of katG were found, which is evidence of the rare occurrence of these mutations in clinical isolates, although they were reported previously by other PF-4708671 chemical structure authors [47, 48]. Fourteen (31.8%) INHR isolates did not show mutations at the four loci analyzed. This discrepancy between the phenotypic results and the genotypic drug resistance tests could be attributed to the presence of other mutations located either outside the selected target region or the selected genes. Several others studies have reported that mutations in inhA or its promoter region are usually associated with low-level resistance of INH. Moreover,

INH-resistant isolates with inhA selleck mutations can have additional mutations in katG, conferring higher levels of INH-resistance [11]. All mutations found in fabG1-inhA promoter region were not associated with phenotypic resistance. The substitution of G to C at position -47 first described by Homolka and al. [21] in an INH-resistant strain has been found in both susceptible (24/44; 54.5%) and resistant isolates

(5/44; 11.4%). Thus, this mutation seems to not correlate with INH-resistance. The mutation -102 C → T not yet described is also not relevant to INH-resistance since it was found only in susceptible isolates. The analysis of SM-resistance mechanism revealed that none of the SM-resistant strains carried a mutation in the rrs gene although those mutations have been described as main resistance mechanism that confer high level SM -resistance [12]. Clinical isolates showing no mutations in rpsL or rrs gene have been reported in the literature [49]. A previous investigation from Cameroon encountered rpsL or rrs mutations in SM-resistant isolates from the Central Region of Cameroon [50]. In contrast in the current investigation only rpsL mutations were associated with SM-resistance. This indicates that Selleck MCC-950 further studies are necessary to delineate the molecular markers for SM-resistance. Mutations in the rpsL locus have been hypothesized to be an alternative mechanism of SM-resistance like mutations in the gidB[51] or efflux pumps [13]. Overall, we detected gidB mutations in 18.