Mulualem Tadesse1, Dossegnaw Aragaw2, Belayneh Dimah3, Feyisa Efa3, Kedir Abdella2, Wakjira Kebede4, Ketema Abdissa4, Gemeda Abebe2. 1. Mycobacteriology Research Center, Institute of Biotechnology Research, Jimma University, Jimma, Ethiopia; Department of Medical Laboratory Sciences and Pathology, Jimma University, Jimma, Ethiopia. Electronic address: mulualemt.tadesse@gmail.com. 2. Mycobacteriology Research Center, Institute of Biotechnology Research, Jimma University, Jimma, Ethiopia; Department of Medical Laboratory Sciences and Pathology, Jimma University, Jimma, Ethiopia. 3. Jimma University Specialized Hospital, Jimma University, Jimma, Ethiopia. 4. Department of Medical Laboratory Sciences and Pathology, Jimma University, Jimma, Ethiopia.
Abstract
OBJECTIVE/ BACKGROUND: The nature and frequency of mutations in rifampicin (RIF) and isoniazid (INH) resistant Mycobacterium tuberculosis isolates vary considerably according to geographic locations. However, information regarding specific mutational patterns in Ethiopia remains limited. METHODS: A cross-sectional prospective study was carried out among confirmed pulmonary tuberculosis cases in Southwest Ethiopia. Mutations associated with RIF and INH resistances were studied using GenoType MTBDRplus line probe assay in 112 M. tuberculosis isolates. Culture (MGIT960) and identification tests were performed at the Mycobacteriology Research Center of Jimma University, Jimma, Ethiopia. RESULTS: Mutations conferring resistance to INH, RIF, and multidrug resistance were detected in 36.6% (41/112), 30.4% (34/112), and 27.7% (31/112) of M. tuberculosis isolates respectively. Among 34 RIF-resistant isolates, 82.4% (28/34) had rpoB gene mutations at S531L, 2.9% (1/34) at H526D, and 14.7% (5/34) had mutations only at wild type probes. Of 41 INH-resistant strains, 87.8% (36/41) had mutations in the katG gene at Ser315Thr1 and 9.8% (4/41) had mutations in the inhA gene at C15T. Mutations in inhA promoter region were strongly associated with INH monoresistance. CONCLUSION: A high rate of drug resistance was commonly observed among failure cases. The most frequent gene mutations associated with the resistance to INH and RIF were observed in the codon 315 of the katG gene and codon 531 of the rpoB gene, respectively. Further studies on mutations in different geographic regions using DNA sequencing techniques are warranted to improve the kit by including more specific mutation probes in the kit.
OBJECTIVE/ BACKGROUND: The nature and frequency of mutations in rifampicin (RIF) and isoniazid (INH) resistant Mycobacterium tuberculosis isolates vary considerably according to geographic locations. However, information regarding specific mutational patterns in Ethiopia remains limited. METHODS: A cross-sectional prospective study was carried out among confirmed pulmonary tuberculosis cases in Southwest Ethiopia. Mutations associated with RIF and INH resistances were studied using GenoType MTBDRplus line probe assay in 112 M. tuberculosis isolates. Culture (MGIT960) and identification tests were performed at the Mycobacteriology Research Center of Jimma University, Jimma, Ethiopia. RESULTS: Mutations conferring resistance to INH, RIF, and multidrug resistance were detected in 36.6% (41/112), 30.4% (34/112), and 27.7% (31/112) of M. tuberculosis isolates respectively. Among 34 RIF-resistant isolates, 82.4% (28/34) had rpoB gene mutations at S531L, 2.9% (1/34) at H526D, and 14.7% (5/34) had mutations only at wild type probes. Of 41 INH-resistant strains, 87.8% (36/41) had mutations in the katG gene at Ser315Thr1 and 9.8% (4/41) had mutations in the inhA gene at C15T. Mutations in inhA promoter region were strongly associated with INH monoresistance. CONCLUSION: A high rate of drug resistance was commonly observed among failure cases. The most frequent gene mutations associated with the resistance to INH and RIF were observed in the codon 315 of the katG gene and codon 531 of the rpoB gene, respectively. Further studies on mutations in different geographic regions using DNA sequencing techniques are warranted to improve the kit by including more specific mutation probes in the kit.
Authors: James Peek; Mirjana Lilic; Daniel Montiel; Aleksandr Milshteyn; Ian Woodworth; John B Biggins; Melinda A Ternei; Paula Y Calle; Michael Danziger; Thulasi Warrier; Kohta Saito; Nathaniel Braffman; Allison Fay; Michael S Glickman; Seth A Darst; Elizabeth A Campbell; Sean F Brady Journal: Nat Commun Date: 2018-10-08 Impact factor: 14.919
Authors: Patrick K Arthur; Vincent Amarh; Precious Cramer; Gloria B Arkaifie; Ethel J S Blessie; Mohammed-Sherrif Fuseini; Isaac Carilo; Rebecca Yeboah; Leonard Asare; Brian D Robertson Journal: Antibiotics (Basel) Date: 2019-01-02