<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kim SY</submitter><funding>National Research Foundation of Korea</funding><pagination>6108</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7969740</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(1)</volume><pubmed_abstract>We evaluated the association between 16S rRNA gene (rrs) mutations and susceptibility in clinical isolates of amikacin-resistant nontuberculous mycobacteria (NTM) in NTM-pulmonary disease (PD) patients. Susceptibility was retested for 134 amikacin-resistant isolates (minimum inhibitory concentration [MIC] ≥ 64 µg/ml) from 86 patients. Amikacin resistance was reconfirmed in 102 NTM isolates from 62 patients with either Mycobacterium avium complex-PD (MAC-PD) (n = 54) or M. abscessus-PD (n = 8). MICs and rrs mutations were evaluated for 318 single colonies from these isolates. For the 54 MAC-PD patients, rrs mutations were present in 34 isolates (63%), comprising all 31 isolates with amikacin MICs ≥ 128 µg/ml, but only three of 23 isolates with an MIC = 64 µg/ml. For the eight M. abscessus-PD patients, all amikacin-resistant (MIC ≥ 64 µg/ml) isolates had rrs mutations. In amikacin-resistant isolates, the A1408G mutation (n = 29) was most common. Two novel mutations, C1496T and T1498A, were also identified. The culture conversion rate did not differ by amikacin MIC. Overall, all high-level and 13% (3/23) of low-level amikacin-resistant MAC isolates had rrs mutations whereas mutations were present in all amikacin-resistant M. abscessus isolates. These findings are valuable for managing MAC- and M. abscessus-PD and suggest the importance of phenotypic and genotypic susceptibility testing.</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Association between 16S rRNA gene mutations and susceptibility to amikacin in Mycobacterium avium Complex and Mycobacterium abscessus clinical isolates.</pubmed_title><pmcid>PMC7969740</pmcid><funding_grant_id>NRF-2016R1A6A3A11930364</funding_grant_id><funding_grant_id>NRF-2019R1I1A1A01041381</funding_grant_id><pubmed_authors>Kim DH</pubmed_authors><pubmed_authors>Moon SM</pubmed_authors><pubmed_authors>Lee NY</pubmed_authors><pubmed_authors>Kim SY</pubmed_authors><pubmed_authors>Song JY</pubmed_authors><pubmed_authors>Jhun BW</pubmed_authors><pubmed_authors>Koh WJ</pubmed_authors><pubmed_authors>Huh HJ</pubmed_authors><pubmed_authors>Shin SJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association between 16S rRNA gene mutations and susceptibility to amikacin in Mycobacterium avium Complex and Mycobacterium abscessus clinical isolates.</name><description>We evaluated the association between 16S rRNA gene (rrs) mutations and susceptibility in clinical isolates of amikacin-resistant nontuberculous mycobacteria (NTM) in NTM-pulmonary disease (PD) patients. Susceptibility was retested for 134 amikacin-resistant isolates (minimum inhibitory concentration [MIC] ≥ 64 µg/ml) from 86 patients. Amikacin resistance was reconfirmed in 102 NTM isolates from 62 patients with either Mycobacterium avium complex-PD (MAC-PD) (n = 54) or M. abscessus-PD (n = 8). MICs and rrs mutations were evaluated for 318 single colonies from these isolates. For the 54 MAC-PD patients, rrs mutations were present in 34 isolates (63%), comprising all 31 isolates with amikacin MICs ≥ 128 µg/ml, but only three of 23 isolates with an MIC = 64 µg/ml. For the eight M. abscessus-PD patients, all amikacin-resistant (MIC ≥ 64 µg/ml) isolates had rrs mutations. In amikacin-resistant isolates, the A1408G mutation (n = 29) was most common. Two novel mutations, C1496T and T1498A, were also identified. The culture conversion rate did not differ by amikacin MIC. Overall, all high-level and 13% (3/23) of low-level amikacin-resistant MAC isolates had rrs mutations whereas mutations were present in all amikacin-resistant M. abscessus isolates. These findings are valuable for managing MAC- and M. abscessus-PD and suggest the importance of phenotypic and genotypic susceptibility testing.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2026-05-10T03:27:41.805Z</modification><creation>2025-04-05T10:30:00.327Z</creation></dates><accession>S-EPMC7969740</accession><cross_references><pubmed>33731862</pubmed><doi>10.1038/s41598-021-85721-5</doi></cross_references></HashMap>