The <i>ahpC</i> c-54t compensatory mutation is not always a valid surrogate for isoniazid resistance in <i>Mycobacterium tuberculosis</i>.

ABSTRACT: Thirteen commercial genotypic antimicrobial susceptibility assays interrogate mutations upstream of ahpC to infer isoniazid resistance for Mycobacterium tuberculosis. We demonstrate that relying on one of these compensatory mutations (i.e., ahpC c-54t)-rather than causative resistance mutations in katG that ahpC compensates for-can result in systematic false-resistant results for isoniazid with the Cepheid Xpert MTB/XDR and suboptimal treatment. The WHO mutation catalog should be refined to address this scenario.

SUBMITTER: Szel V 

PROVIDER: S-EPMC12135522 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature