Antibiotic treatment and selection for glpK mutations in patients with active tuberculosis disease

We read with great interest the paper by Safi et al. (1) describing frameshifts in glpK ’s homopolymeric tract (HT) of seven cytosines (7C) as a potential cause of antibiotic tolerance. These results have implications for tuberculosis (TB) treatment, but other forces than antibiotic pressure may be responsible for the emergence of glpK mutations (1, 2). We raise the possibilities of selection in vitro, selection in vivo from nonantibiotic host...