P. Abel zur Wiesch

This study shows that higher rifampicin peak concentrations accelerate the slow phase of bacterial decline in tuberculosis, supporting heteroresistance as the mechanism.

This study models how antibiotic mechanisms affect resistance mutation fitness, finding that drug type has little impact on resistance selection but that heterogeneous binding enables secondary mutations under certain conditions.

This paper develops a computational model to predict antibiotic dose-response relationships from drug-target binding parameters and validates it with clinical isolates.

This study uses transposon-insertion sequencing to identify genes required for EHEC growth in vitro and in vivo, revealing new factors critical for intestinal colonization.