Claire V. Mulholland

This paper introduces a Persister Enrichment Model (PEM) to study multidrug persistence in M. tuberculosis, showing that drug sequencing and maltokinase-dependent carbon distribution influence antibiotic tolerance.

This study shows the mycobacterial ATP burst is an experimental artifact caused by cell lysis, not a biological response, and presents it as a tool for screening cell wall-disrupting drugs.

The paper identifies a metabolic deficiency causing PDIM loss in Mycobacterium tuberculosis and shows how nutrient supplementation can restore PDIM production and virulence.