There are 17 million new biofilm infections every year in the U.S.A., which lead to 550,000 fatalities (R. Wolcott, S. Dowd, Plast. Reconstr. Surg. 127, 28S (2011), and biofilms are difficult to treat due to the presence of persister cells (K. Lewis, Curr. Top. Microbiol. Immunol. 322, 107 (2008)). Persisters arise due to metabolic inactivity (K. Lewis, PNat. Rev. Microbiol. 5, 48 (2007); Kwan, et al. Antimicrob. Agents Chemother. 57, 1468 (2013); T. K. Wood, et a., Appl. Environ. Microbiol. 79, 7116 (2013)) and are highly tolerant against all traditional antibiotic classes, which are primarily effective against actively growing cells. Bacterial persistence is a non-hereditary phenotype. (W. Bigger, Lancet 244, 497 (1944)) which occurs both stochastically (N. Q. Balaban, et al., Science 305, 1622 (2004) or through environmental influence (Kwan, et al. (2013), N. Möker, et al., J. Bacteriol. 192, 1946 (2010); Y. Hu, et al., Environ. Microbiol., 17, 1275, (2015); T. Dörr, et al. PLoS Biol. 8, e1000317 (2010); N. M. Vega, et al., Nat. Chem. Biol. 8, 431 (2012)) in a small sub-population of all tested bacterial species (K. Lewis, Curr. Top. Microbiol. Immunol. 322, 107 (2008)) (˜1% during stationary phase and in biofilm cultures); (K. Lewis, Curr. Top. Microbiol. Immunol. 322, 107 (2008); K. Lewis, Nat. Rev. Microbiol. 5, 48 (2007)). Few distinctly new antibiotics have been discovered recently (Antibiotic discovery and development. T. J. Dougherty, M. J. Pucci, Eds., (Springer, New York, N.Y., 2012), and current antibiotics are ineffective against persister cells. Thus, there is an ongoing and unmet need for improved approaches to treating infections that comprise persister cells. The present disclosure meets this need.