Hit 'Em Quick, Hit 'Em Strong

See allHide authors and affiliations

Science  12 Oct 2012:
Vol. 338, Issue 6104, pp. 173
DOI: 10.1126/science.338.6104.173-b

Clinicians are very aware of the increasing failure rate of currently available antibiotics to treat persistent infections. In fact, we know little about how populations of bacteria respond to antibiotics, but we do know that the efficacy of antibiotics in several classes depends on the initial density of the bacteria at infected sites, regardless of whether resistant mutants arise or whether protective mechanisms are triggered in the pathogens. It makes sense that the presence of a greater number of bacteria capable of breaking down a fixed dose of antibiotic will allow a greater proportion to escape the effects of the drug. But what happens if the bacteria can't disable the antibiotic? Tan et al. took kanamycin, an antibiotic that targets the bacterial ribosome, and discovered that this drug indirectly induces a heat shock response to the mistranslated proteins, which degrades the ribosome. The denser the bacterial population, the more the antibiotic is titrated and the greater the chances that more bacteria will escape after a period of recovery, or lag, to regrow. It's not so simple though, because clinicians often administer pulses of antibiotic to avoid toxicity effects on patients and the emergence of resistance. But it is also important that they get the dose and treatment times optimized around the lag times, otherwise bacteria may escape again.

Mol. Syst. Biol. 8, 10.1038/msb.2012.49 (2012).

Navigate This Article