Immune cells inadvertently help bacteria form persistent infections

Rocky Mountain Laboratories, NIAID, NIH

Antibiotic resistance can probably be considered the problem of the century. As infectious diseases evolve the ability to evade or disable more of our drugs, we're struggling to come up with alternative approaches to get them under control. Bacterial infections can often persist despite repeated antibiotic treatments, like the C. difficile that inspired one of the first fecal transplants in 1999.

But antibiotic resistance isn't always to blame for persistent infections. Antibiotic resistant bacteria arise from heritable mutations in classic Darwinian fashion. If a bacterial population is exposed to an antibiotic and one cell has a genetic mutation that allows it to survive, all of its fellow cells will be killed but the survivor will grow and divide. All of its progeny will inherit the mutation and therefore the resistance.

In contrast, some persistent infections can arise from special cells—persisters—that slow down their metabolism and cell division. Persisters aren't killed by antibiotics, but these cells leave behind progeny that can actually be susceptible to the drugs. How do bacterial cells become persisters? In one case, by getting eaten by immune cells.