An important mechanism for the spread of bacterial resistance to antibiotics is identified

An important mechanism for the spread of bacterial resistance to antibiotics is identified

The abuse of antibiotics is commonly (and rightly) associated with the development of bacterial resistance to antibiotics. It is a well recognized principle that underlies attempts to limit antibiotic use to only the most necessary conditions, and to eliminate the prophylactic use of antibiotics in animal husbandry. Like any selection factor, antibiotics can help to cull a population so that only the most resistant survive. But, as with all things, the actual mechanism of resistance may be more insidious than now believed.

Researchers found that when E. coli, a common intestinal microbe that occasionally causes illness, becomes resistant to an antibiotic, it can share a molecule called indole with its more vulnerable neighbors. Indole is known to help bacteria tolerate "stress". The researchers found that in a population of E. coli most individual bacteria were less resistant than the group as a whole, and a few were more resistant. The indole was "shared" by the more resistant bacteria with the other bacteria, increasing the resistance of the group as a whole. Indole has two "benefits". It helps to turn on cellular pumps to push the antibiotic out of the bacteria, and it protects against damaging molecules called free radicals.

But, of course, the issue was even more complex. The resistant bacteria were found to have numerous genetic mutations that made them more resistant to the antibiotic. When exposed to the antibiotic, their indole production did not vary; they kept making indole, and in essence sharing it with their neighbors. In contrast, the less resistant bacteria stopped making indole when exposed to the antibiotic.

This strategy may have evolved to help bacteria survive transient stressors. By preserving the colony as a whole, the researchers suggest, the strategy may keep beneficial mutations in the gene pool. Diversity of the gene pool may help the population as a whole survive various stressors.

The paper can be found at