Sure, bats and dolphins use sonar. But bacteria? Microbiologists recently found that a particularly virulent strain of the bacterium Enterococcus faecalis deploys a sonarlike system to “hear” the approach of other cells, then kills them with a blast of toxin. The bacterium is a leading cause of hospital-acquired infections.
E. faecalis normally resides benignly in the contents of the lower intestine but can produce an infection if it gets into a wound. Even so, it is fairly easy to fight off. The toxin-packing version of E. faecalis is far more sinister. That rogue strain has an arsenal of nasty genetic traits acquired in hospitals, including resistance to virtually any antibiotic. People infected with it are five times more likely to die from it than those with the more benign version.
Until now, no one knew what triggered the bacteria to release toxin. Harvard Medical School ophthalmology researcher Michael Gilmore and his colleagues found that E. faecalis constantly produces two kinds of molecules, one large and one small. If there is no cell to kill in the vicinity, the molecules stick to one another and drift away. If a cell appears, the large molecules cling to it, freeing the small ones to bounce back to the bacterium alone, sounding the alarm to release toxin.
The discovery, Gilmore thinks, may be the microbe’s Achilles’ heel. Blocking the small molecule would silence the sonar. But even the garden variety of E. faecalis is rugged and hard to kill, says Gilmore. “They are kind of like the cockroaches of bacteria.”
