The world is full of Good Samaritans; you’ll find many of them in your own body. James J. Collins, a biologist at Boston University, has found that small numbers of drug-resistant bacteria help their vulnerable counterparts survive antibiotic onslaughts, even at a cost to themselves.
Collins and his colleagues exposed one culture of Escherichia coli—some strains of which colonize the human and animal gut; others of which are notorious for causing disease outbreaks—to increasing amounts of an antibiotic over time. When they periodically analyzed the levels of drug resistance in the colony, they saw something unexpected: although the entire population was thriving in the presence of the drug, only a few individual bacteria were actually resistant. “We were really surprised to see that the levels of resistance of the individual isolates were considerably lower than the population as a whole,” explains Collins, who published his results recently in Nature. (Scientific American is part of Nature Publishing Group.) Further analysis revealed that the resistant mutants were secreting a molecule called indole that thwarts their own growth but helps the rest of the population survive by activating drug-export pumps on the bacterial cell membranes.
The findings could spur scientists to develop better antibiotics. If indole allows pathogenic bacteria to withstand antibiotics, it may be possible to thwart drug resistance by blocking indole signaling with small molecules, Collins says. Alternatively, “the findings suggest the possibility that scientists could one day use indole or an indole-based therapeutic, if proven safe, to help beneficial bacteria outcompete pathogenic bacteria in the urinary tract or intestinal system,” says Mark Anderson, chief scientific officer of Emeryville, Calif.–based NovaBay Pharmaceuticals, which develops drugs for antibiotic-resistant infections.
The results may also change the way doctors track infections in their patients. If a bacterial population can become antibiotic-resistant even when only a small number of individuals have the appropriate genetic mutations, doctors who collect and analyze small bacterial specimens from patients may underestimate just how resistant the infection is as a whole, Collins notes. “These unicellular organisms can function as a multicellular organism of sorts,” he says. Thus, isolated samples may not be representative of the big picture.
This article was originally published with the title Nice Germs Finish Last.