Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [54]
Over those eighty-five years their wild cousins have gone on with their own lives. They have continued to colonize guts, and they have evolved as well. The microbes that live inside us today are not the same as the ones that lived inside people in 1920. We are the source of much of that change.
The most obvious way we have changed E. coli is by trying to fight infections with drugs. E. coli and other bacteria have responded to those drugs with a rapid burst of evolution. They can now resist drugs that once would have wiped them out. Scientists are now left scrambling to find new drugs to replace the failed ones, and there’s little reason to think E. coli and other microbes won’t evolve resistance to them as well.
While some scientists have observed E. coli evolve in their laboratories, we have also launched a global, unplanned experiment in E. coli evolution. Like laboratory experiments, the rise of resistant E. coli is offering its own clues to the workings of evolution. Resistance can evolve through the familiar course of random mutations and natural selection. But in some ways, E. coli is not fitting into the conventional picture. In the evolution of resistant E. coli, some researchers claim to have found evidence that the microbe can alter the way it mutates to suit the conditions it faces. And while Darwin erected his theory on the idea that organisms inherit traits from their direct ancestors, E. coli has acquired much of its resistance to antibiotics from other species of bacteria, which can trade genes like business cards. These discoveries are significant not only because they may help in the battle against drug-resistant pathogens. They may also reveal forces that have been shaping life for the past 4 billion years.
The era of antibiotics began suddenly, but it followed a long, slow prelude. Traditional healers long knew that mold could heal wounds. In 1877, Louis Pasteur found that he could halt the spread of anthrax-causing bacteria by introducing “common bacteria” in their midst. No one knew what the common bacteria did to stop the anthrax, but scientists gave it a name anyway: antibiosis, the ability of one creature to kill another.
In 1928, Alexander Fleming, a Scottish bacteriologist, discovered a molecule that could kill bacteria. He noticed that one of his petri dishes had become contaminated with mold. There were no bacteria near it. He ran tests on the mold and discovered that it could halt the spread of bacteria. Yet it did not harm human cells. Fleming isolated the mold’s antibiotic and named it penicillin.
At first, penicillin did not look like a promising drug. For one thing, Fleming could extract only tiny amounts of it from mold, and it proved too fragile to be stored for very long. It took ten years for penicillin to live up to its promise. Howard Florey and Ernst Chain at Oxford University figured out how to coax the mold to make enough penicillin to test on mice. They infected mice with streptococci and injected some with penicillin. The treated mice all survived, and the others all died. In 1941, Florey and Chain persuaded American pharmaceutical companies to adopt their penicillin production scheme and expand it to an industrial scale. By 1944, wounded Allied soldiers were being cured of infections that would have killed them a year before. In the next few years, a rush of other antibiotics came along, mostly derived from fungi