Microcosm_ E. Coli and the New Science of Life - Carl Zimmer [67]
Other strains of E. coli have evolved into different sorts of pathogens, and their genomes still record that transformation. Horizontal gene transfer, lost genes, and natural selection all were at play in their histories as well. Scientists who study E. coli O157:H7, the strain that can be carried in spinach or hamburgers, have done a particularly good job of reconstructing its evolution step by step. Its ancestors started out as far gentler pathogens, but about 55,000 years ago, they began to be infected with a series of viruses, each installing a new weapon in its arsenal. The devastating toxin that makes E. coli O157:H7 so dangerous, for example, is encoded on a gene that lies nestled among the genes of a virus. The virus is such a recent arrival in the E. coli O157:H7 genome that it still makes new viruses that can escape the microbe.
Scientists who study E. coli O157:H7 face a strange paradox, however. Other disease-causing strains of E. coli, such as Shigella, are highly adapted to living in humans and are rarely found in other species. But E. coli O157:H7 is just the opposite. It rarely turns up in humans (for which we can be grateful), but it lives in many cows and other farm animals. In us it can be deadly, but in them it causes no harm at all. It has adapted to them, in other words, as a benign passenger. The fact that O157:H7’s toxins make us deathly ill is just an evolutionary accident, because we are not their normal host.
If E. coli O157:H7 doesn’t make toxins to exploit us, then, why do they carry the toxin genes around? Some researchers have suggested that the bacteria make the toxin to help their animal hosts. At the University of Idaho, scientists have found that sheep infected with E. coli O157:H7 do a better job of withstanding a cancer-causing virus than sheep without that strain. They speculate that E. coli O157:H7’s toxins stimulate the ovine immune system, or perhaps even trigger cells infected with the cancer-causing virus to commit suicide before they can form tumors. But it’s also possible that the toxins are a defense for the bacteria themselves. When protozoans attack E. coli colonies, the ones that make the toxin can fend off the predators.
While E. coli O157:H7 may not have evolved to adapt to our bodies, we have still played a part in its rise. Studies on its genome show that it is a very young lineage; all of its most common forms are less than a thousand years old. Scientists suspect that by domesticating animals, humans created the conditions in which E. coli O157:H7 could thrive. Its hosts now spent much of their time penned together on farms, where the E. coli O157:H7 that they shed with their manure had a much better chance of infecting a new host than if the cows were off in the wild. E. coli O157:H7 exploded with the growth of cattle herding in recent centuries, first with the arrival of cows in the New World and more recently as cows have been packed together into feedlots. The bacteria haven’t just become more common thanks to us; they may also have been evolving faster, because viruses have been able to move from microbe to microbe, producing new strains of E. coli O157:H7.
While some harmless strains of E. coli have evolved into deadly parasites, evolution has flowed the other way as well. Some of the most benign strains of E. coli descend from pathogens. One strain of E. coli,