Next week the paperback edition of my book Microcosm: E. Coli and the New Science of Life will be published. In the book I approach E. coli as a microscopic oracle that can reveal great secrets about how life in general works. This is not actually a rhetorical stretch; over the past century scientists have put a spectacular amount of work into understanding this bug. And, as I write in the book, E. coli continues to offer surprises. In celebration of the arrival of the paperback Microcosm, I’m going to take a look at some fresh-out-of-the-oven research on E. coli that may change the way you think about life as a whole.
There’s no better way to kick off Microcosm Week than with some chocolate chip cookies. Or, to be specific, some raw cookie dough carrying a dangerous cargo of toxic E. coli.
The name ” E. coli ” embraces a veritable empire of bacteria. While all E. coli share the same backbone of certain genes, they can be divvied up into a vast number of strains, each with a distinctive genetic profile. Many of those strains are harmless. You have a couple dozen strains of E. coli dwelling inside you right now, quietly grazing on the extra sugar in your gut. But some strains are extremely nasty. One strain, known as E. coli O157:H7, can stick to the walls of the intestines and build needles through which it can inject molecules into host cells that can alter them in many ways, so that the cells disgorge food the microbe can eat. Typically this manipulation leads to painful, bloody diarrhea but little more. On rare occasion, however, the bacteria unleash toxins that can spread through the blood stream, killing cells and leading to kidney failure.
At the end of June the Centers for Disease Control detected E. coli O157:H7 in a batch of Nestle chocolate cookie dough. It’s a mysterious new move from a mysterious microbe. The normal host of E. coli O157:H7 is livestock–especially cows and sheep. In those animals, this strain doesn’t seem to do much harm and may even benefit its host. Studies on the evolution of E. coli O157:H7 suggest that it emerged and spread in parallel with the spread of cattle over the past 1000 years. The bacteria can spread from cow to cow by passing out of one host with their droppings. The bacteria can survive for months in a barn or a corral, and can then get blown onto grass or other food eaten by another cow. People can get sick from an infected cow if its intestines are nicked during slaughter and the bacteria can contaminate the muscle. That’s why you should always cook hamburgers all the way through–just a few microbes are enough to get you sick.
Yet some of the worst outbreaks of E. coli O157:H7 have not been caused by tainted beef. In 1996, for example, radish sprouts contaminated with E. coli O157:H7 infected thousands of school children in Japan. And now the bacteria have turned up in cookie dough. There’s no official word for how the bacteria got from a cow to a cookie (or at least, a cookie in the making). But chances are good that the story is going to be complicated, in a way that’s both disturbing and fascinating.
I base that prediction on the last headline-making E. coli outbreak, in 2006. Then it was spinach that was ferrying the bacteria, not cookie dough or sprouts. Over the course of two months, 205 people got sick from tainted spinach, and 15% of them developed the more dangerous form of the infection (called hemolytic uremic syndrome). That was over three times the average rate in previous outbreaks, and so scientists have taken a closer look at these particular bacteria–this sub-sub-strain, as it were, to figure out what made it so nasty. The scientists published their preliminary results last year (about which I wrote a piece for Slate), but now they’ve just published their detailed analysis in the journal Infection and Immunity.
The new study drives home a remarkable lesson: the bacteria that caused the spinach outbreak was different in many ways from other E. coli O157:H7. It changed in two ways.
Way #1: New mutations arose spontaneously in individual microbes, were passed down from ancestors to descendants, and then spread through the population by natural selection or a more random process called genetic drift. These mutations altered genes that carry out many functions in E. coli, from the chemical reactions it uses to break down food to the shape of its membrane. It also has mutant genes for cellulose and for hair-like projections from its surface, both of which have proven important to E. coli O157:H7’s ability to stick to surfaces, like those of sprouts.
Way #2: It turns out there are also a lot of genes in the spinach outbreak bacteria that are not found in any E. coli O157:H7. Some aren’t even found in any other E. coli. These genes did not evolve through the familiar rise of new mutations in old genes. Instead, the bacteria picked them up from other species at some point in the past few years. Viruses, for example, can accidentally pick up genes from one host and then insert them in the genome of a different host.
The genes acquired by the spinach E. coli include one encoding a protein that can twist the DNA in your cells so that they can’t send out alarms to your immune system. Another imported gene allows the bacteria to suck in the iron-bearing molecules in your blood. And two other genes bears a striking resemblance to a pair of genes found only in a species of bacteria that grows on plant roots.
Those genes are particularly interesting. The plant-dwelling bacteria uses their genes to manipulate the biology of their plant hosts, such as stimulating the roots they live in to grow. It’s possible that when the spinach E. coli picked up these genes, they helped the bacteria thrive by letting them grow on plants. In other words, this particular kind of E. coli didn’t just get swept away from its ordinary home inside a cow. Along with genes for living inside mammals, it has also picked up genes that help it live on plants. And it made that transition only very recently.
We’ll have to wait to see if the cookie E. coli has evolved its own peculiar set of genes. But as I write in Microcosm, this kind of evolutionary history–a mix of mutations handed down through the generations along with genes moving from one species to another–is hardly unique to a few outbreaks of food poisoning. In fact, these intertwined processes have been shaping life, our own included, for billions of years.