In ordinary times, no person is an island. We are connected to other people through touch and words but also through the exchange of species, most benign, some even beneficial—on our bodies, in our homes, and more generally in our daily lives. These species may be bacteria, fungi, protists, and even small animals. You kiss a loved one and transfer life from your lips to their cheek, a shimmer of species.

But now we are aware that the kiss can be dangerous or even deadly. As we isolate ourselves in order to reduce the connections in the web, what happens to the whole society of viruses, bacteria, and mites that exists on and between us? What happens when each person, or at least each home, becomes an island?

This is something ecologists and evolutionary biologists have studied for several hundred years now. On islands, with enough time, some species become more common, some go extinct, and some evolve. Charles Darwin famously gained insights into the workings of evolution by considering the differences among species of birds isolated on different islands of the Galapagos archipelago. With collaborators, I have looked at similar issues in face mites and bacteria in armpits.

First, there are species that become rarer. We know from thousands of studies of fragments of forest that, as forests are cut into smaller and smaller pieces, species go extinct. For species that live on bodies, it seems likely that the fewer people who live in your home, the more likely it is for any particular body-loving species to go extinct. If it goes extinct on you, it has fewer places from which to recolonize. In normal times, species pass from one person to another, one being to another, when we touch. Roller derby players who bump into each other exchange skin bacteria. The more you bump, the more you share. But in our isolation, we bump and share with fewer people and so colonization is less likely and extinction more permanent. Indeed, this is what we hope happens with the virus that causes COVID-19: that by disconnecting from one another, we give it no island close enough to land upon.

In forest fragments, losses occur in a predictable order: Predators go extinct first, when there are too few prey. Indoors, leopard mites that eat dust mites that eat our skin as it falls from us everywhere we go are almost certainly more likely to go extinct before the dust mites themselves. So too skin or gut microbes that depend on other skin or gut microbes, the wolves of our bodily Yellowstone.

Species evolve more rapidly, as we know from studies of islands, if they have large populations and multiply rapidly. And if these populations become isolated and face different conditions, they tend to diverge. By studying the microbiome, we can see evidence of previous separations among humans. Lice species diverged genetically among populations of Paleolithic humans as they spread around the world. Similarly, I’ve collaborated with my friend and colleague Michelle Trautwein to study divergences among face mites. Of the two most common species of face mites, Demodex brevis nestles deeply in pores, while Demodex folliculorum lives more shallowly. We think that the deep dweller is less able to move among humans, spending so much of its time in its cave. As a result, it is more likely to diverge among human populations during times of separation.

That would take years or even generations in quarantine. But before that, we would expect the bacteria that live inside the mites to diverge on the island of each person. Each mite hosts a large population of rapidly multiplying bacteria in its gut microbiome. And the viruses—even more numerous and rapidly multiplying—that attack the bacteria that live inside the mites that live on your face would diverge even faster still.

We are not only “gardening” our microbes by subtracting from their web, absentmindedly weeding; we are also giving them additional new foods with our new quarantine regimes and hobbies, and lack thereof.

Consider, for a moment, your armpits: They have a special organ called an axillary organ, containing apocrine glands, whose sole function is to feed bacteria. These bacteria produce aromas that wick along the armpit hair (which are different from other body hair and appear to serve no function other than such “wicking”). While we don’t yet understand why the axillary organs evolved (chimpanzees and gorillas also have them), they clearly show a social relationship between primates and bacteria that is somehow about sending messages via smell to other primates.

When you wear antiperspirant, you alter the messages that your armpits send. Specifically, as a study my colleagues and I did several years ago shows, you favor fast growing, weedy Staphylococcus bacteria in your armpit that are not very stinky. Conversely, if you don’t wear antiperspirant, you favor a slow-growing, stinky, old-growth microbial community, like those found in chimpanzee and gorilla armpits—something like the redwoods of the armpit. These two communities, the weeds and the redwoods, send different messages to other people.

What those messages mean and how they are interpreted, we don’t know. We are at the step in the science in which we have discovered a language, but not decoded it. But if you are alone in your apartment and not putting on antiperspirant or deodorant, you are gardening an ancient wilderness of species similar to those found in the armpits of chimpanzees and gorillas. These species aren’t harmful and may even be beneficial, so go ahead and let them blossom.

Then there’s the relationship you may be forming with sourdough bread, which is a great deal more complex and reciprocal than it seems. Several years ago, my colleague Anne Madden and I did an experiment on sourdough starters, the microbial communities composed of bacteria and fungi that are used to leaven bread. Though all leavened breads were once produced using starters, they have a mysterious element: Where did the microbes in them come from? One possibility was that the microbes came from the bodies of the bakers themselves, as is the case with many fermented foods, like beer yeast, which comes from the bodies of wasps.

To test this hypothesis, we had bakers from around the world use the same ingredients to make a sourdough starter. We held all the ingredients constant, except for the hands of the bakers and the air in their bakeries. As it turned out, the individual bakers and/or their bakeries did have a modest effect on the microbes in their starters and thus on the flavors of the resulting bread. In other words, you can taste the baker in the bread.

But we were surprised to find that the story was more complicated than that. We swabbed the hands of the bakers (after they went about their ordinary morning ablutions) to learn what they might be contributing to the bread. Their hands were unlike those of any people yet studied. Lactic acid bacteria are key to the flavor of sourdough starters, making them acidic. In most studies, the proportion of lactic acid bacteria on peoples’ hands is small, around 3 to 6 percent. On the bakers’ hands, though, up to 70 percent of the bacteria were lactic acid bacteria. The baker’s hands also had much more yeast than the hands of other folks. In short, the bakers’ hands looked like sourdough starters. Their daily immersion in bread had changed their microbes. Sure, you could taste the baker in the bread, but the bread had also remade the baker.

The curious reciprocity between the microbial world of our foods and the microbial world of bodies also shows up in yogurt, whose bacteria are originally from human mouths and the guts of mammals. In commercial sourdough bread, the most commonly used bacteria appears to have come from the gut of a rat. Many fermented drinks around the world, such as chicha in the Amazon, rely on human body microbes for fermentation. As with sourdough, these fermentations influence our bodies, changing our microbiomes, affecting what we can digest and how we smell. We forget that we, too, are gardens.

Actual outdoor gardens also have the potential to change the species on our skin. We know from studies in Finland that children whose outdoor environments include a greater variety of plants tend to have more kinds and different kinds of bacteria on their skin, including bacteria that help to keep them healthy. Exposing yourself to the wild microbes of the garden and forest can have a big impact on your body’s wildlife, though we don’t know how much exposure it takes to make a difference. One sample of the skin of a child who grew up in the Amazon rainforest, living a hunter-gatherer lifestyle, found more kinds of skin microbes on the forearm of that child than the total number we observed in a study we did of the belly button microbes of hundreds of Americans. How much would you need to garden to achieve such an effect? I suppose the answer is a lot.

Another big player in your microbial life is your dog, with whom you may be spending more time. Whether or not you have a dog is the single biggest predictor of which bacteria are floating through the air in your house. Children who live with dogs tend to acquire some dog gut microbes. Whether the same occurs with adults is less clear. I don’t advise intentionally acquiring dog microbes. But we know that kids, especially in cities, that grow up with a dog in the house are less likely to develop some allergies and asthma. Something about a dog in the house, microbially, can be good.

As for cats, the jury is still out. One microbe, called Toxoplasma gondii, associated with cat feces, can get into human brains and lead to changes in human behavior. In the garden of your daily life, it is definitely a bad weed.

I look forward to the day in which we can reconnect and share, anew, communities of microorganisms with others. In the meantime, I’m ever more aware of the thousands of species on my own body, in my own house and yard—virtually none of which have been studied, and many of which, though we spend so very much time with them, do not even yet have names.

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Why these two facts seemed among the most important things to teach 12-year-olds in the 1990s is not exactly clear, but it stands to reason that at least the latter fact came from inherited wisdom. This middle-aged teacher in Arkansas had likely heard about botulism in canned food from his own mother and grandmother, seizing upon it as this singularly cool fact, relevant in the kitchen and in the science classroom. The terror of the botulism bacteria and the chaos it could wreak belied the boring, innocuous image of the tin can.

By the time I was sitting at that molded plastic school desk, it was hard for Americans to imagine anything less scary than canned food. In a nation of Lunchables and DunkAroos, we believed in the power and safety of the food industry, of which canned food was a part.

But I later became a student of history and, by a funny turn of events, began to study the history of canned food. I learned of a time when cans were novel and unfamiliar, and when they inspired distaste, fear, and panic. These experiences still shape America, and how it eats, today.

Canned food got its start in the opening years of the 19th century in France and moved to America by 1825, but only began to enter average American homes in the years after the Civil War. The war exposed millions of soldiers to canned food, and they brought the taste home with them. But the new industry also struggled to convince American consumers to consider its products viable and trustworthy. There were many reasons why early consumers weren’t all that interested in trying these new offerings. For one, the long hours that cans of food were boiled left the contents mushy, with an unattractive texture and taste.

But even before tasting the food, many Americans were skeptical. To people accustomed to seeing and touching and smelling the foods they were about to eat, these hard-sided, opaque metal objects did not seem like food. The new method of industrial production and new way of eating felt foreign to American consumers, who had grown up eating food that was more local, more perishable, and easier to fit into existing categories. As the United States entered an era of industrialization and urbanization, the unfamiliar can embodied this time of rapid change.

In the half-century after the war, innovations followed as the canning men—and they were mostly all men—built their business from the ground up, hoping to overcome consumer resistance. The canners perfected machinery to build the cans and process the fruits and vegetables; they organized professional trade groups; they worked with agricultural scientists to breed crops better fit for the can; and they invited government regulation as they helped craft pure food laws.

One central problem that the canners worked to address was spoilage. Even though the canning process killed existing bacteria and created a vacuum seal to keep more bacteria from getting in, the method wasn’t always foolproof. If the temperature of the water bath was too low, or it boiled unevenly, or the pressure was insufficient, or the cans weren’t processed long enough, or the seals were weak—or if there were any other flaw in the process—spoilage could occur. Canners thus invested in bacteriology and public health oversight. With the acceptance of germ theory in the late 19th century, canners embraced this new awareness of the microbial life that could wreak such outsized havoc, seeing it as a key to solving their spoilage issues. Beginning in the 1890s, the industry sponsored scientific work to address bacterial contamination. Before long, canners felt they had gained control over this microscopic foe.

Most canned food spoilage is fairly obvious—either the can itself becomes deformed or its contents are visibly spoiled—and relatively harmless, perhaps leading to digestive upset or mild illness. But there was one rare kind of bacteria that was far from harmless: Clostridium botulinum.

This bacteria produces botulinum, the deadliest toxin known to humankind, which can’t be detected by sight, smell, or taste. Botulism doesn’t itself cause cans to be externally deformed, neither dented nor bulging, but those external signs often suggest an insufficient canning process, which can breed both botulism and other kinds of bacteria that have more visible effects. Botulism is also anaerobic, meaning it thrives in oxygen-free environments, precisely like that of canned food. Though it was rare, botulism terrified canners.

Their worst fears materialized in late 1919 and early 1920, when a series of deadly botulism cases struck unassuming consumers throughout the country, killing 18 people in Ohio, Michigan, and New York, with smaller outbreaks in other states. The deaths were traced back to canned black olives, a mainstay of hors d’oeuvre plates and a delicacy often reserved for special occasions. The olives had been packed in California and then shipped across the country to far-flung destinations, the result of a newly nationalized commercial food system.

The National Canners Association and California Canners League sprang into action, recognizing the particular vulnerability of this moment. These botulism deaths—widely publicized in mainstream media outlets—threatened to undermine the still-shaky foundation of the canned food business, fueling consumers’ deepest fears about these processed foods.

The canners worked on two fronts. Even as they sought to displace responsibility and downplay media coverage of the deaths, they launched an expensive research and inspection campaign that would lay the groundwork for the American food safety system.

In early December 1919, the canning and olive industries came together to fund a Botulism Commission of scientific experts tasked with producing specific strategies for safely processing olives to prevent such a crisis from happening again.

After much negotiation, the Botulism Commission’s findings led to strict regulations for the processing of olives—240 degrees Fahrenheit for at least 40 minutes—and a statewide inspection service, funded by the industries, but overseen by the impartial California State Board of Health. By 1925, many of these standardized practices had expanded to other food products, covering sardines, tuna, and all vegetable products except tomatoes.

In the process, three distinct groups—scientists, canners, and government officials—established a set of relationships. As they got to know each other and worked through their competing commitments and quirks, they built the network that would underpin the nation’s food system.

Because the canning industry had taken a lead role in this network, many critical consumers were mollified, leading to acceptance of canned food, and later processed food, in the decades to come.

This small story of a food scare and an emerging industry’s embrace of food safety regulation encapsulates the larger story of American commerce in the 20th century. In solving the problem of botulism, an industry threatened with destruction instead came back with a set of practices that not only revolutionized canned food, but the entire relationship between science, government, and the food industry in America today. In this early phase, the canners were as much a player in policing themselves as were external regulators.

By the time I heard that questionable information about botulism from my science teacher in the 1990s, I was part of a food system awash in processed foods. By then, dented cans—or any cans—were very unlikely to harbor botulism bacteria, which had been largely brought under control by those new processing methods and regulations. This paved the way for our contemporary American food culture, in which we eat and unthinkingly trust processed food.

Yes, the country still experiences occasional and ongoing food safety outbreaks. But rarely are these from canned food, which—along with the vast array of food products that line our lunchboxes and grocery store shelves—has escaped the reputation that first inspired my teacher’s inherited wisdom generations ago.

Of course, the definition of osmosis is still pretty much the same.

The post The Deadly Toxin Outbreak That Spurred America’s Food Safety System appeared first on Zócalo Public Square.

In a shift similar to when we realized that the sun did not revolve around the Earth, our place on the planet has turned inside out: We live in the germs’ world, now. Increasingly, new diseases are textbook cases of how our old textbooks didn’t describe our real relationship to microbes.

Take Elizabethkingia anopheles, which has mysteriously sickened 61 people, mostly in Wisconsin, since last fall. All were already ill. Twenty people have died, which is a very high rate. Elizabethkingia anopheles is found in dirt, in mosquito guts, and pretty much everywhere else. The Centers for Disease Control and Prevention have sent epidemiologists to Wisconsin, Illinois, and Michigan, and they’ve interviewed survivors, tested fellow patients, and even collected samples of skin care products used by those infected—without finding a clear mode of transmission, or a thread connecting one infection to another. Exploring the history of what we do and don’t know about E. anopheles tells a story about the curious mix of hope and danger in our bacterial companions.

The Elizabethkingia bacterial genus was first discovered by Elizabeth O. King, a CDC microbiologist in 1959. Using fluid from the spinal cords of children, many of whom had died of meningitis between 1948 to 1958, she isolated the likely cause under her microscope: a bacteria with “slender, slightly curved rods. Short, straight forms with rounded ends are also present.” She grew colonies of them on petri dishes, where they appeared “smooth, entire, glistening, gray-white and butyrous”—which means butter-like. She found what they were capable of by subjecting them to chemical tests and antibiotics, and then injected them in rabbits, mice, and hamsters. Elizabeth King’s original name for the genus referenced its yellowish color (Flavobacterium), and the name for its species referenced the infant meningitis it was associated with (meningosepticum). But in 2005 the genus was renamed Elizabethkingia after her.

Until 2008, Elizabethkingia kept a pretty low profile. It was associated with the occasional case of meningitis, scattered in different countries, but otherwise not much thought was given to these rod-shaped bacteria. And then, Swedish malaria researcher Ingrid Faye identified another strain of Elizabethkingia in the gut of a mosquito in Africa in 2008. Named after the mosquito, the bacteria was called Elizabethkingia anopheles.

These days, microbiologists don’t spend much time describinermiteg the shape of bacteria, or how they look in a petri dish. Instead they sequence their genes—which is exactly what Jiannong Xu, an associate professor at New Mexico State University, did. By analyzing its genes in 2011, Xu and his team came to understand that E. anopheles is a key player in the mosquito’s gut, which made it a potential player in the fight against malaria.

In fact, if you were a mosquito in the market for a gut-residing bacteria, you’d hire E. anopheles straightaway! This strain of bacteria contains genes that help break down blood cells. And then, because digesting blood can lead to oxygen poisoning, E. anopheles ingeniously makes antioxidants, too. But day-to-day, when the mosquito is just feeding on sugary nectar, the bacteria helps digest that. And finally, it has a large bag of tricks that make it resistant to antibiotics: a thick cell wall, special pumps that push toxins out of the cell, a set of genes that short-circuit many common antibiotics. A whole tool kit for avoiding death.

I asked Xu why these bacteria have such powerful antibiotic capabilities. “The mosquito’s gut is a collection of bugs inside a bug: a world inside a world,” he said. The gut bacteria have evolved to live together and kill harmful invaders. They’ve divided up the tasks: Some members of the community have strong antibiotic properties themselves—to slay the enemy—so the antibiotic resistance genes essentially protect the gut’s traditional residents from their own weapons.

Xu has spent the last 20 years studying how mosquitoes’ immune systems work, which is much more than an academic question. When they take blood from humans, female mosquitoes take on malaria-causing parasites without damaging their own immune systems, incubate the parasites, and pass them back to humans. There has long been a hope that we could either encourage mosquitoes to breed less enthusiastically, kill the malaria themselves, or engineer some other biological change that would lessen the threat of malaria. In any case, the benefits of understanding this immune process are large: Malaria kills 1.2 million people every year and about half the world is vulnerable to catching it. Initially, it looked as if manipulating E. anopheles might be a good way to keep malaria in check, and Xu got a grant to do just that.

Once scientists knew how to identify E. anopheles, though, it started showing up in surprising places: in a sick newborn in Bangui, Central African Republic, in 2011, then an intensive care unit in Singapore, and then two babies in Hong Kong. Scientists determined that some cases were spread from mother to infant, but not by mosquitoes, despite its name and coziness with the insect. Meanwhile, since 2004, epidemiologists had noticed that cases of the original Elizabethkingia meningoseptica seemed to be rising among babies and people with weak immune systems in hospital settings, where the bacteria’s large set of genes for antibiotic resistance were a clear advantage.

So who was the real E. anopheles? Had the bacteria suddenly changed to infect humans, or had it been the bad bug all along? When the CDC re-analyzed some past infections that had seemed like meningoseptica, they realized they were actually anopheles. “It’s difficult to draw conclusions about the history of E. anophelis since it was just identified as a separate species in 2011,” said John McQuiston, who is the team lead in the CDC’s Special Bacteriology Reference Laboratory, via email. He added that there is no evidence that the infection is spread via mosquito bites.

The story of Elizabethkingia anopheles is typical of the paradox we’re now in: Since 2008, we’ve doubled the genetic data we have about our world every 7 months. Genomic data is growing much faster than Moore’s Law—which says that computer speeds double every 18 months—and even more than our count of stars. It’s gotten to the point where some biologists want to replace the phrase “astronomical growth” with “genomic growth.” But more data open up more questions than they answer.

And genes are just one part of the new information we have: The internet brings us news of infections in places we never thought to look. Mosquitos and diseases also are traveling farther and faster—by boat, by plane, as well as with a changing climate. (They could even be traveling by hand cream!) But understanding how these places are connected by these ubiquitous bacteria will take much longer.

Amidst this bounty of high-tech discovery, it’s important to remember that new technology is not the answer to every problem. I asked New Mexico’s Xu how his anti-malarial research was going. He said that E. anopheles had proven hard to work with, though another team had made some progress. And he sounded a bit skeptical. “It’s relatively easy to engineer bacteria, but we don’t know whether it would work in nature. We know what mosquitoes do in the lab, but we don’t have an ecological sense of how they acquire bacteria and we need that information.” In the meantime, it had become clear that there was a simpler solution to reducing malaria—mixing sugary mosquito bait with a toxic chemical seemed to kill mosquitos more cheaply, and with fewer complications, than re-engineering their guts. “In general, low-tech works better than high-tech,” Xu said with a laugh.

The post Meet the Deadly Bacteria Whose Story Is a Curious Mix of Hope and Danger appeared first on Zócalo Public Square.

Long before you drove a car or ordered a drink, you declared your independence by embracing E. coli. Just a few hours after you were separated from your mother, this strain of bacteria swam into your intestines and set up housekeeping. While you slept, it triggered vital elements of your immune system, and prepared the environment for the arrival of other good bacteria. It also set about manufacturing vitamin K, and keeping harmful bacteria at bay.

You might think that E. coli exerts its will through big numbers, but that’s not the case. It is much less than one percent of your gut’s 9 trillion microbial cells. You have just a billion E. coli, each merely one micrometer wide and two micrometers long. (For comparison, a human hair is between 17 micrometers and 181 micrometers thick.) As for the toxic E. coli, it takes hardly any of those to make a person mortally ill. Ten will do do the trick. Ten! One of E. coli’s recipes for success is reproducing really quickly, sometimes doubling population in 20 minutes.

Another of E. coli’s tricks is sharing code—like open source software developers and DJs. E. coli has a fancy toolkit for acquiring and trading DNA, including viruses and pieces of circular DNA that, Frisbee-like, can transfer DNA from one bacterium to another.

When microbiologist Dr. Pina Fratamico joined the USDA in 1990, she started researching a newly discovered E. coli strain that lived harmlessly in cows’ intestines but caused terrible diarrhea and kidney failure in humans. O157:H7, as the strain is named, had picked up the code for the kidney toxin from a virus (aka bacteriophage) had the ability to invade bacteria. Meanwhile other pieces of DNA, a group of genetic recipes for increased virulence called “pathogenicity islands,” had made their way into the cell. Rather than riding in on a virus, the problematic DNA was either inserted into the cell’s chromosome or remained as DNA rings, and the codes (virulence genes) carried by this newly acquired DNA made the bacterium more dangerous.

In 1993, O157:H7 showed up in hamburger at Jack In the Box, sickening more than 600 people and killing four children. That outbreak caused the USDA to declare the O157:H7 an “adulterant” in beef, and processors and restaurants changed their practices.

As humans changed their behavior, E coli kept on switching DNA and evolving. In 2011, a batch of bean sprouts in Germany harbored a new strain of E. coli carrying a toxin and novel way to adhere to intestinal cells sickened 4,000, caused kidney failure in more than 800, and killed 53 people. That strain was resistant to antibiotics. In 2012, the USDA began testing beef trimmings for six new toxic strains in addition to O157:H7. Keeping a few steps ahead of her nemesis is Dr. Fratamico’s job, so now she’s looking into another type of E. coli that may spend time in poultry before causing urinary tract infections and pneumonia in humans. “E. coli are very intelligent about illness. They want to survive,” says Dr. Fratamico. “We’re always trying to find the emerging strains and develop methods to detect them, but they’re smarter than we are.”

E. coli’s resourcefulness, and its willingness to dance with humans in laboratories has, ironically, given us the super-human power of recombinant DNA. The lab strain K-12 was isolated from the stool of “a convalescing diphtheria patient” in Palo Alto, California, in 1918. K-12 then went to Stanford and (along with three other strains) became the pet of labs around the world, leading to 11 Nobel prizes. More importantly, scientists learned to take advantage of those Frisbee-like plasmids to insert DNA that would trick E. coli into producing useful things, including insulin that diabetics can use.

Another scientist who has revealed the powers of E. coli is Richard E. Lenski of Michigan State University. Nearly 28 years ago today, on February 24, 1988, Lenski thawed a frozen sample of E. coli from his lab’s freezer, and put 0.1 milliliter in each of 12 little flasks. Overnight, the E. coli in the flasks snarfed up all the glucose in their broth while producing seven generations of E. coli. The next day, Professor Lenski removed 0.1 milliliter again from each flask and put them in 12 clean flasks with more glucose broth. Unlike many wild strains of E. coli, the strain that Lenski studied didn’t have plasmids and phages that allow cells to exchange genes. So when he put them in their flasks it was as though he’d taken away all of their smartphones and GameBoys and other toys and left them in a bare room with only a gulp of sugary drink. Lenski hoped to see how they evolved using only random mutations and natural selection, not gene sharing. “Evolution is like a game that combines luck and skill and perhaps bacteria could teach me some new games,” he wrote. The experiment was supposed to last 2,000 generations or about a year.

But it still hasn’t stopped. Twenty-eight years and 64,000 generations later, the experiment is still going. It’s not just an evolutionary casino, though, it’s also a time machine because every 500 generations the lab froze a sample from each of the 12 vials. Lenski has always wondered what it would be like if he could bring a Neanderthal back to life and and have him try to play chess or football—these frozen samples are his tiny time travelers.

When the project started, Lenski thought that evolution would go quickly at first, as the bacteria evolved to fit into their flask-niche environment, and then plateau. But what Lenski and his team found is that the bacteria kept evolving and improving with a curve describing their fitness trending ever-upward. Evolution is a bottomless well of innovation.

And something else really interesting happened. E. coli normally lives on glucose. Every night, the growing population in the flask would gobble up all the glucose, oblivious to the fact that there happened to be another food in the broth called citrate. Lenski calls it a “lemony dessert,” and until 2003 the bacteria skipped dessert. And then in one of the 12 flasks, they had a mutation and those bacteria started sitting down to lemon merengue pie every night.

Lenski’s long-running experiment became a sort of petri dish for smart students with skills in mathematics, modeling, and genetics, drawn to his 12 flasks and thousands of frozen samples. One of them, Zachary Blount, realized that they could trace the lemony-simpatico mutation back through the frozen samples and re-evolve it. It was like they were playing Groundhog Day with the bacteria, giving the Bill Murray character chance after chance. And in the process they were able to run evolution backwards and forwards, trying to find its underlying physics.

The research is more than theoretical: the type of work that Lenski and his students and colleagues have done has helped the FBI identify genetic differences between strains after the 2001 anthrax attacks and is helping others learn how bacteria evolve in the lungs of people with cystic fibrosis.

As Lenski reflected on his years with the experiment, he said, “How exciting is life in one tiny glass flask!” That got him thinking about the teeming activity that takes place on Earth: If every human, and a lot of cows and pigs and so on, have a billion or so E. coli in our guts, then there are more than a hundred quintillion E. coli or more out there—all mutating and evolving madly, full of potential.

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