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It’s nearly here! In just over a month, my first book—I Contain Multitudes—will be published in the US, with the UK edition following shortly after. It’s about the astonishing partnerships between animals and microbes. It’s a natural history book about the hidden side to humans, wasps, squid, hyenas, beetles, koalas, worms, and more. It’s like a David Attenborough series shot through a really good microscope. You can pre-order it here.
Coincidentally, the publication date of August 9th is a fairly momentous one for me. It (more or less) marks the ten year anniversary of my career as a science writer, which began when I created this blog in August 2006. Two of my very first pieces were about microbe transplants that can make mice fat, and sexually transmitted bacteria that give superpowers to aphids; both stories feature in the book. So, in many ways, I Contain Multitudes is the culmination of not just all my reporting on this topic, but of everything I’ve learned as a writer.
If you’ve enjoyed my work over the years, I hope you’ll check the book out. Any support you can give would be greatly appreciated, whether it’s leaving reviews on Amazon or Goodreads, tweeting about it, posting on Facebook, buying copies for friends and family, or anything else that takes your fancy. But above all, I hope you like reading it; I certainly loved writing it.
Early buzz has been pretty positive. Kirkus and Publisher’s Weekly both gave it starred reviews, with the former calling it “some of the finest science writing out there” and “an exceptionally informative, beautifully written book that will profoundly shift one’s sense of self”. Wired, io9, The Week, and On the Point all listed it as one of their summer picks.
For most of human existence, microbes were hidden, visible only through the illnesses they caused. Even today, many people think of microbes as germs to be eradicated, but those that live with us—the microbiome—are invaluable parts of our lives.
I Contain Multitudes lets us peer into that world, allowing us to see how ubiquitous and vital microbes are: they sculpt our organs, defend us from disease, break down our food, educate our immune systems, guide our behavior, bombard our genomes with their genes, and grant us incredible abilities.
With humor and erudition, Ed Yong prompts us to look at ourselves and our fellow animals in a new light: less as individuals and more as the interconnected, interdependent multitudes we assuredly are. When we look at the animal kingdom through a microbial lens, even the most familiar parts of our lives take on a striking new air. We learn the secret, invisible, and wondrous biology behind the corals that construct mighty reefs, the glowing squid that can help us understand the bacteria in our own guts, the beetles that bring down forests, the disease-fighting mosquitoes engineered in Australia, and the ingredients in breast milk that evolved to nourish a baby’s first microbes. We see how humans are disrupting these partnerships and how scientists are now manipulating them to our advantage. We see, as William Blake wrote, the world in a grain of sand.
I Contain Multitudes is the story of these extraordinary partnerships, between the familiar creatures of our world and those we never knew existed. It will change both our view of nature and our sense of where we belong in it.
“Beyond fascinating. An amazing book. It’ll change the way you think about the world. It’ll change who you think you are.” —Helen Macdonald, author of H Is for Hawk
“Ed Yong is one of our finest young explainers of science-wicked smart, broadly informed, sly, savvy, so illuminating. And this is an encyclopedia of fascinations-a teeming intellectual ecosystem, a keen book on the intricacies of the microbiome and more.” —David Quammen, author of Spillover and Song of the Dodo
“A marvelous book! Ed Yong s brilliant gift for storytelling and precise writing about science converge in I Contain Multitudes to make the invisible and tiny both visible and mighty. A unique, entertaining, and smart read.” —Jeff VanderMeer, author of the Southern Reach Trilogy
“Ed Yong has written a riveting account of the microbes that make the world work. I Contain Multitudes will change the way you look at yourself and just about everything else.” —Elizabeth Kolbert, author of The Sixth Extinction
“I Contain Multitudes changes you the way all great science writing does. You become disoriented, looking at the world around you in a new way. With vivid tales and graceful explanations, Ed Yong reveals how the living things we see around us are wildly complex collectives.” —Carl Zimmer, author of Parasite Rex
“Ed Yong has done something beautiful, and unlikely: he’s rendered the unseen world of bacteria thrilling, captivating and highly entertaining. This is a much-needed guide to the hidden kingdom that dominates life on Earth. It cuts through all the hype of microbiomes with a scientifically steady hand, but told with an infectious sense of awe.” – Adam Rutherford, author of Creation
“With a simply wonderful book, Ed Yong opens the doorway to a hidden world around and inside us. He’s smart, he’s witty, and he’s at the cutting edge. You could not get a better guide.” – Tim Harford, author of The Undercover Economist Strikes Back and Messy
“This compelling and beautifully written book will change the way people look at the world around, and within, them. Certainly among the best books in an increasingly crowded field and written with a true passion for and understanding of the microbiome.” — Rob Knight, author of Follow Your Gut and professor at University of California, San Diego
“Yong has captured the essence of this exciting field, expressing the enthusiasm and wonder that the scientific community feels when working with the microbiome.” — Jack Gilbert, professor at the University of Chicago
Speaking events (details to be confirmed)
August 10th – New York, Strand Bookstore with Robert Krulwich
August 13th – New York, Festival of the Unknown with Maria Konnikova
Swordfish steaks frequently appear on menus and dinner plates around the world. But even though many people have hooked, hacked apart, and devoured these majestic fish, few truly understand their bodies. Indeed, until John Videler from Leiden & Groningen University started studying swordfish, no one knew that they had a fist-sized gland in their heads, which slathers lubricating oil over their famous pointed snouts.
Videler has been studying the physics of swimming fish for most of his career, and swordfish were particularly intriguing to him because they’re such superlative swimmers. It’s commonly said that they can reach speeds of 100 kilometres per hour (62 miles per hour), and although the provenance of that estimate is dubious, there’s little doubt that they are really, really fast. So in 1994, while teaching a diving course in Corsica, he bought a swordfish bill from a local fisherman and started studying it.
When a swordfish swims, layers of water flow along the surface of its bill. As it picks up speed, these currents threaten to break away, creating swirling areas of turbulence that increase the drag upon the animal.
But Videler found that the bill is rough, like sandpaper. This limits any turbulence to a thin layer close to the bill, and prevents the larger, destabilising eddies from forming. The bill is also pitted with small, interconnected holes near its tip, which stop water pressure from building up at the fish’s front end—again, this reduces drag by preventing turbulence.
By then, Videler was hooked. He got two more swordfish from the same fisherman, and persuaded Ben Szabo—the head of radiology at Groningen University—to put them in a medical MRI scanner. The team scanned the fish heads between 2 a.m. and 5 a.m., when the machine was available.
At first, the images were confusing and hard to interpret. But when Videler dissected the heads themselves, he noticed a large oily gland above the base of the bill and between the animal’s eyes. And sure enough, there it was on the scans.
He thought nothing of it until 2005, when a student named Roelant Snoek came to him with an interest in swordfish. Videler told him about the gland, and suggested that it might connect to the fish’s olfactory system, influencing its sense of smell. But Snoek couldn’t find any such connections.
After much frustration, he finally worked out the gland’s true purpose by accident. While taking photographs of a swordfish head, he accidentally dropped a lightbulb onto it. The bulb illuminated a web of tiny blood vessels inside its skin, and Snoek showed that these were connected to the gland. The vessels then open out into the fish’s skin via tiny pores, each just a fraction of a millimetre wide. Snoek proved this by heating the gland with a hair-dryer; once hot, the congealed oil became liquid and oozed out the fish’s pores.
So Videler thinks that the gland is yet another drag-reducing adaptation. Its oil repels water and allows incoming currents to flow smoothly over the surface of the bill. That depends on the oil staying warm, but swordfish have a solution for that, too. They have modified some of their eye muscles into heat-producing organs that warm their blood and sharpen their vision as they hunt. This same heating effect could liquefy the drag-reducing oil, allowing it to ooze out of the glands just as the fish have the greatest need for speed.
The oil might explain another weird feature of swordfish anatomy. They are among the only fish with a concave hollow at the front of their heads—an slight inward-curving bowl that, counter-intuitively, ought to increase drag. “I’ve been puzzling about that for years,” says Videler. He now thinks that the hollow is shaped so that water flowing past it creates an area of low pressure, which sucks the oil out of the fish’s gland.
If he’s right, it means that a fast-swimming swordfish automatically lubricates itself.
This makes a lot of sense, but it’s still a hypothesis. “We still have to find some way of doing experiments to visualise the flow of water [over the bill],” Videler admits. “We can’t do that on live swordfish,” since these animals are impossible to keep in captivity. But he hopes that other scientists could run fake swordfish—sandpaper skin, pores, oil, and all—in water tunnels to see how they perform.
An epidemic is moving across the United States. It has invaded 35 states and sickened 324 people, including 88 children. It has put 66 people into hospitals, and one of the sick people has died. And the Centers for Disease Control and Prevention, responding as it always does to outbreaks that menace Americans, is struggling with how to stop its advance—because the things causing the epidemic are widely distributed across the country, come from many places, and are hard to trace back to their source.
And also, are super-cute. The cause is backyard chickens.
Since January, and continuing into June, there have been seven separate outbreaks of Salmonella—each caused by a different strain of the bacterium and each stretching over multiple states, from 16 down to seven—that have been proved to originate in live chicks and ducklings bought by mail or in feed stores and kept at home or at a school.
Baby chicks and ducklings and the birds they grow into may not sound like much of a threat. But in addition to the 324 cases they have caused this year (so far; the CDC plans to update the case count in the next two weeks), backyard poultry caused 252 cases of illness last year, 363 cases in 2014, 514 cases in 2013 (including 356 cases caused by one Salmonella strain); and 334 in 2012. That is 1,757 cases in 5 years.
If that doesn’t seem like much, consider that 2013-14 saw the largest recent outbreak of Salmonella caused by raw poultry, traced back to chicken produced by the California company Foster Farms. That outbreak generated an enormous public health response, months of media coverage, and lawsuits. It caused 634 known cases. Over the same time period, backyard poultry sickened 877. Yet those illnesses seem to still be flying (sorry) under the radar.
“If you ask someone, ‘Can you get Salmonella from eating undercooked poultry?’ they are absolutely going to say Yes,” Megin Nichols, a public health veterinarian in the CDC’s foodborne outbreak response and prevention branch, told me. “But if you ask them, ‘Can you get Salmonella from touching your backyard chicken?’ they don’t necessarily know that.”
Some of that disconnect may be cognitive dissonance. People buy backyard chickens to opt out of an industrial food system they perceive as unhealthy—so it takes some mental gymnastics to confront that the birds providing homegrown eggs (and sometimes meat) might be hazardous too. But, Nichols said, it might also be lack of awareness—that Salmonella, which resides in chickens’ guts even when birds look healthy, and exits their bodies in their droppings, can spread all over them as they perch and take dust baths and preen.
“On their feet, on their feathers, on their beaks,” Nichols said. “And in the areas where they live and roam. So people are exposed when they clean the coop or otherwise maintain the poultry environment. But we also see people, especially young children, cuddling and snuggling them and kissing them.”
Finally, add in that most people don’t know Salmonella, along with other foodborne illnesses, doesn’t only cause a few days or weeks of lying flat and sticking close to the bathroom. An increasingly solid body of research links it to lifelong illnesses from arthritis to digestive problems to circulatory damage that leads to high blood pressure, kidney failure and stroke.
Casey Barton Behravesh, a veterinarian with a public health doctorate who directs the CDC’s “One Health” office, said this is a new problem. Exposure to live poultry used to be rare, and pretty predictable: It occurred when children were given fuzzy newborn chicks in Easter baskets. “Then in the early 2000s, we noticed a growing trend of more and more outbreaks occurring, not linked to little chicks and ducklings, and not among kids getting sick,” she told me. “It was adults getting sick, people who reported having backyard flocks, which was something we had never seen before.”
People are being made ill because they don’t recognize they are at risk—but the structure of the industry, and the systems set up to monitor it, aren’t helping. The federal program that surveys diseases in live chickens, the USDA’s National Poultry Improvement Plan (NPIP) was set up to protect chicken health, not human health. So it tracks Salmonella strains that make chickens sick, but not the ones that cause human outbreaks, and until recently, it focused on the vast commercial poultry trade where those strains would cause costly damage.
Denise Brinson, a veterinarian who is the NPIP’s director, told me that because of the backyard-associated outbreaks, the agency has worked with the CDC to create a program addressing small suppliers. In 2014, it began allowing hatcheries that supply the backyard trade—which sell birds to feed stores and hardware stores, as well as direct to consumers—to join a testing program scaled to the size of their businesses and to advertise that they have NPIP certification.
But to look for that, would-be poultry buyers have to know where the birds are coming from, and that turns out to be more difficult than it should be. Federal investigators including Behravesh documented in 2012 and 2014 that the process of getting chickens to market isn’t a supply chain, it’s a tangle. Birds come from 20 different hatcheries in the US, but many of those hatcheries have contract farmers doing the daily work, and then combine those clutches to make up the millions of birds they ship each year. Because some hatcheries specialize in only certain breeds, they also may “drop-ship”—buy and ship birds from other hatcheries—to make up orders as well.
And at the sales end, birds from different farms and hatcheries may be commingled in the same store pen—increasing the possibility that Salmonella can spread among them, and making traceback to the birds’ origin an extraordinarily difficult task.
All of which means the onus is on individuals to protect themselves: owners of live poultry in backyard or schools, people who visit those owners, even people who handle baby chicks in the stores where they are sold. The CDC’s advice is to keep separate clothes and shoes to wear for feeding birds and cleaning their coops; make sure anyone who touches the birds or their area washes their hands right away; and remember that, no matter how adorable they are, backyard poultry are a food source, not a pet. Despite the temptation, they shouldn’t be smooched or snuggled—especially not by young children, whose immature immune systems put them at greater risk of infection.
“We do think that raising backyard poultry can be a fun and educational experience,” Nichols said. “But it is not the right experience for everyone.”
Every year, in northern Myanmar, thousands of farmers pull tonnes of Cretaceous amber out of the ground, and send the glistening nuggets to local markets. For six years, Bo Wang from the Chinese Academy of Sciences and his colleagues have visited the markets and sifted through 300,000 of the glistening nuggets. It was a lot of work. Then again, it takes a lot of work to find animals that spent their whole lives trying not to be found.
Within the amber, Wang’s team identified dozens of ancient insects that camouflaged themselves by adorning their bodies with junk. They had short bristles and elaborate feathery tubes, onto which they stuck sand, soil, wood fibres, bits of ferns, and even body parts of other insects. They were the earliest animals that we know of to camouflage themselves, some 100 million years ago.
Many living creatures still embellish their bodies in debris. The aptly named decorator crabs, for example, look like walking bundles of algae and seaweed. The larvae of caddisflies live in tubes made of rock, sand, plants, and other underwater detritus, bound by silk. And one grisly species of assassin bug wears a coat made from the corpses of its ant prey.
VIDEO: Carrier crabs are known for toting objects around—sometimes seaweed or a broken shell, and occasionally a shield made of a live sea urchin.
The larvae of lacewings are especially prone to carrying debris. These youngsters are voracious predators of aphids and other bugs, and they in turn are hunted by wasps, spiders, and other cannibalistic lacewings. By coating themselves in trash, they gain a disguise—or, at worst, a physical shield.
This behaviour is an ancient one. In 2012, Ricardo Pérez-de la Fuente described a 110-million-year-old larval green lacewing that dressed itself in junk. Like its modern relatives, it had long legs and sickle-shaped jaws. But its trash-carrying structures were unusually elaborate: a few dozen tubes, longer than its own body, each of which branched into smaller, trumpet-shaped fibres. The creature was effectively carrying a wastepaper basket on its back. As I wrote at the time:
“De la Fuente called it Hallucinochrysa diogenesi, a name that is both evocative and cheekily descriptive. The first part comes from the Latin “hallucinatus” and references “the bizarreness of the insect.” The second comes from Diogenes, the Greek philosopher, whose name is associated with a disorder where people compulsively hoard trash.”
The creature was effectively carrying a waste-paper basket on its back.
At the time, the Hallucinochrysa was a singular oddity. “[The amber piece] is not well-preserved, and the insect is not complete,” says Wang. “Some people think that there isn’t robust evidence to support its camouflaging behaviour.” He begs to differ. His team has now identified 39 similar specimens, including 34 from Burmese amber and five others from French and Lebanese samples.
Two of them, both green lacewings, share the same extreme structures as Hallucinochrysa: elaborate baskets of tubes sprouting from their backs. One of the larvae was carrying the remains of other insects in its basket. These were likely its prey: lacewing larvae inject their victims with a liquefying saliva and then suck their juices out, leaving behind an empty husk. They then use their long jaws to place the bodies on their backs, and become wolves in sheep’s clothing. The ancient lacewings probably did the same.
The other specimens belonged to three different families of insects—two groups of lacewings, and one lineage of assassin bugs. Much like their living counterparts, they used short hairs on their flanks and backs to entangle a wide range of debris, including sand grains, bark pieces, and scorpion fragments. They carried fern hairs, too. Specifically, they carried hairs from a group of ferns that specialised in re-colonising forests that had been scorched by fires. As I wrote at the time of Hallucinochrysa’s discovery:
“Ironically, those same fires would have stimulated the trees to produce more resin, which would have trapped many an insect in liquid tombs that eventually fossilised into amber. Hallucinochrysa may have blended into the forest of its time, but its beautiful remains tell us a surprising amount about what those forests were like. And the forests, in turn, set up the perfect conditions for Hallucinochrysa’s body to endure to this day.”
There he sits, unnoticed, at the edge of Central Park: a flop of hair across his forehead, chin up, eyes blazing. He doesn’t have a body, just a torso resting on a pedestal that says, in simple, bold block letters: HUMBOLDT. No first name, like he’s that famous.
Humboldt? Humboldt who? About 150 years ago, that was like asking Madonna who? Or Beyonce who? Or Napoleon who? Everybody knew. He was spectacularly famous.
On September 14, 1869, though he’d been dead for ten years, all over the world people celebrated his 100th birthday: In Alexandria, Egypt, there was a fireworks display. Crowds gathered in Melbourne, Adelaide, Moscow, and Mexico City. In Berlin, the day was declared a local holiday and—in the rain—80,000 people showed up to salute him. In America, 15,000 gathered in Syracuse for a mile-long parade, and President Grant attended a Humboldt birthday in Pittsburgh with 10,000 people.
… the cobbled streets were lined with flags, City Hall was veiled in banners and entire houses had vanished behind posters bearing Humboldt’s face. Even the ships sailing by, out on the Hudson River, were garlanded in colourful bunting …
… and that afternoon, 25,000 onlookers came to watch the new bust—the one that now stands on 77th Street and Central Park West, the one nobody notices today—get unveiled. Humboldt, even dead, was that big.
So who was he?
Alexander Von Humboldt, born in Prussia, was an explorer who climbed the Alps and the Andes, sailed up the Amazon and Orinoco rivers, criss-crossed Siberia, but more than his feats of daring, more than his studies of gasses, magnetism, stratigraphy, his greatest gift was to describe what he’d seen. His books, his drawings, his vivid tales of adventure were so popular, that schoolkids knew him, and his lectures were packed.
His five-volume masterpiece, called Cosmos, argued that deserts, mountains, and forests, as different as they look, operate by the same rules, and that the Earth was a unity, a single ecology. His fans included Jefferson, Bolivar, Goethe, Darwin, Emerson, Thoreau, Whitman, Edgar Allan Poe. The composer Berlioz called his writing “dazzling.”
And then, having reached the peak, a world-wide celebrity, you can almost hear a long, deep ‘pffffffffftttt’ as his fame began to leak away, until many, many decades later, the deflation complete, we find him on a street corner, a quiet hunk of bronze next to a weekend hot dog stand.
Fame is a funny thing.
Every century has its celebrities who spark, fizzle, and vanish. But the thing about Humboldt is that he was prescient, important, the sort of granddaddy of ecological science, and yet, so many of the famous men who praised him are still famous, highly recognizable names and faces, and him—not.
Is there something about science fame that’s different? There are, of course, the immortals: Galileo, Copernicus, Newton, Darwin, Einstein. Einstein we can see when we hear his name. There’s his hair, the photo of him sticking out his tongue.
The other giants are pre-photography, so if I say “Newton,” you might picture an apple falling, but maybe not a face.
Statesmen get their faces on coins. Scientists don’t have to be visible. They can be represented by ideas: Copernicus by a sun surrounded by planets, Darwin by that progression of apes. You don’t have to know what scientists look like to honor them. You can even use an imposter.
Case in point (and this one is a whopper).
In 1900, chemists from all over the world decided it was time to celebrate Antoine Lavoisier, the “Father of Chemistry,” with a statue in Paris. Lavoisier—who had named oxygen, designed the metric system, and discovered the idea of conservation of mass—had also been guillotined during the French Revolution. And now, more than a hundred years later, his fans thought, let’s rehabilitate our man, give him a statue.
Money was raised. The French government put up 50,000 francs; the tsar of Russia made a big contribution. Small donations poured in from all over ($580 from the U.S.); the statue was commissioned, cast, and unveiled. And so Parisians got their Father of Chemistry, arm outstretched, in front of the Eglise de la Madeleine, near his old Parisian home.
Except—someone noticed, that wasn’t Lavoisier. By some error, the sculptor of the piece had mistakenly copied the face of another Frenchman, the mathematician and philosopher Marquis de Condorcet, so that was Condorcet’s head, not Lavoisier’s, looking out at the city. Wrong guy.
What to do? No one had the money to make a new statue, so Paris shrugged, and the while the pedestal said, this is Lavoisier, the statue said no, I’m not—and life went on.
But there’s more. The Marquis de Condorcet didn’t have a good French Revolution either. He was imprisoned and died, probably poisoning himself rather than face the mob. His granddaughter was doing some housecleaning later, and offered a small bust to an American diplomat who worked for Thomas Jefferson. The bust, presumably of M. Condorcet, was sent to the American Philosophical Society in Philadelphia, where it was proudly displayed …
There it sat for more than a hundred years, until a curator from the Louvre, the French museum, happened to be visiting Philadelphia, saw the bust, and said, hey, that’s not Condorcet.
His hosts said, well, who is it then? He recognized the face from sculptures and paintings: That’s Antoine Lavoisier, the father of chemistry.
This shouldn’t have happened. After all, if you look at the two men, Condorcet is kinda pudgy, ruddy cheeked, with a prominent bump on his nose. Lavoisier (on the right ) is thinner, his nose sharper, more imposing. They don’t look the same.
But maybe that’s the point. Who cares what scientists look like? It’s their ideas that matter; their discoveries, not their faces. I wouldn’t expect to recognize the Marquis de Condorcet or Antoine Lavoisier or Alexander von Humboldt—heck, I can’t tell Madison from Monroe, but I am a little surprised the the name Humboldt rings so few bells these days.
After all, Humboldt’s big idea, that our planet, for all its differences, is a single complex ecology—vulnerable, fragile, precious—was a bold idea in the 1840s, and is even more important now. Maybe it can’t be summarized in a simple image—a falling apple, or a parade of apes, (though Carl Sagan did a pretty good job with his “little blue dot”)—but Humboldt deserves better.
And who knows? The tide can turn. Reputations bounce back. There’s a new Humboldt biography out. It was a New York Times ‘top ten’ book of 2015; plus he’s got a 250th birthday coming up in 2019, so his name may get a bit more buzz, and if buzz creates buzz, I can imagine a few years from now, instead of saying “Let’s meet on 77th by the hot dog guy,” folks might say, “Let’s grab lunch next to the Humboldt statue …”
… and when that happens, I will be smiling a very quiet smile.
The scientists who this week reported dangerous drug resistance in seagulls aren’t the only researchers looking for mcr-1, the gene that confers protection against the last-resort antibiotic colistin.
Since the discovery of the gene was announced last November by English and Chinese researchers, microbiologists the world over have been scouring their “collections”—the thousands (or more) of bacterial isolates they keep in frozen storage—to see whether the sample banks contain any evidence that the gene has passed through. Almost 100 instances of finding the gene have been announced, many of them out of such collections, some from five or more years ago—and that has researchers quietly convinced that more are coming, and that MCR resistance may be more widely distributed than we know.
If their hunch is correct, then that would be trouble. MCR resistance resides in gut bacteria, chiefly E. coli, and can lurk in the intestines an undetermined period of time. Someone who unknowingly carries the bug could pass it to others in a chain of transmission that would go undetected until, in some unlucky person, an infection blooms.
Last weekend, MCR and the urgency of determining how far it has spread was the talk of the hallways at ASM Microbe, the largest infectious-disease conference of the year. During the conference, I grabbed some time with Barry Kreiswirth, a professor of medicine at Rutgers University and founding director of the Public Health Research Institute Center there. In the 2000s, Kreiswirth’s lab led the discovery of the last wave of dire superbugs to hit the United States: a form of the bacterium Klebsiella pneumoniae known as KPC because it was resistant to the formerly last-ditch drugs carbapenems. (Losing carbapenems made medicine take colistin, a very toxic antibiotic, off the shelf where medicine consigned it in the 1950s.)
Kreiswirth and his lab have made three of the almost 100 MCR discoveries made so far, all in China thanks to Chinese collaborators. They are now searching their collections to see whether there are domestic discoveries to be made. (I edited and condensed our conversation.)
Maryn McKenna: You’re very accustomed to superbugs. Tell me why, from your perspective, the arrival of mcr-1 is alarming.
Barry Kreiswirth: The problem with resistance such as KPC, and now MCR, is that the resistance DNA is on mobile elements, plasmids. That’s a whole different game from stopping the spread of an infection from one person to another. Plasmids move. They move from one strain to another. They move from one bacterial species to another. You can have a person that has an E. coli and a Klebsiella in their gut, and those bacteria will actually swap their plasmids, from E. coli into Klebsiella and vice versa. Trying to control that type of epidemic is completely different. We don’t have a strategy, because you can’t stop plasmids moving.
MM: You have begun looking for this already?
BK: We have published three papers. The most striking one was, we had a colleague from China in my lab who, when he went back to China, took out any colistin-resistant strains and screened them for the presence of mcr-1, and found it. Now everyone is looking for mcr-1 genes retrospectively, and finding them. That means that there’s probably a fairly large reservoir out there of strains carrying mcr-1. But we don’t have a clue how big that reservoir is. We don’t know how much, we don’t know where. Why is this concerning? Because colistin, even though it’s not a very good drug, it’s still one of our salvage drugs for carbapenem resistance. If we lose that, we’ve lost another antibiotic, and we don’t have many. You know the old joke, the horse is out of the barn. In this case, the pig’s out of the barn.
We don’t have a clue how big that reservoir is. We don’t know how much, we don’t know where.
MM: Because the resistance originated with pig farms.
BK: China uses colistin in animal feedlots—which is sort of the history of antibiotic resistance; in the U.S. as well as in Europe, we have a history of using antibiotic remnants in animal feed, so that story is not new. But the Chinese don’t use colistin to treat [humans]. And because they don’t use it, they don’t test for resistance to it. The problem is, this is a global community, and other people do use colistin [in human medicine]. And you can’t stop strains or people moving from China to elsewhere.
MM: Where do you think the biggest concern should be now?
BK: My doomsday scenario is that someone in medicine is going to start thinking, Do we do high-risk procedures? Some of what we do now is remarkable. If you ever talk to the guys who do bone-marrow transplants, God. As one doctor said to me, “We kill the patient and then bring them back to life.” If 50 percent of liver transplant patients die of a bacterial infection, what’s the point?
MM: Aside from searching the bacterial collections that you hold—which by definition is looking backward, to when the samples were taken—what else could be done to define how much trouble we’re in?
BK: We don’t do a good job of screening healthy people [for pathogens], mainly because people don’t want to fund it. I would love to have a project where we could start screening. But those are difficult studies to do. They’re hard to get funded. There are a lot of logistics. For an example, my wife’s a nurse practitioner, and we tried to do a study of the prevalence of community-acquired MRSA. We made an attempt to go to doctors’ offices. But how do you do an [institutional consent] with 50 different offices? And then [obtain consent from] every patient that walks in? No one’s paying them to do that. For MCR, we hope to be able to screen liver transplant patients, bone-marrow transplant patients. When you consider how much those procedures cost, additional screening would be trivial. So that’s one intervention I think we could do.
A superbug that’s resistant to the absolutely last-ditch antibiotic colistin has been reported in seagulls on two continents—pinpointing one way, though almost certainly not the only way, that this dangerous drug resistance is moving around the world.
Since last November, when researchers in England and China announced the discovery of bacteria able to survive colistin, there has been an explosion of people looking for that resistance, and finding it. Scientists have published almost 100 reports of colistin resistance—known as MCR and conferred by a gene that’s been dubbed mcr-1—in almost two dozen countries.
It has been found in human patients, including a woman in the United States in May; in livestock, which get the drug on intensive farms, and are probably the original source of the problem; and even in pets.
Now, in letters to the Journal of Antimicrobial Chemotherapy, two research teams in Lithuania and Argentina report that they trapped birds and swabbed their butts, or scooped up seagull droppings, and found the resistance-conferring gene in E. coli being carried by two species: herring gulls in Lithuania (Larus argentatus) and kelp gulls in Argentina (Larusdominicanus).
Both teams think the birds probably picked up the resistant E. coli by eating garbage, which may have contained sewage or medical waste. (The organisms in the South American gulls also contained another important type of antibiotic resistance, known for short as ESBL.)
This isn’t the first time that gulls have been identified as possible carriers of antibiotic-resistant bacteria. In 2011, French researchers found multi-drug resistant E. coli in seagull droppings in Miami Beach, and those researchers and others earlier found resistant bacteria in gulls in Portugal, France, Russia, and Greenland.
The point in all those stories, as well as in the new reports, is that gulls migrate, from hundreds to thousands of miles depending on the species—so they could serve as a vehicle for carrying resistant bacteria somewhere new.
Gulls migrate, from hundreds to thousands of miles, so they could serve as a vehicle for carrying resistant bacteria somewhere new.
“The lifestyle of gulls allows them to carry and disseminate pathogenic and resistant microorganisms despite country borders,” the Lithuanian researchers say in their report. “Water contaminated by feces of birds should be foreseen as an important risk factor for transmission of resistant bacteria.”
The undetected movement of bacteria is especially important in the case of MCR, because the discovery of colistin resistance is truly alarming. Colistin is an old drug that medicine consigned to the back of the shelf in the 1950s because it is toxic, and only recently started using again because so many other antibiotics have been undermined by overuse in medicine and agriculture.
The gene that creates colistin resistance is on what is called a plasmid, a loop of DNA that isn’t bound up in chromosomes but can move easily between bacteria. That has scientists worried that the gene could move into disease organisms that already possess resistance to other antibiotics, creating a superbug that would be completely untreatable.
So far, mcr-1 has been found in the United States three times: in two stored samples from slaughtered pigs that were stashed in a U.S. Department of Agriculture database, and in a 49-year-old woman in Pennsylvania, not identified by name, who went to a clinic for help with a urinary tract infection.
At a meeting Tuesday afternoon in Washington, D.C., of the Presidential Advisory Council on Combating Antibiotic-Resistant Bacteria, federal officials relayed that the woman has recovered from her infection, but still continues to carry the highly resistant bacterium in her system. Dr. Beth Bell, director of the National Center for Emerging and Zoonotic Diseases at the Centers for Disease Control and Prevention, also said that 99 of the woman’s family members and close contacts have been checked, and none of them are carrying bacteria containing mcr-1, reinforcing the mystery of how the resistant bacteria reached her.
Bell and representatives of the U.S. Department of Agriculture said the gene remains rare in the U.S.: The CDC has checked more than 55,000 stored samples collected from patients, animals, and food, and the USDA is checking 2,000 additional samples that it has stored. So far, that search has revealed only the two samples from pigs that were slaughtered in Illinois and South Carolina.
The officials commenting Tuesday agreed that there may be no way of tracing the path that MCR took to reach the U.S.—the bacteria may have spread from another person, or on food—and that the key thing now is to build surveillance systems that alert health planners as it moves.
“The good news is we found it,” observed Dr. Martin Blaser, a professor of medicine and microbiology at NYU Medical Center and chair of the Presidential council. “The bad news is, it’s here.”
Here’s the footprint of an Earthling a long, long way from home.
You know the one—it’s Neil Armstrong’s boot print on the surface of the moon. “A giant leap,” he called it. Well, here’s another leap—arguably just as “giant,” though a touch more obscure. It was discovered in a dark slab of rock that hangs on the edge of the North Atlantic in a remote corner of Newfoundland …
It’s an impression left by another Earthling, an odd-looking ocean dweller that lived roughly 565 million years ago and that was maybe the first creature—certainly the first we know of—to use its own muscles to move from where it was to someplace new.
We call them Ediacarans, or more properly, ‘ediacaran organisms’. They’re a weird family, some flowerlike, some like little plops of mud, this one a little like a palm leaf or maybe a ribbed pancake …
“… did something virtually unprecedented on this planet—it shivered, swelled, reached forth, scrunched up, and in doing so, at an imperceptibly slow pace, began to move across the sea floor, leaving a trail behind it.”
The path it carved that day in the ocean mud—now frozen and fossilized—is the oldest trail we’ve ever seen on Earth, laughably small compared to Neil Armstrong’s journey, but it’s The Beginning, our beginning, the very first evidence of animal-like locomotion.
A volcano must have poured lava on a patch of ocean millions of years ago, freezing every living creature in place, until slowly the earth shifted, and the rock layer surfaced, then got sculpted and exposed, so now if you go to Mistaken Point on the Newfoundland coast, you can see scores of them, fern-like, blob-like, pancake-like …
This is a famous site, well-known to fossil hunters. But, as sometimes happens, new eyes can find what everybody else missed, and when a young paleobiologist from Oxford, Alexander Liu, came by in 2008 and scrunched down to see what he could (this is him lying sideways on the rocks, shoes off, booties on to protect the fossils) …
… he noticed what first looked like a slime trail, a thumb-wide path that crossed the rock surface …
Moor visited more recently, and when he ran his fingers over this same fossil pathway (there were a bunch of them on those rocks) he wrote, “They bore the distinct texture of life. Their surface was patterned with a series of nesting arcs: ))))))”
You can see these clearly at the upper end, but they’re in the middle too …
Those may be the traces of a suction cup foot that these creatures probably used to fasten themselves to rocks or flat surfaces on the ocean bottom. Sea anemones behave that way today: They latch onto flat ground but occasionally pry themselves loose and take lumbering “steps” when it’s time to travel.
In 2009, Alexander Liu and colleagues wrote a paper suggesting that these ancient creatures were not floating or squirming or rolling or reaching. No, they were “crawling.” These were primitive proto-steps, and you can see each step as a series of nesting parentheses.
Critics said they could just as easily be tracks made by pebbles tossed by waves, but when the experts looked, most concluded Liu is right. Those aren’t pebble tracks. Those are trails—our earliest evidence of locomotion, of life on the move.
Why Go Anywhere?
The question is, Why bother? Why move?
Were they hunting food? Looking for sex? Fleeing a predator? Or—and here I get back to Neil Armstrong—were they just on a walkabout, wondering what lies beyond the next hump of sand?
There wasn’t a lot going on in the ocean 565 million years ago. The Earth was recovering from a deep chill that left the sea bottoms, Moor writes, “devoid of predators,” empty-ish. Same for the sea. There wasn’t much to look at: “Perhaps a primitive jellyfish would have passed overhead like a living cloud.”
With no pressing reason to move about, I’m thinking that maybe what pushed these pioneers to travel was (how to put this?) a touch of restlessness, a behavior that would be passed down the great chain of life as animals moved in greater arcs, butterflying their way to Mexico, flying from Canada to the tip of Argentina, circumnavigating the globe, lifting off the planet, and, ultimately, landing on the moon.
That’s why we move, I like to think: to see, to stretch, to have more choices.
But when Moor asks this same question (“Why do we, as animals, uproot ourselves and go somewhere else?”) he doesn’t go to restlessness. The creatures that invented locomotion, paleobiologist Liu tells him, probably wanted security—a clean, flat surface to cling to. Surfaces crack, shift. When life becomes too hard where you are, you go to where it’s easier.
They didn’t want adventure, they wanted comfort.
The two explanations sound opposite, but they’re not. No place stays safe forever, not even our little blue planet. At some point, out of restlessness or desperation, it doesn’t matter which, you have to do that thing that the pancakes invented 565 million years ago—you don’t have a choice. Nature knew that early. So Earthlings learned it early.
You either move—or you die.
So we moved. And we never stopped.
Robert Moor’s new book On Trails: An Exploration(it will be out in a few weeks) is a meditation on paths—not just the paths that ancient creatures made, but also ant paths, elephant paths, footpaths, the paths in our brains and in our machines. Moor, a guy who likes to walk, does the full Appalachian Trail from Georgia to Maine, walks along highways, loses a trail full of sheep, messes with ants, befriends all sorts of fellow walkers, and as he wanders, he wonders how paths form, change and last. Hanging with him you meet a host of different byways, get in (and out) of trouble and the experience is not just enlightening, it’s sweaty, hot, cold and … well, to say it plainly … fun.
How does a frog save itself when it hasn’t even been born?
Every red-eyed tree frog must confront this dilemma. The frogs lay their eggs on plants that lie over ponds. After a week, the tadpoles hatch and drop into the water—at least in theory. In practice, many of the defenceless, immobile, exposed, yummy eggs are devoured by snakes or wasps. Fortunately, they have a solution: super-fast hatching.
WATCH: These red-eyed tree frog tadpoles quickly hatch to escape a parrot snake’s appetite.
For most frogs, hatching is a slow process. The tadpoles release enzymes that break down the jelly coatings of their eggs over the course of several hours. But red-eyed tree frog eggs can hatch in seconds, if the need arises. Karen Warkentin discovered this ability in 1995, and she has spent the last 20 years exploring it. She has shown that the frogs can hatch early to escape snakes, wasps, flooding, drought, and infectious fungi.
The trick comes at a cost: the premature hatchlings are smaller and more vulnerable to threats in the water, but at least they survive aerial dangers some 80 percent of the time.
That explains why the frogs have evolved their rapid-hatching trick, but not how the trick works. Throughout her work, Warkentin didn’t know. She assumed that since the process was so fast, the embryos couldn’t be releasing enzymes as other frogs do. Instead, by thrashing about inside the egg, they were probably strong-arming their way out.
To see exactly what they do, graduate student Kristina Cohen filmed the youngsters using a high-speed video camera. On the slowed footage, she noticed that an embryo can create a hole in its egg without touching anything. It starts shaking, while opening and closing its mouths. Soon, fluid starts to leak from the part of the egg directly in front of the embryo’s snout. It then lodges its snout against the point of rupture, and expands it by wriggling, eventually propelling itself through.
To confirm that the whole sequence begins without contact between the tadpole and its egg wall, Cohen waited until the embryos started to shake, and then turned them around inside their eggs by nudging them with a blunt rod. Even though they had moved, the rupture would form at the place where their snouts used to be.
The frogs, it turned out, were using enzymes after all. But rather than releasing those enzymes gradually, they stockpile their supply. By studying the embryos under a powerful microscope, Cohen found that they have a dense cluster of glands in their snout. Each is full of small packets that contain egg-dissolving enzymes. When danger threatens, the embryos can release these all at once, pressing fast-forward on the hatching process.
“They could do it in six seconds,” says Cohen—and in other experiments, “we’ve recorded them getting out in less than that.”
This is one of several studies showing that embryos are not just passively awaiting their emergence into the world. They are already part of it.
There it is, at the edge of my yard, struggling. It’s only one, maybe two feet tall, with a single pair of leaves—a baby maple sapling, so skinny, so fragile, and yet… little plants get help, and not only from the soil below and the water nearby.
The truth is much more startling, and more marvelous, than that. In his classic book The Trees in My Forest emeritus biology professor Bernd Heinrich describes how plants—especially in springtime—are fed, literally, by the whole planet. Think of a giant spoon stretching across continents, spilling nutrients into hopeful little startups.
I’m not crazy. Here’s what Heinrich says is happening.
In April, May, and early June, if you look very closely, you’ll notice that the branches of any little sapling are getting a bit longer—a smidgen of an inch higher—as it climbs toward the sun. It’s adding new wood cells to itself, long, narrow cells called tracheids. The cells vary in size depending on the species of tree, but they look roughly like this:
Wood cells form long chains that sit side by side … like this …
It’s the pace of the cell-building that made my jaw drop. Springtime is the growing season, and a plant gets taller like a tower does, by adding units, brick by brick, or, in our sapling’s case, wood cell by wood cell. Wood cells are small, and parts of a wood cell are even smaller, so they have to be manufactured fast—and furiously.
There are ten million bricks in the Empire State Building. Plants use sugar molecules instead, strung together in chains. There are about two billion cellulose (sugar) chains in a single wood cell, each composed of a thousand sugar units. That means every wood cell has (two billion times a thousand) two trillion sugar molecules. That’s a lot of bricks to make—and the plant has to work fast. Very fast. All around it, other trees are about to leaf out, blocking out the sun. Spring is its big, short chance for light, so the pace turns frantic.
In a 30-day period one wood cell will add an average of 2 x 10,000,000,000,000 sugar units, which works out to 771,600 sugar units per second (2,592,000 seconds/30 days) per wood cell.
Let me say that again: 771,600 units, every single second.
Now let’s get even smaller—let’s count atoms. How does a plant make sugar? Basically, it eats air.
Our atmosphere is rich with carbon dioxide. So imagine a bunch of carbon dioxide molecules floating by a leaf. The leaf opens its pores, the CO2 drifts in, and then, powered by sunshine, it re-engineers a bunch of molecules, splitting water, rearranging atoms, building new sugars, and spitting oxygen back into the air.
So our plant is harvesting raw carbon straight out of the air, then building carbon molecules. Each one requires six atoms. Count them if you like.
So, mathematically, if our plant is building 771,600 carbon molecules per second, six atoms per molecule, that means that the little sapling at the edge of my yard in springtime is chomping down 4.6 million carbon dioxide molecules every second! For 30 straight days!
“These staggering numbers suggest a story,” Heinrich says in his book.
The carbon dioxide wafting in the air outside your window right now could come, literally, from anywhere on the planet. The total mass of the Earth’s atmosphere is about 5.5 quadrillion tons, and it’s all in motion, sweeping, Heinrich says, “across the continents in a matter of days.” The breeze on your cheek right now might include atoms that two days ago were crazily distant. Just take a look at this beautifully rendered animated wind map from NASA’s “Dynamic Earth: Exploring Earth’s Climate Engine.”
With air moving so freely and so swiftly, Heinrich imagined that the newest wood cells in his garden (“say in a twig of a maple seedling next to my cabin”) might have been built from molecules that only a day or two earlier had been in exotically different places, like say, from “a decaying log in the Amazon … ”
… or from a car on a distant freeway …
… or from a coal-burning plant far away …
… or from a hornbill exhaling somewhere in Asia …
… or from a baboon exhaling through it’s magnificent (and pipelike) nose in Africa …
And now, entirely by chance, they find themselves plucked from the moving air and strung together in a conga line made by a baby maple in a North American garden, hanging at the far end of a freshly growing twig.
And there they will stay for, well, maybe 100, 150 years, surrounded by more plucked atoms, stuck in place as the branch of a maple tree, until one day, the tree topples over or the branch drops to the ground, the beetles and fungi move in and munch those atoms apart so they become soil or beetle droppings and then, after a long while, take to the air again. It’s a slow dance, but as Heinrich says, every tree in every garden is a soup of earthly air frozen into wood cells. “Each wood cell of every tree in my forest is in a give-and-take with the rest of the world.”
Or as I put it: Every plant breathes in the whole planet.
Bernd Heinrich has written of woods, trees, buds, seasons, and the animals that live around his cabin in Maine. The Trees in My Forest, published in 1997, is now a classic. The math in this column comes from Heinrich. He has written many books since then.
Wood cells, or tracheids when they form, are thick with sugars, but when the cells mature, they hollow out, leaving only the cell walls. These are aligned, end to end, forming continuous tubes for fluids to flow through. I wrote not so long ago about how forests scrub our planet’s atmosphere every year of much excess CO2, which is a very different and equally beautiful planetary dance, and you can find that blogpost here.
In the early 19th century, coal-fired factories and mills belched a miasma of soot over the English countryside, blackening trees between London and Manchester. The pollution was bad news for the peppered moth. This insect, whose pale speckled body blended perfectly against the barks of normal trees, suddenly became conspicuous—a white beacon against blackened bark, and an easy target for birds.
As the decades ticked by, black peppered moths started appearing. These mutants belonged to the same species, but they had traded in their typical colours for a dark look that once again concealed their bodies against the trees. By the end of the century, almost all the moths in Manchester were black.
As British air became cleaner and trees lighter in colour, the black moths faded back into obscurity. But in their brief reign they became icons of evolution. As geneticist Sewall Wright put it, they are “the clearest case in which a conspicuous evolutionary process has actually been observed.”
The story has endured a fair amount of controversy. Creationists asserted that the blackening of the moth was just a case of shifting gene frequencies rather than an outright change from one organism into another, ignoring that the former is the very definition of evolution. They also seized onto technical disputes between scientists themselves, over whether the moths’ colours really made any difference to their vulnerability to birds. The latter dispute was resolved through some groundbreaking experiments by the late Michael Majerus.
And now, Arjen van’t Hof and Pascal Campagne from the University of Liverpool have strengthened the peppered moth’s iconic status even further by identifying the gene behind its classic adaptation. And in a wonderful twist, the gene turns out to be a jumping gene—a selfish bit of DNA with the power to hop around its native genome.
Back in 2011, the Liverpool team, led by Ilik Saccheri, bred and compared dark and light moths to identify the gene or genes responsible for the shadowy look. They narrowed their search down to a small section of the insect’s 17th chromosome—one containing 13 possible genes. Since then, having studied more moths, they’ve homed in on one particular gene called cortex.
In almost all the dark moths, the cortex gene contains a unique stretch of DNA that’s missing from all the light individuals. It has all the hallmarks of a jumping gene, including the ability to make an enzyme that cuts it out of its original location and pastes it elsewhere. The moth’s genome contains up to 255 copies of this gene, which the team calls carbonaria. It clearly gets around a bit.
And on one particular jump, it landed in the middle of cortex. This fateful event, which nestled one gene (carbonaria) within another (cortex), is what darkened the moth’s body. Van’t Hof and Campagne estimate that it probably happened somewhere around 1819—a couple of decades before entomologists first saw the dark moths in the wild.
The timing fits, but other details are less clear. For example, how exactly did carbonaria cause the dark colours? Genes encode instructions for building proteins—tiny biological machines that perform various jobs around an animal’s cell. You might guess that carbonaria changed the instructions in the cortex gene, leading to the production of a different protein with new capabilities. But not so—the jumping gene actually landed in a part of cortex that gets discarded, and never contributes to building proteins.
Rather than changing what the cortex gene built, the team suspects that carbonaria changed when and where it is activated. Indeed, with the jumping gene in place, cortex switches on very strongly at the point in the larval moth’s life when it starts producing its adult wings. It’s unclear why that happens, or how it leads to dark wings, but for now, it seems that cortex affects the development of wings and that carbonaria changed how it did its job.
Indeed, in a separate study, Nicole Nadeau and Chris Jiggins from the University of Cambridge showed that cortex controls the patterns of the beautiful Heliconius butterflies, probably by influencing the development of their wing scales. By fiddling with this gene, natural selection has repeatedly tweaked the palettes and patterns of insects.
The alarm over the arrival of a grave new superbug in the United States is obscuring part of the story that is crucial to understanding what might happen next. Here it is: The woman who was carrying an E. coli containing resistance to the last-resort antibiotic colistin went for medical care because she had what felt like a routine urinary tract infection, a UTI for short.
The discovery of colistin-resistant bacteria is worrisome: Researchers have been watching for the arrival of this new superbug for several months. But that it was found in urine sample puts the discovery into a larger context. Highly drug resistant urinary tract infections happen potentially hundreds of thousands of times a year just in the United States. A small, dedicated corps of researchers has been trying for years to emphasize that these infections represent a serious danger, an unexamined conduit of bacterial resistance from agriculture and meat into the human population, and have mostly been dismissed.
Now that the new-new superbug has thrown light on the problem, will someone listen?
The Centers for Disease Control and Prevention weighed in Tuesday with a statement and a press briefing with health officials from Pennsylvania, where, last week, military researchers said they found the mcr-1 gene in an E. coli bacterium carried by a woman living there.
There are up to 8 million urinary-tract infections in the U.S. each year, and probably at least 10 percent, or 800,000, are antibiotic-resistant.
The MCR gene is important because it represents a breach in the last line of antibiotic defense: It confers protection against colistin, one of the oldest antibiotics out there, and one of the few that continues to work even against bacteria that resist multiple other drugs. Colistin was seldom used in people until recently because it is toxic, but agriculture has been using it enthusiastically for decades, which has seeded resistance through the bacterial world.
And those highly drug-resistant bacteria are turning up in urinary-tract infections. Why UTIs? Because E. coli bacteria are carried in feces, which can easily spread to the urethra and cause urinary-tract infections, especially in women. I’ve written about this several times; the long version in MORE magazine, and, even longer, in a collaborative investigation between the Food and Environment Reporting Network, the Atlantic, and ABC News.
The short version is this: Up to 8 million urinary-tract infections occur in the United States each year, and each year, a growing and significant proportion—hard to measure, but probably at least 10 percent, or 800,000—are antibiotic-resistant.
This has been happening with such frequency that it has actually changed medical practice. Medical specialty societies have been advising doctors for several years now that they should always do a test to determine which antibiotic will work for a UTI, rather than prescribing based on a standard checklist.
But only a few researchers have investigated why that tide of resistance is rising. What they have found is that these resistant UTIs infections are not random and singular, but instead constitute a focused epidemic, caused by particular sets of E. coli that bear the same resistance signatures as ones found in meat animals given antibiotics.
This idea has had difficulty gaining traction, because UTIs are usually dismissed as a minor problem, something that causes a few days of annoyance and requires a few days of antibiotics to fix. (And, not coincidentally, because they overwhelmingly happen to women.) But when UTIs go untreated—which is effectively what happens when the antibiotic administered for them doesn’t work —they climb up the urinary system from the bladder, into the kidneys, and thence into the bloodstream.
At that point, the minor problem becomes literally life-threatening. And resistant UTIs are not only a problem for the individual sufferer: They also pose the possibility of infecting others, if the original victim goes into a hospital for treatment and carries the resistant organism unrecognized in their system.
One reason it has taken so long to recognize this problem is that there is no single surveillance network that could capture all the resistance patterns in all those UTI sufferers, and compare them. There is also the problem of belief: It’s just difficult to imagine that something as minor as a UTI could be the signal of something as grave as a widespread epidemic.
Because of that, the MCR finding in Pennsylvania could end up being fortunate—no only for detecting a grave development early, but also for shining a light on a danger that has been growing, unrecognized, for a while.
“Stung by a tarantula hawk wasp? The advice I give in speaking engagements is to lie down and scream.” Justin Schmidt, creator of the Schmidt Sting Pain Index, has written a book and it sounds amazing.