Unnatural Selection: How We Are Changing Life, Gene by Gene

Unnatural Selection: How We Are Changing Life, Gene by Gene

by Emily Monosson


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Gonorrhea. Bed bugs. Weeds. Salamanders. People. All are evolving, some surprisingly rapidly, in response to our chemical age. In Unnatural Selection, Emily Monosson shows how our drugs, pesticides, and pollution are exerting intense selection pressure on all manner of species. And we humans might not like the result.

Monosson reveals that the very code of life is more fluid than once imagined. When our powerful chemicals put the pressure on to evolve or die, beneficial traits can sweep rapidly through a population. Species with explosive population growth—the bugs, bacteria, and weeds—tend to thrive, while bigger, slower-to-reproduce creatures, like ourselves, are more likely to succumb.

Monosson explores contemporary evolution in all its guises. She examines the species that we are actively trying to beat back, from agricultural pests to life-threatening bacteria, and those that are collateral damage—creatures struggling to adapt to a polluted world. Monosson also presents cutting-edge science on gene expression, showing how environmental stressors are leaving their mark on plants, animals, and possibly humans for generations to come. 

Unnatural Selection is eye-opening and more than a little disquieting. But it also suggests how we might lessen our impact: manage pests without creating super bugs; protect individuals from disease without inviting epidemics; and benefit from technology without threatening the health of our children.

Product Details

ISBN-13: 9781610914987
Publisher: Island Press
Publication date: 10/28/2014
Pages: 200
Product dimensions: 5.90(w) x 9.00(h) x 0.90(d)

About the Author

Emily Monosson is an environmental toxicologist, writer, and consultant. She is an adjunct professor at the University of Massachusetts, Amherst, author of Evolution in a Toxic World: How Life Responds to Chemical Threats, and the editor of Motherhood, the Elephant in the Laboratory: Women Scientists Speak Out.

Read an Excerpt

Unnatural Selection

How We Are Changing Life, Gene by Gene

By Emily Monosson


Copyright © 2015 Emily Monosson
All rights reserved.
ISBN: 978-1-61091-499-4


Discovery: Antibiotics and the Rise of the Superbug

"I see resistant staph all the time," says nurse practitioner Maggie G. Her enormous blue eyes convey both the compassion and the weariness of someone who has seen it all. Over the course of 25 years, the Western Massachusetts nurse has treated farmers, hill-town hippies, and teens seeking treatment for STDs and fevers, as well as men, women, and children who walk for miles and wait patiently with festering wounds and suppurating tumors in the Sierra Leone clinic that she visits once a year. One constant throughout all of Maggie's experiences is methicillin-resistant staph, or MRSA. Back in the late eighties, when Maggie was just finishing nursing school, MRSA was rare. But over the years she has witnessed the rise of this drug-resistant bug, tending to countless cases—one of the most memorable involved a young camp counselor whose infected toe turned into a life-threatening hole in her heart. When we spoke, Maggie was working with recovering addicts at a psych hospital. MRSA spreads so easily in needle-using addict populations through needle sharing or festering open wounds that Maggie says addicts are often treated "presumptively"—meaning the staff doesn't always test but assumes drug resistance. It's a reasonable assumption. In some places, nearly 50 percent of the needle-using population may be positive for community-acquired MRSA.

First recognized as a "healthcare-associated infection" limited to patients and caretakers, MRSA made its way out of the hospital into the community a decade or so ago. The bacteria can spread from mother to daughter, throughout a high school locker room by way of an infected towel, from pet to owner, and between hospital patients on the hands of a caregiver. It is a parent's worst nightmare: a small bite or scrape turns into an angry red trail streaking up a child's leg, and one antibiotic after another fails. A once easily treatable infection is now potentially fatal. Of the roughly 75,000 Americans who become infected with MRSA each year, an estimated 9,700 will die.

We live in dangerous times. Infectious diseases are rapidly evolving beyond our medicinal reach, returning us to the pre-antibiotic age. In just over a century, we have rendered impotent some of our most precious therapies, and there is plenty of blame to go around. Whether it be doctors pacifying pushy, anxious parents; the agricultural industry preventively treating livestock, or worse, simply encouraging livestock growth; or hospitals fending off recalcitrant infection—we have all contributed to the rise of the superbug. Each year nearly 37 million pounds of antibiotics are used in the United States. Some 7 million pounds go down the throats of our kids, up the arms of hospital patients, and into infected addicts; a few hundred thousand pounds are consumed by our pets; and the rest is used by the ag industry. And though MRSA is the poster-bug for resistance, it has plenty of company. A once-curable pneumonia recently killed seven patients at a well-regarded national hospital. Tuberculosis that is completely drug resistant has surfaced in India, Italy, and Iran. In Japan, a strain of gonorrhea has shaken free from all antibiotics. That a fully antibiotic-resistant STD may once again rage throughout the world ought to strike fear into all of us, even those who consider ourselves beyond its reach—if not simply because "you just never know," then because some bacteria can easily swap resistance genes. And that means that resistance in a venereal disease may one day transfer to a bug that causes pneumonia or a skin infection. Bacteria may be among the most primitive life forms on earth, but they have proven to be among the most formidable opponents.

The story of antibiotic resistance is one of great advances and impending loss. It begins a little over a century ago with two of the most important discoveries in modern medicine: that disease can be caused by bacteria, and that bacteria can be killed selectively. Yet almost as soon as antibiotics hit the market, one after another began to fail. Antibiotic resistance touches us all, so it is a good place to begin an exploration of evolution in our time.


Before we can cure (or better, prevent) disease, we must recognize the cause. The French chemist Louis Pasteur was just a boy in 1831 when cholera killed nearly 20,000 souls in Paris, roughly 250 miles (400 kilometers) from his hometown. These were the days when epidemics raged—infecting and killing until new victims were too few in number to sustain the spread of disease. Cholera killed millions worldwide. Bubonic plague flared up every few hundred years or so, at one point taking over a third of Europe's population. There was plenty of disease to go around, particularly in dense and well-traveled populations. When Pasteur entered the world, physicians and scientists attributed the cause of infectious disease in large part to "miasma"—poisonous vapors in the air. Disease, like the winds, weather, and the stench of a fetid river, seemed to travel, hovering here and there for days, months, or years before moving on. A few practitioners insisted that disease spread through contact as a tangible entity rather than some amorphous gas—but without proof, the miasma theory ruled. Louis Pasteur's research eventually focused on revealing the invisible causes of disease, moving medicine from the intangible to the treatable. With the goal of preventing spoilage in wine, Pasteur showed that exceedingly small ITLµITLorganisms—"germs"—infected wine and other fermented products.

When he published the results in the 1860s, many believed that infection, whether of wine, meat, or a human body, arose spontaneously. Pasteur disproved spontaneous generation and unveiled the true nature of infectious disease, rendering it vulnerable to attack. It is not difficult to imagine making the connection between a festering piece of meat and an infected wound. In the hospital wards of nineteenth-century Europe, too often patients succumbed to bacteria that spread through the hands, tools, and clothing of surgeons. Joseph Lister, a contemporary of Pasteur's and a founding father of modern surgery, summed it up when he noted that "the same probe was used for the wounds of all patients during rounds to look for pockets of undrained pus." In our germophobic society such a scenario is hard to imagine. Inspired by Pasteur's work and his own observations of the wounds that did heal, Lister developed and encouraged the use of surgical antiseptics. (Listerine, marketed in the late nineteenth century as everything from a mouthwash to floor cleaner, was not Lister's invention but rather was named after the surgeon.) Together with Pasteur, Lister worked to raise awareness of the tangible nature of infection and the very real potential to prevent it, urging surgeons to wash their hands and sterilize their tools, and perhaps change their blood-and-guts-stained coats once in a while. Prevention was one of the first outcomes of Pasteur's discovery. But all too often, prevention is not enough.

A decade or so after Pasteur's discovery, the German physician Robert Koch developed a series of steps to isolate and identify the causative agent of infectious disease. Koch's so-called postulates remain critical to disease sleuthing today. Anthrax, a common disease of farm animals in Koch's district, was the first bacterium to be caught in the act. The microbe poisons the blood by secreting toxin and forms spores that enable it to lie in wait for decades for a suitable host. By culturing bacteria from infected animals, re-infecting healthy animals, and once again isolating the original bacterium, Koch declared anthrax guilty not by association but by causation. If you have ever had the back of your throat unceremoniously scraped and cultured to confirm that you've got strep, you might thank (or curse) Koch. Louis Pasteur may have led medical science to infection's doorway, but it was Robert Koch who provided the keys to identify the diseases that had stalked humanity for hundreds if not thousands of years. By the end of the century, pathogenic bacteria—staph, strep, anthrax, diphtheria, tetanus, and syphilis—emerged from the shadow of "miasma," made visible by the advances of Pasteur, Koch, and others. We now know that a staggering number of bacteria live within us, on us, and around us. We know things about bacteria that would stun those medical giants, including the fact that the bacteria we carry on and within our bodies outnumber our own cells by a factor of ten. Most are harmless, many are essential, and some can kill us.

The fraction of bacteria that make us sick, the pathogens, are products of an eons-old process of coevolution. They invade and use our bodies, and we fight them off. Simply defined, pathogens are microbes that cause disease through infection. If there is one shared feature among pathogens, it is strength in numbers. Should the staph bacteria inhabiting a speck of skin on an addict's arm or a child's elbow gain entrance, whether by needle prick or playground scrape, an initial infection of hundreds can explode into millions if not billions of cells within hours. As the invasion progresses, the immune system kicks in, combating and destroying the trespassers. Sometimes that does the trick; other times the infection wins and we get sick. Visit any pre-twentieth-century cemetery filled with the graves of the young and you can sense the urgency that must have spurred Pasteur, Lister, and Koch to put an end to infection. The power of singling out infectious bacteria was not lost on Koch, who envisioned a day when medicine wouldn't just prevent but cure, leaving the host alive and well. Just one year before Koch's death, the first antibiotic drug was introduced to the world.

Target Practice

Antibiotic (or, more accurately in this case, antibacterial) use is chemical warfare waged on a microscopic field. The trick is to destroy the pathogen, yet leave our own cells unharmed. But there is a catch. Having shared a common ancestry for over a billion years, our cells have much in common with bacteria, which makes identifying a specific target akin to playing "Spot the Difference." Even in these days of genomics and advanced analytical chemistry, it is a difficult game. Singling out bacteria at the turn of the last century would have been like playing the game blindfolded.

And so scientists exploited the very few differences they could see. By the late 1800s, industrial chemical dyes had begun to make the invisible visible, tagging biological structures with red, blue, and purple. For the first time ever, a physician could both differentiate animal cells from bacterial cells and distinguish one class of pathogen from another. If chemical dyes clung to one cell type while ignoring another, could these chemicals also be used to kill pathogens while leaving host cells unharmed? Was there a way "to aim chemically"?

Turn-of-the-century German physician Paul Ehrlich was the first to investigate this central question. Connecting the dots between chemistry, bacteriology, and medicine, Ehrlich assembled a team and took aim at one of the more infamous diseases of the day, syphilis. After running hundreds of chemicals synthesized by the German dye industry through their paces, the scientists discovered that compound number 606 was the winner, curing infected rabbits with a single dose. It was 1909, and within a year number 606, renamed Salvarsan, made its way to the clinic. Syphilis, a chronic and potentially fatal disease for the ages, had become curable. Salvarsan singled out a pathogenic bacterium and, when it was administered properly, caused relatively little collateral damage. The antibiotic age had just begun: synthetic products were poised to make their way into medicine cabinets, hospitals, and our bodies. The uneasy relationship between human and bacterial pathogen, shaped by millions of years of coevolution, was about to change. But it would take two world wars before humans finally gained the advantage.

As the twentieth century dawned, Pasteur's, Koch's, and even Ehrlich's discoveries notwithstanding, eating, drinking, or getting a simple puncture wound could still send one to their grave. Syphilis was but one disease, and hygiene could only go so far in disease prevention. Infections we rarely think about today—cholera, typhus, strep, and staph—continued to run their course, killing and maiming. For pathogens, World War I, like so many other wars, was a war of opportunity. As bullets and bombs shredded skin and tore limbs from bodies, infectious bacteria thrived. Aspiring physicians had few options but to amputate infected limbs and watch helplessly as young men died. If they didn't die from infected wounds, there were plenty of other diseases, like cholera and typhus, waiting in the wings. Gerhard Domagk, a volunteer and medic in the German army, had ample opportunity to observe the quick work that bacteria made of men. Years after the war, inspired by Ehrlich's vision of a "magic bullet" cure, Domagk turned his attention to finding the magic in industrial dyes. The target was Streptococcus, a common cause of skin infections that could quickly take a turn for the worse. One red dye proved particularly effective at curing strep-infected mice, yet any fanfare would have to wait for human testing. But before those tests could be completed, an odd twist of fate intervened. Domagk's six-year-old daughter, Hildegard, fell ill with a life-threatening infection. She had punctured her hand with a sewing needle. Hospitalized with fever and infection progressing up her arm, she faced the standard treatment—amputation with no guarantee of survival. Desperate, Domagk treated Hildegard with the dye. Days later she recovered. It soon became apparent that the dye targeted not just strep but a number of other infections as well. Within a few years, the dye, packaged and sold as Prontosil, became the first commercially available sulfa drug. Its derivatives remain in use today. The discovery offered a cure for illnesses from child-bed fever to pneumonia, skin infections, and gonorrhea. It was 1935, and for the first time in human history a whole range of once–fatal infections could be cured. Less than five years later, Domagk took home a Nobel Prize.

Two chemicals discovered nearly two decades apart, both products of a chemical industry delirious with newfound ability to synthesize novel chemicals and scientists willing to test one after another, offered a world of change. Yet evolution had already produced a far more effective antibacterial chemical, as Scottish physician Alexander Fleming would discover.


Like Domagk, Fleming returned home from World War I bent on disease prevention, only to discover by sheer accident one of the most valuable antibiotics of the century. His is the now-classic story of accidental discovery: a summer vacation trip, stacks of petri dishes dotted with colonies of staph bacteria left in the sink, an observation, and the historic follow-up. Cleaning the lab after returning from vacation, Fleming noticed that an invisible conflict was playing out on plates that been left to molder. Where spots of one particular mold contaminated the plates, bacterial colonies failed to grow. Fleming's genius was to ask why this particular mold (subsequently identified as a Penicillium) cleared the surrounding bacteria. Follow-up studies showed that it produced soluble chemicals that killed not only staph but an assortment of other bacteria.

What Fleming couldn't have known was that penicillin hit bacterial cells where it really hurt—the cell wall. Like a chicken-wire frame for a papier-mâché sculpture, the wall protects bacterial cells from bursting under their own internal pressure. If the wall is compromised, bacteria pop like overfilled balloons. Bacteria like staph and strep with thick cell walls are most sensitive, while others with thinner cell walls, like Salmonella and coliform, are less sensitive. Our animal cells lack cell walls and so avoid damage. Penicillin is a tribute to the ingenuity of nature. When bacterial cells grow and divide, the wall is broken down and rebuilt. Penicillin prevents that molecular frame from linking back together.


Excerpted from Unnatural Selection by Emily Monosson. Copyright © 2015 Emily Monosson. Excerpted by permission of ISLAND PRESS.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Table of Contents

Introduction: Life Changing Chemicals
PART I. Unnatural Selection in a Natural World
Chapter 1. Discovery: Antibiotics and the Rise of the Superbug
Chapter 2. Prevention: Searching for a Universal Vaccine
Chapter 3. Treatment: Beyond Chemotherapy
Chapter 4. Defiance: Rounding Up Resistance
Chapter 5. Resurgence: Bedbugs Bite Back
PART II. Natural Selection in an Unnatural World
Chapter 6. Release: Toxics in the Wild
Chapter 7. Evolution: It’s Humanly Possible
PART III. Beyond Selection
Chapter 8. Epigenetics: Epilogue or Prologue?

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