Excerpted from Big Chicken by Maryn McKenna, published by

National Geographic Partners on September 12, 2017. Copyright ©

2017 by Maryn McKenna. Available wherever books are sold.

EXCERPT OF CHAPTER 1

For most people, antibiotic resistance is a hidden epidemic unless they have the misfortune to

contract an infection themselves or have a family member or friend unlucky enough to become

infected. Drug-resistant infections have no celebrity spokespeople, negligible political support,

and few patients’ organizations advocating for them. If we think of resistant infections, we

imagine them as something rare, occurring to people unlike us, whoever we are: people who are

in nursing homes at the end of their lives, or dealing with the drain of chronic illness, or in

intensive-care units after terrible trauma. But resistant infections are a vast and common problem

that occur in every part of daily life: to children in day care, athletes playing sports, teens going

for piercings, people getting healthy in the gym. And though common, resistant bacteria are a

grave threat and getting worse. They are responsible for at least 700,000 deaths around the world

each year: 23,000 in the United States, 25,000 in Europe, more than 63,000 babies in India.

Beyond those deaths, bacteria that are resistant to antibiotics cause millions of illnesses—two

million annually just in the United States—and cost billions in health care spending, lost wages,

and lost national productivity. It is predicted that by 2050, antibiotic resistance will cost the

world $100 trillion and will cause a staggering 10 million deaths per year.

Disease organisms have been developing defenses against the antibiotics meant to kill them

for as long as antibiotics have existed. Penicillin arrived in the 1940s, and resistance to it swept

the world in the 1950s. Tetracycline arrived in 1948, and resistance was nibbling at its
effectiveness before the 1950s ended. Erythromycin was discovered in 1952, and erythromycin

resistance arrived in 1955. Methicillin, a lab-synthesized relative of penicillin, was developed in

1960 specifically to counter penicillin resistance, yet within a year, staph bacteria developed

defenses against it as well, earning the bug the name MRSA, methicillin-resistant

Staphylococcus aureus. After MRSA, there were the ESBLs, extended-spectrum beta-lactamases,

which defeated not only penicillin and its relatives but also a large family of antibiotics called

cephalosporins. And after cephalosporins were undermined, new antibiotics were achieved and

lost in turn.

Each time pharmaceutical chemistry produced a new class of antibiotics, with a new

molecular shape and a new mode of action, bacteria adapted. In fact, as the decades passed, they

seemed to adapt faster than before. Their persistence threatened to inaugurate a post-antibiotic

era, in which surgery could be too dangerous to attempt and ordinary health problems—scrapes,

tooth extractions, broken limbs—could pose a deadly risk.

For a long time, it was assumed that the extraordinary unspooling of antibiotic resistance

around the world was due only to misuse of the drugs in medicine: to parents begging for the

drugs even though their children had viral illnesses that antibiotics could not help; physicians

prescribing antibiotics without checking to see whether the drug they chose was a good match;

people stopping their prescriptions halfway through the prescribed course because they felt

better, or saving some pills for friends without health insurance, or buying antibiotics over the

counter, in the many countries where they are available that way, and dosing themselves.

But from the earliest days of the antibiotic era, the drugs have had another, parallel use: in

animals that are grown to become food. Eighty percent of the antibiotics sold in the United States
and more than half of those sold around the world are used in animals, not in humans. Animals

destined to be meat routinely receive antibiotics in their feed and water, and most of those drugs

are not given to treat diseases, which is how we use them in people. Instead, antibiotics are given

to make food animals put on weight more quickly than they would otherwise, or to protect food

animals from illnesses that the crowded conditions of livestock production make them vulnerable

to. And nearly two-thirds of the antibiotics that are used for those purposes are compounds that

are also used against human illness—which means that when resistance against the farm use of

those drugs arises, it undermines the drugs’ usefulness in human medicine as well.

Resistance is a defensive adaptation, an evolutionary strategy that allows bacteria to protect

themselves against antibiotics’ power to kill them. It is created by subtle genetic changes that

allow organisms to counter antibiotics’ attacks on them, altering their cell walls to keep drug

molecules from attaching or penetrating, or forming tiny pumps that eject the drugs after they

have entered the cell. What slows the emergence of resistance is using an antibiotic

conservatively: at the right dose, for the right length of time, for an organism that will be

vulnerable to the drug, and not for any other reason. Most antibiotic use in agriculture violates

those rules. Resistant bacteria are the result.

Experimenters began trying the then new miracle drugs in animals almost as soon as

antibiotics were achieved in the lab in the 1940s—and concern about that use dates just as far

back. From the start, in protests that were downplayed for decades, a few perceptive researchers

warned that resistant bacteria would arise in livestock, find a way off farms, and move silently

through the wider world. The shortest route off farms is in the meat that animals eventually

become: In the year Schiller got sick, 26 percent of the Salmonella found on supermarket
chicken by government testing was resistant to at least three separate families of antibiotics. But

resistant bacteria also leave farms in manure, in storm runoff, in groundwater, in dust, and via the

skin and clothes and microbial hitchhikers of people who work on farms and live there. When

those organisms escape, they disperse in a manner that is impossible to track, and they cause

illness and alarm far from the farms where they originated.

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While the CDC’s scientists were tracing the salmonella outbreak that had Schiller in its grip, a

set of researchers on the other side of the world were pursuing another resistant pathogen.

Scientists in China had been running a project in which they checked hogs raised on intensive

farms—the kind of properties where animals are confined permanently in buildings and

antibiotics are used routinely—to see whether they were carrying resistant bacteria. In July 2013,

they found a pig outside Shanghai harboring a strain of the bacterium Escherichia coli in its

manure. That was normal, because E. coli’s multitude of strains make their homes in the guts of

most animals. But the content of this E. coli was unusual and alarming. It was hiding a gene no

one had seen before, conferring resistance to a drug called colistin.

If colistin sounds unfamiliar, there is a reason. It is an old drug, discovered in 1949, and for

decades medicine disdained it as a clumsy, toxic relic of a cruder era of chemistry. Physicians

rarely used it, and no one prescribed it outside of hospitals. But because colistin sat for so long at

the back of the shelf, disease organisms never encountered it either, and never developed

defenses against it. In the mid-2000s, the advance of resistance undermined a critical, powerful
class of drugs called carbapenems, which are used to cure multidrug-resistant organisms—

Klebsiella, Pseudomonas, Acinetobacter—that cause dire infections in hospitals. Against these

newly hardy bacteria, colistin was the only antibiotic that still worked reliably. Suddenly the

clunky, unwanted compound from the past was crucial to preserve.

There was one catch, however: While medicine had been disdaining the drug, agriculture had

adopted it. Because colistin was an old compound, it was cheap, so it made an inexpensive

preventative for the kind of gut and lung infections that could happen to animals in crowded

barns. Colistin is not used in animals in the United States, but European and Asian countries used

millions of pounds each year. No one thought this was a problem, because medicine had not

wanted the drug and because resistance seemed unlikely to develop, requiring a genetically

tricky maneuver that no one had ever observed.

But what the Chinese researchers found in 2013 upended the serene assumption that colistin

was secure. The new gene they found in the pig was on a plasmid, self-contained loops of DNA

inside a cell that spread not just by inheritance when cells divide, but by jumping from one

bacterium to another. This meant that colistin resistance could be disseminating through the

bacterial world unnoticed—and in fact, it was. Within three years, epidemiologists in Asia, and in

Africa, Europe, and South America, would identify the resistance-conferring gene in animals, the

environment, and people in more than 30 countries.

That included the United States. The resistance-conferring gene, dubbed MCR, appeared first

in a woman in Pennsylvania who was carrying it unknowingly, and then in men in New York and

New Jersey who also did not know they were carriers, and then in a Connecticut toddler, and

more. None of those people were ill with colistin-resistant infections; that was true for most of
the people carrying the rogue gene. Rather, they were an epidemic waiting to ignite, held in

abeyance because the use of colistin in medicine was still rare. The spread of colistin resistance

across the world was a time bomb with a fuse of uncertain length, and it had been created and

disseminated by antibiotic use on farms.

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One other thing was happening in autumn 2013 while the CDC was grappling with drug-resistant

salmonella and the Chinese microbiologists were pursuing colistin resistance. The U.S.

government, for the first time in its history, was moving to put federal controls on agricultural

antibiotics.

The United States was late to this. England recognized the danger in the 1960s, and most of

Europe followed its lead beginning in the 1980s. Copying those countries, the FDA had made

one attempt in 1977, but it was defeated by congressional interference and never tried again.

Thirty-six years later, emboldened by the election of President Barack Obama, the agency

proposed making one type of agricultural antibiotic use, the weight-conferring doses known as

growth promoters, illegal in the United States.

The FDA would have a battle ahead of it. American farm animals were consuming 32.6

million pounds of antibiotics in 2013, four times what human patients were receiving. But the

agency also had irrefutable evidence that curbs were needed. Not only was resistance rising; for

the first time, no new drugs were entering the market to replace the ones being lost.

Pharmaceutical companies were contending that antibiotics were no longer profitable to make,
and they had good reasons. By widely accepted industry math, it takes 10 to 15 years, and about

a billion dollars, to get a new drug to market—but resistance was using up antibiotics so quickly

that companies could not recoup their investments or collect any profit before a drug lost

effectiveness. And if a new drug was so effective that medicine elected not to deploy it but to

hold it on the shelf against a future emergency, then the companies made back nothing at all.

The FDA locked in its new policy in December 2013. It gave agriculture three years to adapt

to relinquishing growth promoters and bringing other antibiotic use under the control of

veterinarians. Its reforms became final on January 1, 2017, but how effective they might be will

not be proven for years.

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The events of autumn 2013—the massive salmonella outbreak, the recognition of colistin

resistance, and the U.S. government’s belated attempt to exert some control over farm antibiotic

use—mark a turn in a story that has been unfolding for almost 70 years. Antibiotics were first

added to animal feeds in the late 1940s, in the surge of soaring confidence in science that

followed the end of World War II. They remained a crucial component of meat production for

decades even though more and more voices warned against the practice: first lone scientists who

were mocked for raising the alarm, then small report-writing committees, then large medical

societies, and finally governments, attempting to defy one of the largest, most globalized

industries in the world.

 Antibiotics have been so difficult to root out of modern meat because, in a crucial way, they

created it. The drugs made it irresistible to load more animals into barns and protected animals

and their growers from the consequences of that crowding. The escalating spiral of production

drove down prices, making meat a cheap commodity, but it also drove down profits,

undermining independent farmers and fostering the growth of global corporations.

That history, beginning with the positive effects of antibiotics on agriculture and

continuing with their much more abundant negative ones, is most evident in the parallel story of

poultry. Chickens were the first animals to receive what came to be called growth promoters, and

the first in which scientists demonstrated that daily antibiotic doses could protect birds from

diseases of close confinement. They are the animals most transformed by the post–World War II

mission to feed the world at any cost. Today, a meat chicken’s slaughter weight is twice what it

was 70 years ago and is achieved in half the time. Across those decades, chickens went from a

scarce and expensive Sunday treat to the meat that Americans eat more often than any other and

that is growing fastest in consumption around the world. Until recently, the transformation of

chicken was a point of pride. “Here is good news for both farmers and meat eaters. Antibiotics

provide more meat with less feed,” Fortune magazine reported in 1952. The USDA boasted in

1975: “Broiler production is industrialized in much the same way as the production of cars.”

Yet after the events of 2013, chicken turned against its own history. Some of the largest

production companies in the industry renounced antibiotic use. Some of the largest food service

retailers in the United States committed to carrying only birds raised without routine drugs.

Medical centers, college campuses, school systems, and restaurant chains joined the refusal,

pushed by advocates and by parents who had awakened to the danger to their kids. At a point
where the cattle and hog industries were digging in their heels to resist FDA policies, poultry

rushed to the front of the line and called it a parade.

The intertwined histories of the advent of agricultural antibiotics, and the rise and

transformation of chicken, are mostly a story of hubris: of the romance of innovation, the

seduction of profit, and the failure to anticipate unintended consequences. But they also tell a

story of how an industry can assess its own dark past and adjust its path, and they offer hope that

food production in the rest of the world might be kept from sickening millions more victims like

Rick Schiller, and from making the same mistakes that the United States and Europe made.

To understand both stories, it is necessary to go back to their beginnings: to the earliest

days of the antibiotic era, and a moment when it was urgent to find a new way to feed the world.