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Secret Agents: The Menace of Emerging Infections
Chapter 3
Food Fright
In the autumn of 1996, Laurie Girand, a marketing consultant in Silicon Valley, came home from a Fiji vacation to find her three-year-old daughter Anna in constant stomach pain. “My tummy hurts. My tummy hurts,” the usually resilient child kept saying. Within days, Anna was in the hospital, severely anemic, her red blood cells looking like shredded circles under the microscope. Doctors diagnosed her with hemolytic uremic syndrome, or HUS, a sometimes fatal complication of foodborne infection. The bacterium behind the disease, E. coli O157:H7, is usually linked to undercooked hamburgers—Girand vaguely remembered a huge Jack in the Box outbreak of a few years earlier. But her daughter hadn’t gotten sick from eating hamburgers. Only as Anna lay in a hospital bed, ashen-faced, glassy-eyed, waiting for a blood transfusion, did Girand and her husband hear a news account that apple juice had been linked to an E. coli epidemic. Manu-
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factured by Odwalla, Inc., its selling point was that it was unpasteurized, and presumably more wholesome. The apple juice had been a treat from Anna’s grandmother while Girand and her husband were away. And though Girand didn’t approve of apple juice—too many empty calories—for a long time she had been feeding her daughter Odwalla unpasteurized carrot juice. “I was under the seriously mistaken impression that feeding our daughter unpasteurized juice would be healthier for her,” Girand says. “Odwalla’s slogan at the time was: ‘Drink it and thrive.’”
Though anemic for months, Anna recovered. But in Colorado, a child had died, while nearly 70 others, mostly children six and younger, had become severely ill in what was, until then, the country’s biggest juice-associated outbreak. Catalyzed by the near-tragedy, Laurie Girand started giving speeches to parents and writing letters to government officials. But shocking as the Odwalla outbreak was, it was not sufficiently instructive. Three years later, in the nation’s biggest juice outbreak, Salmonella in unpasteurized Sun Orchard orange juice struck nearly 500 victims and killed one. A few months later, the company had to recall another tainted lot. “I can’t believe,” Girand says, “since I am a marketing person, how badly I was fooled by industry marketing.”
One of the most insistent marketing messages we hear, trumpeted by both industry and regulators, is that the United States has the safest food supply in the world. Yet according to the CDC’s best calculations, each year 76 million Americans—nearly one in four, and that’s a lowball estimate—become infected by what they eat. Most find themselves for a few days dolefully memorizing a pattern of bathroom floor tiles. About 325,000 land in the hospital. Two million suffer drawnout, sometimes lifelong medical complications from unwittingly eating a contaminated morsel. More than 5,000—about 14 a day—die from indulging in what should be one of life’s great pleasures. The “world’s safest food supply” regularly doles out E. coli O157:H7 in hamburgers, Salmonella in alfalfa sprouts, Listeria in hot dogs, Campylobacter in Thanksgiving turkeys.
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Change is what ushers new disease-causing organisms into our lives. And in the past few decades, there have been profound shifts in what we eat, where our food comes from, how it’s made, and who makes it. Fifty years ago, grocery stores stocked about 200 items, 70 percent of which were grown, produced, or processed within a 100mile radius of the store. Today, the average supermarket carries nearly 50,000 food items, some stores as many as 70,000. Agriculture and food manufacture have grown into global economies of scale, producing megaton quantities that, if contaminated, increase the potential for widespread epidemics. More fresh fruits and vegetables come from abroad, where sanitary standards may not be as high as in the United States. And our meals are increasingly cooked by people untrained in the techniques of safe food preparation.
This is not your grandparents’ “food poisoning”—a now-quaint term that originated early in the twentieth century, when dramatic gastrointestinal distress was usually traced to toxins, especially staph toxins, that had grown on spoiled foods such as cream-filled pastries or chicken salads left out too long in summer heat. Literally cases of food “intoxication,” these infections struck suddenly and fiercely, usually within two to six hours after the meal. When local health officials worked up these classic “point source outbreaks,” they would inevitably find that a knot of victims had all eaten a single dish, and that cases sharply climbed and then plummeted as the well of exposed individuals dried up. Point source outbreaks haven’t faded away; big-city health departments face dozens every year. In 1997, for instance, Salmonellatainted hams from a church fundraising dinner in St. Mary’s County, Maryland, sickened 700 people and killed an elderly woman. Today, however, the modest church picnic has given way to a giant food bazaar created by massive consolidation and global distribution. One contaminated tidbit—a shred of meat from an infected steer mixed with hundreds of other carcasses for hamburger, an iced box of tainted lettuce dripping down on the rest of an outbound lot, a soiled production line of cereal shipped coast-to-coast under 30 different brand names—spreads disease far and wide.
The pathogens in science’s crosshairs have also changed—in part
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because improved technology permits scientists to see some for the first time, and in part because evolution has selected for more noxious creatures. Twenty years ago, today’s most fearsome threats were overlooked or yet-to-be-discovered. Campylobacter jejuni, now known to be the most common bacterial agent in food, was considered a rare, opportunistic organism because lab workers didn’t see it hiding among less fastidious bacteria growing in culture. A small, delicate, spiralshaped microbe, it corkscrews its way into mucous membranes of the intestinal tract “with a speed that cannot be matched by other bacteria,” according to one scientist’s report. Listeria monocytogenes, the most deadly agent in our food supply, killing one in five victims it infects, wasn’t even suspected of spreading through food. E. coli O157:H7, a potent threat to children and the aged, was identified only in 1982—and even then remained a medical curiosity until the infamous 1993 Jack in the Box hamburger outbreak. Norwalk virus, the top cause of foodborne illness in this country at 23 million cases a year, remained largely elusive until molecular tests revealed it in the 1990s. All of which suggests there are novel disease-causing agents still hiding incognito in our food. Even with modern diagnostic tools, in 81 percent of foodborne illnesses and 64 percent of deaths, doctors don’t know what organisms to blame—in part because they don’t know what organisms to look for.
To doctors and scientists, some of these bugs—particularly E. coli O157:H7—are scarier than anything seen before. “Foodborne pathogens are not purely a bit of nausea and vomiting and diarrhea,” says David Acheson, an E. coli researcher at Tufts University School of Medicine. “They can kill a previously healthy person in the space of a week.” Evolutionary biologists fear that our efforts to eliminate pathogens on the farm and in processing—by, for example, using disinfectant rinses—may paradoxically help select for more durable and virulent strains.
Meanwhile, more of us are more vulnerable to foodborne microbes. Individuals with impaired immunity—the very young, the very old, and people with cancer, organ transplants, diabetes, AIDS, and other conditions that weaken the body’s defenses; all told, about a
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quarter of the population—are more apt to succumb to these infections. Men and women over 65, who in the next three decades will make up one-fifth of the population, produce less acid in their stomachs, eliminating the first line of defense against enteric pathogens; federal officials predict that the aging population could increase foodborne illness by 10 percent in the next decade. Americans are popping more prescription and over-the-counter antacids than ever, and in so doing, giving pathogens entrée to the nether regions of our digestive system where they do the most damage.
Depending on the organism, the palette of symptoms associated with foodborne disease can include diarrhea, cramps, fever, nausea, and vomiting (the notable exception is Listeria, which can cause miscarriage, meningitis, and other nonabdominal problems). But that’s just the beginning. In some people, researchers have discovered, the gastrointestinal distress that comes and goes with a foul meal may hang around in another form much longer. Salmonella can trigger reactive arthritis, an acute joint inflammation. Campylobacter jejuni may cause as many as 40 percent of cases of Guillain-Barré syndrome, a severe neurological disorder that can bring temporary paralysis and long-term nerve damage. Other complications include thyroid disease, inflammatory bowel disease, and, should someone survive the struggle against E. coli O157:H7, permanent kidney damage from hemolytic uremic syndrome. In these cases, contaminated food seems to provoke an uncontrolled autoimmune reaction. Up to 3 percent of foodborne disease victims—an enormous number, given the total caseload—may suffer lifelong physical problems.
Any depiction of emerging foodborne infections is necessarily panoramic, complex, and accompanied by more questions than answers. This discussion is no exception. As you will discover, debates about questions of farm management, government regulation, and individual versus institutional responsibility may elicit two—or three or four— diametrically opposed arguments that all seem persuasive. “Foodborne illness is more complex than people understand. The more I learn, the less I realize I ever knew,” says Mike Osterholm, a former Minnesota state epidemiologist who has probably launched more successful food
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outbreak investigations than any other public health official in history. “The very nature of the ever-growing and complex food supply chain, and the desire of consumers to have many different kinds of foods available at a moment’s notice, has allowed for a whole new spectrum of pathogens to arrive on the scene.” What’s more, says Osterholm, DNA fingerprinting has pulled back the covers from foodborne out-breaks, showing that “many of the old conclusions we had drawn about what was happening are not valid.”
For those of us who don’t think about it for a living, it’s easy to underestimate the risk of falling ill from food, since the problem is largely invisible—hidden, one supposes, behind the bathroom door. CDC epidemiologists have factored in this cultural aversion by using numerical multipliers that translate the relatively few cases reported into a far higher and more accurate count of victims who never see a doctor. For instance, for every person known to suffer an infection caused by Campylobacter or Salmonella or Cyclospora, there are 38 who have eluded the net of public health officials; for every confirmed case of E. coli O157:H7, there are 13 to 27 doubled-over victims. Keep this in mind when you read news stories about foodborne epidemics. The scores of confirmed cases mentioned in wire service stories may actually represent hundreds or thousands of silent sufferers.
Foodborne infections are ubiquitous, sneaky, and regularly sold short. At the CDC, the foodborne and diarrheal diseases branch investigates more outbreaks than any other group in the agency. According to Paul Mead, a medical epidemiologist, “The paradox of foodborne illness is that, on a per meal basis, it’s extremely rare. It’s like getting hit by a meteor.” But in the very act of eating, says Mead, “You’re standing in a meteor shower three times a day from the time you’re weaned until you die.”
Secret Agent O157: The Evolution of a Killer
Every pathogen has a story, but the biography of E. coli O157:H7 is especially instructive because it shows how chance favors the prepared germ—and how we are giving certain disease-causing organisms
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more chances than a rigged roulette wheel. Though E. coli O157:H7 has turned up in unpasteurized apple cider in 1991, 1996, and nearly every year since the Odwalla outbreak, it is best known as the agent behind “hamburger disease.” Hamburgers, in fact, are Rolls-Royce conveyances for O157. Think of your next Big Mac as the end product of a vast on-the-hoof assembly line. The story begins on hundreds of feedlots in different states and foreign countries. The animals are shuttled to slaughterhouses, where they become carcasses. The carcasses go to plants that separate meat from bone. The boning plants ship giant bins of meat to hamburger-making plants. The hamburger-making plants combine meat from many different bins to make raw hamburgers. At this point, your burger is more fluid than solid, because ground beef continually mixes and flows as it’s made, its original ingredients indistinguishable. Grinding also multiplies surface area, so that the meat becomes a kind of soup or lab medium for bacteria. Finally, from the hamburger-making plants, these mongrel patties are frozen and sent to restaurants. A single patty may mingle the meat of a hundred different animals from four different countries. Or, looked at from another perspective, a single contaminated carcass shredded for hamburger can pollute eight tons of finished ground beef. Finding the source of contamination becomes impossibly daunting. (Making juice is also like making hamburgers: one bad apple can ruin a huge batch.) In the Jack in the Box outbreak, investigators found that the ground beef from the most likely supplier contained meat from 443 different cattle that had come from farms and auction in six states via five slaughterhouses. As the meat industry consolidates and the size of ground beef lots grows, a single carcass may have even more deadly potential. In 1997, Hudson Foods was forced to recall 25 million pounds of ground beef for this very reason: a small part of one day’s contaminated beef lot was mistakenly mixed with the next day’s, vastly spreading the risk.
E. coli O157:H7, the organism that this endless mixing amplifies, is a quiet tenant in the intestines of the 50 percent or so of feedlot cattle it infects, but a vicious hooligan in the human gut. In the bowel, Escherichia coli, rod-shaped bacteria first described by German pedia-
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trician Theodore Escherich in 1885, perform a vital task by keeping disease-causing bacteria from taking over. For many decades, that knowledge obscured the fact that some forms of E. coli trigger violent disease. E. coli O157:H7 (the letters and numbers refer to immune system–provoking antigens on the body and on the whiplike flagella of the organism) was discovered in 1982, during an epidemic spread by undercooked patties from McDonald’s restaurants in Oregon and Michigan. The outbreak wasn’t highly publicized; even some scientists perceived O157 as more of an academic curiosity than a harbinger of bad things. Eleven years later, the Jack in the Box hamburger chain promoted its “Monster Burgers” with the tag line: “So good it’s scary.” These large, too-lightly-grilled patties killed four children and sickened more than 700 people—bringing the exotic-sounding bacterium out of the lab and into public consciousness. In fact, however, by the time of the Jack in the Box tragedy, 22 outbreaks of E. coli O157:H7, killing 35 people, had already been documented in the United States. Suddenly, fast food hamburgers—a staple of American culture—were potentially lethal.
What makes E. coli O157:H7 so fearsome is the poison it churns out—the third most deadly bacterial toxin, after those causing tetanus and botulism. Known as a Shiga toxin, because it is virtually identical to the toxin produced by Shigella dysenteriae type 1, it is a major killer in developing nations. The distinctive symptoms of E. coli O157:H7 are bloody diarrhea and fierce abdominal cramps; many victims say it’s the worst pain they ever suffered, comparing it to a hot poker searing their insides. Between 2 and 7 percent of patients— mostly young children and the elderly— develop hemolytic uremic syndrome, which can lead to death. HUS sets in
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when Shiga toxins ravage the cells lining the intestines. The bleeding that ensues permits the toxins to stream into the circulatory system, setting up a cascade of damage similar to that of rattlesnake venom. The toxins tear apart red blood cells and platelets, leaving the victim vulnerable to brain hemorrhaging and uncontrolled bleeding. Clots form in the bloodstream, blocking the tiny blood vessels around the kidneys, the middle layer of the heart, and the brain. As the kidneys give out, the body swells with excess waste fluids. Complications ripple through all major organ systems, leading to strokes, blindness, epilepsy, paralysis, and heart failure. Though doctors can manage HUS symptoms, and are working on new ways to stymie the toxin, they currently can offer no cure or even effective treatment.
For public health officials, the emergence of E. coli O157:H7 is an object lesson in how a new pathogen can lie low in the environment, biding its time until humankind changes a certain activity and in so doing rolls out a red carpet. Like other emerging pathogens, such as the AIDS virus, O157 had struck long before it caught the attention of public health officials. In 1955, a Swiss pediatrician in a dairy farm area first described HUS, which physicians today consider to be a gauge of E. coli O157:H7 infection. Over the ensuing years, the number of cases kept rising, suggesting that O157 was quietly spreading. In 1975, doctors took a stool sample from a middle-aged California woman with bloody diarrhea, cultured the apparently rare bacterium and sent it to the CDC, where it sat in storage until the McDonald’s outbreak prompted researchers to scour their records for earlier evidence of the vicious organism. In other words, for nearly 30 years before the first bona fide epidemic, E. coli O157:H7 had turned up in scattered, sporadic cases of bloody diarrhea. It was out in the meat supply, but not in high enough concentrations to catch health officials’ notice.
Where did E. coli O157:H7 come from in the first place? Scientists have pieced together a long, rather provocative history. Genetic lineages suggest that about 50,000 years ago, O157 and another closely related serotype—O55:H7, which causes infant diarrhea in developing nations—split off from the same mother cell. Since then, O157 has
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taken part in a series of biological mergers and acquisitions that left it as vigorous as one of today’s giant pharmaceutical houses. Indeed, a 2001 study showed that O157, composed of more than 5,400 genes, picks up foreign DNA at a much faster rate than do other organisms. At some point, it acquired two deadly Shiga toxin genes after being infected by a bacteriophage, a tiny virus that insinuates its DNA into the chromosome of a bacterium. In the microbial world, phages are like squatters in Amsterdam, casually taking up residence in new bacteria, perhaps as a response to environmental stresses such as ultraviolet light or toxic chemicals. Bacteriophages are also the villains behind some of the most deadly human plagues; the genes coding for the cholera toxin, for instance, were borne on a phage. So what surrounding pressures compelled the phage carrying the Shiga toxin genes to light out for a new home in E. coli? In experiments on mice, Tufts University researcher David Acheson may have found the answer. When Acheson gave the animals low levels of antibiotics, the phage virus wildly replicated itself, and its magnified forces were more likely to infect other bacteria. Antibiotics also spurred the phage to pour out clouds of Shiga toxin. Acheson speculates that when farmers began the practice of feeding cattle small doses of antibiotics to spur growth, beginning in the 1950s—perhaps not coincidentally, when the first reports of sporadic HUS in children came out—they may have unleashed O157. More backing for this theory comes from epidemiological evidence. E. coli O157:H7 is a disease of affluent, developed nations— which also happen to be the ones that feed growth-promoting antibiotics to livestock.
What worries Acheson and other scientists is that the restless phages that manufacture Shiga toxin may jump to other disease-causing bacteria. Actually, they’ve already proven they’re disposed to do this, having set up home in about 200 other strains of E. coli. One of these, E. coli O111:H8, in 1999 caused a massive epidemic of nausea, vomiting, bloody diarrhea, and severe stomach cramps at a high school drill team camp in Texas, sickening dozens of the 750 teenage girls who attended. Though investigators never did find where the organism was hiding, they suspect it was either in the ice the girls used to
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soothe their parched throats during the drills or somewhere in the salad bar. Shiga toxin phages have also landed in Enterobacter and Citrobacter—other bacteria that stir up intestinal disease. To find out just how prevalent these mysterious strains of dangerous E. coli may be, Acheson analyzed ground beef samples from 12 supermarkets in Boston and Cincinnati. The results came as a shock. He found Shiga toxin in a quarter of the samples—toxin produced not by O157:H7, but by other kinds of E. coli. And this may not be the end of their roving, Acheson warns. “Suppose something like Salmonella developed the ability to produce Shiga toxins. That could be an extremely deadly pathogen.” Not only is Salmonella common, but, more than E. coli O157, it has a talent for quickly invading the bloodstream, meaning it could speedily convey Shiga toxins throughout the body like tiny poison-tipped missiles. Even more problematic, the antibiotics normally used to treat E. coli O157:H7 infections may actually aggravate the illness, by kicking phages into overdrive and stepping up their production of toxins, leading to hemolytic uremic syndrome.
Along its evolutionary path, E. coli also became acid resistant, so impervious to a low pH environment that it can survive the incredibly sour bath in the human stomach. Grain-feeding cattle, which supplanted traditional hay feeding after World War II, may have made the bacteria more acid resilient. Because of this acid tolerance, as few as 10 organisms are enough to cause infection. Having acquired a mean set of toxin genes, acid resistance, and other virulence properties, all E. coli O157:H7 needed to become a truly fearsome threat was access. That it acquired by spreading in domesticated cattle and then entering the gears of modern industrial meat production, all within the past 25 years. Unfortunately, O157 may have left the door open behind it. Other strains of E. coli, “if tweaked in the right way” by phages and the mobile rings of DNA known as plasmids, could negotiate the same path, says Tom Whittam, a biologist at Pennsylvania State University who has studied O157 evolution.
Research is under way on vaccines that would prevent cattle from carrying O157, and on feed additives—including competing intestinal bacteria—that would eliminate the pathogenic organism in livestock.
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Or are all outbreaks related to other meta-outbreaks that we are now more able to discern?”
Even if investigators were able to tie together individual cases and outbreaks in a grand theory of everything, they wouldn’t necessarily be able to act on that knowledge. Few investigations end as neatly or as gratifyingly as the case of the Shigella-ridden parsley. Sometimes DNA fingerprinting raises more questions than it answers, or presents bureaucracies with challenges that they either won’t or can’t face. Unlike in criminal investigations, DNA fingerprints aren’t enough to close a case of foodborne illness, since there is a tiny chance that identical bacterial fingerprints may come from unrelated sources. Epidemiologists must also prove that the patients all ate a particular food and, for liability reasons, federal regulators must prove that the product was indeed contaminated.
The sometimes tricky business of closing a PulseNet case was underscored during an outbreak in the United States in late 1998. That November, the CDC received calls from several states reporting an increase in Listeria monocytogenes cases. Named for the British surgeon Joseph Lister, the father of modern hospital antisepsis, Listeria— a small bacterium that tends to line up side by side, like a regiment of recruits—is almost impossible to eradicate once it makes its home in a meat processing plant. Ubiquitous in the environment, it is found in soil, water, sewage, decaying vegetation, and many species of birds and mammals. Reports of Listeria are usually the kickoff for frustrating and ultimately fruitless investigations because the organism has a long incubation period; the lag time between eating a contaminated food and developing symptoms can be one to two months. That makes gathering food histories difficult, since most people can’t remember what they ate yesterday, let alone eight weeks ago. More perplexing, the symptoms of listeriosis don’t always suggest foodborne infection. In fact, not until 1981—after an outbreak in Canada killed 41 percent of those infected, and 34 women suffered stillbirths or miscarriages or gave birth to ill infants—did researchers even realize Listeria was transmitted by food. The victims had eaten commercially prepared cole slaw made from cabbage grown on a farm where listeriosis had killed
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sheep. If a mother’s infection spreads to the fetus through the placenta, Listeria can cause meningitis in infants and newborns. Listeria infection in the nervous system causes a severe headache, stiff neck, loss of balance, and convulsions. All told, Listeria monocytogenes kills 1 in 5 people it infects, making it one of the most deadly foodborne agents known. Each year in the United States, more than 2,500 persons fall ill and more than 500 die. But while between 2 and 7 percent of processed meats carry Listeria, some strains may be less virulent than others, which is why there aren’t constant Listeria outbreaks. “Chances are most Americans eat Listeria monocytogenes at least once a week,” says the CDC’s Paul Mead, “and yet they don’t get sick that often.”
The 1998 case was one of the deadly strains. By late November 1998, the death toll was mounting. Investigators had no clue where the disease was coming from. Questionnaires eventually ferreted out what the victims had in common: hot dogs. But which brand? Many had been mentioned. Here, a lucky break—also the legacy of DNA technology—pointed investigators toward the answer. That fall, Cornell University happened to have taken genetic fingerprints from pieces of smoked chicken that had sent several members of a New York family to the hospital. The DNA fingerprint perfectly matched the hot dog outbreak strain—and both, it turned out, came from Bil Mar Foods, a division of the Sara Lee Corporation, the biggest purveyor of packaged meats in the country.
By mid-December, 15 people scattered across the country had died in the outbreak and scores were ill—though with the slow trickle of reports from state health departments, the CDC wouldn’t be able to add up the numbers for weeks. Ultimately, the agency calculated that the outbreak killed at least 21—15 adults and 6 stillbirths or miscarriages—and made more than 100 sick in 22 states. But the CDC and USDA tussled over whether there was enough evidence to implicate the company—while CDC insisted there was, USDA officials fretted about the legal consequences of wrongly accusing Sara Lee. Understandably confused by the government’s mixed signals, Sara Lee officials called Mike Osterholm, then the Minnesota state epidemiologist,
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who had been at the helm of many high-profile foodborne illness investigations. Osterholm was convinced the company should carry out a recall. As he explained to the Washington Post, in a typical metaphorical flourish, “I said to Sara Lee that this was like driving down a highway and seeing a herd of deer. You can put on the brakes now and you’ll still hit them. Or you can hit them at full speed and the deer will come through your windshield.”
On December 22, Sara Lee recalled 15 million pounds of hot dogs and deli meats. But the USDA, contrary to its own policies, did not deliver a timely warning to the public; instead, it allowed Bil Mar to issue a weakly worded press release that did not mention the serious nature of the illness, or the deaths. A few days later, the CDC team isolated the Listeria strain found in a package of unopened hot dogs in the refrigerator of one of the Michigan patients—a woman who had given birth to a child with sepsis. The strain matched the bacterium that was quietly killing Americans.
But the government’s earlier timidity had deadly consequences. In the midst of the holiday season and as presidential impeachment dominated the news, Americans never really took note of the outbreak. In Columbus, Ohio, Lisa Lee and her fiancé, unaware of the recall, continued eating Sara Lee deli meats. Lee was in the fifth month of her first pregnancy, expecting twins. That January, feeling feverish and wretched, she went to an emergency room, where a doctor diagnosed her with flu and sent her home. A few days later, she returned with a high fever. After unsuccessfully trying to stop her contractions and prevent miscarriage, doctors induced a long labor. Lee gave birth to twins, a boy and girl, both stillborn. “If we knew it as soon as Sara Lee knew it,” she told an interviewer, “we might have had a chance.”
As it happened, employees at the Bil Mar plant did know about the contamination, long before the recall. The plant had had trouble with condensation in the hot dog production room. When franks are cooked to a high temperature and then chilled, steam rises to cooling elements in the ceiling. Those cold, moist conditions make a perfect home for Listeria—a psychrophilic, or cold-loving, bug—which thrives on walls and ceilings and can survive for years on biofilms and metal
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surfaces. When the steam condenses, it rains down on whatever happens to be sitting on the production line, washing Listeria along with it. On the July 4th weekend, Bil Mar workers had ripped out cooling units from the ceiling and, because the units were too big to push out the door, cut them up with a chain saw before forklifting them away. Immediately afterwards, routine bacterial samples came back positive. The construction probably raised dustborne Listeria that drifted through the factory to the deli meat section, under the same roof but three acres away. From the plant, Listeria was dispatched across the country. In response to this dramatic foodborne epidemic—the most lethal in the United States in 15 years—the USDA in 2000 took steps to require Listeria testing in processing plants. In 2001, Sara Lee pleaded guilty to a misdemeanor charge that it had produced and distributed tainted meat. It agreed to pay $4.4 million to settle civil and criminal charges.
Food Fights
The very things that make America’s food system extraordinary— its mammoth production levels, its stunning variety of imports, and its low cost—are what compromise safety. Mass production spreads risk, imports bring global pathogens to our doorstep, and historically low cost makes farmers and regulators reluctant to pursue safety measures that could raise prices. It’s not the ideal way to cultivate the world’s safest food supply—a claim that food safety advocates say is overblown anyway. Denmark, Sweden, and the Netherlands, for instance, have taken far more vigorous steps to eliminate pathogens.
Even if America’s were the safest, it’s not safe enough. So whose fault is that? Throw together all the parties involved in food safety— scientists, company officials, regulators, advocacy groups, victims and their families—and the discussion inevitably boils down to this: How much responsibility for preventing foodborne illness belongs to the individual and how much to government and industry? Those who lean toward individual responsibility point out that it’s often mistakes close to home—either yours or someone else’s—that inflict the
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damage. Most cases of Campylobacter, for instance, simply come from undercooking poultry or letting the raw bird or its juice touch another food. Most cases of E. coli O157:H7 come from eating ground beef heated only to pink or pallid gray. “Raw meats are not idiot-proof,” says USDA microbiologist Nelson Cox. “They can be mishandled and when they are, it’s like handling a hand grenade. If you pull the pin, somebody’s going to get hurt.” But while some might question the wisdom of selling hand grenades in supermarkets, Cox believes that blame grows less actionable the farther back you go in the food chain. “Who are you going to sue?” he asks. “Are you going to sue Kroger? Or are you going to sue the man who transported it? Are you going to sue the man who processed it? Or the one who grew it? Or had the breeder flocks? I think the consumer has the most responsibility but refuses to accept it.”
Admittedly, food abuse is rampant. Surveys show that more than one-quarter of respondents don’t wash cutting boards after cutting raw meat, nearly a quarter prefer their hamburgers pink, and half eat raw or undercooked eggs. The faster we forget the lessons of an agrarian culture, and the more we rely on packaged and microwavable food, the more we are apt to mishandle raw ingredients in our own kitchens. Moreover, changes in work and family life have led us to cook less and eat out more—Americans spend half of their food dollar away from home, and nearly 14 percent on fast food—exposing us to the ministrations of young and often even more naive food handlers. A 1999 study from Los Angeles found that large restaurants—those with more than 400 seats—were more than seven times as likely to have a complaint lodged against them as a restaurant with fewer than ten seats. It
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wasn’t just because the restaurants had more customers, but because they had varied menus, creating more chances for cross-contamination behind those swinging kitchen doors.
Inexperienced kitchen help who may not receive training in sanitation or hygiene are also perfectly positioned to broadcast their own foodborne ailments. Because wages in these jobs are low, and insurance and sick leave nonexistent, “people are encouraged to work while they’re sick,” says Kirk Smith, who supervises foodborne disease investigations at the Minnesota Department of Health. In addition, many food workers emigrate from countries where intestinal infections are endemic. For all these reasons, employees suffer unusually high levels of enteric disease. While up to 0.5 percent of individuals in the general population may carry an intestinal parasite, in restaurants that have triggered foodborne outbreaks, up to 18 percent of food handlers have been shown to suffer intestinal infections. The public health literature is replete with reports of kitchen workers sowing foodborne epidemics, from Shigella to Campylobacter to hepatitis A viruses. Though shellfish from polluted waters are a major source of Norwalk virus, a nasty ailment that begins with sudden projectile vomiting, so are infected kitchen workers who are less than meticulous—such as the bakery worker in Minnesota in 1982 who used his bare hands and arms to stir 76 liters of butter-cream frosting, an unconventional culinary technique that made 3,000 pastry lovers sick. In 1988, the largest home-grown epidemic of Shigella came to light when 21 players on the Minnesota Vikings football team suddenly became ill after a charter flight to Miami, a trip on which they had partaken of cold meat sandwiches. After media coverage of the outbreak, hundreds of calls poured in to the Minnesota Department of Health from other air travelers complaining that they, too, had gotten sick. Investigators ultimately tracked the outbreak to 219 airline flights depositing travelers in 24 states, the District of Columbia, and four other countries—jaunts on which as many as 35,000 travelers ate contaminated sandwiches. One or more employees in the flight kitchen—who couldn’t afford to lose a day’s pay—had worked while sick with diarrhea from shigellosis.
It’s these hidden, unsuspected sources of food poisoning—from
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long-contaminated meat and produce, from infected food handlers, from unpasteurized apple and orange juices—that have persuaded food safety advocates that fallible humans simply can’t act as the bulwark against dangerous pathogens. In the United States, at least 12 federal agencies have a hand in food safety, fiefdoms that sometimes work in efficient synchrony but often in a kind of all-thumbs opposition. Though the system has become a sprawling mess, it did make sense during the era of malfeasance when it was created. In 1906, Congress passed the Pure Food and Drugs Act, which established the duty of the federal government to regulate foods other than meat and poultry, and to prohibit the interstate sale of food that was misbranded or adulterated with chemical preservatives—a structure that’s now the Food and Drug Administration. And in response to Upton Sinclair’s 1905 novel The Jungle, which graphically depicted Chicago’s meatpacking industry, lawmakers passed the Meat Inspection Act of 1906. That law set sanitary standards for slaughter of animals and for meat sold in interstate commerce and led to daily inspection in slaughterhouses, using “organoleptic” means—sight, smell, touch—to ferret out problems.
Back when the nineteenth century became the twentieth, of course, “clean” didn’t mean free of microscopic pathogens, since many were not known at the time. Because of this technological lag, the public and the courts later came to consider disease-causing organisms in meat and poultry an unavoidable risk. As late as 1974, in a case in which the American Public Health Association sued the U.S. secretary of agriculture for violations of the Wholesome Meat Act, a U.S. court of appeals endorsed this fatalism, writing that Salmonella and other organisms were “inherent” in meat and that it was the consumer’s responsibility to work around those hazards: “American housewives and cooks normally are not ignorant or stupid and their methods of preparing and cooking of food do not ordinarily result in salmonellosis.” Not until 1994 did a district court break a new precedent, declaring that “E. coli is a substance that renders ‘injurious to health’ what many Americans believe to be properly cooked ground beef” and therefore “fits the definition of an adulterant.”
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Shaped by case law and political wire-pulling, the USDA and FDA have dramatically evolved from their origins. The USDA is now responsible for monitoring meat, poultry, and commercially processed egg products, with a policing force known as the Food Safety and Inspection Service (FSIS). The FDA is charged with ensuring that all other foods are safe, nutritious, sanitary, wholesome, and honestly labeled. This jigsaw puzzle sometimes doesn’t fit. For example, while the FDA oversees shell eggs, the USDA has authority over egg products. While the FDA oversees plants producing cheese pizza but rarely inspects them, the USDA has jurisdiction over plants producing pepperoni pizza and inspects them every day. And while the USDA is responsible for meat and poultry safety, its inspectors can look only for microbes that cause animal—not human—disease. The two agencies also share monitoring of imported foods, again with very different approaches. While the USDA must certify an exporting country’s meat and poultry inspection program, the FDA has no such power and instead relies on a tiny staff to do physical inspection and chemical analysis of food at ports of entry—inspections that can’t possibly keep pace with the huge rise in imports. The FDA inspects less than 1 percent of the foods and ingredients imported from other countries.
Today, the centerpiece of the federal food safety system is the HACCP program—for Hazard Analysis Critical Control Point. HACCP (pronounced has´-sip) is a system of process control that evolved out of methods designed to protect astronauts from food contamination. The model is an eminently rational one. It identifies critical contamination points all along the path from farm to fork—in shipping, processing, wholesaling, retailing, and kitchen handling— eliminates those hazards, monitors the effects, and then sets even more stringent standards. But it may hand over too much responsibility to industry to police itself. In 2000, the General Accounting Office, a research arm of Congress, issued a report recommending that the government tighten enforcement of sanitation standards in meat and poultry plants, and give the USDA the authority to levy fines against plants that don’t meet these standards. The GAO also estimated that 85 percent of foodborne infections comes from fruits, vegetables, seafood,
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and cheeses: items regulated by the thinly staffed FDA, an agency with only a tenth of the inspection force of the USDA.
Critics of American food safety policies have insistently called for a single independent government agency to replace the current patchwork of bureaucracies and fiefdoms that are often at cross-purposes. CDC officials privately grumble about the USDA’s and FDA’s foot-dragging and the bureaucratic hurdles that spring up the instant an outbreak investigation is launched. “Until a few years ago, the attitude of the Department of Agriculture was that if a pathogen didn’t make the animal sick, it wasn’t their business—it was your business,” says Carol Tucker Foreman, a former USDA official who now heads the Safe Food Coalition, an advocacy group in Washington, D.C. “You have diffuse authority and a political structure that says: Do not impose any cost on the farmer. You don’t go tell the American farmer that he has to rebuild his stock pens, redo his water supply, alter completely the way he houses and ships animals to market. Look at the people who make up the House and Senate agriculture committees: Nobody’s on those committees because his or her first interest is food safety. They’re on those committees because their first interest is to make sure farmers make a profit.”
Meanwhile, industry and regulatory officials counter that CDC investigators operate with a naive, narrow-minded zeal. Egg industry officials, for instance, complain that the Clinton administration and the CDC focused attention on eliminating Salmonella enteritidis in eggs only because SE outbreaks almost always originate with that single food, making it a conveniently neat target—unlike E. coli O157:H7 or other forms of Salmonella, which pop up all over. “Some of the people that we interact with from CDC . . . say things . . . without ever having personally been on a farm,” observes the USDA’s program leader for the National Animal Health Monitoring System, Nora Wineland. “I would take it with a very large grain of salt.” So deep is the antagonism at times between the federal agencies involved in food safety that Wineland has even wondered aloud whether the many cases of disease that CDC officials are convinced are foodborne actually come from food at all. It’s perfectly plausible, Wineland says, that someone could
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get a Salmonella infection by preparing food on a kitchen counter where the family cat may have just been prowling. “And where’s that cat been?” Wineland asks. “When you try to think about where people could pick up these bugs, the possibilities in my mind seem nearly endless.” It’s an argument that makes CDC investigators see red.
The finger-pointing goes in all directions. Public health officials blame farmers and industry for sanitation problems that they believe perpetuate the chain of infection. Farmers blame slaughterhouses and processing plants for contaminating their products. Microbiologists studying animal diseases insist that fresh produce is the biggest threat today. And the tension between blaming consumers for foodborne disease and blaming corporations and government never goes away. “It’s the blame game,” says Mike Osterholm, adding that rhetoric doesn’t go far. “Today, if I gave some of these advocacy groups a billion zillion dollars and told them to raise cattle and bring them to market and get them to the consumer without E. coli O157:H7, they couldn’t do it. And if I gave a billion zillion dollars to a meat packing plant and told them, ‘You can’t have any Listeria, period—zip, zero,’ they could do a lot to minimize it but they couldn’t reduce it to zero.” Osterholm wonders, in fact, if the problem could ever be dispelled at the source. “The bottom line is, if everybody did their job perfectly well, given the level of technology that’s readily available, you’d still have problems.” Food recalls, he adds, almost always come too late. “It’s like shutting the barn door after the cow is out.” Unlike many public health experts, Osterholm has pushed hard for a last-stage technical fix: irradiation of ground beef, poultry, and eventually of fresh produce, all of which he likens to the commonsensical pasteurization of milk.
Ultimately, preventing foodborne infections will take scientific and political courage—sparked, most likely, by personal stories. In 1993, Alexander Thomas Donley, age six, was one of four children who died from eating a Jack in the Box hamburger. E. coli O157:H7 first made him curl into a fetal position from abdominal cramps. Then, one after another, his organs failed. Screams of pain were followed by silence as toxins liquefied his brain. He suffered tremors and delusions and finally a massive seizure. His body swelled as his kidneys shut down. “I
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was so horrified and so shocked and so angered by what happened to him,” says his mother, Nancy Donley, now the president of Safe Tables Our Priority, or S.T.O.P., a Chicago-based advocacy group. “I had no idea that there was any problem in our food supply. I loved my child more than anything in this world. And then to find out that he died because there were contaminated cattle feces in a hamburger. And to find out that had been recognized as a problem for a while. Why hadn’t it been fixed?”
Donley believes in the value of teaching consumers to handle food safely, but she doesn’t think education is enough. The best way to prevent foodborne illness, she says, is to mount a strong attack on the farm and then vigilantly follow up every step along the path to the table. It’s an approach that goes against the grain of many political interests. Not long ago, testifying before a congressional subcommittee, a senator reminded her, as have countless industry and government officials over the years, that the United States has the safest food supply in the world. Donley stared at him and said, “Senator, I beg to differ with you.”
Representative terms from entire chapter:
health officials
