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3 SALMONELLA READING IN TURKEY

FOODBORNE INFECTIONS, FOCUSING ON SALMONELLA

TO SOMEONE not well versed in the literature on food poisoning, the title of this chapter might sound like a headline in a supermarket tabloid about a literate fish discovered in Istanbul. In fact, the report that carried this title described an outbreak of gastrointestinal disease among hospital food-service employees related to infection with a particular strain of the bacteria Salmonella first recognized in Reading, England, and therefore named after that place. Salmonella are often named after the places where they were first discovered. If the Salmonella were to have their own family picnic, there would be some 2,500 of them, from all over the world. There are Salmonella named after Aberdeen and Adelaide, Caracas and Dublin, all the way down the alphabet to Zanzibar. These names could result in mind-bending medical headlines, involving, say, Salmonella uganda invading New York. Microbiologists have recently tried to remedy this problem by giving all the Salmonella that attack the gut a middle name, enterica. This system may please the classifiers, but it doesn’t do much for those who just want to give their gut problems a proper name. In this book, I have stuck with the old names, just because they require fewer words.

If we take a global view of our existence on this planet—that is, that we are all part of the living, breathing organism that British scientist James Lovelock has called Gaia—then the bacteria, parasites, and even natural toxins that make us sick are as much at home here as we are. They are not here to make us sick, any more than we are here to destroy the rain forests. If evolutionary microbiologist Lynn Margulis is correct, then people are entirely composed of various kinds of bacteria, and each of us is a synergistic colony of microbes, a cross between priest-archeologist Teilhard de Chardin’s grandiose vision of the universe becoming God and an amazing, lumbering grade-B horror movie attempt of the universe to understand itself. “What a piece of work is man!” said Shakespeare. Indeed.

The sicknesses we suffer are a side effect of an imbalance in human-microbial relations, some distortion in our collective ecosystem, resulting in the migration of disease-causing microbes from their natural homes into our food, and from there into our bodies. More often than not, the ecosystem distortion or cause of the bacterial migration is human in origin. Perhaps the easiest way to explore foodborne infections as a complex social-ecological issue is to look closely at the emergence and behavior of Salmonella epidemics over the past few decades.

On June 24, 1984, a seventy-one-year-old lady went to a family picnic in Moncton, New Brunswick. Little did she know, when she ate her morsel of cheese, that she was to be part of a great Canadian historical event, celebrated in bacterial circles and rued in milk producers’ circles for many years to come. On June 27, this modest, grandmotherly woman came down with nausea and diarrhea. Although some folks have been known to react in similar fashion to family picnics, this woman did not think family events were quite that bad. On June 28, she started vomiting; by June 30, things were getting worse, and she ended up in the hospital, from which she emerged shaken but alive on July 5.

That same day, the cheese manufacturer, in Prince Edward Island, issued a national recall of its products, which were distributed across Canada under various brand names. What the woman in Moncton did not know was that she was near the tail end of a six-month epidemic of salmonellosis that attacked more than two thousand people in the Maritimes and Ontario. The investigation of this epidemic, the largest of its kind in Canada, had progressed more slowly than it should have for various reasons. Not all the investigators saw the value of sound epidemiologic methods and did not always include a comparison, or control group, in their investigations. Cheese was not always considered a real food by those who got sick; they thought of it as a snack and thus did not include it in their food history questionnaire. The cheese involved was distributed to most Canadian provinces under eighteen brand names, making it difficult to trace. Finally, the number of bacteria in the cheese was very low. One Canadian researcher estimated, based on a series of case studies, that people in this epidemic got sick by eating fewer than half a dozen of these microscopic bacteria.

The organism involved in this epidemic, a strain of Salmonella typhimurium, was traced back to the factory where the cheese was made. There, it turned out, one of the workers decided to turn off some valves manually, even though an electronically controlled flow-diversion valve was in place. As a result, raw milk that was supposed to go to the pasteurizer ended up in the cheese vat, and 2,700 people got sick. The milk with the Salmonella in it was traced to one teat on one cow on one farm. She was a good producer, but she had chronic mastitis, not caused by Salmonella, although she was shedding it.

Most of the agents that cause food poisoning have a natural home—that is, they have evolved a niche for themselves where, like most of us, they carry out their recycling and respiratory functions with minimal trauma to their immediate neighbors. Over the years, a high proportion of outbreaks of foodborne disease in Canada and the United States has been traced to chicken, turkey, pork, and beef. Other Salmonella prefer pigeons, gulls, and people.

As in any respectable family, there are a few black sheep and troublemakers that will stir up a good gut incident no matter where they are. However, in its natural home setting, Salmonella organisms, like most of the agents that cause foodborne disease, often live like good quiet farmers in the hinterlands of their chosen animal hosts. The Maritime cow with the bacteria dripping from her teat is typical.

That year, 1984, George Orwell’s year of doom, was a bad year for salmonellosis in Canada. In September 1984, for instance, the Pope helicoptered in to visit the Jesuit mission of Sainte-Marie among the Hurons near Midland, Ontario. Of the more than sixteen hundred police officers who provided security, five hundred ate the roast beef boxed lunch offered by volunteers. Within the next twenty-four hours, as they headed home, just about every one of those police officers got sick. Newspaper reports describe police sick with severe diarrhea and vomiting on buses and motorcycles, finding bathrooms where they could, running from squad cars into the woods. In the weeks that followed, twenty-seven (over 6 percent) of the infected officers developed reactive (secondary) arthritis—pain and swelling in many of their joints. Some of them ended up with permanent joint damage. This painful arthritis, which is sometimes associated with eye and urinary tract inflammation, is a known consequence of infections with foodborne organisms such as Salmonella, Campylobacter, and Yersinia. Reactive arthritis used to be called Reiter’s syndrome, after the physician who discovered it in 1916. Unfortunately, Dr. Reiter later went on to a less-than-glorious career doing experiments in the Nazi death camps—hence the new name for the disease.

The 1984 outbreaks in Canada were a sign of things to come from the Salmonella gang. In the spring of 1985, some 16,000 people in and around Chicago were reported to have acquired Salmonella-associated diarrhea and vomiting after a small technical mix-up in a dairy processing plant. After an intensive investigation, the estimate of casualties was raised to almost 200,000. Only a few months before, the plant had been hailed as one of the safest and most modern in the United States (and by implication, of course, the world). In this case the cause appeared to be a structural flaw in the technology itself, which, as in Prince Edward Island, had allowed some unpasteurized milk to slip into the system. After the epidemic the plant, the largest in U.S. history until then, went bankrupt.

In 1994 an estimated 224,000 people got sick from Salmonella typhimurium. Tanker trucks in Minnesota that had been carrying liquid raw eggs were subsequently used to haul ice cream premix. The tanks had apparently not been well cleaned out. All the eggs were in one basket and guess what? Somebody dropped it.

When I’m teaching, I like to tell the parallel story, which also took place in 1994, of the old Mennonite couple at the St. Jacobs farmers’ market who sold a homemade delicacy called cook cheese. Apparently, they didn’t properly clean out a barrel that had been used to store chickens. Eighty-two people got sick. It was big news locally. It was sad for the old couple, but the problem could be handled locally and provided an excellent opportunity for education. There are still many such small outbreaks around the world. The major advantage, from a public health point of view, is that you can identify the farms, talk to the farmers, and improve the situation with a few simple recommendations. Trace-backs, responses, and regulations are much more difficult at economies of scale; they require more sophisticated (and expensive) molecular laboratory techniques and tend to evoke industrial-type solutions, like food irradiation, which mostly increase problems rather than solve them.

Several other trends have emerged in recent years. First, even if they are not large, outbreaks of salmonellosis and other foodborne bacteria are becoming more widespread as they cross borders and oceans. We are in the midst of a Salmonella pandemic. Because of mass distribution of food, and because food from many sources gets mixed up, relabeled, and redistributed at various points in the system, outbreaks are more difficult to trace back to where they started. Second, even though the bacteria involved are considered to be adapted to animals, they are also being connected with fresh produce. The sh*t is everywhere: fresh sprouts of all sorts, cantaloupe, chip dips, minced beef, powdered milk, lettuce, tomatoes, and pigs’ ears (fed as treats to dogs that then infect people) are some of the sources of human infections. Finally, some of the newer strains of Salmonella are resistant to a wide variety of antibiotics.

Salmonella typhimurium DT104, which sounds like the name of a small warship, first emerged in cattle in the United Kingdom in the early 1980s and then went pandemic in the next couple of decades. This organism is more likely to kill both people and animals than other members of the Salmonella extended family and is resistant to most of the antibacterial drugs one might wish to launch against it. Fortunately, although it has become widespread in North America and Europe, it does not (yet) appear to be common.

Trying to understand the emergence and spread of Salmonella is a lesson in the complex dynamics of social-ecological systems we think we control. Although a few of them prefer one host (typhi in people, cholerae-suis in pigs), most Salmonella are both liberated and cosmopolitan. S. panama came into the United Kingdom by way of dried eggs during World War II and from there migrated into pig feed and from there into people. S. eastbourne rode the cocoa bean boats from Africa into eastern Canada and brought its sweet tenesmus dances to children all over Canada and the United States in contaminated candy. Among the many we might reflect upon, the story of Salmonella enteritidis may be one of the more instructive.

Chickens and turkeys often carry a few Salmonella in their intestines or on their feathers, without any apparent ill effects. Tens of millions of people have gotten sick from similarly few Salmonella over the past few decades, and many have died. We are currently on the slowly declining tail (we hope) of a global pandemic of salmonellosis, mostly from chickens and mostly S.enteritidis. But bacteria are, from an evolutionary point of view, considerably more “fit” than the rest of us, and the emergence of S. enteritidis furnishes a cautionary tale.

In the early twentieth century, two serologically related Salmonellas—S. gallinarum, which causes diarrhea in chicks, and S. pullorum, or fowl typhoid, were quite common in poultry flocks in Europe and North America. Veterinarians noticed two important things about these organisms: they were adapted to domestic chickens and waterfowl, and they made the birds (but not people) sick. The first characteristic made the disease vulnerable to a “test and slaughter” method of eradication—a kind of mass-slaughter/napalm operation that many animal disease control people seem to find attractive (someone should do a psychological study on that); the second characteristic was strong motivation to carry out such a program. The eradication of fowl typhoid has been a success story; the disease is rare in any country that boasts a “modern” poultry industry.

About the same time as this Salmonella was eliminated from poultry, another Salmonella—S. enteritidis—wandered over from its natural home in rodents and took up residence in the vacated ecological niche. Not many disease specialists know much about ecology, so this shift in bacterial ecology was not widely investigated. The notion that various species of all types and sizes in the world are interconnected, and that ecological niches are not really vacated but just filled with other species, makes disease treatment and control seem, well, complicated.

In any case, the vets didn’t worry too much about it, since enteritidis doesn’t make chickens sick. It does make people sick, however, but veterinarians and physicians have a long history of not talking much to each other. By the late 1980s, there was a global pandemic—in people, not chickens. Enteritidis was even more clever than scientists imagined, since it lived inside the ovaries of the birds laying the eggs, and they got it from their closely guarded and very valuable parents, the so-called breeder flocks. These flocks are the source of most of the world’s commercial chickens. People didn’t even have to be dirty to get sick. All that hand washing and all those chemicals for naught! All those great genetics! How could a bacterium be so vile and anarchistic?

In 1988, Edwina Currie, then a junior health minister in the British government, drew attention to a problem with S. enteritidis in eggs. After Edwina made her announcement, sales of eggs in the UK fell by 60 percent overnight, and many egg producers went out of business; Edwina herself was relieved of her job. By 1994, Edwina was back in the news, helping to launch a celebrity-chef cookbook called My Perfect Omelette and claiming that British eggs were now the safest in the world. That may well be, but the global pandemic of salmonellosis is not over yet, and the organisms keep coming up with new chemical-evading stratagems as fast as those chemicals can be devised.

S. enteritidis continues to adapt. An epidemic in Canada and the United States of an unusual molecular strain, PT 30, was traced to raw whole almonds in 2000 and 2001. (The PT refers to “phage type”; phages are viruses that infect bacteria and can be used to trace them.) PT 30 is an uncommon strain in foodborne diseases, and almonds are an uncommon vehicle for infection. Investigators looked everywhere for an animal source, since Salmonella are not supposed to live out there in the wild without an animal host. They couldn’t find any animals near the nut farms. One of the researchers has suggested that the bacteria have been growing in the soil, which, because the almond growers have been growing trees at much higher densities than was once thought possible, is richer in nutrients than was once thought possible. If this supposition is true, then people have pushed the bacteria down new, interesting, and (for consumers) dangerous evolutionary paths.

Most Salmonella do not travel first class, as the ones inside the eggs have. Usually, they hang around in the dust and feces in the chicken barn, cling to the outside of the eggshell, and only get into the eggs after the eggshells have been washed. A 2006 survey in Europe found that in some countries, such as the Czech Republic, Poland, and Spain, more than 70 percent of egg-laying flocks are infected with Salmonella. With the exception of the Nordic countries (which have all but eradicated the disease in animals), other industrialized countries have lower, but still substantial, levels of contamination. In washing the eggs, people remove not only the visible dirt but also the less visible protective layer that the hen has secreted over her baby’s shell. The invisible bacteria are left intact and ready to invade through the pores of the egg, which they do as the shell dries.

Salmonella in cattle may move from the rural backwoods of intestinal living to adopt suburban lifestyles in lymph nodes. Even people can carry the organisms without being sick. Mary Malone, the infamous cook called Typhoid Mary, was one of many such people who have spread infections without themselves being sick. How we deal with such people (or animals) raises all the great questions of private rights versus public good that are at the heart of public health. Should people be quarantined? Cautioned? Charged with mischief?

A few bacteria do not usually cause much of a problem. What brings the masses out into the streets, however, is stress. Crowding the chickens or pigs together, and piling them into trucks to go to the slaughterhouse, brings Salmonella into the bracing, rebellious air, infiltrating feathers, splotching skin, and multiplying and filling the earth. If animals are not contaminated before they get into the truck to go to slaughter, they probably are afterward. Various studies find significant degrees of contamination in retail meats in Canada, the United States, and Europe (with the exception of the Nordic countries). Even if the prevalence gets down to, say, 1 percent, you, as a consumer, don’t know which 1 percent that is.

With all the scalds and disinfectants in modern packing plants, a lot of bacteria on the chickens do meet their end at the slaughterhouse. But with the crowds out full force, there are always a few million to spare, and bacteria love to multiply. Some of those millions get siphoned off into the meat by-products and from there get into the animal feeds and go back to the quiet life on the farm. The rest of them head off to the bright city lights, weddings, family reunions, papal visits, hospitals, and nursing homes.

From the point of view of the bacteria, bigger is better; the more intensive and large scale the livestock operations, the more extensive and devastating the foodborne disease, as well as the ecological problems. Salmonella in the family cow no longer need to content themselves with recycling through the same boring small family but get a free ride across the country and around the world. The notion of bacteria coming through in the eggs really only becomes frightening when one considers that a few major companies supply all the source birds for the egg industry. Monocultures and world trade are tailor-made for bacterial survival: the economies of scale are the economics of pandemics.

Another way to help the Salmonella along at the farm is to feed the animals antibiotics, which kill off the other neighborhood bacteria. The hardy and often drug-resistant Salmonella, never being ones to waste an opportunity, move into the homes we have cleaned out with our preemptive public safety measures. This tactic also works at home; you can sometimes lure a latent case of salmonellosis out of the closet by taking penicillin. Because of the massive amounts of antibiotics used in both people and animals, some people fear that drug-resistant Salmonella might take over the world. Drug-resistant bacteria, however, are adapted to live in a drug-filled environment, and if we cut back on our profligate antibiotic use, they would not give us problems.

If the bacteria can almost count on a quiet home on the farm, opportunities to spread from animal to animal abound on the truck to market. Even more opportunities arise at slaughter, and they most certainly can look forward to sloppiness in the kitchen. The counter becomes contaminated with bacteria when the turkey is put down there for dressing. Those that accompany the bird into the oven usually get killed off, but a healthy population lurks on the counter and repopulates it. If the counter is not contaminated, then your hands, or the knives, are. (What do you do about that itch on your scalp just before you handle the dinner? Just a little scratch won’t hurt, will it?) It is best, from a bacterial point of view, if you let the meat sit on the counter for a while, just to incubate.

Salmonella get turned on by that sort of warm, moist situation. They tumble over themselves in incestuous delight, doubling their populations every half hour or so. Other bacteria are even speedier. E. coli, a common gut bacterium, doubles every fifteen to twenty minutes, and Clostridium perfringens, which tends to favor meaty gravies and causes a passing diarrhea, is a copulatory sprinter at an eight. to ten-minute doubling time. I am told by a microbiologist colleague that, with unlimited food and ideal warmth, one cell could multiply to a colony of clones four thousand times the mass of the earth in twenty-four hours. Fortunately, the cells run out of food before they reach that size.

If poultry are a haven for Salmonella, hamburgers are heaven for a veritable menagerie of bacteria. Bacteria generally sit on the surface of meat, which includes the turkey’s armpits but not the heart of a steak. When we make hamburger, we take the surface bacteria and integrate them into the larger community of meat. Hamburgers, then, are really just cases of diarrhea and vomiting waiting for stomachs to happen, unless you cook them, and cook them well. Some of America’s finest foodborne disease outbreaks have been tracked back to hamburgers.

Like most of us, Salmonella prefer temperatures that are warm but not hot and will survive freezing but not boiling. They abhor the caustic wit of bleach and the acidic tongue of tomato juice, but they are adaptable enough to make a go of it in the most soiled of environments.

Hopelessness in the face of universal pollution is sometimes used as an argument by polluters to continue polluting; in the case of antibiotic resistance in bacteria, however, the situation is not at all hopeless. Bacteria can change rapidly; the same characteristics that allow them to develop antimicrobial resistance will also lead them to drop much of that resistance. Not burdened with rules of socially acceptable reproductive behavior, they can evolve and adapt as quickly to a drug-free life as they have to drugs. If Solomon had advised us to go to the bacteria, where quick, guiltless, cooperative change is the watchword, instead of to the ants, where regimented war prevails, who knows what the shape of human civilization might be today? The short of it is: things will get better if we change our ways.

Countries such as Sweden and Denmark have been systematic and aggressive in addressing Salmonella problems. Through a mixture of legal requirements and commercial inducements, Salmonella has been reduced and all but eradicated on farms, at slaughterhouses, and in the human population in these countries. So improvements are possible, but they are going to take some realistic, complex, systems thinking, firm commitments, and perhaps some deep cultural changes. For some of us, becoming more Swedish would, after all, not be so bad.