Vaccinated (11 page)

Jennifer Seavers was fourteen years old when she went out for Mexican food to celebrate a friend's birthday. Although Jennifer didn't like Mexican food, she didn't want to miss the party. So in October 2003 she and a dozen girls from Ambridge High School sat down to plates of nachos, fajitas, and tacos at a Chi-Chi's restaurant in Beaver, Pennsylvania, twenty-five miles northwest of Pittsburgh. Within a few weeks, one of Jennifer's friends came down with fever, stomachaches, muscle pain, weakness, nausea, and vomiting. Her urine turned dark brown, her skin turned yellow, and she couldn't breathe without feeling as if she was being stabbed just below her ribs. Frantic, the girl's parents took her to the doctor, whose blood test revealed the diagnosis: hepatitis A.

Jennifer knew that she had dodged a bullet. “I feel really lucky that I didn't get sick,” she said. “But I know a lot of people who did.” Jennifer's friend was one of many. The first case of hepatitis occurred on October 2, 2003. During the next few weeks, several more people in that area got sick. By November 3, local health officials confirmed that there was an outbreak of hepatitis and asked Chi-Chi's to shut its doors. Because the time from exposure to the virus to the appearance of first symptoms can be as long as seven weeks, everyone who had eaten at the restaurant from September to November was at risk; Chi-Chi's had served eleven thousand meals during that time. By November 5, the number of people infected had risen to eighty-four; by November 6, to a hundred and thirty; and by November 7, to two hundred. On November 7, Jeffrey Cook, an auto-body restorer from Aliquippa, Pennsylvania, died following a liver transplant in a desperate attempt to save his life.

Health officials were sure that the outbreak was caused by a restaurant employee, and during their investigations they found several employees with hepatitis. But all had been infected at the same time as their customers, not before. The timing wasn't right. The virus was coming from somewhere else. By November 11, the number of people infected had risen to three hundred, and two more people were in critical condition. By November 12, after forty more people became ill, investigators finally closed in on a likely source. Earlier that year, public health officials had interviewed thousands of people during outbreaks of hepatitis A in Georgia, Tennessee, and North Carolina. They had asked people who had and hadn't gotten sick what they had eaten. Then they had carefully checked the ingredients of each of those foods. One item kept appearing on the list of hepatitis A victims: green onions (scallions). Investigators found that restaurants had imported their green onions from Mexico, a country with a high rate of hepatitis A infection. Richard Quartarone, a spokesman for the Georgia State Health Department, said, “Because they're multilayered, green onions are very difficult to clean. The only way to be 100 percent sure that you've killed the hepatitis in the green onions is to cook them. But they're often used as a garnish, so you don't cook them.” Chi-Chi's, which had imported its green onions from Mexico, immediately pulled them from the menus of their ninety-nine other restaurants from Minnesota to the mid-Atlantic. But it was too late.

By November 13, the number of cases had risen to four hundred, and the outbreak claimed its second victim, Dineen Wieczorek, a customer service representative for Ikea. She had eaten at Chi-Chi's on October 6 to celebrate her wedding anniversary. Her daughter, Darleen Tronzo, recalled, “One meal. One meal, that's all it took. And people eat out every day. I eat out every day. You never think something like this could come of it.” By November 14 the number of cases had risen to five hundred, and the outbreak claimed its third victim, John Spratt, an employee at a payroll processing company. Spratt had eaten at Chi-Chi's with his daughter. They had both ordered the chicken fajitas. But Spratt, not his daughter, had chosen to eat the condiments that came with the meal—a choice that killed him.

When it was over, the hepatitis A virus outbreak at Chi-Chi's had infected about seven hundred people and killed four. Although this was the largest outbreak of hepatitis A in the United States, it wasn't the largest outbreak in the world. In 1989 in Shanghai, hepatitis A virus in uncooked polluted clams from the East China Sea had infected more than three hundred thousand people and killed forty-seven. Clams, like mussels and oysters, can filter as much as ten gallons of water an hour, concentrating the virus a hundredfold relative to its concentration in the ocean.

At the time of the outbreak at Chi-Chi's, a vaccine that could have prevented the tragedy had been available for eight years. Critical to the development of the first hepatitis A vaccine was Friedrich “Fritz” Deinhardt.

In the mid-1960s, Fritz Deinhardt was an unknown researcher. Born in Gütersloh, Germany, he attended the University of Göttingen and received his medical degree from the University of Hamburg. After completing both an internship and a residency in Hamburg, Deinhardt came to the United States, where he met his wife, Jean, and later became the chairman of microbiology at the Presbyterian St. Luke's Hospital in Chicago. In 1965, while working at St. Luke's, Deinhardt sampled the blood of a thirty-four-year-old surgeon whose initials were G. B. The surgeon had been ill with hepatitis for three days, his skin and eyes had turned yellow, he couldn't eat without vomiting, and he was tired and listless, unable to work. To capture the surgeon's virus, Deinhardt took the blood and injected it into the veins of white-lipped, hairy-faced marmosets—small, squirrel-like monkeys found in South America. Within a few years, marmosets would become an endangered species. But before the United States government prohibited research on marmosets, Deinhardt imported them, bred them, and, with the help of his wife—who fed milk to the babies—raised them. A few weeks after Deinhardt had injected marmosets with the surgeon's blood, all of the animals fell ill with hepatitis.

Despite his apparent success at isolating a hepatitis A virus, the American military, which funded Deinhardt's studies, was skeptical of his results. They asked Hilleman what he thought of Deinhardt's work. Although Deinhardt could be difficult to deal with—aggressive and argumentative—Hilleman stood by his friend, recalling that “[Fritz] took samples of blood from a surgeon with the initials G. B. and isolated a virus from that. He reportedly had hepatitis A. [Deinhardt] showed he had transmitted the virus to marmosets. All the time that the military was funding that, they would ask me, ‘Do you think that he's doing anything? Do you think he's right?' I said ‘Fritz Deinhardt is very bright. And who in the hell are you going to get to do the hepatitis A work if Fritz doesn't do it? You've got to fund him.' I had no reason to believe at the time that he hadn't isolated hepatitis A virus.”

On April 30, 1992, at the age of sixty-six, Fritz Deinhardt died of cancer. One of Deinhardt's obituaries, in reference to his work on marmosets, stated, “It was here that the first roots of meaningful specific studies of hepatitis A were begun. This breakthrough discovery was the epicenter of all hepatitis A investigations, opening a window to that which followed, and initiating a trail to the reality of [a] vaccine. Were it not for these seminal marmoset findings, we might still be struggling with the mysteries of hepatitis A.” But Fritz Deinhardt had never studied hepatitis A virus. He had isolated a very rare virus now called hepatitis G virus, an uncommon cause of disease in humans. Although he was unknowingly studying a different virus, Deinhardt was right about the marmosets; they were an excellent model for the study of hepatitis A.

Following Deinhardt's lead, Hilleman injected blood from a nine-year-old Costa Rican boy with hepatitis into the vein of a marmoset. Several weeks later he detected hepatitis A virus in the marmoset's liver. But marmosets were becoming increasingly harder to find. He needed other cells in which to grow his virus. And Hayflick's cells were the only ones that worked.

During the next thirteen years Maurice Hilleman became the first person to detect hepatitis A virus and hepatitis A antibodies, the first to grow the virus in fetal cells, the first to weaken it (as an added margin of safety), and the first to kill it with formaldehyde. Then he became the first to show that his weakened-then-killed hepatitis A vaccine worked in animals. Confident, he was ready to test it in people. When he tested his measles, mumps, and rubella vaccines, Hilleman had needed people at high risk for those diseases, so he had chosen institutionalized, mentally retarded children. Now he needed people at high risk for hepatitis A infection. Fortuitously, at around the time that Hilleman was looking for a place to do his studies, Alan Werzberger visited Merck. Werzberger was a physician at the Kiryas Joel Institute of Medicine.

In 1974, to accommodate their growing population in the Williamsburg section of Brooklyn, a group of Hasidic Jews moved to the Hudson Valley, fifty miles northwest of New York City. The village that they established, Kiryas Joel, transformed a quiet rural setting into a bustling urban center, with bearded men wearing black coats on hot summer days and women in head scarves pushing baby carriages past signs written in Hebrew. They brought a unique way of life from Brooklyn. Inhabitants of Kiryas Joel married at eighteen and had large families. By the early 1990s, about eight thousand people lived there.

The village of Kiryas Joel stood out for yet another reason: it had unusually high rates of hepatitis A. Typically, when infants and young children are infected with hepatitis A virus, they don't suffer any symptoms of the infection. But when older children, teenagers, and adults are infected, they often suffer severe disease. At Kiryas Joel, the living conditions allowed for easy transmission of the virus from younger children to older children. “The high birth rate, large family size, [and] day care center–like school atmosphere permitted close contact between younger and older children,” said Werzberger. “[We had] difficulty maintaining constant control over what the [younger] children did with their hands, from peremptory hand washing to surreptitious dips into communal school food.” “They all bathed together in these community pools,” recalled Phil Provost, Hilleman's co-worker on the hepatitis A vaccine at Merck. “It was a traditional practice in the community. But there was a lot of hepatitis A virus contamination in those pools. That's how they were spreading it.” From 1985 to 1991 local physicians cared for three hundred children infected with hepatitis A virus at Kiryas Joel. The virus infected 70 percent of all residents.

Hasidic boy living at Kiryas Joel receives an experimental hepatitis A vaccine while Alan Werzberger (left), who conducted the clinical trials, looks on, 1991.

The task of testing Hilleman's weakened-then-killed hepatitis A vaccine fell to Alan Werzberger. First, Werzberger found a thousand children who had never been infected with the virus. Then he divided them in half; one half received a shot of vaccine, the other a shot of placebo. Three months later he found that hepatitis A virus had infected thirty-four children in the study, all of whom had received placebo. In a paper published in the
New England Journal of Medicine
, Werzberger concluded that Hilleman's hepatitis A vaccine was 100 percent effective.

Since 1995, when Merck licensed its hepatitis A vaccine, the incidence of the disease in the United States has declined about 75 percent.

 

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Maurice Hilleman made their vaccines using Hayflick's cells, they didn't consider their actions to be immoral. Fetal cells were attractive because they were free of contaminating animal viruses, easy to grow in the laboratory, and highly susceptible to every known human virus. They were, in many ways, ideal cells in which to make vaccines. At the time they were being made, no one complained: not the media, the public, religious groups, the FDA, the NIH, or the WHO. Also, the woman who had provided her fetus to Leonard Hayflick for use in vaccines had requested the abortion. But times have changed. Now some groups—like those headed by Debi Vinnedge—see vaccines made from fetal cells as immoral.

Vinnedge sees a simple solution. Now that we have more sophisticated methods to detect contaminating viruses, we can remake these vaccines in animal cells. It wouldn't be easy. First, companies would have to find the right animal cells in which to grow these viruses. Then they would have to effectively weaken or kill the viruses, test these new vaccines in progressively larger trials (including tens of thousands of children), construct or refit buildings in which to make the vaccines, solicit FDA approval in the United States, and solicit approval from other regulatory agencies throughout the world. Because these diseases are now uncommon, it would be difficult or impossible to conduct trials large enough to prove that they worked. And because these new vaccines might not work as well, these trials could be considered unethical. Furthermore, from the point of view of regulatory agencies, these companies would be making new products that would have to be subjected to the standard scrutiny of a new product. Regulatory burdens would be immense; each new vaccine would cost at least $800 million to make. These new vaccines wouldn't increase sales, just costs. And these costs would have to be absorbed by taxpayers, medical insurance premiums, and international health agencies.