The Fatal Strain (9 page)

 

 

 

One day before Hoi-ka died in May 1997, Hong Kong’s public-health laboratory at Queen Mary Hospital had received a specimen of fluid from his windpipe. The sample was one of more than eighty collected every day from patients at the city’s hospitals and clinics. They were all sent to the lab, a small but hectic facility on the seventh floor of the clinical pathology building, erected on a hillside overlooking the western approaches to Victoria Harbor. The waters below were crowded with freighters emerging out of the mists of the South China Sea. Inside, the staff busily tested the samples, sorting them for flu, hepatitis, HIV, and other viruses, categorizing them by subtype when appropriate.

The technicians suspected that Hoi-ka was suffering from influenza and placed his specimen in a cell culture designed to grow the virus. When they looked at it a little later under a microscope, sure enough, it was flu. But what sort? Using an antibody test, they determined it was a kind of influenza A. They assumed it was one of two run-of-the-mill subtypes, either H3N2 or H1N1. The lab had chemical reagents to identify each of these seasonal strains. Yet every time they ran the test, they came up empty. They were stumped.

Dr. Wilina Lim was the adept yet unassuming chief of the virology lab. She spoke in quick, clipped sentences and had a no-nonsense manner that won her the respect of colleagues. Lim was sure the boy’s sample had to be seasonal flu. Since she never expected it to be something utterly new, she wasn’t particularly worried. Lim concluded that one of the ordinary strains must have evolved ever so slightly, which would explain why her lab’s reagents no longer picked it up. Still unaware that the boy had died, Lim decided to divvy up the specimen
and ship these samples out for further analysis in specialized flu labs overseas, including the CDC in Atlanta and Mill Hill in London. She also sent a sample to a veteran Dutch virologist named Jan de Jong, who worked at an institute outside Utrecht in the Netherlands. Though they had never met, Lim and de Jong shared a fascination with odd and offbeat viruses and over the years had compared notes from time to time.

More than two months passed. Lim never heard back. Then, on a Friday in early August, she got a call from de Jong. He was coming to Hong Kong, arriving in two days, and would like to see her. He didn’t say why. Lim assumed he was just passing through. She said she’d be pleased to finally meet him. She reserved him a room at the Ramada Hotel in Tsim Sha Tsui, a teeming quarter of narrow streets jammed with shops hawking clothes, shoes, and electronics, where the air was pungent with the smells of tropical cooking and the night skies blazed with neon.

First thing Monday morning, she picked him up. They set off for Queen Mary Hospital. De Jong wanted to see her lab. Lim was behind the wheel of her Nissan, seated on the right like all drivers in Hong Kong, de Jong to her left.

After five minutes, as they approached the harbor tunnel, de Jong looked over and asked, “Do you have any idea what virus you sent me?”

“No, I don’t know,” she responded. She was betting it was some idiosyncratic version of the common H3 strain.

“It’s an H5.”

“What?” she asked. “H5?”

Lim was bewildered. She had never come across an H5 strain. She wondered to herself, “Where did this H5 come from?”

De Jong didn’t say much more about the test results during the ride, but privately he had a suspicion. It could be contamination or some confusion in classifying samples. That was why he wanted to inspect her lab, why he had come all the way to Hong Kong. But once they arrived at the hospital, he quickly saw her operation was well run.

A few hours later, Lim called Margaret Chan, the health department director. The scientists at the CDC in Atlanta, which had
independently reached the same results, had yet to inform Hong Kong of their findings. So Lim’s news came as a shock.

“Are you sure?” Chan pressed. “H5N1? I have never heard of H5N1 infecting people.”

“That’s why I’m calling you,” Lim explained.

“Please educate me,” Chan told her.

Chan’s expertise was not infectious diseases. Her early medical interest had been pediatrics, followed later by women’s and family health issues. In reality, she had never intended to be a doctor at all. Growing up in Hong Kong, Chan had trained to be a teacher and for a year taught English, math, and home economics to elementary school students. But when her sweetheart, David, left for Canada to attend college in 1969, she followed him to the far side of the world and enrolled in a Catholic women’s college in Ontario. Before long, they were married. When David then decided to brave the rigors of medical school, she concluded the only way to assure his continuing attention was to become a doctor, too. Chan had little background in college science. But she did have the late-night tutoring of her new husband. After receiving their medical degrees from the University of Western Ontario, she and David returned to Hong Kong. Chan joined the government in 1978, rising quickly through the ranks of the health department. Sixteen years later, she was running it.

Chan has a charm that makes her seem taller than her modest height. Her manner is eminently self-assured yet empathetic. Her black hair is coiffed and her preferred lipstick bright red. Her brown eyes radiate warmth from behind large, round lenses. She speaks with authority, whether lecturing on health-care politics or the therapeutic qualities of her mother’s recipe for pork tenderloin soup. (Chan swears it’s good for stamina. Years later, after leaving Hong Kong and rising to the top post at WHO, she would get the Chinese herbal ingredients shipped to her in Geneva.) But in a realm of outsize egos, she is quick to admit what she doesn’t know.

When Chan heard about the test results, she asked Lim to bring de Jong over to see her at the health department. The next day, Chan took the visiting researcher out for lunch at the Hopewell Centre, a circular, sixty-story skyscraper that for a time had been Hong Kong’s
tallest building. Over a lunch of dim sum, she continued to press him for an explanation.

“What is the implication of this?” Chan asked.

“Dr. Chan,” de Jong answered, “if this is true, we are heading for something really serious.”

 

 

 

By the time the CDC team arrived in Hong Kong, Chan’s health officers were already hunting for clues, trying to pinpoint the source of the boy’s infection. But even a seasoned sleuth like Fukuda would find them elusive. Hoi-ka had died three months earlier, and the trail was getting cold.

The investigators got their first break when they learned the virus had already been implicated in a previous outbreak. Earlier that year, a baffling plague had raced through three farms in the rural north- west of Hong Kong. Every single bird at one farm had fallen over dead. So did most of those at the other two. About five thousand chickens had crashed out. Researchers from Hong Kong University, who studied influenza at a veterinary lab in Queen Mary Hospital, were stumped. They forwarded samples to a high-security lab run by the U.S. Department of Agriculture in Ames, Iowa. “It was one of the most highly virulent influenza viruses we’d ever worked with,” recalled Dennis Senne, a USDA microbiologist. “We’d never seen anything like it before. We’d never seen anything that killed so quickly.”

Senne inoculated ten chickens with the virus to test its pathogenicity. Some died within a day, the rest a day later. At first Senne couldn’t believe the virus was responsible. “We thought they’d somehow suffocated in the cages,” he said. But when researchers examined the dead birds, they found the lungs had been devastated. Genetic analysis revealed the culprit was an H5N1 flu virus. The discovery surprised the researchers back in Hong Kong, since this stripe of flu had never before troubled the city’s poultry. Yet they didn’t bother to stroll over to the adjacent building where Lim had her public-health lab and share the chilling news. Why should they? This virus had never been known to infect people. It was considered strictly avian.

When Fukuda learned in August there’d been an outbreak among
birds, he was convinced it was somehow related to his case. Yet he wasn’t sure how. The infected farms were clear across Hong Kong in Yuen Long, more than fifteen miles from the boy’s home, and Hoi-ka had been nowhere near them. The investigators searched his apartment and found bird droppings in the air-conditioning ducts. Was this the missing link? Or was it the live poultry market they discovered close by? The evidence was at best circumstantial.

The trail soon led to the boy’s nursery school. Several weeks before he fell sick, the staff had brought in three baby chicks and two ducklings to help the children get closer to nature. The cages were placed on the ground and the youngsters encouraged to peer inside, even to touch the birds. That was in the spring. By the time the investigators arrived in August, both ducklings had died, as had two of the chicks. The final chick had been removed, and no one knew where it was. There were no samples to take, no evidence that the birds were the source of infection. But suspicions ran strong.

On the remote chance they’d detect some vestige of virus, health officers scraped up dirt and dust from the school grounds for testing. The lab analysis found no trace. The investigators asked after the health of other children at the school and the staff. But there had been no unexplained absences. Nor had there been any other unusual illnesses.

In fact, there seemed to be practically none anywhere in Hong Kong. Fukuda and his colleagues examined medical records from hospitals and clinics from around the city, searching for atypical respiratory cases that might signal a swelling wave of infections. They visited intensive-care doctors and medical directors, urging them to report patients who were ending up on respirators with undiagnosed ailments. The phones started ringing, but they were all false alerts. “We didn’t see a big upsurge in respiratory illnesses going through the city,” he recalled. “We weren’t hearing about kids dying of mysterious illnesses.”

The team had even gathered two thousand blood samples, including several dozen from Hoi-ka’s schoolmates and teachers, to check for antibodies indicating exposure to the virus. These would ultimately all test negative except for a few from otherwise healthy poultry workers. The virus had gone silent. Fukuda’s anxiety about a nascent
pandemic began to ebb. “This is perhaps an odd infection that we don’t quite understand where this one child became infected,” Fukuda thought. “Perhaps it’s a one-off, a freak event.”

Yet even as he prepared to wrap up the probe and head home, he couldn’t put his mind to rest. Was this the end or the beginning? Could this virus still spark a global epidemic? He didn’t know how to answer the question.

 

 

 

Before Fukuda left Hong Kong, he met health department officials one last time. “We don’t fully understand what happened,” he admitted to them. “Look, we don’t know how this virus works. We don’t know what’s going to happen.” He urged them to step up surveillance for additional cases in city hospitals. He privately wondered whether he’d be back.

There was no doubt the threat would ultimately return. Flu pandemics are inevitable. Divining precisely when one will strike may be no easier than predicting the timing of earthquakes and hurricanes, but global epidemics are just as certain.

Three times in the twentieth century, novel flu strains crossed the species barrier from animals to humans, then circled the globe. The Spanish flu in 1918 claimed about 50 million lives, according to official estimates. But because many deaths occurred in far-flung corners of the world, beyond the range of medical chroniclers based in the United States and Europe, scientists and historians now believe the true toll could have reached 100 million. This plague killed about 675,000 Americans, more than the American death toll in all the wars of the twentieth century. Until recently, Spanish flu was considered the worst-case scenario. Bird flu has made the experts reconsider.

A better-case scenario is illustrated by the two subsequent pandemics, the Asian flu in 1957 and Hong Kong flu in 1968. Together, they claimed an estimated 3 million people worldwide. What distinguished the Spanish flu from its successors was how sick it made people, not whether it made them sick in the first place. In rough terms, all three pandemics were equally contagious, infecting a quarter to a third of the world’s population. The coming pandemic will
likely do the same. Even in the mildest scenario, hospitals and other medical care will buckle.

It is not just precedent that makes a flu pandemic inevitable. There is a dynamic to the virus that accounts for the historical pattern of recurring pandemics, and that dynamic continues to hold today. Influenza is among the most capricious and mutable of viruses, and it is this very unpredictability that makes a pandemic a sure thing.

All viruses, influenza and otherwise, can be grouped by the nature of the genetic material at their core. Some are built around DNA, or deoxyribonucleic acid. These viruses contain an inherent self-correcting mechanism that discourages the microbe from mutating. When the virus reproduces, this genetic spell-check detects inadvertent changes in the code and fixes them. But other viruses, including all influenza, are built around a second form of genetic material, RNA, or ribonucleic acid, and lack this proofreading mechanism. As a result, many of the copies contain subtle and not-so-subtle errors.

Among viruses, flu is exceedingly sloppy, constantly spinning off mutant progeny. Most of these copies are defective, with mutations that impede their ability to spread and reproduce. But a different kind of accidental change, instead of undermining survival, can take the virus in a new, more perilous direction.

The flu virus reproduces so vigorously that there are enough viable copies to propel it forward. The other copies, those with damaging mutations, are cast aside, as the virus is swept along a path of ever-shifting forms and threats. Ultimately, the virus hits upon precisely the set of mutations needed to infect people and spread like a common cold, the recipe for pandemic. It’s just a matter of chance. Each time the virus replicates, it’s a roll of the dice. Each new bird that’s infected, each person who’s exposed, each one who’s sickened is another toss. Throw the dice enough times and they’re sure to come up snake eyes.