Dowes Ginting, the most wanted man in Sumatra, lay dying. He had abandoned the Indonesian hospital, where he had seen his family succumb one after another, and fled deep into the mountains, trying to outrun the black magic, seeking refuge in a small, clapboard home beyond the cloud-shrouded peak of the Sinabung volcano. For four straight nights, a witch doctor hovered above him, resisting the evil spell.
The medicine man mumbled the unintelligible words of an incantation. He doused Dowes with cooking oil and massaged his tormented muscles. He placed a hefty chunk of betel nut in the corner of his own mouth and chewed, his lips staining red from the juice of the mild stimulant, and then, with the precision of a surgeon, spit the concoction gob by gob over his patient’s head, face, and chest and along his arms and legs. To relieve the surging fever, the witch doctor applied a pasty preparation of pounded rice and ginger called beras kencur to the man’s damp flesh.
Dowes, a wiry thirty-two-year-old with a mop of dark hair and a whisper of a mustache, seemed at times to improve. His breathing grew less labored and his coughing less wrenching. At these moments, Dowes would hope his affliction was nothing more than the respiratory troubles he sometimes had as a teenager. But other times his condition would suddenly deteriorate. The witch doctor had to repeat the treatment several times in the course of a single night. He even lit some kemenyan, a pungent incense made from the balsamic resin of local trees and burned only when battling the most intractable spirits.
When the nighttime therapy was finished, Dowes would retire to a house just next door on a rise overlooking the village of Jandi Meriah. While the witch doctor’s home was little more than a shack with a faded white exterior and rickety brown shutters, the neighbors’ was more substantial. It had a jolly pink tile facade with a green tile terrace and even a working toilet. It belonged to relatives of Dowes’s wife, and for the four days he sheltered there, they looked after him, washing him and cooking his meals. Mostly, he slept. But when he felt ambitious, he sat on the terrace and looked down on the rusting, corrugated metal roofs of the village and the tall stands of coconut palms.
It was to this remote hideaway that Dr. Timothy Uyeki tracked Dowes in May 2006. Uyeki had been dispatched to Indonesia by the World Health Organization after the agency’s office in the capital, Jakarta, had put out an urgent call for reinforcements. Influenza specialists suspected that Dowes was carrying a novel flu strain. And he was on the loose.
Since bird flu had first jumped the species barrier from animals to humans in Hong Kong nine years earlier, the strain had infected more than two hundred people, yet it had reassuringly shown little aptitude for spreading from one person to another. Now the outbreak ravaging this one Sumatran family suggested the contrary. It was the largest cluster of confirmed bird flu cases in the world to date and the strongest proof yet that the virus could be passed among people. If the virus that Dowes was harboring had mutated into a more transmissible form, tens of millions of people worldwide could die.
Investigators would ultimately conclude that the Sumatra outbreak was not sparked by an epidemic strain. The toll would be confined to the Gintings. But the outbreak was the closest thing yet to a dry run for an emerging epidemic.
The experience was sobering. This was more than just a stress test of the world’s emergency response. The episode, more generally, would cast doubts on some of the biggest bets humanity has been placing, raising profound questions about whether the WHO formula of brilliant scientists, courageous investigators, and modern technology was potent enough to break history’s inexorable cycle of pandemics.
In the tight-knit world of highland Sumatra, it did not take long for Uyeki and a pair of Indonesian colleagues to trace the fugitive through his extended family, catching up with Dowes three days after he slipped into Jandi Meriah. Uyeki entered the front room of the hilltop refuge and spied Dowes lying by the window. He was sprawled on a thin, pink mattress against the wall, chest bare, his head propped up on a pair of pillows. His eyes were open. They were dark and sunken, and beneath them hung heavy bags left by the long nights of misery and magic. Above him, the curtains were open. Morning sunlight filled the room.
The patient’s wife and several other family members took seats on a red rug along the far wall and eyed their visitors suspiciously. Uyeki sat down by the door. He started by offering his sympathy for the losses they’d already suffered. He explained he was looking for information. He wanted to help. It was a hard sell. Outsiders, even fellow Indonesians, were a rare sight in the village. They were viewed with distrust, even hostility.
Uyeki, an American, was an old hand at this kind of fieldwork. During his career as an epidemiologist with the U.S. Centers for Disease Control and Prevention in Atlanta, he had responded to Ebola in Africa, SARS in Asia, and anthrax attacks in Washington.
But flu was his passion. He had signed on to CDC’s influenza branch in 1998 and was instantly dispatched to investigate an unusual summertime outbreak on cruise ships in Alaska that sickened thousands of tourists and tourism workers. In 2002 he headed off with an international team to the island nation of Madagascar, where thirty thousand villagers had come down with a baffling respiratory infection and hundreds had died. Though it was never publicized, some communicable disease specialists at WHO feared that at that very moment a global flu pandemic was hatching, not somewhere in Asia but in that African country’s remote rural highlands. Uyeki pitched his tent there and camped for five days in continuous rain, collecting samples from the sick. The test results were ultimately reassuring, revealing that the outbreak was caused by an ordinary seasonal flu strain, exacerbated by Madagascar’s crowded conditions, malnutrition, and cold, wet winter.
Uyeki is evangelical about flu. He calls it the Rodney Dangerfield of diseases. He is outraged that for years the virus was unable to garner much attention from researchers and policy makers despite its proven ability to kill tens of thousands of Americans each winter and potentially millions in a pandemic. He is emphatic about this point, as he is about many things. He is perpetually engaged and chronically restless. He keeps his sleeves rolled up and sneakers on his feet. Even into his late forties, this abundant energy, coupled with his intense brown eyes and dark, uneven bangs, lent him a boyish aspect.
Uyeki is also a practicing physician, a trained pediatrician, and, as he sat in that doorway in Sumatra, he understood that he was dealing with more than just the devilish twists of microbiology. He also had to attend to stigma and loss. “These were people who had already suffered a great tragedy,” Uyeki later recalled. “This was a family that was trying to grieve. You needed to be empathetic and sympathetic. You feel a little reluctant to keep pushing.”
As he spoke with the relatives, Uyeki tried to make eye contact, hoping to win their trust. But out of the corner of his eye he also studied Dowes. The ailing man had pulled himself into a sitting position. There was something odd about his breathing. His chest muscles seemed to be working too hard, too fast. Before long, Uyeki fell silent. He looked down at his watch. Then, for a full minute, he observed Dowes, counting each breath. A healthy man would breathe about fourteen or sixteen times in a minute. But Dowes exceeded that in half the time. Uyeki counted up to thirty-six. He knew then that the patient had pneumonia. It was almost certainly bird flu. But he’d need a specimen of virus to be sure.
Uyeki delicately advised the family that he wanted to take a sample.
“No blood,” one relative objected.
“I’m not going to draw blood,” Uyeki assured them. His aim was to swab the man’s nose and throat.
“No equipment,” a relative insisted, making clear they’d be horribly offended if Uyeki donned his protective gear.
It was a terrible demand. This was a monster of a virus that had killed most of those it infected. Flipping a coin would give better odds of survival. It was so deadly that scientists studying the virus were required to wear protective suits and work in special limited-access laboratories behind double doors with reverse ventilation to siphon off contaminated air. In the field, investigators were instructed to wear full outfits, including respirator masks, goggles, surgical caps and gowns, shoe coverings, and gloves. Uyeki usually snapped on three layers of gloves just to be sure. He always carried the complete gear in his backpack. This was going to be a tough negotiation.
“OK,” Uyeki offered, “I won’t wear a gown and I won’t wear goggles.” He would compromise. “But I’m going to wear a respirator and gloves.” He figured the main hazard would be breathing in the virus or getting it on his bare flesh.
“Nothing,” the relative repeated.
“No, this is what I’m going to wear,” Uyeki responded, motioning to his face and hands.
They went back and forth. Eventually the family relented. Uyeki slipped on what he considered the minimum protection, a mask and gloves.
Uyeki had wanted one of the Indonesian doctors to help him take samples. But his colleague was petrified, rightfully so. He was just a local country doctor who had never confronted such a cruel and exotic killer. Uyeki tried to reassure him. Uyeki produced another mask and pair of gloves from his backpack and passed them to his reluctant partner, then explained step-by-step what they were about to do.
On Uyeki’s instruction, the Indonesian physician lifted a Q-tip-like swab to Dowes’s left nostril and gingerly inserted it. Then he handed it back to Uyeki, who carefully snapped off the top, placed it into a tube containing sterile media for transporting virus samples, and screwed on the cap.
Next Uyeki sampled the right nostril himself, repeating the procedure.
Finally Uyeki prepared to take the throat specimen. This would be tougher. He would have to reach into the windpipe with the swab and fish out a glob of mucus. It would be absolutely loaded with virus. The pathogen had already been replicating inside its host for a week, and Dowes would be teeming with infection.
Uyeki squatted beside him and leaned right in. The doctor’s eyes were just inches from those of his patient. Uyeki lifted the swab. Then, he carefully inserted it through the open mouth and down Dowes’s throat.
The sensation must have tickled. For at that very moment, Dowes coughed. And when he did, it was right in Uyeki’s face.
Uyeki didn’t blanch. But inside, his stomach dropped. “Oh, this is not good,” Uyeki fretted to himself. Despite the mask, most of his face was exposed. His mind raced. He instantly thought about his unprotected eyes. He knew other types of avian flu viruses had been contracted through the eyes. Could the same be true for this strain?
He tried to stay focused. He had long since learned to remain calm no matter what. Countless times in his career he had resuscitated children when one slight miscue or false start might mean their death. This time he stared past his own mortality. Later, after leaving the village, he would urgently dose himself with antiviral drugs, taking four times the usual amount prescribed for prophylaxis, and acknowledge he’d made a mistake. He would promise himself never to forgo goggles again.
But now he had to rein in his rising anxiety. Slowly, he withdrew the swab from the Dowes’s mouth and backed away.
Uyeki placed the final, hard-won sample in a tube. With a Magic Marker, he labeled all the specimens. Next, he removed his gloves, then those of his Indonesian partner. He stuffed them in a bag he had brought specifically for disposing of dirty material. He sealed it tight.
Then he turned back to the row of family members seated along the wall with another request. He told them he now wanted to briefly examine Dowes and asked for permission.
“All I want to do is listen,” Uyeki appealed, showing them his stethoscope. “I just want to listen to him. No blood. I’m not going to do a full exam.” They agreed.
Squatting next to the mattress, he listened to Dowes’s chest. He listened with the patient sitting up and with the patient lying down. Uyeki heard an odd crackling sound, a kind of coarse gurgling each time Dowes inhaled and each time he exhaled. Uyeki had heard this in other patients, but never this loud. It was the sound of fluid, of a man drowning.
“He has pneumonia and he has it in both lungs,” he reported to the relatives. “I strongly recommend he go to a hospital.”
From beneath his straight black bangs, Uyeki’s detective eyes watched them, trying to gauge their reaction. But he knew what the answer would be. The relatives refused. They insisted that Dowes had to complete two more days of traditional treatment. Uyeki had no choice but to defer to their wishes. He didn’t want to make a scene. Nor did he have any way of forcing them to comply. Though he had come to the village with a security officer, the escort’s charge was limited to keeping Uyeki safe should the locals turn unruly. So after only two hours in the village, the medical team was back on the road in their four-wheel-drive vehicle, skirting the volcano, bound for the district capital of Kabanjahe twenty-five miles away.
But before they left, Uyeki urged the relatives to get Dowes to a hospital if his condition worsened. Uyeki suspected it would. It was clear Dowes was going to die. Uyeki did not realize how quickly.
It had been nearly a year since Indonesia had confirmed its first human cases of bird flu. A government auditor in the suburbs of Jakarta and his two young daughters had died abruptly in July 2005. The outbreak was unnerving on several counts. Not only were disease specialists unable to determine the original source of infection despite weeks of investigation, but the sequence of the three cases strongly suggested that the virus had been passed from at least one victim to another. Perhaps most worrisome was that the virus was now striking people in Indonesia at all. The strain had already been exacting a toll elsewhere in Southeast Asia, but Indonesia, a country of vast size, sprawl, and poverty, was the most daunting front so far.
Then, less than a month later, the world got some surprisingly good news from a pair of international research teams. By applying cold, hard numbers and sophisticated computer models to the outbreak in Southeast Asia, the two teams had each determined that the world could nip a human flu epidemic in the bud given the right mix of antiviral drugs, quarantines, and social controls. This would be unprecedented. Mankind had never before been able to stem an emerging influenza pandemic but throughout history always had to ride out the storm, waiting for the plague to burn itself out. Now, armed with high-speed computers, advanced statistics, and modern medical science, humanity might be able to bend nature to its will.
At Imperial College London, computational biologist Neil M. Ferguson led a group of researchers in simulating an emerging epidemic in rural Thailand. They chose Thailand because detailed demographic data was available. But the researchers said the conclusions could equally apply to similar low-density communities in Southeast Asia. Starting with a single human infection, Ferguson and his colleagues found that the virus remained limited to the local area for about thirty days before shooting like buckshot across the rest of the country over the following two months. They said this created an opportunity to contain a nascent pandemic at its source if about 2 million courses of the antiviral drug oseltamivir were rushed to the scene and dispensed to those within three miles of the initial outbreak. Oseltamivir is marketed by the Swiss drug company F. Hoffmann-La Roche Ltd. under the brand name Tamiflu. Officials would also have to shutter schools and workplaces to limit human contact and would have to place the entire area under quarantine.
A separate team led by Ira M. Longini Jr., a biostatistician at Emory University in Atlanta, ran a slightly different model that also simulated an outbreak in a theoretical population based on data from northeast ern Thailand. These researchers likewise examined the impact of antiviral medicine, limits on human contact, and quarantine and came essentially to the same encouraging conclusions. Their analysis was even more optimistic, finding that no more than 1 million courses of Tamiflu might be needed.
Together, these two studies, published almost simultaneously in the rival journals Nature and Science, offered the WHO a strategy for confronting a pandemic. It was perhaps the only hope, and WHO was quick to integrate the findings into its emergency planning. “No attempt has ever been made to alter the natural course of a pandemic at its start and the behavior of influenza viruses is hard to predict. Nevertheless, the rapid containment approach is considered one of the key elements of pandemic influenza preparedness,” WHO wrote in describing its new strategy.
But the researchers made clear that success rested on some very perilous assumptions. The nature of the virus itself was a crucial variable. If the epidemic flu strain were good at reproducing itself, say for instance if each sick person on average infected at least two others, containment would be unlikely. If, however, the strain were less contagious, with each sick person infecting fewer than two others, chances of checking the disease would be better.
Success depended equally on the speed and effectiveness of the response. Ferguson’s team stressed that health authorities would have to almost instantly recognize the initial case of an epidemic strain and detect most of the subsequent ones. They would also have to identify nearly everyone who may have had contact with the victims, including relatives, schoolmates, work colleagues, and anyone else who had ridden in the same bus, shopped together in same market, eaten in the same restaurant, or prayed in the same mosque, temple, or church, and then get Tamiflu into their hands. The drugs would have to reach an overwhelming majority, preferably more than 90 percent. Longini’s group concluded that containment could only work if “the stockpile were deployed at the source of the emerging strain within two to three weeks of detection.” Any longer and the highly infectious virus would breach the containment zone, confronting the world with an unstoppable epidemic.
WHO’s emergency containment plan incorporated this narrow window, stressing that success depended on mass administration of antiviral drugs within three weeks of the “timely detection” of the first case of this new epidemic strain. A twenty-day supply of Tamiflu would have to reach 80 percent of the targeted population, defined as everyone within at least three to six miles of every detected case, or between ten thousand and fifty thousand people in each area at risk. This would require a massive global undertaking to tap international stockpiles of Tamiflu, airlift the drug into the country, ship it to the hinterlands, and distribute it among the locals. (If the outbreak occurred in a city, such efforts would be pointless. The population density would offer so much dry tinder to the virus that a global conflagration would be unavoidable.)
WHO would rely heavily on the government of the stricken country to quickly detect and honestly report any suspicious outbreaks, initiate the containment effort, and then efficiently transport antiviral drugs to the affected area, no matter how remote. Movement in and out of the containment zone would be sharply restricted. Cooperation from the community would be essential. People would have to stay put, stay home, and take their medicine as prescribed. The sick would be isolated, those exposed to them quarantined. Lab testing of their samples would be crucial for tracking the evolution of the outbreak and calibrating the response. To succeed, this highly disciplined operation would have to last a month or more. “It will require excellent surveillance and logistics mechanisms as well as an ability to ensure compliance with policy directives,” WHO acknowledged.
The power of the computer simulations was awesome, and the chances they promised humanity to dodge a pandemic were previously unimaginable. But what would happen when they collided with the realities of Asia?
In the weeks before Dowes was tracked to his mountain hideaway in May 2006, he had watched sickness burn through his family. It had taken his older sister, his younger sister, and three of their children. His own ten-year-old son had held on longer than most. Dowes and his wife barely moved from the boy’s bedside, but eventually, after suffering eleven days of fever and ever-greater difficulty breathing, he, too, succumbed.
The members of this Sumatran family had perished despite the efforts of the best hospitals in the island’s main city of Medan, the third-largest in Indonesia. Though overseas laboratory analysis in Hong Kong had confirmed the cause was bird flu, Dowes did not believe it. When his relatives took antiviral drugs as prescribed for bird flu, they only got worse. When they gave blood to be tested for the virus, they only grew weaker. Nearly everyone who entered the hospital was fated to die, not to survive. So when Dowes fell sick two days after his son’s death, he decided to make himself scarce.
The outbreak in his family had already attracted international attention because of the cluster’s size. The WHO had sent Uyeki to Indonesia along with the agency’s premier epidemiologist, Dr. Tom Grein. An intrepid German investigator, Grein had repeatedly responded to some of the world’s most terrifying outbreaks, including Ebola and Marburg epidemics in Africa and mysterious clusters of respiratory disease in remote areas of northern Afghanistan and southern Sudan. He and Uyeki had worked together before and were familiar with each other’s routines.
When Dowes fell ill, WHO’s flu specialists surmised he was another link in an unprecedented chain of human transmission. Now his disappearance was setting off warning lights well beyond the islands of Indonesia. He was on the move and potentially contagious with what seemed to be the most transmissible strain of the virus yet. This was the way epidemics started. Indonesian authorities put out a bulletin to local health officers: Find Dowes. Uyeki and Grein had reached Sumatra the very day he went to ground. They joined the hunt.
Dowes and his family had rented a public minibus to smuggle him even deeper into the wilderness. They drove along a rough country road that cut through orange orchards, fields of high corn, and glistening terraces of rice. They passed the occasional brick church, onion-domed mosque, and villagers drying tobacco on wood frames set out in their yards. In places, tall brush brimming with wildflowers pressed up against the roadside. The green slopes of Mt. Sinabung beckoned in the distance, its upper reaches in shadow, the lower ones in crisp sunshine. After several hours they reached their destination.
Jandi Meriah is built on the opposing slopes of a slender valley bisected by the Loborus River, which courses through a deep, lush ravine. A bridge connects the two halves, and a dirt and gravel road ascends each side, meandering through the hamlet to the fields and orchards above. The villagers grow oranges, durian fruit, corn, chili peppers, and chocolate. But Jandi Meriah is particularly famed in North Sumatra province for its witch doctors.
When Dowes arrived at the small, clapboard dwelling three days after falling ill, he could still walk and talk. He was feverish and coughing badly, but he seemed relieved to be there. The reclusive witch doctor, or dukun in Indonesian, agreed to treat him and said there would be no charge. It is believed that demanding payment is the surest way for a sorcerer to lose his mystical gift, though gratuities like cigarettes are always welcome.
The witch doctor’s formal name was Suherman Bangun. The villagers, with a mixture of affection and awe, called him Pak Dirman. Bangun had been born forty-three years earlier in Medan before retreating into the mountains to farm corn and exercise his mystical talents. Though Bangun was a Muslim, many of those who sought his help, including Dowes, were Christian. “His reputation is very famous,” Bangun’s wife, Rintang Boru Ginting, boasted to me when I later caught up with her in the village. “His patients come from many faraway places.” Rintang herself had been his first patient, she recalled. Not long after the birth of their second child, he had removed a tumor from her neck, carving it out with a razor blade, then sealing the flesh by spitting betel nut juice on it and reciting a spell.
Dowes proved to be a more trying case. The nighttime treatments failed to dispel the affliction. Each new dawn found Dowes fighting harder for his breath. Late on his fourth night at the witch doctor’s home, hours after Uyeki had made his futile appeal to the family, Dowes got up to use the bathroom. Since there was no toilet there, his uncle wrapped his arm around him and helped him walk next door. Dowes could hardly breathe. He was staggering, on the brink of collapse. His condition had taken an abrupt turn for the worse since the previous day. “He was almost unconscious,” one relative later recalled.
Bangun advised the family there was nothing more he could do. So the uncle wrestled Dowes to the Suzuki jeep parked out front. Together with an aunt and two cousins, they drove out of the valley and began racing through the dusky daybreak back toward Kabanjahe and the district hospital. Before they made it, Dowes died.
In the highland village of Kubu Sembilang where Dowes and his family had lived, the Suzuki jeep was a rare luxury. The vehicle had originally belonged to Dowes’s father, the patriarch of the Ginting clan, until he died in 2001. Though most everyone in Kubu Sembilang came from generations of hardscrabble peasants, Dowes’s father, Ponten, had also been a gangster. In fact, in that corner of Sumatra, he had been the godfather, running protection and extortion rackets throughout the environs. It was said he had won his power by conjuring evil spirits. His criminal pursuits had earned the family a measure of respect and riches. But the Gintings remained essentially farmers, spending their days in orange and lime orchards and fields heavy with red chili peppers.
Ponten had five children, three boys and two girls, with Dowes in the middle. The eldest sister, thirty-seven-year-old Puji, peddled the family produce at a traditional market in the neighboring town. Villagers from the surrounding area of Karo district came to buy clothes, shoes, and other dry goods from stalls in the heart of the market. Puji’s stand was near the edge with the other fruit, vegetable, and meat mongers, about twenty yards from a kiosk hawking live chickens. After she fell fatally ill, WHO investigators hypothesized she had contracted the flu virus at that nearby poultry stall, though samples later taken in the market all came back negative. Investigators also suggested she could have been infected by contaminated chicken droppings that she used as fertilizer in her garden.
Puji started feeling unwell on April 24, 2006, less than a week before the people of her village were to celebrate their annual harvest festival, Merdang Merdem. She began to cough and her temperature climbed. Her sister massaged Puji’s throbbing muscles and tried unsuccessfully to nurse her to health. Her family decided to proceed with their thanksgiving anyway.
Tradition is an essential ingredient of daily life in the district. The Karo people are Bataks, a distinct ethnic group within Indonesia known for a stubborn streak and a fierce adherence to their own culture and beliefs. In the past, the Bataks were storied as ferocious warriors. Today they are leading officers in the Indonesian military and some of the most formidable lawyers in Jakarta. Inevitably the fearless bus drivers who career through the capital’s tortured traffic are also Bataks. While the Javanese of Indonesia’s main island are refined, aloof, and at times duplicitous, the Bataks can be coarse but also refreshingly candid.
The festival brought together all five Ginting siblings, their spouses, and their children. They gathered at the small house, facing the village soccer field, where Puji lived with her husband and three sons. It was a wooden dwelling with a sun-bleached blue facade and pitched corrugated metal roof crowned by a satellite dish. Chickens rooted around in the dirt out back. Directly next door, her sister lived with her husband, two daughters, and son in a larger, more robust, cream-colored home built from concrete and tile, also capped by a satellite dish. Just beyond that was where her brother Dowes resided with his wife and two sons. His home was the most modest of the three, a small, unpainted clapboard structure.
The celebration began just after sunrise and continued until nightfall, the family feasting on curried chicken and roasted pork served in a spicy sauce prepared from pig’s blood, while the children played in the dirt road out front. In olden times, the harvest festival would last seven days, culminating with a communal feast and folk dancing that doubled as matchmaking for the girls and boys of the village. The holiday had in recent years been condensed to one day. But as they always had, relatives who’d moved away from the village came back to celebrate. So the youngest of the Ginting siblings, a twenty-five-year-old kid brother named Jones, who had left the village to start his own family in the district capital, returned with his wife and two sons.
Once the party finished, it was too late for Jones and his family to go home. They stayed over at Puji’s house, sleeping in the same confined quarters with her and her children and two other relatives. It was a rough night, nine people crammed into one small space with Puji coughing uncontrollably.
Three days after the festival, the family brought Puji to the emergency room at the district hospital. She could hardly breathe, and her skin was turning blue from a lack of oxygen in the blood. The doctors gave her medicine and advised the family to take her to Santa Elisabeth Hospital in Medan, about fifty miles away along the coast, where she was admitted into the intensive care unit. Santa Elisabeth was one of the best medical facilities in Sumatra, a seventy-five-year-old Catholic hospital opened by Indonesia’s former rulers, the Dutch. Inside the colonial structure, the black-and-white marble corridors were spotless. The interior courtyards were meticulously maintained with manicured lawns, sculpted shrubbery, and flowering bushes. Patients and their families waiting in the main lobby, with its high stained-glass windows, spoke only in hushed tones. By contrast with the crowds and chaos at Indonesia’s public hospitals, everything about Santa Elisabeth was orderly and organized. But that wasn’t enough. On May 4, after only twelve hours in intensive care, Puji died. The precise cause of death was never determined. No samples were taken, and no one suggested at the time it could be bird flu.
But by the time Puji was buried a day later, six other family members were already sick. Most had gone to their village’s rudimentary health post complaining of fever and breathing difficulties, but found no relief. As they continued to grow weaker, even talking became a chore.
“The doctors were shocked,” recalled the district health chief, Dr. Diana E. Ginting, who was no relation to Puji and her family. “The chest X-rays were all white.” Their lungs had filled with fluid. The clinic doctor was the first to suspect they had caught a novel flu strain and sent them to Adam Malik General Hospital in Medan, which had been designated by the Indonesian government as the referral facility for all bird flu cases in the region.
As soon as they arrived, it was clear they desperately did not want to be there. “They didn’t accept that it was avian influenza,” recounted Dr. Nur Rasyid Lubis, the hospital’s deputy director and head of its outbreak response team. “They tried to refuse all treatment. We could treat them only because their condition made it impossible for them to resist. But if they had been healthy enough to walk, they all would have run away.”
The family members balked at giving blood for testing. Several initially refused to go to the isolation ward set up for suspected bird flu cases. “None of us believed it was bird flu,” Puji’s sister-in-law later recounted. “We thought it was black magic. Everyone in the family was getting sick and no one else was. Someone had put a spell on our family.”
That account was offered to me by the wife of Puji’s younger brother Jones. I must have given her an inquisitive look because she added, “Black magic is very common in our place.”
True to local practice, relatives and in-laws had streamed out of the mountains to keep vigil at the hospital. They crowded into the large room where their kin were lined up in two facing rows of metal cots and scoffed at the insistent advice of hospital staff that they put on masks and gloves to protect themselves.
Puji’s oldest son died just one day after being admitted to the hospital. One of Puji’s sisters succumbed next.
As Jones watched his kin perish in the beds around him, he confided to his wife, “If I stay here, I’ll be dead.” Jones’s fever had topped 102 degrees and showed no sign of breaking. Fresh X-rays revealed that his left lung had entirely clouded over and his right lung was nearly as bad. He told his wife it was time to leave.
“I was losing hope,” Jones later recounted in a raspy voice, almost a whisper. His stare was blank beneath thick eyebrows, and his cheeks were sunken. He had been a young tough. Now his arms and legs, covered with elaborate swirling tattoos of red and green, had grown emaciated. He had dropped twenty pounds during his struggle for survival, and his tank top hung off his shrunken frame. “I was afraid of the hospital,” he continued. “I thought I was going to die. I can’t remember much, but I remember running away.”
At that moment in the retelling, Jones fell silent. His wife, a chatty twenty-three-year-old with long hair parted in the middle and tied in the back, picked up the thread. “We were watching our family die one by one,” she recalled. “We thought the hospital could not cure him.”
Jones had slipped out of the hospital with his wife and two young sons and hailed a taxi on the street. They told the driver to take them to a congested, working-class quarter of Medan jammed against the edge of the city airport. The houses were jumbled together along narrow alleys. Young men lingered on cramped front porches. Drainage ditches ran past the doorsteps and chickens pecked in the fetid black water. Every few minutes, an airplane would pass overhead with a tremendous roar. A year earlier, an Indonesian jetliner had crashed into the neighborhood moments after taking off, killing at least 149 people, including dozens on the ground, yet the incident was soon all but forgotten outside the quarter. This was the kind of place where Jones could disappear.
Jones also had relatives there to take him in. One, a distant relation, was a doctor with a practice on the main boulevard. Jones went to see him. The doctor examined Jones, prescribed some medicine, and offered an unwelcome diagnosis. “You have bird flu,” the doctor said, urging the feverish fugitive to return to Adam Malik Hospital. Jones balked.
If Jones could not find the answer in the city, he reasoned, he should go home to the mountains. He and his family hired another taxi and fled Medan. They drove deeper and deeper into the jungle, following the steep winding road and treacherous switchbacks up and up and up to the highlands of Karo, where cool breezes offered relief and promise of a cure.
By the time health officials in Sumatra realized they had a problem, it had already been two weeks since the eldest Ginting sister, Puji, fell sick, and six others were already desperately ill.
District health and veterinary officials drove to Kubu Sembilang and summoned the villagers. “Bird flu is here, now, among you,” an animal-health officer told the hundreds of people who gathered at the village hall. “To break the chain of infection, we have to depopulate your livestock.”
The cooperative spirit lasted precisely one day. Trouble began when provincial veterinary officials drove up from Medan, pulled rank on their local counterparts, and announced that all the samples taken from local poultry were negative for bird flu and the mass cull, though prudent, had been unnecessary. The villagers were livid.
Kubu Sembilang was in revolt by the time a team of disease investigators from the provincial government arrived in the highlands later that week. Local officials pleaded with them to go home. “We’re frightened something might happen to you,” one local health officer warned them. “You might be attacked.” The investigators retreated.
A day later, the provincial team returned reinforced by disease specialists who had flown in from the national health ministry in Jakarta. This time they managed to enter Kubu Sembilang. But the villagers refused to answer any questions: What was the possible source of the infection? How did the victims catch it? Was anyone else in the village sick? After several frustrating days, the team from the national health ministry withdrew to Jakarta and never came back. They were too scared. Villagers had threatened to stab them.
“We chased them away,” Puji’s brother-in-law admitted to me when I met him a few weeks later. The man had a hard face and bitter eyes. His tone grew more menacing the longer I peppered him with questions. “There is no such thing as bird flu. It’s bullshit,” he continued. “This is all simply black magic.”
That last line was recited to me over and over as I explored Kubu Sembilang. There were no sick chickens in the village and only one sick family. What else could it be but an evil spell?
A neighbor laid it all out for me. “This is something supernatural,” began Tempu Sembiring, a fifty-year-old orange grower with a balding pate and salt-and-pepper mustache. An unlit cigarette bobbed between his lips as he recounted the tale. “Their father used to be the chief gangster in this area. He took his power from a spirit called Begu Ganjang at a holy place in Simalungun. This is revenge for worshipping at that place.”
According to Batak lore, Begu Ganjang can be conjured by offering him the liver, heart, and gizzard of a red rooster wrapped in four banana leaves along with seven pieces of chili pepper and chunks of banana. These are to be placed around the perimeter of a late-night ceremony, at the four points of the compass. The rooster’s blood is drained into a coconut husk at the center and then the spirit summoned. He is believed strongest at a mystical site in the district of Simalungun on the shores of Lake Toba, in the heart of the Bataks’ highland domain. Once called, Begu Ganjang will do his master’s bidding, delivering wealth and protection. But the spirit will remain faithful only as long as periodic oblations are offered, and unpaid debts to Begu Ganjang can be collected from kin in blood.
“Ponten was quite powerful,” Sembiring continued, lowering his voice to a whisper as he mentioned the patriarch’s name. “When he died five years ago, his friends came all the way from Jakarta. The condolence flowers stretched all along the road. They stretched from there,” he said, pointing at the Ginting homes in the distance, “all the way to here.” He scanned his finger past the soccer field, the village church, and the dirt track leading up into the orchards. “The family had to be sacrificed. It is a payback for what happened in the past.”
The village of Kubu Sembilang was in full rebellion as the investigation moved into its second week. WHO had received final lab confirmation that the outbreak was caused by bird flu. But Karo district residents objected that their poultry were not to blame, and, in mid-May, half a dozen farmers beheaded a chicken and drank its blood to demonstrate that their birds were healthy. A week later, with Indonesian officials designating Karo a bird flu-infected area, scores of poultry traders furious over the potential loss of revenue descended on the provincial capital, Medan, again slaughtering chickens and drinking their blood in protest.
The WHO team’s initial effort to visit the village was “significantly delayed” by security concerns, according to an internal agency report. “It was later learned by WHO that quite strong hostility was expressed by some villagers, including a threat to bodily harm of laboratory staff,” the report said.
When the WHO investigators, accompanied by Indonesian health officials, finally entered the village nearly three weeks after Puji fell sick, they recruited twenty local volunteers to monitor fellow residents for fever and set up a temporary health post on the soccer field, offering free medical care. The investigators bravely pieced together the chronology of the outbreak. They tried to collect samples from family members to see how widely the infection had spread. But, the WHO team reported, “Such requests were universally refused.” The investigators traced those who had contact with the victims, providing them Tamiflu for protection. But many of those who were closest to the Gintings refused to take it.
Before I’d set off myself for Kubu Sembilang, I had worried I’d also get a hostile reception. A relative of the Gintings in Medan had given me the name of an uncle in case I needed help. When I got to the village, the man was away. But an aunt and cousin politely greeted me and invited me into the spartan eatery they ran, offering roasted pig and blackened dog. Then they served me up an earful.
“The doctors gave us Tamiflu but we didn’t take it,” recounted the aunt, Mamajus Boru Karo. She was thirty-eight years old with long filthy hair, parted in the middle. Her face scrunched up as she retrieved the unpleasant memory. “Why should we take it? We don’t have bird flu.”
“The doctors said we should take it as a precaution,” offered Sanita Ginting, the twenty-nine-year-old cousin, her brown eyes opening wide.
“We’re healthy,” Mamajus retorted. “If we took it, we could die.”
Sanita nodded in agreement and acknowledged she, too, had thrown aside the medicine. Seated at a scuffed table by the window, her gaze drifted toward the semipaved street outside. A few goats, chickens, and dogs scavenged among the potholes for discarded morsels of food. A highland breeze chased scraps of litter down the road. Sanita’s attention returned to the cramped, concrete room with its chipped green paint. She, too, was getting agitated.
“We were scared of the health officials and of the WHO,” Sanita admitted. The doctors had given her relatives medicine and shots, and yet they got worse and worse until they died. “It’s possible they murdered them with injections.”
“Why would they do that?” I asked.
“To keep them from infecting anybody else,” she answered.
I looked at Mamajus. She was seated cross-legged on a wooden chair in the doorway. She concurred.
“Of course we’re suspicious,” Mamajus said. “They told us it was bird flu even before they had any lab results. They were just making it up.”
“They think we are stupid people, uneducated,” Sanita interjected. “We didn’t go to advanced schools like them so they think they can say anything. But if no poultry are sick, how can it be bird flu? It’s irrational. We can think even if we’re stupid. Where’s the proof?” Then came the refrain: “It was black magic.”
When I had spoken earlier with provincial health officials, they told me they had tried to take blood samples from everyone who had contact with the victims.
“I didn’t give a sample,” Sanita responded.
“I didn’t give a sample,” Mamajus echoed. “I don’t know anyone in my neighborhood who gave blood samples.” She paused, glancing at Sanita for confirmation, and then continued, “We got angry. We said, ‘Why do you want to take our blood? That’s only for sick people.’ ”
Without specimens from the villagers, the world’s picture of this unprecedented outbreak was, at best, incomplete. I decided to ask the health officials from Karo district itself. They were the ones closest to the scene and fluent in the local dialect. I finally caught up one evening with Dr. Diana Ginting, the health department director, for a talk literally in the shadows. She was still on duty despite the late hour, her jacket pulled tight against the chill, because a new bird flu outbreak in poultry had been confirmed hours earlier. As we sat on the dimly lit steps of the government building in Kabanjahe, the once-sleepy parking lot in front of us had been transformed into a war zone. The district was mobilizing for a mass cull, marshalling scores of uniformed security forces and civilian officials to carry out the late-night operation.
As Dr. Ginting distributed surgical masks to the gathering forces, she recalled what had earlier transpired in Kubu Sembilang. The doctors had tried to calm the people and coax them into giving blood. “It wasn’t easy,” Dr. Ginting said. “They kept wanting to know why.” When the medical staff had put on masks in preparation for drawing blood, many villagers took offense. Nearly everyone refused. Across the province, health officers were eventually able to collect thirty-two blood specimens, including many from doctors and nurses who had treated the victims. But in Kubu Sembilang itself, investigators ultimately took just two samples, from a neighbor and the local midwife. “The people here are very difficult,” Dr. Ginting said. “Maybe we weren’t good enough at convincing them.”
Tortured by the diagnoses of big-city doctors, Jones, the youngest of the Ginting siblings, had bolted the hospital, fled the suffocating back alleys of Medan, and absconded for the highlands of his ancestors. But he arrived shadowed by death and local officials.
He initially sought out a witch doctor who lived in a hamlet amid the cornfields about ten miles from his home. This healer poured some water into a cup and recited an incantation. Then he gave it to Jones to drink. Next, applying the standard treatment for a fever, the medicine man prepared a paste of beras kencur from crushed rice and galangal (a root similar to ginger) and rubbed it on his patient’s face and body. The remedy did not work. Jones was on fire.
His neighbors were not happy to see Jones when he returned to his home in the district capital, Kabanjahe. They were terrified of the curse. They had also heard that Jones had become the target of a major manhunt. The provincial health department, alarmed that a contagious patient was on the loose, had asked local officials to track him down and ship him back to the hospital in Medan. The word on the street was that police had also joined the hunt for Jones and his family.
“They’ll arrest us if we don’t go back,” Jones’s aunt warned him.
Jones objected, “If I go back there, I’ll die for sure.”
Jones and his wife debated what to do. The family told Jones they would defer to his wishes. But with his condition deteriorating, he was no longer in any shape to keep running.
After three days on the lam, Jones was readmitted to Adam Malik Hospital, a sprawling urban medical complex of white buildings with red tile roofs that, like many public hospitals in Indonesia, was in need of a little convalescence of its own. The corridors were clean, but their tile floors were chipped and the air was sour. Many of the fluorescent lights were out. While groundskeepers kept busy raking the lawns, the grass was perpetually overgrown, and many of the bushes were draped with drying laundry. The hospital was named for a former Indonesian vice president. But a letter had fallen off the sign over the main entrance so that it now read ADA MALIK, which is Indonesian for THERE’S MALIK!
Though Jones had surrendered to health authorities, he was not done fighting. He refused to take Tamiflu or accept intravenous medication and injections of antibiotics. As hard as it was to breathe, he would rip the oxygen mask off his face. The nurses were terrified of him. When they came close, he would wrestle them away, flexing his tattooed biceps, or lunge at them with a fork.
The doctors treating him in the special “red zone” set up for bird flu patients looked around and found a young resident physician whose family was from Karo district. He could speak to Jones in his local dialect. Soon the resident won a measure of cooperation. But only a measure. Jones began taking his medicine but still resisted giving the blood samples required to monitor his progress. “He thought it would make him weaker. For people like him, one drop of blood is worth a plate of rice,” one doctor told me.
The red zone was demarcated with a red line painted on the hallway floor outside the two rooms where the most infectious patients were segregated. Hospital staff donned masks, helmets, rubber gloves, gowns, and boots before crossing the line. But as Jones slipped in and out of consciousness, now hooked up to a ventilator, more than a dozen unprotected family members pitched camp on the outdoor terrace just beside his room. They filtered in and out of the ward all day long, wearing neither masks nor gloves despite the timid protests of the medical staff. “We weren’t afraid of catching the disease,” his wife explained. “If we have to die, we’ll die. No one else would look after him. Even the nurses were reluctant to look after him.”
Dr. Luhur Soeroso, the silver-haired chief of the pulmonary department, took a deep interest in Jones. “This is a very rare case,” he told me as he thumbed through the patient’s file. When I met Soeroso, he had an air of composure and comportment that seemed out of place amid the bedlam beyond his office door. He wore a pink shirt with a pair of Mont Blanc pens in his breast pocket and a red tie fastened with a gold clip. On each hand he wore a gold ring, one inlaid with small diamonds, the other with a large black stone. He had just completed writing an article about Jones that he was hoping to publish in the New England Journal of Medicine. While all the other family members who caught bird flu had died within twelve days of falling sick, Soeroso noted that Jones was still alive and battling the virus six weeks later.
Jones was also unusual because he had developed brain abscesses after three weeks in the hospital and was suffering from severe headaches, mental distraction, and crippling muscle pain. Soeroso attributed this to a secondary infection caused by parasites that Jones had long ago picked up in his village. The intense battery of antibiotics and other medication had depressed his immunity, allowing the parasites to attack the central nervous system. He had tested positive for a parasitic infection called toxoplasmosis. A CT scan had revealed multiple pockets of pus in his brain.
The family’s stubborn resistance to blood tests had made treatment difficult. But then the medical staff struck a deal with the family. If Jones would agree to give blood specimens, the family could invite a witch doctor to the hospital to see him.
Agenda Purba was laboring in his rice paddy when the Mitsubishi van drove up. He looked over to see who it was. Several passengers were strangers, but he recognized at least one man from his village. The visitors said they had a sick relative in Medan and needed Purba’s help urgently.
“Can’t you bring the patient to me? I have no way to get there,” Purba demurred.
“He can’t leave the hospital,” one visitor responded. “We’ll take you to him.”
Purba was in no mood to make the long trek to the coast. It was already late in the afternoon. “I’ll give you the right ingredients so you can do it yourself,” he said.
“No, please, can’t you do it the first time?” the visitor pressed.
Purba thought it over and agreed. “But on one condition,” he added. “Bring me all the way home again.”
Along with Suherman Bangun, Purba was one of the most prominent witch doctors in the village of Jandi Meriah. He was a skinny fifty-six-year-old with disheveled, graying hair and an oddly elongated face, carved with deep creases. A few wispy white beard hairs sprouted from his chin. His manner was agitated, almost manic, and when he spoke, he would look into space and squint, his heavy lids settling over melancholy, light brown eyes.
Even as a boy, Purba had realized he was special. He could always climb the tallest coconut trees in the village. But it was only when he turned twenty-one that he became a mystical healer. “I got the inheritance from my grandfather. He had this power. Before he died, he gave me the power by touching my left arm,” Purba told me, rolling up his sleeve, extending his arm and tapping it with his right knuckles to illustrate the bequest. “I can still communicate with him through dreams.”
Within years he became famous for his specialty: curing hernias. “If someone’s colon is sticking out their anus, I chew up some betel nut and spit on his stomach,” Purba explained with the cool detachment of a doctor describing an upcoming outpatient procedure. “I don’t have to touch him. I just light a cigarette and hold it. When it burns down to my fingertips, that’s the moment the colon goes back inside the body. But I can make it happen whenever I want. If I say you’ll heal tomorrow, you’ll heal tomorrow. If I say ‘heal now,’ you’ll heal now.” Over the years, Purba claimed his reputation had attracted patients from as far as Medan and even Java island. “I can do hernias, snakebites, and scorpion bites,” he boasted. “But I don’t do broken bones.”
Before Purba had driven off to Medan, he’d rushed home to slip on his one clean shirt and say good-bye to his wife. She’d insisted he promise to stop along the way and eat something, reminding him he’d been under the weather and needed to keep up his strength. He promised. “I didn’t want her to get angry at me,” he recalled.
The van pulled out of Jandi Meriah about an hour before sunset and reached Adam Malik Hospital six hours later. It was midnight by the time Jones’s relatives had hoisted the ailing young man from his bed and carried him out to the terrace for the ceremony, setting him down in a chair. Purba began to prepare the ingredients. He laid out twenty-one betel pepper leaves, each about the size of his calloused palm, arranging them in rows. Then, into each, he deposited palm blossoms called mayang, some pasty white lime called kapur sirih, reddish brown chunks of an astringent called gambir produced from local vegetation, and bits of the orange-colored betel nut from an areca palm called buah pinang.
Purba asked Jones his name. Jones told him, and the witch doctor began to chant over the leaves, praying for the young man’s recovery. Then Purba lifted the first of the stuffed leaves to his lips. He chewed it up, puckered, and softly spit it onto Jones’s forehead. Bending over the patient, he gently blew the slime over the flesh. The witch doctor lifted the second leaf, chewed it up, and spit it onto Jones’s chest, repeating the same procedure. He continued until he had finished all the leaves, slathering the torso, arms, legs, hands, and feet, alternating between left side and right, making particularly sure to cover all the joints.
“Afterward, he looked better,” Purba recounted. “I asked him how he felt. He said he felt better. He felt relieved.” Purba told him to go back inside the ward and go to sleep. Then he passed a bag of ingredients to the family, instructing them to repeat the same spitting procedure four times a day: in the morning, noontime, afternoon, and night. Finally Purba asked to be taken home to his village. It was dawn when he got back.
Just three days later, the Mitsubishi van reappeared beside Purba’s paddy. The family had used up all the ingredients. They wanted Purba to return to the hospital and personally repeat the ritual. He again acceded to the request.
None of the staff at Adam Malik hospital ever objected to either of the late-night rituals or cautioned Purba that he might be exposing himself to a killer disease. No one suggested he take Tamiflu. No one sampled his blood or monitored his health. But had they tried, Purba would have considered it silly. He knew for a fact the source of the illness striking Jones and his family, and it certainly was not bird flu.
“I know the truth because I speak to the spirits,” the witch doctor told me as we chatted on a wood bench in a thatched shelter on the village outskirts. “I know that Jones’s father made a deal with another, black-magic witch doctor. Both of them have died. But I can communicate with the spirits, so I know what happened.” According to Purba’s detailed account, Jones’s father, Ponten, had petitioned a witch doctor in the Alas River valley to help him become rich and powerful by conjuring the spirit of Begu Ganjang. The witch doctor had obliged. But Ponten never rewarded the witch doctor as promised. “The father broke his vow,” he continued. “Now the family has to pay. Now the whole family has to die.”
But Purba added that he had been able to shift the course of fate. He alone had been able to stay the execution of the remaining family members. “I’m the one to save Jones,” he said. He grinned, baring a mouthful of teeth stained black by decades of betel nut. “There will be no more casualties. Seven is enough. I drew a border around them at the hospital.” Purba stood up to demonstrate and etched a line in the dirt with the tip of his flip-flop. “It stops here,” he assured me, “because I protected the family with my magic line.”
Jones was discharged from Adam Malik Hospital ten weeks after he had been admitted. It had been a long, torturous stay. Besides losing weight and developing brain abscesses, he suffered what doctors reported was permanent lung damage. He had also become exceedingly bored during his convalescence. As his strength returned, he had begun to wander, repeatedly slipping out of the infectious disease ward for a coffee in the hospital’s small cafeteria, potentially putting other patients and staff at risk.
“I never expected to come home,” Jones recalled when I met him less than a week after he was discharged. “It was too long in the hospital. I lost hope.” He was still taking medicine, and the doctors had instructed him to come to the hospital for a checkup every week for the next six months. So he, his wife, and their two sons had returned to the crowded, working-class neighborhood near the airport and temporarily moved in with an aunt. Jones would spend much of his time sleeping on a thin woven mat on the floor, which was where I found him when I first came to visit. He gradually roused himself and sat up on the mat. But his gaze remained vacant. Only when I asked about his plans did he smile. “I want to go back to farming, back to my orchards and grow oranges,” he said softly.
Jones was now the head of the Ginting family, the sole surviving son. But he did not know that. No one had yet had the heart to tell him that during his own long recovery, his older brother Dowes had died.
Throughout the Ginting family’s ordeal, senior Indonesian officials dismissed any possibility that the virus had been passed from one person to another. They were afraid the world might conclude this was the start of an epidemic and isolate Indonesia, crippling tourism, staggering the economy, and inciting panic. Health Minister Siti Fadilah Supari later boasted about how she’d convinced her president, Susilo Bambang Yudhoyono, that CNN reports about human transmission of the virus in Sumatra were lies. “From the lessening of the tension in his face, I knew that he trusted me,” she later wrote. Supari would continue to maintain over the coming years there had been no human spread, at times accusing those who disagreed of trying to sabotage Indonesia.
But WHO’s flu specialists were quickly convinced that nearly all the stricken family members had actually caught the disease from one another. Most had fallen sick so long after the eldest sister, Puji, that it was highly improbable they had caught it from the same source as she. More likely, Puji had infected them.
Dowes, however, could not have caught the bug from Puji. He had taken ill too long after the others. If Dowes had the virus, he had caught it while caring for his son, who had caught it from Puji. That would be an ominous precedent, marking the first time the virus had been found to hop from one person to another and onto a third. But until samples from Dowes tested positive for the strain, this would only be speculation. There were no hospital specimens for him, unlike for most of his relatives. There were just the samples that Tim Uyeki and his colleagues collected when they located Dowes on the hilltop in Jandi Meriah.
Before leaving the man’s bedside, Uyeki had taken the tubes and wrapped them with a cold pack in double plastic bags, which he then put in his backpack for the return trip to Kabanjahe. There, on a cement landing just outside the district office, he repackaged the samples. He made sure the vials were closed tightly and relabeled them so it was clear for the laboratory what they contained. He placed them, along with new cold packs, into a plastic bag, which he put inside another bag and then inside another. A provincial health officer drove this hazardous delivery out of the mountains, back to Medan, where a waiting WHO official carried them on to an evening flight to Jakarta. It was about 11:00 P.M. when this official arrived by taxi at Indonesia’s national health laboratory. The samples were split up, half to be tested by Indonesians and half at a U.S. Navy lab in the capital. The scientists worked through the night.
That evening, a senior WHO official in Jakarta e-mailed the agency’s regional headquarters in New Delhi reporting on Uyeki’s success in finding the fugitive, Dowes, and obtaining the samples. The outcome of the tests would be crucial. “If he turns out to be positive, then we will have to consider going in for rapid containment measures,” the official wrote. These would involve an intensified investigation, widespread distribution of Tamiflu, and possibly, for the first time, a mandatory quarantine of the affected villages.
His missive received an urgent rebuttal. It came not from the regional office but from the top, from the chief of the global influenza program at WHO’s main headquarters in Geneva. “In response to the possibility of a rapid response raised in the e-mail, my sense from various communications is that the level of suspicion and hostility in the area is high. Trying to mount a rapid response, especially one involving many outsiders and oseltamivir coupled with quarantine and isolation, seems most likely to lead to a very bad outcome, especially in terms of more suspicion and hostility and rumors,” wrote Dr. Keiji Fukuda, the global influenza chief. Only if the virus spread beyond the Ginting family should a rapid response be considered, he said. Fukuda was not optimistic about its prospects even then. “If intense social mobilization doesn’t quickly reverse the population’s suspicion,” he added, “we would probably have to contemplate a heavy security force/military backed operation which is, I suspect, very unappealing to us all.”
Uyeki had come down for breakfast at his modest hotel in the Sumatran highlands when, at 7:00 A.M., he got a call on his cell phone. Both labs had results. The specimens had indeed tested positive for the virus.
Fifteen minutes later came a second call. Dowes was dead. His body had just arrived at Kabanjahe Hospital, and people there were reportedly in panic. Uyeki was worried they’d blame him for the death since he’d worked on Dowes only hours earlier. “OK,” Uyeki responded, “we’re on our way.”
When he arrived, he found the relatives were actually quite calm, even relieved. They’d been advised by the witch doctor, Purba, that seven people would succumb and Dowes was number seven. That meant the dying was over.
Tom Grein, as a seasoned veteran of Ebola and other hemorrhagic fever outbreaks in Africa, knew what to do next. He and Uyeki asked the local health staff for supplies: large-gauge needles, formaldehyde, rubber boots, chlorine bleach, and a backpack sprayer, the kind used for insecticide. They suited up in their gowns and other protective gear. They used the needles to take additional lung tissue specimens, blood, and other samples from the body. Then they donned the boots and filled the sprayer with bleach. They sprayed the corpse to disinfect it, setting aside the man’s wristwatch to give to his family, placed the body in a black plastic bag, and hauled it over to a waiting coffin. They closed the coffin, sealed it, and disinfected it. They disinfected the hospital room. They disinfected each other. And when they were almost done, they disinfected the Suzuki jeep that had had transported Dowes to the hospital all too late.
In Jandi Meriah, Uyeki and his Indonesian colleagues had left behind boxes of Tamiflu with instructions that relatives, the witch doctor and his wife, and anyone else who’d been exposed take the tablets for protection. Health teams also distributed the drugs in three other villages, providing medicine to the Gintings’ neighbors, their relatives, and the driver and conductor of the minivan that brought Dowes to Jandi Meriah. A total of fifty-four people who might have been infected by him were placed under voluntary quarantine and asked to remain in their homes, or at least in their villages, for two weeks. Few listened.
Heni Boru Bangun, a forty-seven-year-old in-law, was among those who had the closest contact with Dowes, helping to care for him when he was in hiding. She had stayed in the same house with him for four days. Less than a week after he died, Heni broke quarantine, traveling to the next province to visit her mother.
I asked Heni whether she had taken the Tamiflu she’d been given. She said she had finished only two of the ten tablets required for a full course. “I was afraid of the side effects,” Heni explained. I looked at her adult son, who had been watching me suspiciously. “They gave me ten tablets but I only took three or four,” he volunteered. His wife, who had also helped look after Dowes, had declined to take any.
Heni disappeared into the back room of her house and returned with the thin white box of Tamiflu. She opened it and dumped the contents on the wood floor. Out tumbled the eight remaining yellow and white tablets still in their wrapper for me to see—and, with them, some harsh truths about our hopes for bending nature to our will and forestalling a pandemic.
According to the computer models that underpin WHO’s planning, the difference between success and cataclysm is measured in days, and the conditions for snuffing out an emerging pandemic are unforgiving. Yet in the dry run of North Sumatra, the virus had been spreading among the Gintings long before it was diagnosed, and in some cases, rather than seeking medical care, they ran. When public health officials finally responded, they were repeatedly chased off. The victims and their contacts refused to share information and samples vital for containing an outbreak, likewise rebuffing appeals to take antiviral medicine, obey quarantine, or even take rudimentary steps to avoid exposure to those stricken. It was as if the highlanders had done everything imaginable to accelerate the spread of the disease.
“If this were a strain with sustainable transmission from human to human, I can’t imagine how many people would have died, how many lives would have been lost,” said Dr. Surya Dharma, who was head of communicable disease control for North Sumatra.
If there was any encouraging news from North Sumatra, it was only this: the novel strain had not spread beyond the one family. In its current form, the virus was still tough to catch. But influenza viruses inexorably mutate. It had now, for the first time, demonstrated the capacity to jump not only from one person to another, but also onto a third.
Only nine years earlier, flu specialists had assumed that this strain couldn’t infect anyone at all. When it had, alarms sounded around the world.
Keiji Fukuda had been anticipating this call his entire career. It came in August 1997, when he was busy caring for patients at San Francisco’s Mount Zion Hospital, deep into a clinical rotation he would do a couple of weeks each year to keep his skills as a physician sharp. After he came off the wards, a hospital staffer mentioned that the CDC, where Fukuda worked most of the year as the country’s top influenza investigator, had been trying to reach him.
Fukuda suspected something was wrong. He quickly returned the call, which had come from a laboratory in the CDC’s influenza branch, and the lab director filled him in on some tests her scientists had just completed on a sample from Hong Kong. It looked as though someone had been infected by a new virus, a novel strain of flu called H5N1. The victim had died.
“It was a jolt,” Fukuda recounted. “It was an unusual call. But it was the call you are kind of always waiting for in the field of influenza.”
His mind instantly started to race. This was a strain that had never before infected humans, at least as far as scientists knew. That meant no one had immunity to the pathogen and everyone could be vulnerable. “How many other people have been infected?” Fukuda wondered to himself at the time, adrenaline pumping. “Are we missing anyone else? Right now, what’s going on?”
It took a few hours to arrange a larger conference call. The CDC hooked in Fukuda along with Dr. Nancy Cox, the chief of the influenza branch, who had been tracked down while vacationing with her family at a horse ranch in Wyoming. Flu was their field, some would say their obsession, and they instantly understood what was at stake. “The idea of a pandemic coming on is one of the things you know is always possible,” Fukuda said. “Perhaps this is the start of that pandemic.”
Joining them on the call from Hong Kong was Dr. Margaret Chan, a Canadian-trained doctor who ran the city’s health department. She had never spoken with Fukuda before. Nor did she know much about pandemic flu. Over the next decade, she would become intensely familiar with both, gaining a perspective on influenza shared by few on Earth. But in 1997, it was all new. Chan peppered the CDC specialists with questions. “Is this a big threat or not?” she asked. They admitted they weren’t sure. They explained that the lab might have made a mistake. Even if the test result was accurate, it might reflect merely a single, isolated infection. But they cautioned her that the case could also be a harbinger of something larger. Chan was quick to appreciate the horrific implications. She told them she needed help. Hong Kong couldn’t get to the bottom of this alone. Before the call was over, Fukuda knew he was bound for Asia.
Fukuda finished his rotation in San Francisco, then headed home to pack. He and his wife and two young daughters lived in a suburb of Atlanta, where he had worked for the CDC since 1990. In 1996, he had become chief of epidemiology in the influenza branch.
Fukuda had been bred for the job. His parents were both doctors. His mother was Japanese, his father Japanese American. Born in Tokyo, Fukuda became a New Englander at age three when his family moved to Vermont so his father could take up a medical post there. The future flu hunter earned his own medical degree at the University of Vermont and did his residency in San Francisco before studying public health at the University of California-Berkeley. Influenza became his calling at a time when few infectious-disease specialists paid it much mind. Starting in the 1980s, HIV-AIDS exploded on the American scene and monopolized much of the scientific attention and research money. Like others in the small influenza fraternity, Fukuda felt “his bug” was slighted. Even short of pandemic, seasonal flu was a proven scourge. “It certainly wasn’t on the radar screen,” he lamented. “People dying year in and year out in fairly large numbers in many countries and still it remains invisible.” Among flu researchers, it was a common grievance.
Yet among them, Fukuda was rare. His fervor was a quiet one. When I met him nearly a decade after the first H5N1 case, his buzz cut was graying but his round face was still youthful. He was one of the few veteran flu specialists whose brow was clear of lines and furrows. I concluded this was due not to any deficit of passion but rather a balance of passions. (Fukuda, who claims he is only a mediocre musician, had decorated an entire office wall with pictures of antique cellos.) His manner is authoritative but reserved. He is brilliant in analysis but measured and soft-spoken in delivery. He is ever polite, even when his colleagues spy irritation smoldering behind his rectangular-framed glasses. Above all, he is calm and calming. So when he worries, those around him get scared.
Fukuda arrived in Hong Kong late one sultry August evening at the head of a small CDC team. By the next morning he was already cloistered at the city health department, mapping out a systematic investigation into the outbreak.
The victim had been a three-year-old boy named Lam Hoi-ka, who had died in the spring. He had been a healthy youngster, the second son of an affluent Hong Kong couple. The father owned a company that manufactured decorative candles at a factory in mainland China. The mother was in charge of the firm’s marketing. They lived in a satellite town called Tseung Kwan O in the lower reaches of the New Territories, an expanse of former wilderness just beyond the congestion of old Kowloon that the Chinese had ceded to the British crown colony of Hong Kong a century earlier. Tseung Kwan O is really more city than town, a modern, highly planned community with scores of high-rise apartment towers, some as tall as fifty stories, amid American-style shopping malls and brightly painted schools and kindergartens. The town sits on a bay of the same name, which means General’s Bay. But the British had called it Junk Bay after the multitude of traditional sailing vessels that once plied the waters. The community is no longer oriented to the sea but toward cavernous rail and bus depots. Each morning, the apartment towers disgorge thousands of office workers, headed for downtown less than a half-hour commute away.
Hong Kong health officers had already visited Hoi-ka’s family. It had been a hard interview. The family was distraught, and it took a long time to explain to them how an entirely new virus could have claimed their son. Investigators had gathered what information they could from the parents and their housekeeper about the boy’s recent history. None of it seemed exceptional. When Fukuda arrived in Hong Kong, he asked to see the family again, but they refused to talk anymore. He didn’t press it.
Fukuda had other angles to explore. His first priority was to determine whether this was simply much ado about nothing. The positive test result for H5N1 was so startling that he suspected it could be the result of a contaminated sample. Perhaps the boy had never been infected at all. So Fukuda and his team traced the precise route of the specimen. They went to Queen Elizabeth Hospital, the primary referral hospital on Hong Kong’s Kowloon peninsula, to see the intensive care unit where the boy had been treated. They checked to make sure that hospital staff had followed proper sampling procedures, and they examined the equipment. They asked whether any other patients had a similar respiratory disease and could have been the source of the virus. They asked about the health and habits of the staff. Perhaps some nurse had tracked the virus in. The team also visited the health department’s lab at Queen Mary Hospital on Hong Kong island, reviewing how the tests were conducted. They explored whether the virus might have been inadvertently introduced by technicians working at a veterinary lab in the adjacent building. After nearly a week of investigating, there was still no evidence of contamination anywhere.
But the conclusive proof came in the lab. The team conducted an analysis using antibodies that would find the virus and cling to it. The antibodies were tagged with fluorescent stain so they could be identified under a microscope. When these were added to a sample from the dead boy’s windpipe, they attached to the inside of the human cells in the specimen. The antibodies did not simply float on top. This meant the virus had truly infected the boy’s cells and was not an accidental visitor.
The cruel progression of the boy’s disease also seemed to confirm he’d been struck by a form of viral pneumonia arising from influenza. As Fukuda pored over the medical records, he learned that Hoi-ka was initially taken to a doctor after coming down with a high fever, sore throat, and dry cough. The doctor prescribed aspirin and antibiotics and sent him home. But the condition worsened. The boy didn’t seem to be thinking right or acting right. He was oddly irritable. He wasn’t his usual alert self. The doctor couldn’t put his finger on what was wrong. So he admitted Hoi-ka to a small private hospital. A day later, he was moved to the intensive care unit at Queen Elizabeth Hospital and put on a respirator, but to no avail. The boy was losing consciousness. His lungs were failing. Five days later, he was dead.
Fukuda read the records and thought, “Wow. This is really bad. No matter what they could have done, they weren’t going to prevent him from dying.” Fukuda was struck by the relentless advance of the disease. “It was clear from the time the child got in. He started getting sicker and sicker and sicker and then he died. You don’t expect to see that in young healthy children.” It reminded Fukuda of the healthy young men he had seen in San Francisco in the 1980s struck down almost overnight by AIDS.
It also made him think of his daughters. He couldn’t keep his mind off them. He wasn’t frightened, not yet. There was just one case. But he felt so sad. How awful for parents to lose a child out of the blue to such a mysterious intruder. “This,” he thought, “is just like a visitation from outer space.”
Hoi-ka’s young lungs had been ravaged. The final diagnosis gave the cause of death as pneumonia and acute respiratory distress syndrome, in other words a severe inflammation of the lungs that culminated in their wholesale destruction. But the virus didn’t stop there. The boy suffered kidney failure, and his blood was poisoned, unable to clot normally. His liver and kidneys also showed evidence of Reye’s syndrome, a separate, potentially fatal disease that can occur when aspirin is taken to treat viral disease.
This was indeed flu. But it wasn’t the flu most people know. Sure, ordinary seasonal flu can put you on your back with a fever, a cough that keeps you up at night, and aches that rack your bones. But in the vast majority of cases, these symptoms pass in just a few days. This new strain meant far more than a runny nose and chills.
Often, viruses will adapt themselves to their human hosts over a period of time. They will soften their edges and temper their nastiest qualities. After all, the objective of any virus is to reproduce itself inside its host and then jump to another so it can continue to replicate. A death that comes too quickly does little to serve these ends.
But H5N1 is an interloper, an unrefined newcomer, all fury without the seasoning of age. In human cells it has discovered a fresh target and it pursues its prey deep into the body, penetrating much farther than ordinary flu. Seasonal flu usually strikes the upper respiratory tract, the nose, and nearby throat. The result is sniffles. This novel virus, by contrast, advances on the lungs themselves, attacking the branches of the bronchial tree and the myriad little buds on their tips called alveoli, where the life-sustaining task of exchanging carbon dioxide for oxygen occurs. The pathogen infects the coating of mucus that protects the membranes of the lungs. But unlike regular flu, which cannot reach much beyond surface cells, this newcomer penetrates into the tissue itself. It thrusts deeper. It spreads farther, often infecting both lungs at nearly the same time. As the pathogen relentlessly erodes the cells of the deep lung, you find yourself increasingly short of breath. Your cough is often bloody and you may bleed from your nose and even gums.
Once inside the cells, the virus begins reproducing madly. Even in the throat, which is at best a secondary target, the amount of virus can exceed that of normal flu. Down in the lungs, there are at least ten times more than in the throat, in some instances even a hundred times more. This is a virus in a hurry. And the human body, which has never encountered anything like it, has no ready arsenal of antibodies to choke off the process.
The body can still marshal its innate, all-purpose defenses. But in doing so, it mounts a counterattack so furious that some scientists believe it’s more lethal than the virus itself. The besieged cells raise the alarm by dispatching messenger proteins called cytokines. These in turn prompt a counterattack by the body’s defensive forces. Immune cells of different stripes, including killer T cells, macrophages, and other white blood cells, flood into the infected lungs, ferociously attacking the virus and the cells that have fallen into enemy hands.
This is the fateful battle on which life could turn. There is no restraint, nothing held back. The body throws everything it has at the intruder without regard to the tremendous collateral damage this causes the lungs themselves. The cytokines keep firing and firing in what scientists call a cytokine storm. (Researchers debate whether the massive response is due to the tremendous amount of virus in the system or the nature of the pathogen itself. Unlike regular flu viruses, which have a way of calibrating the immune response, this strain may not.) Ever more immune cells are summoned to the front and continue to blast away. The carnage mounts. The lung cavities fill with dead and damaged tissue, mutilated mucus cells, and other cellular wreckage. The lungs become rigid as the cells that make liquid to keep the lungs flexible are annihilated. The seal between the bloodstream and the air passages ruptures. Red blood cells and plasma leak into the lungs. The alveoli sacs are swamped with fluid and debris and are no longer able to exchange carbon dioxide for oxygen. If you listen closely, you can hear the liquid crackling. Your breathing accelerates. You desperately press all your chest muscles into helping you suck down precious oxygen. You’re gasping for air. This is the acute respiratory distress syndrome, known as ARDS, that struck Hoi-ka. On a series of X-rays, it appears like a white ghost consuming your lungs. You’re drowning.
But the virus is not content to remain a solely respiratory disease like regular flu. From the lungs, the pathogen sets upon other vital organs. It invades the digestive tract, perhaps when you swallow contaminated sputum, but more likely via the blood. The virus gets into the gut, often causing diarrhea and sometimes vomiting. It can assault the liver and kidneys, as it did with Hoi-ka. It can provoke heart failure. It can attack the eyes. It can even breach the brain and spine, on rare occasions causing encephalitis and related seizures. This virus has shown a singular facility to smuggle itself through the bloodstream and proliferate throughout the body.
Yet in the end, the lungs are where this microbe concentrates its energies and takes its heaviest toll, whether by killing directly or inviting a suicidal counterattack. The lungs are also the means by which it casts its net for further prey. In this one regard, it is much like its seasonal cousin. They both spread their sickness through contaminated droplets coughed or sneezed into the air, one of the most efficient forms of transmission known.
Influenza viruses, like all viruses, defy definition. Are they alive? On one hand, they lack the cell structure shared by all other living things from humans down to the amoebas that students study in science class. But at the heart of a virus is genetic material, the basic blueprint of all life, and viruses share the imperative of all living things to reproduce and pass on their genes before they perish.
The flu virus contains eight pieces of RNA, accounting for all of its genes. These determine everything about the virus: how it’s structured, how it reproduces, how it spreads, who or what it infects, and how sick it makes them. In particular, the genes program the proteins that do all this heavy lifting.
The virus itself is a microscopic sphere studded with two types of these proteins. One is the hemagglutinin, a spiky protrusion that the virus uses to break into the cells of its host. The other is the mushroomlike neuraminidase, which the virus uses to break out again. The two are called H and N for short. Each can take slightly different forms—scientists have so far discovered sixteen H subtypes and nine N subtypes—and the subtle variations that define them can mean life or death to the host. Human antibodies can recognize certain of these surface proteins and disarm them, but they are powerless against those that are totally new.
The flu virus most often enters the human body by hitchhiking a ride on an inhaled droplet. As the virus is whisked through the nose and down the windpipe, it brushes along the cells lining the airway. These cells have special receptors. Some are a poor fit for the specific hemagglutinin subtype that has been inhaled, so the virus keeps going. But some are just right. When the hemagglutinin finds the right receptor, the spiky protein plugs in, allowing the virus to fasten to the outside of the cell like a pirate ship preparing to board another vessel. The human cell seeks to stem the attack by engulfing the virus, then walling it off while trying to digest it with acid. But all the cell has done is speed its own demise. The acid triggers a remarkable transformation of the flu virus. The hemagglutinin turns itself inside out, baring a hidden weapon often likened to a molecular grappling hook. The virus uses this to pull itself even tighter against the cell. The membrane of the virus dissolves, and the viral genes stream into the core of the cell like marauding buccaneers.
A virus cannot reproduce on its own. But once inside the human cell, it finds everything it needs to do so. The viral genes hijack the cell’s own genetic machinery and deliver fresh commands. The innocent cell is soon churning out viral proteins, which are assembled into a brood of new viruses. Within hours, up to a million progeny are ready to explode forth and continue the mission.
But escaping the cell is not so easy. The same receptors on the cell’s surface that first attracted the virus now try to ensnare its offspring. So the neuraminidase steps in to cut them loose, leaving behind the lifeless wreckage of a human cell.
Most flu viruses fall into one of two types, either influenza A or influenza B. While the former can infect a wide array of species besides humans and cause severe illness, the latter tends to be found only in people and is less virulent. Influenza A viruses are further categorized by the proteins on their surface. The strain that struck Hong Kong in 1997 and continues to menace the world today is identified, for instance, by its H5-type hemagglutinin and its N1-type neuraminidase, hence influenza A (H5N1). Like all flu viruses, H5N1 originated in waterfowl, and that’s where most flu strains stay, circulating benignly among wild birds. But over the centuries, a few strains have succeeded in crossing the species barrier, either directly or via intermediate hosts like pigs, to infect people. Over time, these have evolved into the ordinary seasonal viruses that we usually associate with flu, losing much of their bite as humans develop immunity. The prosaic H1N1 strain that in recent years has kept millions of people in bed each winter, for example, is descended from a virus that first infected humans in the early twentieth century, sparking the catastrophic Spanish flu pandemic of 1918. The swine flu strain that erupted in early 2009 is also an H1N1 strain and it too can trace its lineage back to the Spanish flu. But swine flu, which scientists believe emerged only recently from pigs, has diverged so far from other H1 viruses over the years that vaccines against the seasonal H1N1 variant afford little protection against this new arrival.
So what distinguishes avian and human flu strains? Research suggests there may be several factors explaining why some viruses circulate primarily or exclusively in birds while others spread easily among people. Much of the suspicion centers on the receptors in the human respiratory tract. The hemagglutinin of human flu viruses fit better into one type of receptor common in the nose, sinuses, and upper reaches of the airway. Avian viruses, including H5N1, prefer a different type of receptor that is characteristic of birds but relatively rare in the upper airway of humans. Instead, this avian-type receptor is found deep in our lower respiratory system. Scientists surmise this is why H5N1 primarily strikes the lungs, as opposed to the throat and nasal cavity. This could also explain why the virus remains hard to catch, since these avian-type receptors are buried and relatively inaccessible. And when the deep lung does get infected, the virus has a long trip back up the windpipe before being coughed or sneezed into the air, making it hard to spread.
Yet all that separates the world today from an unprecedented calamity could be a slight retooling of the virus, some evolutionary tinkering with the hemagglutinin to make it a better fit for the receptors in the nose and throat, a change in another protein allowing the virus to better replicate in the temperatures of the upper airway, a few other genetic tweaks. Some researchers estimate it would take at most a dozen minor adjustments.
Scientists were aware of H5N1 even before it killed Hoi-ka in 1997. A version of the strain had initially been detected four decades earlier in chickens in Scotland. But no one thought it could jump the species barrier to people. It was strictly avian. That’s why its sudden appearance in the lab sample from Hong Kong was so startling. By making the leap, the virus had satisfied two of three conditions for a pandemic. It was novel—no one had been exposed, so no one had immunity—and it had proven it could infect people. Now it just had to show it could get around.
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.
As if the threat of mutation wasn’t enough, the virus can also take a shortcut through what’s called genetic reassortment. Flu viruses are notoriously promiscuous because of a rare gift for swapping genes with other flu viruses. Though most other viruses can’t do this, flu can go out and acquire entirely new attributes. This is because the genetic material in a flu virus—unlike nearly all other RNA viruses—is composed of separate segments that can each be individually replaced. If two different flu strains infect a person or even a pig at the same time, a new hybrid strain could emerge that is both lethal and has the tools to spread with ease. The poster child for gene swapping is swine flu. It was produced by the recent, seemingly improbable encounter of two different flu viruses: one known to circulate among pigs in the eastern hemisphere and another among pigs in the western hemisphere. The latter strain was a so-called triple reassortant, born from even earlier flu strains originating in humans, birds, and swine.
With the wholesale genetic changes that reassortment allows, it doesn’t require too many rolls of the dice to splice together a pandemic this way. “You can move a whole lot of characteristics in one go,” explained Robert Webster, a veteran virologist at St. Jude Children’s Research Hospital in Memphis, Tennessee, and the dean of avian flu researchers. “Flu is an RNA virus and it’s also a segmented RNA virus. That gives it a double whammy.”
Among flu strains, none unnerves disease specialists as much as H5N1 bird flu. In the decade after it surfaced, the virus spread over a swath of Earth unprecedented for a highly lethal avian virus. It extended its reach among animals, even infecting mammals like tigers and leopards. It grew more tenacious. The disease persisted longer in birds and spread more easily among them than only a few years earlier. The dice were being rolled faster and faster.
Researchers have concluded that the continuing outbreaks “appear out of control and represent a serious risk for animal and public health worldwide.” No matter how many times governments claim they’ve expunged the virus, it returns. In some countries, like Indonesia and China, the disease has become deeply entrenched in poultry, posing a permanent threat of contagion to their neighbors. Global eradication, according to senior animal-health experts at the UN Food and Agriculture Organization, “remains a distant and unlikely prospect.”
Yet this strain is not the only avian virus menacing humanity. A little-noticed but equally novel avian strain called H9N2 has also proven it can infect people, including several in Hong Kong and mainland China since 1999. This pathogen, like its better-known cousin, has quietly spread across the birds of Asia and the Middle East and on to Europe and Africa. Studies have suggested that human cases of H9N2 are more common than generally acknowledged, and human transmission may have already occurred. Most worrisome, scientists say the H9N2 virus is actually a better fit for receptors in the human airway, giving it perhaps an edge in the pandemic sweepstakes. “The establishment and prevalence of H9N2 viruses in poultry pose a significant threat for humans,” an international team of researchers reported.
A separate family of novel strains, the H7s, has meantime been circulating in both North America and Europe. Several of these pathogens have also shown an increased affinity for receptors in the human airway. Researchers have urged “continued surveillance and study of these viruses as they continue to resemble viruses with pandemic potential.”
But the H7s, like H9N2, so far remain fairly benign, far less lethal than H5N1. The latter, with a recorded human mortality rate of about 60 percent, is so savage that most flu specialists agree it is the one to be most feared.
Some medical scholars dissent. Although another flu pandemic is inescapable, they doubt that H5N1 will be the source. They note that years have passed, tens of millions of birds have been infected, and countless people exposed without the virus crossing the pandemic threshold. “If it was going to happen, it would have happened already,” said Dr. Peter Palese, chairman of microbiology at the Mount Sinai School of Medicine in New York. Moreover, he suggested that H5N1 wasn’t nearly as virulent as many of his colleagues claim. “I feel the virus is awful for chickens. But this is not a virus that has been shown to really cause disease in humans except in unusual circumstances when the dosage has been extraordinarily high,” he told me, adding that a person has had to practically sleep with a sick chicken to catch a bad case. Perhaps there is some hidden, immutable attribute of the virus that precludes it from ever spreading easily among people. Maybe the dice are loaded, never to come up snake eyes no matter how many times they’re tossed.
This line of reasoning is comforting but, unfortunately, unconvincing to many other virologists. “Such complacency is akin to living on a geological fault line and failing to take precautions against earthquakes and tsunamis,” wrote a leading team of flu specialists. How much time does a virus need to become a pandemic strain? Scientists don’t know. There’s scant information about the virological events that preceded previous pandemics. Had the 1918 strain been smoldering in animals for many years before it crossed to people? Had the 1957 and 1968 strains been circulating for a long time, bouncing between birds and people, but gone unnoticed because these pathogens did not cause mass poultry die-offs like H5N1? Is a decade a long time for a virus to evolve into an epidemic strain? With severe acute respiratory syndrome (SARS), for example, it wasn’t too long. Malik Peiris, the Hong Kong microbiologist who identified the virus behind the 2003 outbreak of SARS, cites evidence that people were exposed to that microbe for quite a number of years before it finally acquired the ability to be transmitted among humans. Once it did, it spread like fire. Flu could do the same.
“The virus has evolved in alarming ways in domestic poultry, migratory birds, and humans in just the last four years,” Margaret Chan told a conference of American business leaders in early 2007. “Global spread is inevitable.”
Chan’s remarks came a month after she’d become director general of WHO. She herself had traveled far since the scare of 1997. In 2003, after staring down outbreaks of both bird flu and SARS, she had left Hong Kong for Geneva. Before long, she was the agency’s assistant director for communicable diseases and its special envoy for pandemic influenza, which she identified as the most serious health threat facing humanity. By the time she ascended to the world’s top health post in January 2007, she was well schooled in flu and convinced that a pandemic was coming.
“If you put a burglar in front of a locked door with a sack of keys and give him enough time, he will get in,” she later warned at a summit of international health policy makers in Seattle. “Influenza viruses have a sack of keys and a bag full of tricks. They are constantly mutating, constantly delivering surprises.” She cautioned that a pandemic strain would be unstoppable once it became fully transmissible. No corner of the world would be spared. So no country could count on outside relief as with earthquakes or tsunamis. “This will almost certainly be the greatest health crisis experienced for almost a century,” she said.
But back in the fall of 1997, as the mystery of Hoi-ka’s death had faded with Hong Kong’s steamy summer, flu had all but vanished from Margaret Chan’s mind. She was facing a new crisis. A public health clinic in Hong Kong had been mistakenly dispensing toxic mouthwash to sick babies instead of syrup for their fever. Many of the children had developed diarrhea and vomiting. The public was clamoring for an explanation. The scandal captured the city’s grim mood as an historic year approached its end. Months earlier, with the world watching on television, Britain had ended more than 150 years of colonial rule by relinquishing sovereignty over Hong Kong to China. But the sheen quickly came off the handover. The Asian financial crisis that autumn rocked Hong Kong. The stock market crashed. The property market tanked. Tourism dried up. Even the weather was rainier than usual.
In late November, Wilina Lim’s lab received a sample from a two-year-old boy who had been briefly hospitalized in another building at Queen Mary with a fever, cough, and sore throat. The lab staff tested the specimen for seasonal flu. They drew a blank. But now they had the chemical reagents required to check for H5N1. When they ran this test, it came back positive.
Lim called over to the health department headquarters. Dr. Thomas Tsang, a senior medical officer responsible for infectious diseases, got the news. “Not again,” he said to himself, thinking of all the work this would mean.
Tsang led a team of Hong Kong investigators to the boy’s home. It was located in Kennedy Town, an older urban quarter of aging apartment buildings and street-level shops at the westernmost end of Hong Kong island, far from the site of the original case. The neighborhood is tucked between the island’s steep green slopes and the sea, the cranes of Kowloon’s port just visible across the channel. The boy was Vietnamese, the son of a migrant construction worker. Though the youngster suffered from a congenital heart condition, he had succeeded in recovering from the attack of flu and was back in the family’s cramped apartment when Tsang came calling.
The interview was difficult because the parents spoke little other than Vietnamese. It took a lot of patience, and the investigators often resorted to hand gestures to convey the intent of their questions. Tsang asked about the boy’s recent history, in particular whether he’d had contact with ducks, chickens, or other birds. The parents insisted he hadn’t. But when the health officers produced a calendar and went over it day by day with the couple, they noted a Vietnamese festival about a week before the boy got sick. “What did you do for the holiday?” Tsang asked. The mother remembered she had bought a live duck or goose at the market. She had slaughtered it at home, littering the apartment with feathers and feces. To Tsang, the source of infection seemed clear.
Lim had also e-mailed the CDC in Atlanta with the results of this most recent test. When Keiji Fukuda was notified of this second case, he had no doubts this time that the results were correct. “OK, are we off to the races?” he thought darkly. The initial case was no longer a freak occurrence. His mind sped through possibilities. “Is this the first of many cases? Are there more cases going on? Is this the tip of the iceberg?” Fukuda packed his bags again and on Friday, December 5, headed with a fellow CDC investigator for the airport. The probe would be under the auspices of WHO, but CDC staff would carry it out.
The flight from Atlanta to Hong Kong takes about twenty-four hours. As Fukuda sat in his economy-class seat, he had a long time to reflect. He reviewed everything he would need to know. He thought about what his years on the trail of influenza had taught him and about the findings of the earlier investigation in Hong Kong. His mind groped for what was crucial, sorting and filtering the information. He sketched out the scientific surveys he’d want to conduct this time. He plotted out what he’d do as soon as he arrived. He didn’t want to waste a second. “Question one, two, and three,” he said to himself. “Are there other people infected? Are they passing it to each other? Is there an animal source?” So far, thankfully, the answer to the first question seemed to be no.
When the plane landed, Tsang met him at the airport. While officers were clearing Fukuda’s passport through immigration and customs, Tsang whisked him into a side room to begin briefing him on the outbreak.
“I’ve got good news and bad news,” Tsang quipped.
Fukuda waited for the rest.
The good news, Tsang said, is that he’d be taking Fukuda to a nice dinner. The bad news was that while Fukuda had been in the air, Hong Kong had confirmed two more cases.
Tsang brought Fukuda to his hotel in the downtown Wan Chai neighborhood, the former red-light district of The World of Suzie Wong, which in recent years had gone through a commercial renaissance. Then they went to work. They reviewed the lab data and the findings from the preliminary investigation, mapping out the next steps. It would be the first of many late nights spent together.
Fukuda and a growing CDC team was set up with an office in Wu Chung House, the imposing thirty-eight-story tower on Queen’s Road East that was home to the health department and assorted other government agencies and private enterprises. From the windows of their corner room on the seventeenth floor, the Americans looked out at one of Asia’s great skylines and each night watched the lights in the opposing buildings go dark. The team consistently worked past midnight, recapping the progress of their probe and debating its mystifying results. Cases continued to surface all over the city with no apparent geographic pattern. The ultimate source of infection remained elusive. “I’ve never been in an investigation where the stakes were both so high and information was so little about what was going on,” Fukuda said. “I don’t think I have ever slept less over a sustained period of time.”
Early each morning, the questions would rouse him, at five o’clock, four o’clock, even three thirty, and he would resume his self-interrogation. “What are we missing?” he pondered. “What are we not asking? Is there anything obvious going on?”
He and his growing team of CDC investigators would meet for breakfast and compare notes on the day. By eight o’clock, they were back at the health department. They had dragged the desks to the center of the room to form a single large rectangular table and covered it with computer printers and laptops they had brought from home. At the far end of this command center was a whiteboard, where they recorded each suspected case, jotting down the age, gender, location, and crucial dates of the illness. The ultimate outcome was marked at the end of each listing. A downward arrow meant death.
The scrutiny from politicians, foreign officials, and particularly the press grew intense. The earlier investigation in August had received little media attention. But when Fukuda returned to the health department in December, the hallways were already crammed with reporters. Walking to the bathroom, he recounted, was an “exercise in photography.” Press conferences became high-pressure events where the subtleties of epidemiology were often lost in the journalistic scrum, buried beneath shouted questions and the forest of microphones. One day after he arrived, Fukuda faced the media. “There’s a possibility these cases are the only cases that appear and the virus completely vanishes. Another possibility,” he added with foreboding, “is that these viruses may increase.” By the middle of December, the number of cases had in fact reached double digits.
Hong Kong residents with little more than sniffles streamed to hospitals and clinics, fearing the worst. In normal times, these health centers took only a few samples each day from suspected flu cases. But now the samples were being wheeled into Wilina Lim’s lab by the trolleyful, at least five hundred specimens every day. And health officials were demanding that the lab analyze them immediately for H5N1, rather than screening them first to see if they were flu at all. The workload overwhelmed the small influenza lab and its staff of two technicians. Lim yanked staff from the hepatitis and HIV labs and put them to work on flu, more than twelve hours a day, seven days a week.
Most samples came back negative. But the few that were positive made a terrifying impression. To Lim, this virus behaved like an alien. Her lab, adhering to international norms, normally tested for flu by culturing the virus in special cells harvested from the kidney tissue of cocker spaniels. Scientists consider these canine cells to be especially good for growing flu viruses, far better than most other types of cells. So it was little surprise when Lim’s technicians placed the virus into the canine cells and it grew. But when they inserted it into a variety of other cells to see what would happen, they were stunned by what they saw under the microscope. “This one, it grows well in all kinds of cells,” Lim recalled. “You can see the cell change very quickly. It seems that whatever cell you put it in, it just grows.”
The long hours were also taking their toll on Margaret Chan, who was often up until the middle of the night speaking with anxious WHO officials in Geneva. But as the face of the health department, she tried to remain cool and upbeat. Once she went too far. Accosted by reporters after delivering a luncheon speech, she was asked whether she still ate chicken despite the flu scare. “Yes, I eat chicken every day. Don’t worry,” Chan told them reassuringly. Her response was scientifically sound, since the virus cannot spread in cooked meat. But to many in panicky Hong Kong, her answer seemed frivolous and out of touch. It sparked a brief furor in the local media, and she later admitted she’d fumbled the public relations.
In the privacy of her office, by contrast, Chan and her senior lieutenants were growing extremely worried. “Has the situation got out of hand?” Tsang recalled them wondering at one meeting. The disease seemed to be spreading exponentially. They suspected it might now be jumping from one person to another. They feared that hundreds of thousands in the city could soon fall sick. They still didn’t understand where the virus was coming from, so they didn’t know how to stop it.
Hong Kong’s senior health officials looked to Fukuda for reassurance. But now he, too, was frightened, and his anxiety showed. Unlike in August, he was in the middle of a storm with no end in sight. Moreover, time was running out. In just a few more weeks, Hong Kong would enter its regular winter flu season, and Fukuda feared that the convergence of prosaic and novel infections would overwhelm the city’s hospitals since there was no easy way to tell them apart. Even worse, if both strains were circulating at the same time, the opportunity for them to swap genes and spawn an epidemic strain would be tremendous. “All of that was very pressing,” he said. “We were racing against time.”
“It was striking that this was not regular influenza we were looking at, whatever it was,” Fukuda later told me. Ordinary flu preyed on the weak: infants, the elderly, and the infirm. But this strain had demonstrated that even the young and healthy—especially the young and healthy—were its targets. “What does it look like?” he asked. “It looks like young people dying from something new. So it really brought us back to 1918.”
The parallels were eerie. Ordinary flu has what scholars describe as a U-shaped mortality curve, with deaths concentrated among the very young and very old and a far lower proportion among those in between. The milder pandemics of 1957 and 1968 adhered to the same pattern. But during the Spanish flu of 1918, more than half the deaths were among those between eighteen and forty. This gave the disease a W-shaped mortality curve, reflecting the heavy toll in the middle of life as well as at the beginning and end. The avian flu outbreak in Hong Kong was much the same. And after the virus resurfaced in 2003, spreading its reach across much of East Asia, the deaths continued to follow this disquieting pattern. The largest toll was among those between ages ten and nineteen, followed by those in their twenties. The overall case-fatality rate was highest among those between ages ten and thirty-nine.
“Most of the time in public health and in medicine,” Fukuda continued, “there’s a fair amount of uncertainty, but you rarely come across issues where there’s a really high degree of uncertainty and what you’re sitting on may be something like a 1918. You feel like, ‘I don’t know what is going to happen. I don’t know what is going on. But what is going on is not good, and what it reminds me of is the worst not-good of the century.’”
Researchers have yet to account fully for why the Spanish flu and avian flu, alone among contemporary flu outbreaks, manifest this W-shaped curve. “Explaining the extraordinary excess mortality in persons 20-40 years of age in 1918 is perhaps the most important unsolved mystery of the pandemic,” wrote researchers at the U.S. National Institutes of Health. The answer could lie with another uncanny similarity between the two viruses. Historical accounts from 1918 and experiments on a version of the Spanish flu strain resurrected in the lab reveal that it also provoked tremendous cytokine storms, those withering counterattacks by the body’s immune system. Scientists speculate that the young and healthy may be most vulnerable because, ironically, they have the most robust immune systems, thus the ones that launch the most vicious and ultimately suicidal responses. These victims may be undone by their own strength.
Scientists’ understanding of this novel bird flu strain is still evolving, and the more they learn, the more they worry. Some now suspect that bird flu is moving down the same path as the virus responsible for the deadliest epidemic in human history. “This is a kissing cousin of the 1918 virus,” warns Michael Osterholm, director of the Center for Infectious Disease Research and Policy and a frequent commentator on the pandemic threat.
Spanish flu, like bird flu, is thought by scientists to have been a wholly avian virus that developed solely through a series of internal mutations, as opposed to the genetic reassortment that spawned the 1957 and 1968 strains in addition to the swine flu of 2009. Some of the mutations discovered in the 1918 virus look familiar. “Notably, a number of the same changes have been found in recently circulating, highly pathogenic H5N1 viruses that have caused illness and death in humans and are feared to be the precursors of a new influenza pandemic,” wrote a team of researchers led by Jeffrey Taubenberger, the American scientist who first fully analyzed the genes of the 1918 virus. Just since 1997, bird flu has become more like the Spanish flu strain. A series of studies shows bird flu has grown more virulent and less susceptible to antiviral drugs. “The H5N1 avian flu viruses are in a process of rapid evolution,” said researcher Elena A. Govorkova in 2005. “We were surprised at the tenacity of this new variant.” A later lab study suggested that bird flu may have already become more ferocious than the 1918 virus, laying even greater waste to the respiratory system and, fiendishly, targeting those lung cells specifically involved with repairing damaged tissue. In September 2006, WHO brought the world’s premier flu specialists to Geneva to scrub the evidence. Malik Peiris, the renowned microbiologist from Hong Kong, told the three dozen participants at this private session something that took their breath away. If the virus continued to develop along the same path, ultimately emerging as a pandemic strain through internal mutation rather than genetic reassortment, its high lethality could persist. He concluded there was no scientific reason for expecting a decrease in the fatality rate, currently at 60 percent of recorded cases. His comments, though later reported by WHO, were largely overlooked by the media. Their import was horrifying. Once the virus evolved into a form easily passed among people, it would be expected to infect a quarter of humanity. So even if the actual fatality rate was only 50 percent after accounting for overlooked mild cases, this could mean the deaths of nearly a billion people.
That figure is so big as to be incomprehensible. Researchers would rather dwell on scenarios more akin to 1918. That strain claimed fewer than five percent of those it infected. If the coming pandemic follows suit, the global death toll would only be 62 million, according to one extrapolation.
The World Bank originally projected that a severe pandemic could cost the world economy $800 billion in the initial twelve months. By late 2008, the World Bank had nearly quadrupled this estimate, concluding that an epidemic would cost about $3.13 trillion during the first year. Even a mild pandemic, like the 1968 Hong Kong flu, would cost $450 billion, and a moderate one like the 1957 Asian flu would reach $1.3 trillion.
The gloom was suffocating in those final weeks of 1997, like the cold, foul mist wrapping Hong Kong’s steep slopes and settling on its myriad islands. A small, tongue-shaped islet called Ap Lei Chau had become the latest focus of the city’s collective anxiety.
Five-year-old Chan Man-kei had been playing with friends at her kindergarten, a brightly decorated school on the ground floor of a public housing project in Ap Lei Chau, when she started throwing up. Her parents had been called. A doctor had referred her to nearby Queen Mary Hospital, where her lab samples tested positive for bird flu. About a week later, on Tuesday, December 16, Hong Kong health officials announced that two of her younger cousins had also been hospitalized in Queen Mary’s isolation ward. They, too, might have the virus.
Hours after that disclosure, Fukuda and Chan addressed the press about the heightened prospect of human transmission. “It’s a possibility in this case and one of the things we are concerned about,” Fukuda acknowledged at the evening news conference. Chan agreed that Man-kei might have infected her cousins. “They live together at Grandma’s and play together,” she said. The health department was trying to crack the case, she told reporters, assuring them, “We are working at breakneck pace.”
Ap Lei Chau was connected to the southern shore of Hong Kong island by a bridge. A decade earlier, the government had erected several dozen brown-and-gray high-rise apartment buildings on the green hillsides of Ap Lei Chau, and about ninety thousand people now lived there, making it one of the most densely populated islands on Earth. Man-kei’s two younger cousins and a third sibling stayed with their parents and grandparents in an apartment barely three hundred square feet in size. This was often where Man-kei spent her days.
When health investigators arrived at the apartment, they were rebuffed. The family patriarch, a sixty-four-year-old watchman, refused to speak with them or provide blood samples to see if he’d been exposed to the virus. Other family members were also reluctant to talk. They were afraid of being stigmatized or shunned by neighbors spooked by this new, mysterious plague. Fukuda arranged to meet one relative secretly at a café, the first of several clandestine interviews health officers conducted over the course of the outbreak. Eventually, they were able to tease out a history of the children’s recent activities, noting what they had done together and what they’d done separately. (Only one of the younger cousins ultimately tested positive for the virus. All three children survived.) But the source of their infection remained elusive.
Chan was frustrated. She couldn’t visit Ap Lei Chau herself because of the media frenzy this would cause. Nor was she getting a good sense of the family and its surroundings from the investigators. She kept sending them back to scare up more details, instructing them to observe the neighborhood at different times of day and different days of the week.
“I want to know exactly what is going on,” she insisted. “What do the children do?”
“They play in the car park,” came the response. “That’s their play-ground.”
Chan wanted to be able to picture the parking lot. She told them to take photographs and draw her a map. They did. Nothing seemed amiss.
But when the team returned to Ap Lei Chau the following Sunday, they spied cages of geese in the parking lot at the base of the apartment tower. There were several stalls near the entrance. Perhaps they’d been there on previous occasions and the children had passed too close. The investigators snapped some photographs and later presented them to Chan. They were all thinking the same thing.
Samples were taken from the grubby cages and tested. “Bingo,” Tsang recalled. “We found a positive swab in one of the stalls.”
They had identified a likely source for the infection. But could it account for both Man-kei and her cousin? Or had Man-kei caught the virus and then passed it to her cousin while they were frolicking on their grandmother’s carpet? Could the virus already be spreading from one person to another? Neither Chan nor Fukuda nor anyone else could ever rule that out.
Hong Kong at Christmas was a city under siege. People were flooding emergency rooms to be tested for the virus. Even medical personnel were calling in sick, fearful they’d been infected. Drug prices had spiked, and panicked calls were overwhelming the health department’s hotlines. Though only a handful of sick chickens had been discovered in the city’s live markets, poultry sales had plummeted, and restaurants were banishing popular Cantonese chicken delicacies from their menus. On Christmas Eve alone, three more suspected human cases had been announced. Now the first of the seasonal flu cases were also surfacing.
There was no holiday break that year for the six members of the CDC team. Fukuda had never before missed a Christmas with his wife and daughters. So the health department arranged a Christmas Day lunch cruise for their CDC guests. But they couldn’t escape the oppressive mood. Word came that four more suspected cases had been identified, the highest one-day total so far.
“I don’t know whether this disease will stop or spread,” Fukuda once again told reporters two days later. He was appearing at a press conference on Saturday, December 27, with Chan and Hong Kong’s agriculture chief, Lessie Wei. There were now about twenty confirmed or suspected cases. The press was demanding to know what more the government would do to stem the crisis. Since poultry were thought to be responsible for most of the outbreaks, would officials have them killed? Chicken hawkers had already been ordered to clean and disinfect their cages. On Christmas Eve, Hong Kong had barred all imports of chicken from mainland China, the primary source of the city’s poultry and a possible origin of the infection. “I feel at this point in time,” Chan responded, “the measures are sufficient.”
The call that changed everything came that night at two in the morning on Sunday, December 28. Chan was at home in bed. It was the agriculture department. There had been a die-off of chickens at Cheung Sha Wan, the city’s main wholesale poultry market. About fifty birds from a batch of three hundred in a single stall had abruptly fallen over dead with swollen chests and necks, internal bleeding, and other symptoms of avian flu. And there was more bad news. A week earlier, a similar outbreak had occurred at a farm in the New Territories. The disease had moved gradually along a row of cages, claiming its victims. The test results had just come back positive for bird flu.
Chan couldn’t fall back asleep. “What is going on?” she wondered. Only days before, city inspectors had toured Hong Kong’s farms and reported that there were no outbreaks. “Margaret,” she told herself, “the size of the problem is bigger than what it appears.”
She didn’t have proof of a widespread poultry outbreak. But if there was one, it could finally explain the unrelenting series of human cases. She thought about the holding pens, nicknamed “chicken hotels,” where Hong Kong’s birds were kept overnight. As demand for poultry had dropped, retailers in the city’s live markets found they couldn’t sell many of their chickens. At the end of each day, birds from various stalls and markets were gathered together before being distributed again for sale in the morning. Chan’s technical advisors had told her this system was perfect for disseminating disease throughout the markets. “Enough is enough,” she thought.
After a long wait for sunrise, she contacted researchers at Hong Kong University. They had begun sampling poultry in the city’s markets just before Christmas. Most of the test results had yet to come back. Chan urged them to take as many specimens as possible and to hurry up. She was about to recommend drastic action but didn’t yet have the scientific evidence to support it. “When you are ahead of the curve in dealing with new and emerging infections, science is always lagging behind,” she later explained. But despite the uncertainty, she wouldn’t wait. “Don’t be afraid to make major decisions,” she told herself. “Don’t be afraid to be wrong.”
Chan spoke that morning with her boss, Chief Secretary Anson Chan, who ran the Hong Kong administration. They scheduled an emergency meeting for later in the day. As health director, Chan would tell her that all the chickens in Hong Kong had to go. But there was no guarantee the city’s political leaders would sanction such a costly measure. “I am prepared, if they don’t accept that, to resign,” she thought. “I will resign, because if the environment does not allow me to do my job to protect the people, then that is the proper action to take.”
Chan’s driver ferried her up to the Peak, the highest point on Hong Kong island and home to a white colonial villa called Victoria House. Once a taipan’s summer retreat, it was now the official residence of the chief secretary.
Chan and agriculture director Lessie Wei briefed the chief secretary on the latest poultry outbreaks. Hong Kong had already closed its borders to imports from China, yet the poultry infections persisted. If the disease continued to circulate among birds, Chan explained, the public health threat would mount, especially if the virus mutated or reassorted. That’s why all 1.2 million chickens in Hong Kong had to be culled. About three hundred thousand ducks and geese that were kept in close contact with the chickens would also have to go.
The chief secretary cautioned that the economic implications were huge. A mass slaughter could severely harm the livelihoods of countless chicken farmers and traders.
“People will not like it,” Chan admitted, “especially when it affects their vested interests.”
The chief secretary continued to press. The poultry sector would demand the government pay compensation. The bill could be tremendous.
“Yes, it’s going to cost money,” Chan agreed.
“What if we don’t solve the problem after killing all of the chickens?” the chief secretary asked.
“Then we need to go after all the ducks and geese,” Chan said.
“And what if we still don’t solve the problem again?”
“I’ll be accountable,” Chan answered. If she needlessly put Hong Kong through the trauma of a mass slaughter, she’d accept the consequences. “I’ll deliver my head on a platter. I’ll resign.”
Finally, the chief secretary accepted Chan’s recommendation. She agreed to take it to Hong Kong’s leader, Chief Executive Tung Chee-hwa.
Within hours, Chan announced that Hong Kong would kill every last chicken. The slaughter would start the following afternoon. They were all to be gone within a day.
From the start, it was clear the slaughter would not go as planned. The government pressed 2,200 public employees into the operation, giving them masks, canisters of carbon dioxide, and orders to gas the birds to death. But these were dogcatchers, park rangers, and other civil servants with no experience in killing birds and unsure even where to find all of Hong Kong’s farms. Day laborers were hired as reinforcements, and even some market traders joined the effort, slitting the throats and snapping the necks of their birds. The result was literally bloody chaos. The chickens clawed and scratched and scampered for safety. Flies swarmed. Farmers resisted. By the end of the first day, less than a fifth of the chickens targeted had been slaughtered, and many of those remained unburied. Television showed plastic garbage bags of carcasses heaped high while stray animals and vermin scavenged through the carnage, spreading fear of contagion. Nearly a week into the slaughter, fugitive chickens still roamed the streets.
Many traders and laborers in the city’s nearly one thousand poultry markets were incensed. On the third day of the slaughter, New Year’s Eve, Chan accompanied Chief Executive Tung to the Cheung Sha Wan wholesale market, an expanse of weathered stalls with rusting corrugated metal roofs in an old industrial quarter of Kowloon. They walked through the parking lot, crowded most other mornings with small trucks heavy with poultry, and toured sheds crammed with wood and bamboo cages, now empty but still caked with droppings. The chickens had gone silent. Instead about two hundred market employees confronted the officials, shouting objections and waving placards with slogans scrawled in red paint.
The South China Morning Post, Hong Kong’s leading English newspaper, captured the prevailing public skepticism. In a front-page editorial, the paper asked whether the mass slaughter would eradicate the bird flu virus and allow poultry sales to recover. “There must be serious doubts whether either of these aims will be quickly achieved, if only because the central question surrounding the spread of bird flu has still not been answered: where does it come from? Until we know the answer, the killing of a million birds cannot hope to quell the public’s understandable fears. And, more importantly, nor can it be certain to stop any more cases of bird-to-human transmission of the deadly H5N1 virus.” A week later, this skepticism turned to harsh criticism over what the Post labeled the “botched” operation. “What is amazing is that the Government should have embarked on this task without any accurate estimate of its scale or duration,” the newspaper editorialized. “Equally astonishing is that it should have bungled matters so badly as to raise the possibility that other animals may have become infected.”
Yet even as the Post published those words, the final chickens were meeting their fate, and Chan was starting to find her vindication. The researchers at Hong Kong University had finished sampling nearly 350 chickens at markets around the city. They discovered the disease was even more widespread than expected. One of every five chickens had been infected.
Chan had accurately identified the source of the crisis. But had she found the solution?
Reporters asked Chan shortly after she announced the slaughter how she would know if it was a success. Chan told them it would have to put a complete stop to human cases. The normal incubation period for flu was a week. To be confident, Hong Kong would wait twice as long. If there were no more cases by the end of the second week of January, she would declare victory.
Just two days into the waiting period, Chan received a report of a new case, a three-year-old boy. “Son of a gun,” she thought. “What is going on?” Chan was scared. But when she reviewed the boy’s history with her staff, they concluded he had likely been infected just before the mass cull began. For two weeks the newspapers counted down the days and the population held its breath. On the final day, two new cases were announced. But these victims, too, had fallen ill before the slaughter.
There were to be no more. The final count stood at eighteen. Of those, six had died. Hong Kong would be the source of no new human infections, not that year and not for the next decade. The city had banished a killer.
Researchers later concluded a pandemic had been averted. This took an unprecedented effort that marshaled some of the world’s leading disease specialists and courageous investigators. It required exhausting lab work in Hong Kong and Atlanta, tapping some of the most sophisticated techniques then available to medical science.
Yet that alone was not enough. Hong Kong had aggressively pursued the pathogen from the instant city health officials learned of it. They took radical action to eradicate the virus though it was a gamble that carried a huge economic cost. The government acted with openness, even when hammered with criticism. As a result, humanity’s first brush with this novel strain would be its most successful. Over the following years, no other government would match this achievement, and the standard set by Chan and her colleagues would too often be honored in the breach.
Hong Kong’s success also lay partly in its nature, rare in Asia. As a small, mostly urban outpost, there were few agricultural interests to contest the imperatives of public health. Nor did most residents of Hong Kong live among livestock. Their main exposure to the virus, researchers later concluded, was at live markets. And though an age-old preference for fresh meat made these markets an integral part of Cantonese culture, the government overcame the inertia of tradition by restructuring them. When they reopened, Hong Kong barred the sale of live ducks and geese, believed to be the original source of the infection in chickens. Live chicken sales resumed, but all imported birds were screened for the virus before entering the markets.
But the virus would prove implacable. Even in Hong Kong, it would resurface in 2001, killing chickens in market after market. As a pre emptive strike, the government ordered a second mass slaughter of all poultry in the markets and imposed a mandatory rest day each month when they would be emptied, unsold poultry killed, and the stalls cleaned before restocking with new flocks. Undeterred, the virus struck yet again the following year. But over that period, it never again jumped to people.
Fukuda eventually would go on to become WHO’s global influenza chief. Yet he always remembered the Hong Kong investigation as the most rewarding in his life. He lauded Chan’s leadership as heroic. He had no way of knowing that nearly a decade later he would be reunited with her in fighting the virus as it spread to much more difficult terrain far beyond the horizon.
The operation, as Dr. Prasert Thongcharoen called his lonely campaign against a killer, started on a hungry stomach. After seventy years of life, he had developed an abiding fondness for farm-fresh eggs and looked forward to those occasions every few weeks when a pair of young friends would present him with dozens of the finest from their family homestead outside of Bangkok. So when they returned to the Thai capital empty-handed one warm December day in 2003, Prasert was disappointed. He also suspected something was terribly amiss.
A distinguished man with silver-and-black hair combed back off a high forehead and eyes keen behind thick aviator glasses, Prasert had accumulated countless honors and accolades during his pioneering career. He had been dean of the medical school at Bangkok’s Mahidol University, chief editor of the Thailand Medical Association’s journal, and a fellow of the Thai Royal Institute. He had also earned a reputation as something of a gourmet. He often cooked for the staff at Siriraj Hospital, where he continued to do research as an emeritus professor, preparing chicken-leg curry and other favorites in the small departmental kitchen. He experimented at home with new recipes, trying them out on his children. He was so passionate about fresh food that he once flew home from Hong Kong with a newly butchered goose in his hand luggage.
The doctor was partial to eggs sunny-side up for his breakfast and had been expecting a fresh batch as usual. Two of his longtime friends, the chief reporter at one of Thailand’s leading newspapers and his wife, had taken advantage of a national holiday marking the birthday of Thailand’s revered monarch, King Bhumibol Adulyadej, to escape Bangkok’s suffocating traffic and hectic pace. They had decamped to their farm about fifty miles to the east amid the mango orchards of Chachoengsao province. After a brief vacation, the couple returned to the capital and came to Prasert with apologies. “What happened?” he asked. The response astonished him: “There are no chickens, so there are no eggs. The farm is usually full of chickens. But the chickens all died. We don’t know why.”
The couple traditionally visited their farm twice a month and for years had been furnishing Prasert with six or seven dozen eggs on their return. This time they brought him only a riddle. It was a grim and disquieting puzzle that would become the focus of a personal crusade. Almost alone, he would press his kingdom’s leaders to admit that a plague was raging in the Thai countryside and threatening to leap beyond the borders. “I had no eggs to eat,” he later told me. “And so the operation began.”
Six years had passed since the novel strain of flu had crossed to people in Hong Kong in 1997, and the virus had been nearly invisible since then. In the interim, the only confirmed human cases in the world had come several months earlier in a Chinese family. At this moment in late 2003, though Asia was on the brink of an unprecedented outbreak in both birds and people, flu was on few minds. The virus, it seemed, had vanished, lulling much of the world into a naive confidence that the pandemic threat had passed.
This would become the pattern. Over the next few years, the H5N1 strain would repeatedly raise its head, surfacing in ever more countries and provoking grave public health warnings anew. Yet each time, the virus would stop short of epidemic and then retreat. Politicians would boast they’d cornered the bug. Media attention would fade. Much of the public would forget.
In 1997, H5N1 had been but one hurdle shy of pandemic, yet that recognition vanished in the silence that followed the Hong Kong outbreak. The virus was a subtype against which no one was immune. It had demonstrated it could infect people. Only the last of the three conditions for pandemic had remained unfulfilled: that the disease could be relayed along a human chain.
It would fall to Prasert to prove that once again, a novel strain was circulating across the landscape of East Asia. Soon after, he would also reveal that the virus had begun to strike his countrymen. And eventually, as the world watched anxiously to learn whether the virus could be passed from one person to another, Prasert would play a central role in confirming it could. Although Prasert held the title of WHO consultant, he waged this campaign mostly by himself. For while WHO’s flu specialists back in Geneva also suspected something was not right, they had to defer, as they all too often must, to the assurances of a sovereign state that all was well.
When I first met Prasert in 2005, the bags beneath his eyes had grown heavy and the lids were sagging. The years had generously etched his forehead with fine lines. But his curiosity and intellect remained acute. He was still Thailand’s most eminent virologist and the man who literally wrote the book on flu in his country. His 1998 monograph on the disease begins, “Influenza has been an epidemic illness since ancient times but the flu virus never remains the way it was. It never stops changing.”
When the Asian flu pandemic of 1957 swept through Thailand, Prasert was just one month out of medical school and beginning his hospital residency. As pandemics go, it was comparatively mild. But for the three months that it throttled Thailand, the flu flooded Prasert’s hospital with the sick and dying. Several dozen of his fellow residents fell victim. The young physician was one of only two healthy enough to attend to patients. Eleven years later, when pandemic revisited Thailand in the form of the Hong Kong flu, Prasert was already emerging as a leading researcher. He devoted his efforts to deciphering the virus’s behavior by scrutinizing the pattern of mass absenteeism at Thai schools and industries.
Prasert received me in his sixth-floor office at Mahidol University’s microbiology department, where he had established the virology program decades earlier. Siriraj Hospital, home to the department, is a teeming complex of white-and-cream towers rising on the west bank of the Chao Phraya River, which winds through the heart of the Thai capital. The dark waters below bustle with low-slung ferries shuttling commuters and shoppers between the shores, carnival-colored long-tail boats popular with sightseers, and the occasional tugboat dragging a sand barge slowly downriver. On the opposing bank shimmer the fairy-tale pagodas and gold steeples of the Grand Palace, the Temple of the Emerald Buddha, and the other signature sites of royal Bangkok. Prasert’s office was cramped but well air-conditioned, a relief from the hospital’s steamy corridors. Several bouquets of silk-and-plastic flowers brightened the room. As Prasert’s assistants brought us coffee, he slipped on the white lab coat of a man still very much involved in scientific inquiry and sank into the cushions of a purple sofa. Then, after offering a few observations about the merits of Thai coffee beans, he began to recount how he had forced his government to come clean.
In November 2003, Thai poultry farmers had begun to complain about a disease devastating their flocks. Their chickens at first seemed depressed and lost their appetites. The hens stopped laying eggs. The birds would soon start to wheeze and cough as the sickness ravaged their lungs. Some would develop diarrhea. Many would stagger around as their brains began to hemorrhage, melting into a bloody cranial mush. They would die suddenly, often overnight, and by the thousands. This disease was killing with a speed almost never seen in Thailand or anywhere on Earth.
Thai agriculture officials investigated and, suppressing the truth, reassured farmers it was nothing serious, just a minor outbreak of fowl cholera complicated by bronchitis. The country’s deputy agriculture minister and livestock chief would both later blame the spiraling death toll on the weather, saying that an abrupt seasonal change had left chickens in a weakened state that made them vulnerable to catching these two infections in tandem. There was no reason to panic. There was certainly no reason, the agriculture officials said disingenuously, for anyone to doubt the quality of poultry raised in Thailand, which at the time was the world’s fourth-largest chicken exporter, annually shipping $1.3 billion worth overseas.
Prasert heard the initial reports and had no reason to disbelieve them. But he was intrigued. Though he had spent years studying infectious diseases, from dengue fever to HIV-AIDS, fowl cholera was entirely new for him. “I just wanted to see about it,” he explained. So in the predawn hours of a December morning, Prasert headed for the wet market that sprawls across more than a dozen acres beside the Bangkok Noi railway station. There, across from the creaky gray train carriages ferrying farmers from the countryside, Thais continue to shop as they have for generations. Prasert ventured into the warren of crowded aisles, slightly stooped, stepping carefully along floors slick with water and mud, past mounds of pineapples, mangos, hairy ramb utan, and lavender dragon fruit, past chili peppers and curry power heaped high in plastic baskets, past pig heads lined up along white tile countertops and catfish slithering in their trays. Even before he reached the chicken mongers, he could hear the repeated thump of their cleavers as they hacked the birds into wings and legs, feet and ankles, liver and intestines. He asked around until he located several peddlers whose families raised poultry in Nakhon Sawan province, about a hundred miles north. Prasert had heard it was at the center of the fowl cholera outbreak.
“They said they didn’t believe it,” he recalled. “They said it wasn’t like fowl cholera. If they have some chickens that are sick with that, they give them tetracycline, and they get better. But these chickens, by the next morning, they’re all dead. So they thought there was something more than that.”
Prasert was unsure what to make of this skepticism and filed away their dissent. “I didn’t pay much attention to that then,” he said. But within two weeks, when his friends came to him with apologies instead of eggs, he remembered what the farmers of Nakhon Sawan had said.
His ears now attuned to reports of ailing chickens, Prasert was starting to hear about a bird flu outbreak in southern China. Though Chinese agriculture officials would not disclose the spreading infection for nearly two more months, in late January 2004, the virus had in fact been circulating there for years. This was no secret to Chinese farmers, veterinarians, and researchers, and the rumor soon reached Prasert. He surmised that the flu virus afflicting Chinese poultry was now making chickens sick in Thailand. He suspected that migratory birds had spread the disease from China. But he still needed proof.
With Thai livestock officials continuing to hide evidence of bird flu, Prasert turned to two colleagues at the Ministry of Public Health. Together they plotted to smuggle poultry samples from the countryside into Bangkok for testing. Since agriculture officials had barred them from visiting chicken farms, Prasert and his colleagues called a farmer in Chachoengsao province, home to the county’s largest concentration of chickens, and recruited him as an accomplice. They arranged for him to wrap two dead chickens in newspaper and then leave them at the edge of his property like innocent rubbish. The pair of health ministry officials would drive out to the province to collect the contraband carcasses.
When the officials arrived back in the capital, they called Prasert. “We’ve got them,” they reported. “What should we do now?”
“Bring them here,” he instructed.
As a medical facility, Siriraj Hospital was not authorized to test animal samples, just those from humans. But Prasert was sure that veterinary labs would refuse to run tests of the dead chickens, fearing government reprisal, or would decline to tell him the results. “We had to do it ourselves. It was a must,” he said. Prasert immediately turned the samples over to lab researchers at his hospital, who began secretly analyzing them for both influenza and fowl cholera.
The proof he was seeking came later that evening, “December 19, twenty-hundred hours,” Prasert recounted, flashing a broad smile. The researchers brought him lab results demonstrating that the birds were infected with influenza. The tests were not precise enough to determine whether the virus was specifically H5N1, which had surfaced in Hong Kong in 1997 and had been circulating in China ever since. Siriraj Hospital did not have the right chemical reagents to tease this information out of animal samples. But Prasert was now sure that something more than fowl cholera and bronchitis was troubling Thailand’s chickens. And if it was bird flu, he was convinced it had to be H5N1. That meant that the people of Thailand and beyond were in peril. They had no natural defense against this novel strain of flu.
Prasert placed an urgent call to senior officials at the health ministry. “I have evidence that this is avian flu,” he notified them. He told them they had to be vigilant. He urged them to prepare for a medical emergency. But he was rebuffed. “For agricultural production, we have nothing to do with that,” one senior health officer responded curtly.
Prasert was aghast. “This is a public health concern,” he scolded, “and I will not close my mouth. I will talk even louder. I’m retired already and no one employs me. It’s not like I’m a government official.”
Prasert was not alone in suspecting the worst. Inside Thailand’s health ministry itself, infectious-disease specialists were already speculating that the strange sickness decimating the country’s chickens was flu. Officials in the ministry’s disease-control department later told me they had heard rumors as early as November 2003 about flu outbreaks among birds in China and Vietnam. So the ministry sent out letters across Thailand alerting doctors in the provinces to be on guard. The public health surveillance system, which Thailand put in place months earlier in response to the SARS epidemic, was urgently revamped to monitor for bird flu. But health officials remained mute in public. They issued no advice on how to avoid the virus, no warning against contact with sick birds. There was no public guidance about how to recognize the disease if you caught it and what to do if you did. No effort was made to import and stockpile Tamiflu, which was considered the main remedy for the virus.
Nor was Prasert the only one with hard lab evidence of a flu epidemic out on the farm. Across town at Bangkok’s elite Chulalongkorn University, researchers had confirmed it was bird flu back in November and even determined that the virus was the H5N1 strain. Associate Professor Roongroje Thanawongnuwech, head of the university’s veterinary diagnostic laboratory, would later disclose that the virus had been found in samples taken from Suphan Buri province, about sixty miles northwest of the capital. His lab used a test called the RT-POLYMERASE chain reaction to reveal the virus’s makeup. Researchers compared their results with GenBank, a public database run by the U.S. National Institutes of Health containing tens of thousands of known genetic sequences, and discovered that the Thai virus was very similar to those previously isolated in Hong Kong and Vietnam. Roongroje later reported that these findings had been turned over to Thailand’s national livestock department. But again the public was not told.
Thai health officials and researchers were cowed. They were under intense pressure to keep mum. At stake were the country’s lucrative poultry business and its export markets, primarily in Europe and Japan. Hundreds of thousands of Thais were estimated to work on thirty thousand poultry farms and in related industries. While some infectious-disease specialists in the health ministry were anxious to sound the alarm, they were silenced by a powerful agriculture ministry whose primary aim was promoting farm interests.
“We were fighting with each other and not the virus,” admitted Dr. Kumnuan Ungchusak, a senior Thai health official, in a remarkably frank lecture delivered in May 2006 at a medical conference in Singapore. As the director of epidemiology in the ministry’s disease-control department, Kumnuan had been uniquely positioned to investigate the threat to human health that began emerging with the mass poultry deaths in November 2003. But he continued, “Nobody dared to speak that this was H5N1.” He urged his listeners from countries facing the epidemic—by that time the virus had spread to birds in more than fifty countries—not to repeat Thailand’s mistake in withholding information. “We should have declared this a couple of months before so we can save a lot of poultry and we can save a lot of lives.”
I was in the audience as Kumnuan recounted his experience and was surprised by his public candor. After he finished, I asked him privately to expand. Why wouldn’t anyone in the health ministry reveal the truth? “At the time,” he explained, “there would be a large impact on exports. There was a lot of reluctance to inform the public about it. This is a very bitter story.” But specifically, I pressed him, who gave the order to keep quiet? “I don’t want to pinpoint,” he demurred.
What Kumnuan remained reluctant to say was that the poultry sector’s pull had extended beyond the ranks of the agriculture ministry to the very top of the Thai government. The industry had influential advocates in the tight inner circle of Prime Minister Thaksin Shinawatra. A telecommunications tycoon turned politician, Thaksin had come to office in a landslide in 2001 vowing to turn around the struggling Thai economy by running it like a corporation. He had indeed succeeded in resuscitating the economy by 2003, achieving some of the highest growth rates in Asia and promising even faster growth in the year ahead. He had also demonstrated his impatience with those who got in the way of his economic juggernaut. Thaksin labeled himself the CEO-prime minister. His critics called him autocratic and vengeful.
In mid-January 2004, nearly a month after Prasert produced proof of a flu outbreak among Thai chickens, Deputy Agriculture Minister Newin Chidchob was still vowing it wasn’t so. “Irresponsible media and some groups of people are trying to spread this rumor,” he told reporters. “There is no bird flu here.” His assurances were endorsed three days later, on January 19, by David Byrne, the European Union’s health commissioner, who was visiting Bangkok on a previously scheduled trip. Part of his job was to protect European consumers, and, after a briefing from agriculture officials, he pronounced Thai chickens to be safe. “There’s absolutely no evidence of the existence of bird flu in Thailand,” Byrne said in remarks he would soon furiously retract.
The next day, as television cameras rolled, Prime Minister Thaksin and his cabinet ministers tucked into a luncheon feast of spicy chicken soup, minced chicken salad, chicken biryani, chicken teriyaki, and grilled, boiled, curried, and fried chicken, capped by a healthy serving of the Thai leader’s trademark bravado. “Come and join us. Are you scared?” the prime minister taunted reporters. With anxiety mounting among consumers, Thaksin’s response was to order up the repast and claim all was well. “It’s the best chicken in the world, Thai chicken,” he offered between bites. “It’s very good. It’s safe.”
But WHO already knew better. A week earlier, on January 14, the agency’s office in Bangkok had received a confidential tip from a government epidemiologist reporting that bird flu had been detected in a recent poultry outbreak and tests had determined it was an H5 virus. Though more analysis was needed, the scientific implication was that the strain was a novel H5N1. This troubling disclosure was forwarded to WHO headquarters in Geneva, where infectious-disease specialists asked the Bangkok office to get more specifics from the Thai government.
These inquiries were repeatedly spurned. WHO’s chief representative in Thailand and his staff were informed by their government counterparts that only the health minister could release details, and she remained tight-lipped. So over the coming days, the WHO team in Bangkok grew increasingly exasperated, venting frustration in e-mails and conversations with Geneva.
WHO had been on edge practically since the new year. Poultry outbreaks of bird flu had already been detected in South Korea, Vietnam, and Japan. Just a week earlier, Vietnam had confirmed human cases, stoking public fear of a flu pandemic for the first time since Hong Kong’s outbreak six years earlier. Could Thailand be the next front? It was crucial to know. Yet there was little the agency could do. It couldn’t force the Thai government to come clean. Nor could WHO itself go public unless the government cooperated.
As a United Nations agency, WHO was established by its member countries and, like other UN bodies, respects their national sovereignty. Though WHO has been growing increasingly assertive in recent years, pressuring governments on occasion to hunt for infectious diseases on their turf and disclose them when discovered, the agency still largely defers to local politics. Even when an outbreak becomes apparent, WHO cannot dispatch investigators to a country without a formal invitation. And even after they get on the ground, these teams are barred from the field until authorized by the country to proceed.
The agency’s critics fault it for becoming a prisoner of its politics. They accuse it of too often bowing before the dictates and deceits of its member countries, of placing a higher price on diplomatic nicety than on truth. But senior WHO officials, including some who have personally braved the world’s most horrible pathogens, scoff at the contention that they’re weak or cowardly. They counter that WHO is a creation of international politics and thus, by definition, a creature of one. Otherwise, they say, WHO and its mission could not exist at all.
Nor is WHO some kind of global health department with an army of doctors, nurses, ambulance drivers, and inspectors. It has no labs or hospitals of its own. The oldest disease-control program at WHO, even older than the agency itself, is its global monitoring effort for flu. The perils of pandemic combined with the economic and health impact of seasonal flu made this initiative an early priority. Yet even this program depends entirely on a network of outside labs—at latest count more than a hundred in eighty-plus countries—to track the evolution of flu viruses and help develop suitable tests, drugs, and vaccines.
Mostly, WHO supplements the efforts of individual governments, offering specialized expertise and scarce materiel like stockpiled vaccines for meningitis and yellow fever. To accomplish this, the agency relies on an extensive network of consultants from around the world, both public and private, to help investigate outbreaks, treat the sick, test samples, train local health staff, and deliver medicine, vaccines, and equipment.
These outside allies are people like Prasert, whose career was devoted to forging the institutions and disciplines of modern medical learning in Thailand that now make his country among the most advanced in the region. Yet there was always time for WHO. On a curriculum vitae stretching for several pages of publications and affiliations, Prasert prominently highlights his position as consultant to the World Health Organization. For over three decades, he served on various advisory committees for the agency, most notably the expert panel on viral diseases. He has run a WHO collaborating laboratory for AIDS research and edited an agency monograph on dengue fever.
In Geneva, senior agency officials describe their role in coordinating all this outside expertise by using words like secretariat, catalyst, and platform. What they mean is that they’re like the salaried fire chief of a vast volunteer brigade.
WHO was born of the optimism that followed the Second World War, when international cooperation in the shape of the freshly minted United Nations and its agencies promised a new chapter in human history. Founded in 1948, WHO set its objective as nothing less than the “attainment by all peoples of the highest possible level of health.” This was an ambitious goal. Yet advances in medical science at the time seemed to be bringing down the curtain on epidemic diseases that long plagued mankind, notably polio and smallpox. By the 1960s, however, WHO suffered a colossal setback with the failure of global efforts to eradicate malaria. It was emblematic of a broader resurgence of infectious disease as microbes mutated, outsmarting new medicines and vaccines, exploiting environmental degradation, poverty, population growth, and humanity’s lapses in vigilance.
As a young American physician, Dr. David Heymann had played a starring role in the eradication of smallpox. He and his WHO team had tracked it to its final havens in India. But soon after, as a new recruit to the CDC, he confronted a pair of entirely new threats. In the summer of 1976, he was dispatched to help investigate a mystery pneumonia spreading through an American Legion convention in Philadelphia. The outbreak, which sickened more than two hundred people and killed nearly three dozen, was ultimately blamed on a previously unknown illness dubbed Legionnaires’ disease. By the end of that same year, Heymann was in Zaire, responding to the first recognized outbreak of a horrible hemorrhagic fever called Ebola. He would end up spending thirteen years in Africa and, during that time, track the Ebola virus deep into the rain forests of Cameroon.
Heymann would later point to 1976—with its outbreaks of Legionnaires’ disease, Ebola, and also swine flu in the United States—as an inflection point in public health history. Man’s conceit was that modern medicine and potent drugs had given him mastery over emerging diseases. But the events of 1976 started to rekindle the world’s concern about these threats, Heymann told me, and the appearance of the AIDS pandemic dashed any remaining illusion of invincibility. “HIV-AIDS really caught the world off guard,” he said. “This really changed the thinking. The world realized the vulnerabilities.”
In 1995, WHO tapped Heymann to establish a program on emerging and communicable diseases. Storm clouds were gathering at all points of the compass: pneumonic plague in India, cholera in Latin America, resurging tuberculosis in Russia and Ukraine, Ebola in central Africa, meningitis across the whole of that continent, and an unprecedented epidemic of dengue fever in nearly sixty countries. Under Heymann, the agency overhauled its intelligence gathering, integrating a system developed by the Canadian health department that mines the Internet for reports and rumors of disease outbreaks. Next Heymann and his colleague Guenael Rodier set up what they called a global strike force, tapping disease investigators from more than a hundred universities, hospitals, and ministries who could get their boots on the ground within two days of any reported outbreak.
Then came SARS. In a matter of weeks in 2003, this novel respiratory disease spread to four continents, striking the economic heart of Asia, putting global air travel in jeopardy, and raising the specter of a worldwide epidemic. WHO’s rapid response contained the epidemic before it became entrenched. This success consolidated the agency’s role in managing outbreaks around the world. That largely explains why WHO, and not the CDC, took the lead in responding to the human cases of bird flu when they erupted in 2004.
SARS was a close call. It underscored the need to rewrite the global code of conduct called the International Health Regulations. The new rules, which took effect in the middle of 2007, require countries to notify WHO within twenty-four hours of any outbreak posing a global threat. Previously, the requirement applied only to yellow fever, plague, and cholera, a legacy of the nineteenth century, when European governments sought to forestall pestilence from the East. Now it was flu, again rising from the East, which posed the greatest menace.
The adoption of the regulations emboldened WHO. “When we come to an assessment that our assistance is needed, we have to push our agenda,” said Dr. Michael Ryan, the burly Irishman who runs the agency’s alert and response operations. But WHO is still ultimately constrained. Governments like the one in Bangkok can continue to tell it to buzz off. “At the end of the day, you are dealing with sovereign states,” Ryan added. “That has to be respected.”
One day before WHO was tipped off to the spreading epidemic in Thailand, a six-year-old boy with symptoms of pneumonia was rushed to Prasert’s hospital. He had a fever of 104 degrees and was desperately short of breath. Within twelve hours, his breathing had grown so labored that the doctors placed him on a ventilator. It seemed at first to do little good, so they kept cranking up the pressure on the device until they could finally achieve an adequate flow of oxygen. An X-ray revealed that the boy’s lower right lung had gone cloudy white, indicating that fluid was flooding the airspaces. The cloud spread a day later to the upper right lung. The next day, it progressed to the left one. The boy, Captan Boonmanut, had been brought to Siriraj Hospital from his home province of Kanchanaburi, located eighty miles from Bangkok near the western border with Burma. Outside Thailand, Kanchanaburi is best known for the Death Railway, built during World War II by Japanese occupying forces to supply its front lines, using Allied prisoners of war and Asian forced labor. At least sixteen thousand POWs perished from disease, hunger, and exhaustion, as did many more of the locals. This brutal chapter was captured in the Oscar-winning film The Bridge on the River Kwai, and the infamous steel-and-concrete bridge still stands, very much in use. But inside Thailand, Kanchanaburi today means rice paddies and chicken sheds.
Captan was a healthy youngster who had a country boy’s love of farm animals. He would often play with the chickens that roamed his backyard. So when he had been handed a rooster during a fateful visit to his uncle’s nearby farm, the boy had hugged it tight. Like many in rural Thailand, the uncle had raised fighting cocks and at first had high hopes for this particular rooster. But when it got sick, the uncle decided to do what most Southeast Asian farmers do with an ailing bird: eat it. Captan’s parents told me how the boy had cradled the bird in his arms and kissed it during the final moments before it was slaughtered and converted to curry.
Captan fell ill within days. A nearby clinic diagnosed the illness as a common cold. When it got worse, his father brought him to the local hospital, where he was given injections of antibiotics. Then, as his fever climbed and his breathing began to race, he was rushed by ambulance to Siriraj Hospital, eventually admitted into the pediatric intensive care unit. His white-blood-cell count was plummeting. So was the level of platelets in his bloodstream. Doctors prescribed broad-spectrum antibiotics on the assumption that his pneumonia was caused by a bacterial infection—but to no effect. The disease was unrelenting. So the doctors shifted their diagnosis to a possible viral infection and began treating Captan with antiviral drugs. They notified Prasert, the hospital’s most respected virologist.
The doctors had learned from Captan’s parents about his history of close contact with poultry. His father had related the tale of the rooster. Family members further reported that all three hundred chickens on the uncle’s farm had eventually died or been culled and that all but one of the chickens at Captan’s home had also succumbed.
Prasert was afraid he knew what this meant, that he was seeing his worst fears materialize in his own hospital. But without definitive test results, he was reluctant to go public. “We had suspicions already but couldn’t say anything. At that time, nobody could reveal information to anyone. The information the government was releasing was that we didn’t have any avian flu,” he said with narrowing eyes and an ironic smile. For all his credentials and earlier bluster, Prasert was wary of tangling with Thaksin and his ministers, at least for now. That very week, the agriculture ministry had threatened to sue another research institute and the media for allegedly damaging Thai national interests by exaggerating the number of chickens that had died nationwide. “What could I do?” Prasert asked. “I’m only a small, old man. Who would believe me?”
Subsequent study would reveal the viciousness with which the virus was assaulting the little boy’s body. The disease was decimating his respiratory system, destroying the air sacs and capillaries in his lungs and inundating them with blood. The virus also invaded his intestines, where it established a beachhead and began to reproduce further. The pressure on the ventilator helping him breathe had to be turned up so high that even this was starting to take a toll.
Shortly after he arrived at Siriraj Hospital, initial tests confirmed that Captan had influenza A. A week later, on Thursday, January 22, another set of results came back and showed conclusively that it was the novel strain. Prasert now had proof that the second condition for a pandemic had been met. The virus was again infecting people.
Time was up. Prasert placed three calls in the following hours to officials at the public health ministry, including the minister and the director general of the Thai center for disease control. He rebuked them: “Bird flu has reached humans already.” He also went public with his laboratory evidence of a flu outbreak in chickens, telling reporters that the H5N1 strain was widespread and the “cover-up” had to stop. His efforts were seconded by a top Thai lawmaker, a physician-turned-politician named Nirun Phitakwatchara. Nirun, a member of the Thai Senate, announced he’d learned from health officials about a second boy, this one from Suphan Buri province, who had also tested positive for bird flu. He accused the government of hushing up the outbreak for the sake of poultry exports. “I think it’s very late but very late is better than not telling the truth,” Nirun told me at the time.
The next morning, Thailand’s Public Health Minister, Sudarat Keyuraphun, hastily summoned the Bangkok press corps. “There are two cases of bird flu, in a seven-year-old boy from Suphan Buri and a six-year-old boy from Kanchanaburi,” she announced, adding that they were in stable condition. She said that everyone who had contact with the boys would be quarantined for ten days. She blamed the delay in disclosing the cases on the time required to finish testing samples.
The agriculture ministry followed right behind by issuing a statement confirming that chickens on a farm in Suphan Buri province had tested positive for the H5N1 strain. Samples from elsewhere in the country were still being analyzed. Newin, the deputy agriculture minister, announced that a mass slaughter of birds in central Thailand was already under way and that Thailand’s poultry exports were to be suspended.
“It’s not a big deal,” Thaksin reassured the Thai public. “If it’s bird flu, it’s bird flu. We can handle it.”
Tamiflu was urgently flown into the country and immediately administered to the sick boys.
Three days later, Thailand confirmed its first fatality from bird flu. In the early hours of Sunday, January 26, after taking an abrupt turn for the worse, Captan died.
Krisana Hoonsin could not sleep the night he paid eight laborers to slaughter all his chickens. He took a pill to help. When he awoke, he discovered that the silence blanketing the flat, lush province of Suphan Buri had enveloped his farm. Morning broke without the cackling and cooing he had known since he was a teenager. “It reminds me I’m not a chicken farmer anymore,” he told me plaintively. “In a week, all the chickens in our district will be gone.”
One day after Thai officials publicly confessed that bird flu had struck, Krisana sat heartbroken in a small, clapboard kiosk erected inches above a fishpond in front of his farmhouse. He wore a loose, black-checked work shirt and had a slight scar on his left cheek. His eyes were bloodshot, his dark brow deeply furrowed, like some of the nearby plots. Between the fingers of his rough right hand, the thirty-eight-year-old farmer clutched a lit cigarette, but he barely puffed. It would burn to a stub. Then, noticing just in time, he would rub it out and light another. This was still January, one of the coolest months in Thailand, but the midday sun was intense, so Krisana had taken refuge beneath the pitched, corrugated metal roof of the simple shelter. It was here that he had often come at dusk, when his chores were finished, and fondly gaze at one of his poultry sheds on the other side of the narrow country road. “My chickens would recognize me,” he recounted. “They would stick their heads up and see me. Now it’s empty.” His voice cracked. “I still think of all my chickens.”
His birds started getting sick two weeks earlier. He reported it to local livestock officers. Though they assured him it was only a minor case of fowl cholera, he was ordered to take draconian measures and put all seven thousand to death. Too upset to execute the sentence himself, Krisana hired a few locals. They marched down the tight aisles of the poultry sheds, wrestled the birds from the raised metal cages, and stuffed them alive into plastic feed and fertilizer sacks. The chickens were left to suffocate, then buried in a pit coated with lime at the edge of his property. “How can I express the feeling to see all our chickens die that way?” he asked. He let his sandals slip from his feet and rubbed his soles against the rough wood planks. “When you do chicken farming, it’s like you’re taking care of your own children. You love them. They love you back.”
I had come to Suphan Buri early that morning with an energetic Thai journalist, Somporn Panyastianpong, who often worked as my translator. Before we left Bangkok, she had stopped to buy us surgical masks and rubber gloves, though the two health officials I had consulted were unsure whether these would adequately protect us. The disease was still so new, its precise lines of attack still uncharted. We drove north along the modern divided highway that connects the sprawling suburbs of the capital with Thailand’s central wetlands. After an hour, shimmering green rice paddies opened up before us, many fringed with coconut palms. Storks, herons, egrets, and cormorants swooped and scavenged amid the neon fields. Peasants in straw hats meandered along the earthen dikes, hoes slung over their shoulders. A few ragged duck herders, barely teenagers, squatted at the edge of flooded paddies while their flocks waded into the murky waters, shaking their dark brown tail feathers and rooting around in the muck, hunting snails.
As we turned off the main road, we began see the scores of metal-roofed chicken sheds that Suphan Buri’s farmers had raised in making their region one of Thailand’s most prodigious poultry producers. These were long, open-sided structures on wooden stilts that all seemed to jut out over ponds and reservoirs. Under an ingenious system, chicken droppings are not cleared away but allowed to fall between the wooden floorboards into the water, which are stocked with carp, tilapia, and barb. The droppings serve as nourishment and save on fish food. The fish themselves often command better prices at market than the birds. But when the chickens die, the fish go hungry.
Now, as we ventured deeper down the rural roads, we drove past one eerily vacant shed after another. A legion of cullers had swept across the countryside ahead of us, killing an estimated 7 million birds over previous days in Suphan Buri and two other provinces. More than five hundred workers from the agriculture ministry were again fanning out across Suphan Buri to continue the mass slaughter. Teams clad in masks, rubber gloves, and high boots were storming through the sheds, cramming squawking birds into sacks and spraying disinfectant from tanks. Hundreds of Thai soldiers and several dozen prisoners were also being pressed into service, many with brightly colored shower caps to protect their heads. Though the government was targeting four hundred more farms on this day, Newin had warned that teams were running short of sacks and burial space. He told reporters that the cullers were now being forced to use the grounds of Buddhist temples.
Krisana’s family had been raising hens in Suphan Buri for twenty-two years in a village called Baanmai. At first, their aim was to produce just enough eggs for income between rice harvests. But when Krisana took over the farm from his father in 1994, the ambitious young man decided paddy was the past and poultry the future. He immediately quadrupled the number of hens to four thousand, adding more in the following years. It proved a lucrative business. He built an airy, two-story house with a solid brick facade. An upstairs veranda with a cheerful blue-and-purple balustrade looked out over the emerald fields. He bought a new Toyota pickup, parked it out front, and hired a farmhand. He never imagined that one day his livelihood would be buried along with his birds in a hole in the side yard.
Over the years, he had grown accustomed to a few chickens dying suddenly and mysteriously. But he had never witnessed the kind of epidemic that had been stalking his province for the last two months. “It got bigger and bigger and spread from one farm to another before it reached our farm,” he recalled. “Every night, three or four chickens would die.” He consulted a veterinarian, who prescribed antibiotics. They had no effect. Local livestock officers could offer no explanation. The provincial livestock chief reprised the official line that the affliction was fowl cholera. But Krisana was starting to suspect something else. When Vietnam confirmed its poultry had been infected by influenza, Thai television carried reports with footage showing the symptoms. The birds suffered from stiff muscles, reddening skin, and chills, then died. “I saw it on the news and saw the same symptoms here, and I was sure it was bird flu,” he said.
Krisana and his neighbors had alerted officials to their suspicions but were ignored. Now the farmers were livid. They were convinced their flocks could have been salvaged by a swifter government effort to quarantine contaminated farms. “They kept denying and denying and denying it was bird flu. If the government had admitted it earlier, they could have contained it,” he said. A thin smile passed across his sullen face. “Instead, farmers kept transporting chickens and eggs from one place to another.”
Slipping on his sandals, Krisana roused himself from his bench inside the kiosk. He led the way around the side of the house to give me a closer look at one of his chicken sheds, empty and deadly quiet. He shuffled along the wooden planks that served as a short causeway. Though the shed had been disinfected, I was still wary of following. I had the surgical mask and rubber gloves with me but Krisana had neither. I didn’t want to be rude. So with some trepidation, I left them in my bag and poked my head ever so briefly inside the entrance. I tried not to breathe.
When we returned to the kiosk, Krisana’s father came out of the house to join us. At seventy-six, Sompao Hoonsin was still vigorous, with thinning gray hair, and age spots on his broad face. He wore a jolly T-shirt with pictures of Winnie the Pooh and Tigger, but his manner was decidedly downcast. In his hand, he carried a small, handwritten note listing the family’s liabilities in blue ink. They totaled nearly $40,000. The family, he explained, netted about $2,500 a month from selling eggs to small-time retailers in Bangkok, and this had long been enough for Krisana to support his wife, three children, and his father, who had raised him alone since he was a boy. But the debts mounted over the previous two years as the price for eggs weakened. They had to put up the house and land as collateral. “Finally,” Sompao said, “things began to brighten.” Prices had picked up since summer, and the weather had at long last turned favorable for laying: not too warm, with a gentle breeze. “We thought we’d be able to get out of debt and buy all our chicken feed without borrowing money,” the elderly farmer continued. “Then suddenly, we had to bury all our chickens. We can’t even earn one penny. All the children in the family, before they go to school, they’re asking, ‘Will we have enough to eat today?’ ”
Often overlooked in discussions about bird flu, amid all the anxiety over a possible human pandemic, are the staggering economic costs already incurred by Asia’s farmers. For the poorest peasants, their few chickens were an insurance policy against hunger in bad times. For those who have proven more successful, like Krisana, the flu plague has jeopardized the investments and aspirations of a generation. Some of the farmers in Baanmai village, seduced by the riches that poultry promised, had gone so far as to ask their children to quit or forgo good jobs in Bangkok to help with the business back home. Now they faced bankruptcy.
A day before I stopped by the farm, Sompao had visited the bank to talk about the family’s debts. He had hoped to defer the interest payments of about $250 a month. Nothing was resolved. Government officials had floated the idea that they might pay some degree of compensation for culled flocks. But even if they did, Krisana vowed he was through with chicken farming. “Once they announced the results of the lab tests, I got worried about my health and the health of my kids. We don’t know if this flu would come back,” he said.
His voice trailed off. A white government van pulled up at the edge of the front yard. Krisana watched as officers from the animal disease control department got out to examine the pit where his birds were buried. Satisfied that they were properly interred, the inspectors got back in and drove off.
Krisana resumed his thought. Perhaps it was time to go back to rice farming. He certainly had abandoned his ambition to keep expanding. Maybe self-sufficiency was the answer, he suggested dejectedly. “You can’t imagine how it feels to sit and stay quiet when you see all you have suddenly disappear,” he went on mournfully. “Everyone around here is in shock. We’ve lost hope in life.”
Earlier in the day, Krisana had heard Thaksin might visit the province with his agriculture minister to inspect the culling operation and reassure local farmers. Krisana hoped they would. He said he had something for them—a lotus leaf. “If an elephant dies, you can’t cover it with a lotus leaf,” he quipped, reciting a Thai proverb. Don’t try to hide a large mistake once it’s in the open. “If a million chickens die, you can’t cover it with a lotus leaf,” he continued, embroidering on the original. He paused and reflected for a moment. Then he added, “I’d give them the leaf. But I’m not sure they would understand.”
Hours after Captan Boonmanut died on January 26 in a nearby ward, Siriraj Hospital convened a seminar to discuss the gathering storm. Prasert was to brief his medical colleagues and review what it would take for H5N1 to spark a human epidemic. The first two conditions had been met. He wanted to discuss the third and fateful one.
Many of those at the seminar were relative newcomers to flu. Prasert reminded them there were two ways a bird flu virus could become transmissible among people. The virus could gradually undergo a series of discrete mutations making it progressively better suited to the human body. This first process was called antigenic drift. The other way, Prasert continued, was antigenic shift, in which the bird flu virus experiences genetic reassortment, swapping genes with an existing human influenza virus and creating an entirely new strain that is both highly lethal and as easy to catch as an ordinary flu bug. This latter transformation could happen overnight, he warned.
It had taken a whole lot of pushing and prodding to get the government to acknowledge that Thailand’s birds were spreading the disease. But now, Prasert told his audience, an equally acute threat could be posed by the country’s pigs. That was because swine could be what researchers called the mixing vessel, in which two flu strains exchange genetic material. Sick pigs in Asia, Europe, and Africa had repeatedly been found infected with a human strain of influenza. Prasert said he was also hearing reports, later confirmed by Chinese researchers, that pigs in China had come down with bird flu. If a pig caught both strains at the same time, the results could be catastrophic.
Over the coming months, as the scourge spread to a third of Thailand’s provinces and across a half-dozen Southeast Asian countries, flu hunters would grow haunted by the prospect that the strain had cracked the code for human transmission. Yet even as the world was reawakening to this threat, Prasert was already probing how the virus might cross this final hurdle.
The next morning, his admonitions made headlines in Thai newspapers. But the reaction was not as he’d hoped. Swine farmers were enraged, fearing for their sales, and some threatened him.
The prime minister was asked by reporters about Prasert’s warnings and brushed them off as the ranting of a mad old man, calling them overly imaginative and without basis in science. “Are the doctor and the media going take any responsibility if the virus does not spread to pigs?” Thaksin asked pointedly.
Dismissing the elderly virologist with a disparaging Thai word, ai, that can best be translated imprecisely as “goddamn,” the prime minister accused the elderly virologist of going too far this time. “It was that goddamn doctor,” he snapped, “saying it all by himself.”
The flu hit America early that year and it hit hard. It was shaping up to be the worst season in twenty-five years. That fall, in October 2003, Tim Uyeki had been summoned back to Atlanta while at an international influenza conference on the Japanese island of Okinawa. His CDC colleagues had urgently notified him about an unusual spike in severe flu cases among children. Texas and Colorado were being struck particularly hard. The culprit was a traditional strain of human flu but a new, unexpected subtype. As autumn turned to winter, the epidemic spread eastward until outbreaks were being reported in most states. The disease was taking an unusual turn in some children, resulting in neurological complications. Even worse, scores of children were dying. Uyeki, as both a pediatrician and influenza specialist, was tapped by the CDC to help run a national effort to identify and detail these fatal cases.
Now, in the waning days of December 2003, Uyeki found himself at his desk. The hallways of the CDC were depressingly empty except for a few other souls on flu duty.
He had been forced to cancel his Christmas vacation. He could have used the downtime. It had been a grueling year, much of it spent on the road. But the mounting pile of pediatric files beckoned. He had to sift them, study them, and try to divine why children were falling victim while the flu’s typical casualties, the elderly, had this time been spared.
When he logged on to his computer on Monday, December 29, he came across an e-mail from Vietnam titled “Urgent.” It was a copy of a request sent to one of Uyeki’s colleagues by a virologist at Hanoi’s National Institute of Hygiene and Epidemiology (NIHE). The Vietnamese scientist, Dr. Le Thi Quynh Mai, reported that Hanoi Hospital was treating a number of children with respiratory symptoms and doctors there were stumped. “We need to know what’s causative of it,” she appealed.
This entreaty was the first hint outside East Asia of a nascent outbreak that would soon transfix the world’s flu specialists. In nearby Thailand, Prasert Thongcharoen had already concluded earlier in the month that bird flu was sweeping his country’s poultry flocks. But he still had no inkling that it had spread to people. That would come three weeks later.
By then, global flu hunters would be streaming into Vietnam on the trail of the novel strain. Their pursuit would widen over the coming months to ever more provinces of Vietnam and then Thailand, the two countries to confirm human infections in 2004. (More countries, including Indonesia, would begin to report them in 2005.) And with each case, investigators would confront that terrible question: Had the virus been passed from one person to another? As the cases persisted and the deaths in Vietnam and Thailand mounted, it became increasingly clear there were indeed likely instances of human transmission. Yet the region’s leaders and the senior brass of WHO itself remained loath to acknowledge publicly that the virus was flirting with the third and final condition for a pandemic.
As Uyeki reviewed the e-mail, he immediately thought of two possibilities, one worrisome and the other worse. “Could the situation be similar to what we are experiencing in the U.S.?” he wondered, thinking about the unusual uptick in seasonal flu. It would hardly be unprecedented for such a strain of human flu to circle the world. “Or,” he pondered, “could these be highly pathogenic H5N1 virus infections?”
He had reason to suspect the latter. Though there was yet no public report of unusual poultry deaths in Southeast Asia, South Korea had officially disclosed a die-off two weeks earlier on a chicken farm outside the capital, Seoul. But Uyeki had little other information to go on. So he replied to the e-mail best as he could, laying out possible diagnoses, suggesting more than a half-dozen different viral infections. Topping the list were influenza of some stripe and an ailment called respiratory syncytial virus infection, or RSV, common among infants. He urged his Vietnamese counterpart to collect samples from the patients and test for those two possibilities.
Uyeki was already acquainted with the Vietnamese doctor and her colleagues in Hanoi. He had first gone to Vietnam three years earlier to collaborate with them on a study looking for evidence of bird flu in live poultry markets. He had stayed in touch, cultivating the relationship as he had with scientists across much of Asia. When SARS broke out in Hanoi in early March 2003, Uyeki returned to help contain the epidemic. He arrived just days after Vietnam’s first case was identified and stayed for a month. Later in the year, he was back yet again, advising the Vietnamese on how to monitor for flu.
When Uyeki first joined the CDC’s influenza branch in 1998, Keiji Fukuda had been on board for two years and had already helped run the investigation into Hong Kong’s H5N1 outbreak. Now the two of them would return together to Asia yet again, trying to decipher whether the new threat was also a passing scare or a harbinger of something far worse.
Uyeki talks about his colleague as he would about an older brother. Both are Japanese American, graduates of Oberlin College in Ohio, and dedicated to a virus that others in Atlanta call “their bug.” They are both among the best at what they do. But while Fukuda is reserved, precise, and methodical, Uyeki is exuberant. Fukuda speaks in carefully crafted arguments, commanding attention with an economy of words. Uyeki’s discourses cascade from topic to topic, detouring through colorful details and intriguing distractions. Fukuda is the kind of man who organizes his day so he can drive his daughter to evening soccer practice. When I last met Uyeki, he was still regretfully a bachelor. His work habits are legend at the CDC. It is not unusual to find him at his desk until one in the morning or later.
So it was no surprise that Uyeki was still in the office when, shortly before midnight on December 29, Dr. Mai’s e-mail reply arrived. “Dear Tim,” she wrote, “these childrens… have fever, cough, difficult breath.” But other symptoms didn’t look at all like flu, she reported. Some of the patients developed diarrhea a few days after the onset of illness and, she added, “died quickly.”
“Died?” Uyeki thought. She hadn’t mentioned that earlier.
Exactly a week later, Dr. Peter Horby got an urgent call on his cell phone. He had driven out of Hanoi that Monday morning to train Vietnamese medical personnel in a nearby province. Horby, a British epidemiologist, had joined WHO’s Hanoi office only a few months earlier after working for several years at the Public Health Laboratory Systems in London, specializing in communicable diseases. He was still learning his way around his new home.
The call was from the director of Vietnam’s National Pediatric Hospital back in Hanoi. He had a mystifying outbreak of respiratory cases. A week earlier, he’d brought these to the attention of senior officials at Vietnam’s health ministry, but they’d brushed him off. So now he was turning to Horby. There was something about the call that told Horby he shouldn’t wait. He broke away from the training session and directed his WHO driver to take him back to Hanoi, directly to the hospital.
The car pulled past the gate and onto the campus of the pediatric hospital, an oasis of soothing greenery and tropical decay in the middle of one of the capital’s most crowded quarters. The institution’s sun-bleached buildings with their ancient wooden doors and paint-chipped balconies were arrayed amid overgrown lawns. Stands of bamboo rose here and there. The grounds were still but for the chirping of birds in the generous shade trees and the occasional sound of a wailing infant. Uniformed nurses walked briskly along the scarred tile walkways. Orderlies in traditional conical hats shuffled past.
Professor Nguyen Thanh Liem, the hospital director, met Horby on his arrival. Three other doctors, including the heads of intensive care and infectious disease, were asked to join them. The doctors told Horby they feared that SARS might again be breeding within their walls. During the previous three months, they had admitted eleven children with unusual respiratory ailments, and seven had died. The other four remained hospitalized. Yet another child, the sibling of one of their cases, had succumbed a week earlier from a similar illness in a provincial hospital.
Horby inquired about the background of the children. There didn’t seem to be an obvious pattern. They ranged in age from nine months to twelve years. They came from a variety of places outside Hanoi, mostly from the countryside but in a pair of cases from town. There were no reported outbreaks in their communities or in their schools.
The doctors escorted Horby to the intensive care unit to see the four surviving children. They had all been healthy just weeks earlier. At first it was just a runny nose, dry cough, and fever. Then the infection grew violent and spread to their lungs. When Horby reviewed the chest X-rays, they were desperately clouded. Their white blood count was low, suggesting the infection was not bacterial but viral. It was likely, Horby concluded, they would die.
“How unusual is this?” he asked the doctors.
“It’s unusual,” Liem replied. “They’re not responding to treatment and we don’t have a diagnosis.”
Horby quickly surmised it wasn’t SARS. That disease had largely bypassed children. It was more likely a pathogen called adenovirus, or perhaps flu. They agreed to conduct more tests on the patients and to press the health ministry about similar cases at other hospitals. WHO would supply masks, gloves, goggles, and face shields to the staff at the pediatric hospital.
A day later, Horby took a call from a journalist asking whether he’d heard reports about a massive die-off of chickens outside Hanoi. He hadn’t. No one at WHO had. “That instantly started ringing alarm bells,” he recalled. “The first day, we thought it was influenza. The second day, we were talking about possible avian flu.”
Dr. Mai at NIHE came to the same conclusion later that week. She had finally succeeded in discovering her causative agent in a sample from one of the children. It was H5N1 bird flu. But WHO still wanted confirmation from an overseas lab with proven experience and turned to Wilina Lim in Hong Kong, the laboratory chief who had worked on the initial human cases in 1997. It took several days to get her the samples. Vietnamese Airlines had balked at transporting them, so another airline had to be found.
The results finally came back on Sunday, January 11. Two children had tested positive for the virus. And so had a third person, the mother of one of the dead youngsters.
WHO put out a worldwide call for reinforcements.
WHO was coming off a monumental victory six months earlier. The containment of SARS, a previously unknown killer that had spread to four continents before it was checked, marked one of the agency’s greatest successes in a half century of history. But it came at a great price.
Agency personnel and their allies from dozens of countries had hustled day and night for months on end, often far from home, to uncover the extent of the SARS outbreak, crack its genetic secrets, and ultimately run it to ground. It was a sprint pace at marathon length. And as the death toll had mounted, so had the pressure. Individual governments made relentless demands on the agency. The global media’s appetite for information was insatiable. The prospect of failure was chilling. After the final two countries, China and Taiwan, were declared SARS free in July 2003, the troops were utterly spent. In Geneva, where crisis had built camaraderie, the agency descended into internal bickering as all the disputes and grievances that had been repressed now bubbled up.
“People were just strung out,” recounted Michael Ryan, who directed WHO’s alert and response program. “Our systems survived. But I use the word survived because it’s like surviving a nuclear explosion. We were still breathing. We were still feeling our limbs to see, were they all there.”
When the threat of pandemic rose anew in January 2004, the agency was still reeling. “We were thinking, ‘We don’t want to do that again,’ ” Ryan said.
That was especially true for WHO in Vietnam, which had been among the first countries struck by SARS and among the first to contain it. Pascale Brudon, the auburn-haired Frenchwoman who headed the agency’s Hanoi office, likened the SARS experience to The Plague, by Albert Camus. She said the tension and sense of personal jeopardy had been profound, especially after the loss of Dr. Carlo Urbani. Urbani, an Italian infectious-disease expert assigned to Vietnam, had investigated the country’s initial SARS case, and his early insights into the pathogen ultimately helped the world defeat it. But not before he, too, succumbed. He had been a popular figure, a hang-gliding, motorcycle-riding musician of a man who, while previously working for Doctors Without Borders, had received the 1999 Nobel Peace Prize on that organization’s behalf. His death was staggering.
When Horby notified Brudon in early January 2004 about what he’d learned at the National Pediatric Hospital, her reaction was, “Oh no, not again.”
In Geneva, Dr. Klaus Stohr was the head of WHO’s global influenza program. He had never doubted that bird flu would resurface, and he was waiting for the moment. “To prevent an earthquake or an eruption of a volcano, you always prepare for it,” he recalled. “But when it happens, you’re still surprised, still shocked.”
Stohr wanted to get his flu hunters on the ground fast. But it was proving difficult to assemble a team. “There were some people, all international experts, who said ‘Why should I go? Why should I jump into the frying pan?’ ” he recalled. They were thinking about their families. They were thinking about Carlo Urbani. “It’s too hot for us to go right in the middle of a possible volcano.” They demurred.
Horby was already on the ground and he, too, was thinking about Urbani. He had assumed some of Urbani’s duties, and like his predecessor, was back in the hospitals, seeing desperately sick patients infected with an uncertain yet catastrophic agent. “It was a very worrying time,” Horby later acknowledged.
But Uyeki, biding his time in Atlanta since he’d first learned of the outbreak two weeks earlier, couldn’t get there soon enough. “You want to help and you want to find out answers,” he told me. “Yeah, I was ready to go right away. Keiji and I, we’re ready to go.”
“What do I need?” Uyeki thought. He stocked up on antiviral drugs to dose himself. He collected his protective gear. As a matter of course, he had already been custom-fitted for N95 respirators, what most people call masks, and he replenished his supply. Then he and Fukuda started turning over their command responsibilities in fighting the seasonal flu still raging at home.
The flu outbreak that began that fall had jolted the American health-care system. It was only seasonal flu, but hospitals and doctors’ offices were flooded with the infirm. Emergency rooms from coast to coast were reporting record numbers of patients, in some cases a hundred a day, and many waiting rooms were standing room only. Some hospitals made other patients give up their beds. Local government officials activated disaster plans. Just a week after Thanksgiving, flu shots already had run out.
But as nasty as that flu season was, again, it was only seasonal flu. In a pandemic, the health-care system could crumble. Just the initial rumblings of a pandemic, the first weeks of the swine flu outbreak in spring 2009, overwhelmed many American hospitals and clinics as patients with little more than common colds, or no symptoms at all, clamored to be checked out. A mild pandemic with a relatively low death rate would still sicken at least a quarter of the population, sending millions of petrified, sniffling Americans to the hospital. In a more severe epidemic, our broader society as we know it could be in jeopardy. That’s the lesson of Philadelphia.
As a young reporter, I worked there for eight years—it was my first big city—and I got to know its streets well. I never realized I was sharing the ghostly geography of the worst calamity ever to befall the United States.
It was September 11, 1918 when the Spanish flu made its first recorded appearance in Philadelphia, striking the Naval Yard at the foot of South Broad Street. The virus had come ashore with scores of sailors transferred days earlier from Boston, a city already under siege. But Philadelphia’s flu epidemic would evince its full fury only later in the month, after the city had experienced perhaps the greatest orgy ever of human-to-human transmission. Soon the city would be the hardest hit in the country, gripped not only by illness but by terror and social breakdown on a scale unprecedented in American history.
As autumn broke in 1918, the eyes of Philadelphians, like those of most Americans, were on the war in Europe. Two days after U.S. forces and their allies launched a decisive offensive in the battle of Argonne Forest, attention shifted to the home front with the city’s Fourth Annual Liberty Loan parade. Billed as the largest in Philadelphia’s history, this procession on September 28 would kick off the city’s campaign to raise money for the war effort. As I study an old photograph of that Saturday afternoon in 1918, I can almost see death marching through my neighborhood, retracing the steps I walked daily. Five uniformed sailors, rifles on their shoulders, escort a festooned float bearing a navy patrol boat past the intersection of Broad and Chestnut. Hundreds of spectators are crammed beneath the classical columns of a building that decades later would become my local bank branch. At least two hundred thousand others pack the route along twenty-three blocks of Broad Street, cheering on the passing pageant of marines, sailors, and yeowomen, steelworkers, shipworkers, and makers of “shot and shell,” with horse-drawn eight-inch howitzers, Boy Scouts, women of charity and relief, and Main Line debutantes riding farm equipment. Never would a flu virus more clearly demonstrate what it means to fully satisfy the third and final condition of a pandemic.
Philadelphians had barely boarded the streetcars for their Monday morning commute when the epidemic exploded. By Tuesday every hospital bed in town was taken. Thirty-one hospitals, and they were all turning people away. In the historic Society Hill neighborhood, the sick rushed to Pennsylvania Hospital, cofounded by Benjamin Franklin. “When they got there, there were lines and no doctors available and no medicine available. So they went home, those that were strong enough,” a neighbor recalled. Five days after the parade, a doctor at Women’s Medical College of Pennsylvania reported that students had begun filling in for hospital staff who were themselves laid low. “The experiences through which we are passing remind one of the historic records of the plague,” wrote Dr. Ellen C. Potter, a medical professor at the college, in a letter to an academic colleague.
Just a week after the parade, on Saturday, October 5, doctors in Philadelphia reported 254 deaths in a single day. Five days later, the daily toll was 759, almost precisely triple. Hundreds of thousands were sick.
Philadelphia General Hospital, in West Philadelphia, was among the first to appeal for help. “Two-thirds of the nursing force were prostrate by the disease with none to replace them in the wards,” reported sisters from the Roman Catholic archdiocese, who time and again answered the call. Almost half the doctors and nurses had themselves been hospitalized. Others had collapsed from overwork. Patients, many violently delirious, were getting minimal care. “Some of the poor sick had had no attention for over 18 hours and some had not been bathed for over a week,” the sisters reported.
Isaac Starr was a third-year student at the University of Pennsylvania’s School of Medicine. After a single lecture on influenza, he was dispatched to staff an emergency hospital opened in a partly demolished building at Eighteenth and Cherry streets. Starr and his classmates hauled twenty-five beds onto each of five floors. These filled right up with victims. “After gasping for several hours, they became delirious and incontinent, and many died struggling to clear their airways of blood-tinged froth that sometimes gushed from their nose and mouth,” he later wrote. Many died without seeing a doctor. Corpses were “tossed” onto trucks, which hauled them away when filled. “The rumor got around that the ‘black death’ had returned,” he wrote.
More emergency hospitals were opening every day in garages, parish houses, gyms, armories, nursery schools, and college frats, but often there was barely anyone to staff them. The city established one of the first at the poorhouse in the Holmesburg section. Its five hundred beds were filled in a day. In the second week of October, when a contingent of nuns came in relief, they discovered only twelve nurses caring for the patients. “One can imagine the distress, neglect and misery of these poor creatures. Some did not have their faces washed for days; their bed clothing had not been changed for a like period of time,” one of the sisters recounted. Patients were moaning, coughing, delirious, some rising from their beds and frantically wandering the wards like specters. With only a single orderly for the whole hospital, the dead could lie unattended for hours until volunteers came to haul them out. “The first day we saw 13 bodies carried out to the dead-house within four hours,” the nun continued. “The odor from this dead-house was something awful.”
Nor was it just the city that was in the crosshairs. The smaller towns in its orbit were also succumbing. In Pottsville, the residence of a wealthy family was converted into a medical facility. “What sights and sounds met us when we entered that room where 84 patients were moaning and crying for help!” one nun wrote. “There were about forty babies in one room, all crying and perfectly helpless, their ages ranging from six days to two and a half years.” All night, the stricken begged for water, ice, or a comforting presence in their final hours. The nun was horrified. “Some,” she said, “were so far gone that worms were crawling out of their mouths.”
On the streets of Philadelphia, cars bearing medical insignia were mobbed. College classes for pharmacy students were suspended so they could help fill prescriptions until drugstore shelves ran bare. Public services broke down. Nearly 500 police officers stayed off the job. About 1,800 telephone employees failed to show up for work, forcing Bell Telephone Company of Pennsylvania to take out newspaper ads warning it could handle “no other than absolutely necessary calls compelled by the epidemic or by war necessity.”
Most people stayed cooped up in their homes, often low on food, at times dying there unattended. What volunteers from Holy Name Parish discovered in one Fishtown home was not uncommon. “In the parlor were the dead bodies of the married son and his wife who had died a few days previously,” a nun wrote. “A daughter was dying in the adjoining room, alone, while her mother was seriously ill upstairs. The only attendant they had was the father who was too sick to realize what he was doing.”
During the second week of October, 2,600 people died of flu in Philadelphia. Another 4,500 died a week later. There was no longer anywhere to put their bodies. At the city morgue, abandoned corpses were stacked three and four high in the corridors and spilling out onto Wood Street. Bodies were piling up on the porches of row houses, in closets and garages, uncollected for days. “The smell would just knock you,” Elizabeth Struchesky remembered decades later.
Police wagons, mortuary trucks, and even horse-drawn carts plied the street, and people were called to bring out their dead. “They were taking people out left and right. And the undertaker would pile them up and put them in the patrol wagons and take them away,” recalled Louise Apuchase, who said her family was the only one in her neighborhood spared by the flu. “Directly across the street from us, a boy about seven, eight years old died, and they used to just pick you up and wrap you up in a sheet and put you in a patrol wagon. So the mother and father [were] screaming, ‘Let me get a macaroni box.’ ” There were no more coffins. “ ‘Please, please, let me put him in the macaroni box. Let me put him in the box. Don’t take him away like that.’ ”
Nor were there enough embalmers. Nor gravediggers. “They had so many died that they keep putting them in garages,” recounted Anne Van Dyke, whose mother had volunteered to shave the corpses.
The highways department finally dispatched a steam shovel to dig mass graves in a field at Second and Luzerne streets. Prisoners were pressed into service to bury decomposing bodies that others refused to touch. The few available caskets were priceless, and people were stealing them. A fresh supply had to be shipped in by rail under armed guard.
By the time the plague had finished claiming 12,897 Philadelphians in late November, the compassion and common decency that bound society together had been shredded. The nuns found babies without milk and adults without water. They even happened across children newly orphaned and abandoned in their homes. One nun later reflected, “It was the fear and dread of the scourge on the part of kindred and neighbors, who ordinarily would have cared for friends.”
Much of the world still knows what it is to live with death. Not to take old age for granted. To see, in fact expect, that children will die. Most Americans, by contrast, have forgotten 1918.
Yet the American health-care system, with its promise of the highest quality care for those who can afford it, is intensive, expensive, and particularly vulnerable to the extraordinary demand for medical care that would accompany even a mild flu pandemic. “It’s a more brittle system,” Fukuda told me. “The ability to meet an upsurge in patients is not one of the virtues of that kind of system. Whereas in a lot of the developing countries, where you have more flexibility in terms of the health-care system, ironically it may be those systems that are able to cope.”
In the United States, the health-care system has been under tremendous financial pressure to operate on the margin. Hospitals have been closing around the country, with the number offering critical care tumbling 14 percent between 1985 and 2000. By 2005, vacant ICU beds were rare. Some of these beds have been removed because of a severe nursing shortage. So, too, intensive care doctors have also been running short. Emergency rooms are being shuttered, about 10 percent of the national total between 1995 and 2005, and a survey of American emergency physicians revealed that almost 90 percent said their departments were routinely overcrowded. Ambulances are commonly diverted from one ER to another—on average, somewhere in the country, of once every single minute.
When researchers from the U.S. Government Accountability Office explored in 2008 whether hospitals were preparing for a mass casualty event like a pandemic, they learned that hospital executives were too preoccupied with day-to-day financial problems. The same researchers reported that federal funding for hospital emergency preparedness had decreased 18 percent from 2004 to 2007.
“Medical economics is really pushing toward downsizing of hospitals, reducing the number of staff, reducing the number of unoccupied beds,” Fukuda said. “When you look at pandemic influenza, which is a one-period-of-time occurrence, that absolute increase in cases cannot be handled so easily. You cannot handle it without having a lot of staff. You cannot handle severe cases without having hospital beds.”
Medicine would run out. Oxygen, crucial for treating those with lung disease, could be gone within days. The producers of medical oxygen are few, and the fleet of tanker trucks required to haul fresh supplies is far too small. There would be a tremendous shortage of ventilators. Most of this equipment is already being used in the everyday treatment of critical-care patients. In a severe pandemic, about 740,000 people would require ventilation, according to the U.S. Department of Health and Human Services, while studies put the existing stock at between 53,000 and 105,000.
Infectious-disease experts now debate whether the industrialized world might actually be more vulnerable today than it was in 1918. After nearly a century of medical progress, how could this be? No doubt there have been some astounding advances in hospital care. The development of antibiotics alone might save millions who would have died in 1918. Many, perhaps most, of the Spanish flu’s victims succumbed not to the virus itself but to secondary bacterial infections that are now treatable.
But consider this: In the United States, 80 percent of all prescription drugs are now produced overseas. They are delivered to drugstores just hours before they’re dispensed. In a pandemic, international shipping could come to a halt as countries impose travel bans and quarantines, companies suspend operations, and employees fall sick or stay home. Once again, pharmacy shelves would run bare. Nor would it just be flu medicine and antibiotics. Within days, medication for heart disease, high blood pressure, and depression would vanish, and insulin for diabetics would disappear. Many hospitals now maintain minimal inventories, receiving three rounds of medicine and other equipment each day. These supplies, too, could evaporate, and with them many forms of critical care.
Since the novel strain reemerged in 2003, Dr. Michael T. Osterholm, the director of the Center for Infectious Disease Research and Policy at the University of Minnesota, has been warning of the perils inherent in modern commerce. The economies of countries like the United States now more than ever depend on just-in-time supply chains and offshore sourcing of essential goods and services. “The interconnectedness of the global economy today could make the next influenza pandemic more devastating than the ones before it,” he wrote. “Even the slightest disruption in the availability of workers, electricity, water, petroleum-based products and other products or parts could bring many aspects of contemporary life to a halt.” With little surge capacity of their own, Osterholm projects that countries facing a major pandemic would run short on everything from soap and lightbulbs to gasoline and spare parts for municipal water pumps, and, of course, food.
Four days after lab tests had come back positive for bird flu in Vietnam, Klaus Stohr in Geneva convened an unpublicized conference call on January 15, 2004, with a half dozen of the world’s leading influenza specialists. He wanted to know what he was up against.
“A critical situation, unprecedented,” said Dr. John Wood, senior virologist at Britain’s national biological institute. “We have to behave as if it could go to pandemic.”
“Very, very serious,” said Dr. Masato Tashiro, head of virology at Japan’s national infectious-disease institute. The likelihood of human transmission is rising, and this, he said, “would be devastating. [Something we] have not yet experienced before.”
Just two months earlier, Dr. Robert Webster from St. Jude Children’s Hospital had coauthored an article for Science magazine warning that the world was unprepared for a flu pandemic. Now the dread scenario seemed to unfolding. But the extent of the outbreaks caught even him by surprise.
“A very unusual event,” Webster said.
These superlatives reinforced Stohr’s concern. Stohr himself was not formally schooled in flu. Trained as a veterinarian in East Germany before the Berlin Wall came down, he had established himself as a national authority on rabies. His work caught WHO’s eye, and he was recruited to the agency, where he was later tasked with restructuring an influenza operation then considered a backwater. He joined the fraternity of flu hunters.
“Klaus was very excited,” a colleague said, recalling those uncertain days in early 2004. “It’s one of the things they wait for their whole life. Pandemic, it’s the big one.”
Reared on the grinding shortages of the Eastern Bloc, Stohr was skilled at marshaling scarce resources. Now he cobbled together a global response from an agency strapped and weary. He massaged the bureaucracy, spinning out long lists of urgent tasks as he walked the halls, assigning them with dispatch. He stoked the enthusiasm and anxiety of his staff with talk of pandemic and helped position the agency to ensure it got a piece of this action.
The CDC had been eager to send in its own team and had already won a nod from senior Vietnamese officials. But WHO, flush with its triumph over SARS, didn’t want to cede control of an emerging pandemic to the big boys from Atlanta. So WHO hurriedly dispatched Dr. Hitoshi Oshitani, its senior East Asian expert on communicable diseases. He was an astute, hard-driving Japanese doctor, a former Africa hand fascinated by diseases of the developing world. He had a humble respect for flu and little patience for politics. But he’d have to tend to both. Oshitani set out to assess the extent of the outbreak and negotiate with the Vietnamese government over permission for a larger team. He insisted that his investigators be allowed into the field. But the Vietnamese health ministry, wary of outside meddling, was reluctant to oblige.
“Avian influenza could be much worse than SARS,” he admonished the skeptical officials. “If this avian influenza becomes a pandemic, it could infect two billion people. Millions of people would die.”
It wasn’t just a line. He personally thought he could be seeing the start of a global outbreak. Oshitani had already helped the world dodge one epidemic by steering Asia’s response to SARS. “Hitoshi suddenly came alive again,” an associate in the regional headquarters recounted. “For people like him, this is what life is about: crises. He immediately understood the implications.” When Oshitani warned that avian flu could dwarf SARS, his exhortation sent shudders through his WHO colleagues. But it also had the desired effect on the Hanoi government.
With the door cracked open, Tom Grein was urgently detoured to Hanoi from a WHO mission in southern China. Grein, who would team up two years later with Uyeki to investigate the Ginting family cluster in Indonesia’s North Sumatra province, became in essence the agency’s player-coach in Vietnam. His was an all-star roster of epidemiologists, virologists, lab technicians, clinical specialists, and veterinary, logistics, and public-affairs experts that would eventually total nearly a hundred personnel. Finally, as part of this international effort, Uyeki and Fukuda were bound for Vietnam along with five CDC colleagues.
Uyeki quickly peeled off into the field. Fukuda remained in the capital, helping set up a command center in a conference room just off the entrance to WHO’s office in downtown Hanoi, and from there he helped direct the response. “We’re not sure what’s going on,” Fukuda recalled, “and we have to sift through this pretty quickly.” He pressed Vietnamese health and agriculture officials to cooperate, to share their intelligence about the outbreaks and ramp up efforts to contain them. “Don’t be lulled into a sense of false confidence about small numbers,” he urged in meeting after meeting. Though only a handful of human cases had been detected so far, the country could be at jeopardy.
Fukuda’s counsel carried weight. He had unique credentials as a veteran of the Hong Kong outbreak in 1997. Yet these dynamics were different. The Vietnamese were not open to the kind of close partnership he’d established with Hong Kong’s health director, Margaret Chan, which had been central to success. The international team itself was also different, larger and more unwieldy than the exclusively American one he’d led six years earlier. But the outbreak itself looked very similar. Again, it was mostly birds infecting humans. In urban Hong Kong, the source had been markets. Here in rural Vietnam, it was mainly farms. Still, for Fukuda, the killer was no longer a stranger but a known assailant.
The cases continued to come, the pace quickening. Healthy, mainly young victims kept turning up with breathing problems, rising fevers, and tumbling white blood counts. Many had diarrhea. Most died. By the third week of January, the virus had opened a second front in the south of Vietnam with initial cases in a young girl and teenage boy. Poultry outbreaks were also accelerating, proliferating faster than Vietnam could slaughter its afflicted birds and extending throughout the region. Under pressure from Prasert Thongcharoen, Thailand finally stopped its dissembling and confirmed both human and poultry outbreaks. By the first of week of February 2004, four more Asian countries had reported infected flocks: Cambodia, China, Laos, and Indonesia. Most of these countries had never been struck by any strain of avian flu before. Never had a highly lethal bird flu strain sparked as many outbreaks at once.
Each evening Pascale Brudon, the WHO’s chief representative in Vietnam, gathered team members in the command center to compare notes and briefly unwind. The workload was tremendous, the days long, and the nights late. Yet it didn’t seem to be enough for Geneva. “We had all of this pressure,” Brudon said, “a lot from headquarters from Stohr, saying that this was going to be a terrible epidemic and it was going to be like Spanish flu.”
The boy’s mother was stumped. So was his grandmother. The thirteen-year-old had been among the very first in southern Vietnam to succumb to this new disease. Yet there had been nothing noteworthy about his habits. The women told Uyeki they didn’t keep any poultry in their home. In fact there weren’t even farms in this suburban enclave of Ho Chi Minh City, the former southern capital still known by most of its denizens as Saigon.
Uyeki had followed the outbreak south, remaining just a week in Hanoi before decamping to Ho Chi Minh. He had tracked the virus to the boy’s home, determined to find the source of infection. “They had no idea what this kid did,” Uyeki said later. “Because, like a normal kid, aside from school, they’re playing. It’s not unusual for a parent or grandmother to have no idea what this kid does after school.” Uyeki could find no evidence of exposure to birds, much less sick ones. Nor was anyone else in the family ill. Could the virus now be lurking somewhere else? Perhaps in a new, undiscovered lair?
Sometimes, on disease investigations, fortune breaks your way. As Uyeki and his colleagues filed out of the family’s home, they were an odd sight, a band of strangers in masks. Quickly, curious neighbors started congregating. They showered the investigators with questions. Then Uyeki started doing the asking.
“Oh, yeah,” one neighbor piped up. “That kid, every day after school, he participates in cockfighting.”
Uyeki’s ears perked up. “Where?” he asked.
The neighbor led them down a narrow, paved street. After a couple of hundred yards, they came upon three or four woven baskets on the roadside, each containing a rooster. A little farther they found several more roosters and then a few more beyond that. This was the staging ground for the fights.
“We found out that this kid, along with other boys, every day after school he’d actually hold the cocks,” Uyeki later reported. “So that’s pretty good contact. If you’re holding the rooster, the rear end or the feathers are pretty close to your face. That is what we believed was his risk.” With this discovery, Uyeki had become the first to identify the threat posed by cockfighting, a popular pastime that over the coming years would be repeatedly implicated in bird flu deaths across Southeast Asia.
Other times fortune breaks against you. Days later, Uyeki and his Vietnamese colleagues pulled into a rural village in Tay Ninh province, about fifty miles northwest of Ho Chi Minh City, to investigate the case of a seventeen-year-old girl who had died of bird flu in a local hospital. They parked their van down the dirt road from her home. Chickens foraged in the dust. Pigs grazed on the roadside. Then, dressed in full protective gear, including baby blue disposable aprons and pants, masks, goggles, shower caps, gloves, and rubber shoe coverings, the team got out of the van and slowly approached the house.
But as they did, they discovered they weren’t the only strangers in town. A Vietnamese television crew had also turned up to interview the family. A crowd was forming.
The girl’s mother and grandmother were sitting in the doorway of their home, little more than a shack of bamboo and metal. They spotted the TV crew. They spotted the group of what could only have looked like space aliens. And the grandmother began to shriek. She was afraid. She was resentful of the intrusion at a time when the family was grieving.
But Uyeki wondered whether there was something more. He asked his translator what the old lady was saying. She was shouting over and over that her granddaughter had died of natural causes, insisting there was nothing untoward about the death. Uyeki suddenly realized the histrionics were meant for her neighbors. “She was trying to reassure them and also trying to deflect any potential stigma,” he concluded. The family was terrified of being ostracized if fellow villagers believed they were infectious or, even worse, cursed. The investigators retreated, deciding the family should be left alone.
As long as the cases were coming one at a time, WHO felt confident that a pandemic virus had not yet broken loose. Each isolated human case was a dead end for the pathogen. Then investigators began to hear about the wedding party.
In late December 2003, a family in the northern province of Thai Binh, a verdant, rice-growing region in the Red River delta, had gathered to prepare for a marriage. On January 3 the couple wed. Four days later, the thirty-one-year-old groom started having trouble breathing. He died in the intensive care unit barely a week after his nuptials. Next his twenty-eight-year-old bride and two younger sisters came down with a cough and fever. Though the wife soon recovered, the sisters were taken to Hanoi, where they were admitted to the tropical disease institute, a six-story cream-colored building on the bustling urban campus of Bach Mai Hospital. Both ultimately tested positive for bird flu.
Bach Mai was already associated with tragedy. In the waning days of 1972, U.S. B-52s had leveled the hospital during a withering aerial campaign against North Vietnam that came to be known as the Christmas bombing. At least thirty people inside Bach Mai were killed in an attack emblematic of the war’s excesses. After the conflict subsided, the hospital was slowly rebuilt, an inch at a time because of unexploded ordnance. Now, a generation later, Bach Mai again commanded the world’s uneasy attention.
Peter Horby went to visit the sisters the day after they were admitted. “They were well,” he recalled. They were walking around and taking the antiviral drug Tamiflu. But soon they started to deteriorate and within nine days were dead.
Horby set out for Thai Binh to learn more about the cluster of cases. “This was the first time we could investigate something like this,” he said. “Everyone was wondering whether it was human-to-human.” He interviewed the mother of the three victims. It was a tough conversation. She was distraught. He questioned neighbors. He tried to reconstruct the chain of events and scrutinized the timing of the cases to see whether everyone could have conceivably contracted the disease from the same, single source.
He learned that one sister had handled a duck while cooking. But she had not personally butchered the bird, considered a practice with a high risk of infection, and in any case the duck had seemed healthy. The bride and the other sister had no such exposure at all. There were no birds around their house or, for that matter, in their immediate neighborhood. They lived in town, not on a farm. But the sisters had cared for their ailing brother who, though never tested, almost certainly died from the disease. Horby deduced that the sisters had likely caught the virus directly from him.
Horby drove back to Hanoi and presented his report. The findings were explosive, especially because WHO had been reassuring the world’s media there was no reason to panic as long as there was no human-to-human transmission.
“We really have to be sure,” Brudon told the team members. “We must be really, absolutely sure.”
For several long evenings, they cloistered in the Hanoi command center scrubbing the evidence. The conclusion was clear. “The team was quite convinced after the careful epidemiological investigations done by some members of the team,” Brudon later wrote, “that we were in front of cases of H to H transmission.” She agreed to release the findings.
Almost instantly, Horby said, “the shit hit the fan.” The agency’s upper echelons had not seen the disclosure coming. The next day WHO’s director general, Dr. Lee Jong Wook, called Brudon. He was furious. He castigated her for endorsing what he thought an ill-considered statement. He said she had rattled the world for no reason.
Team members in Vietnam were stunned by Lee’s response. They were sure their hard work had uncovered a fateful twist in the evolution of a killer virus, and this was their reward? They concluded that Lee had buckled under pressure from some of WHO’s member countries, notably the Thais. With the virus also circulating in Thailand, that country’s government was sensitive about any suggestion that the strain could become epidemic, fearful of the toll this could take on the economy. Thai Prime Minister Thaksin publicly attacked WHO’s statement about human transmission, calling it bad science. “Normally, the ethics of researchers is such that if there is only a slight possibility of something happening, then they will discuss it among themselves. They will not say anything to the public to raise concern,” Thaksin told reporters, assuring them that “the possibility of human-to-human transmission is 0.00001 percent.”
In subsequent statements WHO adopted a far more reassuring tone, minimizing the significance of what the team in Vietnam had discovered. Three leading researchers based in Vietnam, including the director of its National Institute of Hygiene and Epidemiology, later cited the episode, recounting that “temperatures were running high, and any mention of person-to-person transmission of H5N1 was thought by some to be reckless.” They added, “An air of tension… surrounds this disease, particularly in the corridors of power within the international health and political communities.”
WHO would later clarify that “limited” human transmission was not a threat. The concern was “sustained” and “efficient” transmission. But the novel strain had now crossed another barrier. In 1997, it had demonstrated it could jump from animals to people. Back then, investigators in Hong Kong had also suspected that the virus could hop from person to person but never had conclusive proof. Now, nearly seven years later, it had shown convincingly that it could.
As reports of outbreaks among both people and birds continued to pile up, Vietnam resolved to take a terrible gamble. It would seek to exterminate the sickened flocks, the course recommended by international health specialists. But this would mean dispatching thousands of potentially susceptible peasants against an inscrutable enemy. They would fight the virus literally with their bare hands.
Inside the dimly lit coop of one farm outside Hanoi, workers chased the frenzied chickens, trying to pummel them with wooden rods. A bird bolted out the door into the sunlight and a woman lunged, snagging the errant fowl with her unprotected hands. She pounded it senseless, then stuffed its lifeless body into a sack with other casualties. Dozens of survivors scattered, dodging blows. Feathers flew. Droppings kicked up underfoot.
It was early February 2004, and I had arrived in Vietnam days earlier, anxious to see how authorities were tackling the budding epidemic. Poultry outbreaks had been reported across Ha Tay province, home to much of northern Vietnam’s chicken industry. As I approached the village of Phu Cat just south of the capital, an agriculture official in a blue uniform motioned for me to stop my car. He circled the vehicle, spraying the tires with disinfectant to ensure I was not tracking death into his community. Then, for my protection, another official handed me a 3M mask, surgical cap, rubber boots, and a white Kimberly-Clark jumpsuit and instructed me to put them on. He then joined me in the car and guided us into the village.
We pulled up at a two-story shed. Thousands of chickens on this farm had been marked for death because they might carry the virus. A pair of veterinary officials huddled in the driveway. They were clad in broad masks, caps, and thick goggles, as well as protective suits, gloves, and boots. The local government had dipped into its budget to finance protective outfits for officials but could not afford to buy them for the cullers—the very people on the front line. Upstairs on the second floor was the large, low-ceiling coop where farmworkers were running down their prey, stuffing the battered chicken bodies into sacks, and then heaving them out a window into the bed of a truck below. Most of those called to battle wore only cheap rain slickers and flimsy masks.
One young culler emerged from the shed, dirt and bloodstains speckling his sandaled feet. “I didn’t wear boots or gloves. I didn’t buy any,” he told me. Other farmworkers reported the same. “It’s very dangerous for the people, but we can’t buy everything we need to wear,” added a neighbor. “I’m afraid I’ll get infected from the chickens, but I have to do it because I can’t ask anyone else to do it for me.”
WHO officials were becoming alarmed. The workers in this nationwide slaughter were risking their lives. Even more ominously, they were giving the disease a prime opportunity to remake itself inside their bodies, potentially hatching a new strain easily passed among people.
Then, as springtime approached, the virus seemed to vanish abruptly from all of Asia. The outbreaks ceased like a fever breaking overnight. Most of the flu hunters headed home, still puzzled, but few believed they were gone for good.
“We need to think of it like a war,” urged Dutch scientist Dr. Albert Osterhaus in a conference call with WHO.
“We may have no choice than to live with the virus,” added Dr. Les Sims, who had been Hong Kong’s chief vet at the time of the 1997 outbreak. “I don’t believe we are going to get rid of this virus from the region even in the long term.”
Though flu specialists had anticipated the return of the novel strain, they were startled by its sudden reappearance in late June 2004. The virus had always surfaced in the cooler weather, and here they were still in the summer. Despite the unprecedented culling of more than 100 million birds in East Asia, the scourge reappeared on farms across Vietnam, eventually returning to Thailand, China, Cambodia, and Indonesia and spreading, for the first time, to Malaysia. New human cases popped up in Vietnam and Thailand. Researchers were reporting that the virus was widespread in ducks, moving into wild birds, and growing ever more lethal in lab animals. Another study concluded that the strain had gained a permanent foothold in Asian poultry.
In August 2004, Vietnam’s Tuoi Tre newspaper reported that a brother and sister in the southern province of Hau Giang had died under suspicious circumstances. The man, a nineteen-year old high-school student, had just taken his university entrance exam when he fell sick on July 23. Four days later he was admitted to the hospital with a fever, headache, and bloody cough and died after three more days. The local doctors diagnosed the case, apparently incorrectly, as septicemia or blood poisoning and never notified higher government authorities.
A day after he died, his twenty-five-year-old sister, a local teacher, began to complain of headaches, muscle pain, and difficulty breathing. She was dead within a week. A journalist for Tuoi Tre got wind of the cases and publicized them.
The hospital had already discarded samples from the brother, but lab technicians tested those from his sister and discovered she had bird flu. Health officials also reported that a third family member, a cousin, had also died recently but had never been tested.
Alerted, investigators came to the densely populated town deep in the luscious Mekong Delta, but they struggled to find the source of infection. Though the family raised ducks, chickens, and geese, the birds were all healthy. Investigators reported that “no link could be established with deceased or dying poultry.” But they did learn that the sister had initially cared for her ailing brother, possibly accounting for her infection. This revelation, coupled with the sequence of the cases, persuaded some at WHO that for at least the second time, the virus had hopped from one person to another.
“My personal feeling is that this was almost certainly H2H transmission,” a WHO epidemiologist would write in an internal memo later that year.
This time WHO didn’t announce the conclusion at all. Senior WHO figures and Asian political leaders remained unwilling to acknowledge how far this fatal strain had come.
Scott Dowell was America’s sentinel, watching from his post in Bangkok for threats on the horizon, when he got a call in September 2004 from Thailand’s chief epidemiologist.
“We’ve got a weird situation,” Kumnuan Ungchusak began.
He told Dowell that a local hospital had been routinely watching for cases of bird flu when a woman with severe pneumonia came in. She’d been around chickens, so the staff suspected the virus. Investigators from the health ministry were called. It ended up being a false alarm. But as the officials were preparing to leave, a nurse pulled one of them aside and asked about another woman, who had just died. She, too, had had severe pneumonia. No one had suspected bird flu in this case, Kumnuan said, because the woman hadn’t been around any poultry. But then they learned the woman’s daughter had also died about a week earlier in the countryside.
Kumnuan was going to drive up to the province in the morning to check it out. Did Dowell want to come?
Dowell was an American who ran the CDC’s International Emerging Infections Program, headquartered in a sprawling office park that houses the Thai health ministry. Like the listening posts established by U.S. intelligence agencies during the cold war to monitor developments behind the Iron Curtain, Dowell’s operation was on the front lines of a new struggle, watching for novel diseases that could threaten Americans and their national security.
As he and Kumnuan drove north to Kamphaeng Phet province on that Friday morning, the Thai doctor recounted more of the story. An eleven-year-old girl named Sakuntala Premphasri had lived with her aunt and uncle in a remote village about twenty miles off the main road. Their home was set back in the trees, a traditional, one-room house on wooden stilts with a sloping roof. Like everyone else in the village, the family kept chickens, and they ranged freely in the shady space beneath the house, where the girl often played with her friends and sometimes slept. The birds started dying in August, a few at a time. About four days after the last chickens had keeled over, Sakuntala got sick with a cough and sore throat. She felt feverish. Her aunt took her to a local health center for medicine, but the condition worsened. Days later, the girl was admitted to a district hospital with a high temperature, difficulty breathing, and low blood pressure. An X-ray revealed pneumonia in her lower right lung.
When her mother, Pranee Thongchan, learned of Sakuntala’s deteriorating condition, she rushed to the bedside. Pranee, almost a girl herself at age twenty-six, lived more than two hundred miles away in a Bangkok suburb, where she worked in a garment factory. Pranee had asked her husband, a cabbie, to drive her back to the province to see her daughter. She reached the hospital at midnight. There she cradled the limp body of her little girl, repeatedly kissing her and wiping her mouth. Though the girl kept coughing, a duty nurse reported that Pranee kept her face “attached” to that of her daughter, spending the night beside her “cheek to cheek.”
The next afternoon, with antibiotics failing to make a difference and her body descending into shock, the girl was transferred to the province’s main hospital. When she arrived, she was bleeding heavily from her lungs. Blood oozed from her nose and mouth. Three hours later she was dead.
Pranee brought her daughter’s body to a Buddhist shrine near her parents’ home in Khampaeng Phet for three days of funeral rites. On the third day, Pranee herself began complaining of a headache and fever. Pranee went to the district health center for medicine. When she returned to the Thai capital, she felt even worse. It was getting harder and harder to breathe. Ten days after her daughter died, Pranee checked herself into the Bangkok hospital. By then it was too late. The infection had invaded both her lungs, and nothing could save her.
Alone in the car, Dowell and Kumnuan agreed that her case looked a lot like one of human transmission. “If there is transmission in this way, many people will be interested in this case,” Dowell told his colleague.
Kumnuan kept working his cell phone to get more details. He called his subordinates, who were already in the province. Now they were telling him that other family members might also be sick.
“We need to get samples,” Dowell urged. These specimens would not only confirm the virus but could also show whether it was mutating.
Had they taken samples from the mother? Not yet, Kumnuan answered. Kumnuan called back to Bangkok. He discovered that Pranee’s corpse had already been embalmed. At that very instant, the body was at a Buddhist temple in the capital, about to cremated. Kumnuan ordered his officers on-site to do whatever it took to hold on to the body and hurriedly dispatched a specialist who could conduct a limited autopsy on the fly. He got there just in time, snipping out a specimen of lung tissue. It later tested positive for the virus.
When Dowell and Kumnuan finally arrived at Kamphaeng Phet Hospital, Sakuntala’s thirty-two-year-old aunt had just been brought in. She, too, had chills and trouble breathing, and she was having X-rays taken. They went to the radiology department to have a look. Sure enough, her lungs were clouded over. That raised an alarm. They asked to see her. The woman’s condition was serious—her temperature had spiked at over 103 degrees, and samples she gave that day would later test positive—but unlike in the previous cases, would not be fatal. She mumbled to Dowell and Kumnuan that she’d been the one who buried the sick chickens in the yard, wrapping her hands in plastic bags for protection. But that had already been more than two weeks earlier, beyond the incubation period for flu. She also told them she had cared for her dying niece, staying at her hospital bedside until the very moment Pranee had arrived. That was the telling detail.
The following Monday, September 27, the veteran virologist Prasert Thongcharoen chaired a closed-door meeting convened by Thailand’s Ministry of Public Health to review the cases of Sakuntala, her mother, and her aunt. In attendance were government health officials and medical experts from WHO and the CDC. Eight months had passed since Prasert blew the whistle on bird flu in Thailand. Now it was his mission to have his government and international health agencies formally acknowledge what scientists increasingly believed: The virus could spread among people.
This wasn’t the first probable case of human transmission. But the evidence this time was incontrovertible. Sakuntala’s mother, Pranee, hadn’t even been in the same province when her daughter got sick. There was no way they could have caught the bug from the same chickens. In fact, there was no poultry at all in the Bangkok apartment where Pranee lived, nor in the factory where she worked. She had certainly contracted the virus at her daughter’s bedside, and that was the same way the aunt had likely caught it. “It was a clear indication that H5N1 could be transmitted from person to person,” Dowell said later. “Even though a number of us who had studied H5N1 closely over time thought that had probably already occurred, there was a widespread perception that the virus couldn’t be transmitted person to person.”
Dowell told me he faulted WHO and his own institution, the CDC, for too long leading the public to believe that bird flu could not be passed among people. Even if the transmission was limited, it was of grave concern. This was precisely how the virus could become proficient at spreading, he explained. It was through the process of passing from one human to another that a mutating strain could select the genetic attributes required to become a mass killer.
Once the evidence had been presented, Prasert coaxed his colleagues to accept the inevitable conclusion. He had the rare combination of independence, savvy, and scientific credentials to make it happen.
A day later Thailand’s health ministry announced that the Kamphaeng Phet cluster had been “probable human-to-human transmission” of bird flu.
“For the political leadership in Thailand to say there was person-to-person transmission, that hadn’t happened before,” Dowell recounted. “It’s a testament to Prasert and the influence he was able to wield in Thailand.”
WHO released a statement about the Thai cluster that same day, copying the government’s language and for the first time conceding “a probable case of human-to-human transmission.” The virus had crossed a threshold, and so had its antagonists.
But even as they accepted how close H5N1 had now come to an epidemic strain, they had little inkling of what was about to happen. The death of yet another Vietnamese youngster right after New Year’s Day 2005 would mark a new, even larger wave of infections. The virus would extend its reach in the new year as never before. It would soon strike beyond Asia, infecting new continents, multiplying its victims, and confronting the flu hunters with the prospect of imminent pandemic.