End Times: A Brief Guide to the End of the World

by Bryan Walsh

  It was March 2003, and I was in my second year working as a reporter for Time Asia magazine, in my second year out of college. The world was new to me—I had barely traveled outside the United States before I boarded a plane in July 2001 that brought me, two stops and some twenty-four hours later, to this densely populated, vertiginous city of 6.7 million people crammed on the southeastern corner of China. I was lonely and homesick at first, wrung out by the crowds that clung as closely as the heat and the humidity. I spent my first month living in a hostel largely populated by migrant workers from mainland China, and I went to sleep listening to the screams of monkeys in the zoo across the street. But Hong Kong has a way of getting under your skin, and by the spring of 2003 I’d begun to find my place there. I’d even managed to carve out an identity as a journalist, writing about science.

  In the spring of 2003, however, there was one story and one story alone dominating the news: the impending invasion of Iraq. Or at least that was the case for other journalists. Time Asia was the regional edition of Time magazine, and while the map said that Iraq was part of Asia, what mattered to us in Hong Kong were the boundaries drawn by Time’s top editors back in New York, which mandated that Time Asia’s remit ran only as far west as Afghanistan. That spring the pages of our magazine—usually a mix of original articles about Asia that we produced and pieces pulled from the U.S. Time—were full of stories about the preparation for fighting in the Middle East. That left those of us in Hong Kong with not a lot to do. And that may be why we were so eager to pounce on reports of an unexplained respiratory illness that was spreading in the southern Chinese province of Guangdong, which borders Hong Kong.

  I’d been in Hong Kong for less than two years, but I already knew what unchecked infectious disease could do to this crowded city, where the densest neighborhoods stuffed more than 35,000 people into a square mile. In a park down the street from my apartment there was a plaque1 memorializing the last great outbreak of bubonic plague in Hong Kong in 1894, one that killed more than 100,000 people2—greater than 10 percent of the city’s population at the time.3 Not far from the park was what Hong Kongers call a “wet market,” an open-air store that sold live chickens to Cantonese shoppers who liked their poultry so fresh it clucked. Those markets had been at the center of a frightening brush with the H5N1 avian influenza virus in 1997.

  Up to that point, true to its name, H5N1 bird flu was thought to be a danger to bird populations—not human ones. But the virus mutated—as influenza often does—and in April that year Hong Kong became the first city to record human infections of the disease. Eighteen people fell sick, and six ultimately died.

  Those numbers were tiny—that same year 252 people in Hong Kong would die from tuberculosis—but the outbreak alarmed international health officials, not just because of what was happening, but where it was happening. The last global influenza pandemic in 1968 had originated in Hong Kong, and it had begun when a mutated flu virus in birds spread to human beings who had no immunological defense against the new strain. More than one million people around the world would ultimately die. The most likely place an influenza pandemic would emerge was where lots of human beings were in close contact with lots of birds—as might be the case, for instance, in a Hong Kong wet market, where flu viruses could mix and match between species. The initial human H5N1 cases might have meant the start of a new flu pandemic, which is why the Hong Kong government took drastic measures to stem the outbreak, killing all 1.2 million live chickens in the territory.4 It seemed to work—there were no more human cases after the chicken cull. But health officials and flu experts feared that H5N1 would return one day.

  So when news of a mysterious respiratory disease in Guangdong began circulating in February 2003, many assumed the bird flu was back. But this was something else. Soon there were cases in Hong Kong with similar symptoms—fevers, chills, shortness of breath that became so severe many patients were put on artificial respirators. News broke that dozens of doctors, nurses, and students had fallen ill at Hong Kong’s Prince of Wales Hospital. New cases popped up in Vietnam, Singapore, Germany, and Canada. The World Health Organization (WHO) declared the disease a “worldwide health threat” and gave it a name: severe acute respiratory syndrome, or SARS.5

  But even the possibility of a global outbreak of an unknown new disease wasn’t enough to displace the looming Iraq invasion, and that Saturday night, as we at Time Asia closed our weekly issue, there was only room for me to dash off a short piece summarizing the news. My story began: “International health officials are being confronted by everyone’s worst nightmare: a highly contagious, potentially fatal disease of unknown genetic makeup and for which there is currently no antidote or vaccine.”6 Looking back, I can see I had no clue what those words really meant—not yet. If anything I assumed that SARS, like H5N1 in 1997, would flare up and then disappear.

  The next morning I boarded a flight for the United States to attend the wedding of a close friend in Tucson, Arizona. As I left the Tucson airport a local TV news crew stopped me to ask a few questions—not about the disease I had left behind but about my opinions on the Iraq invasion. (For the record, I was against it.) A couple of days later, sleepless and a bit drunk after the wedding, I searched the TV news obsessively, but it was all Iraq, all the time. I fell asleep to the sound of Colin Powell giving yet another press conference.

  Viruses don’t care about the news cycle, however, and by the time I landed back in Hong Kong after eight days away, SARS was everywhere. In an airport drugstore I saw the front page of the South China Morning Post announcing the news that the chief executive of the Hong Kong Hospital Authority had fallen ill with a suspected case of SARS.7 On the high-speed airport train back to the city I found myself observing what would become the defining image of SARS: human faces covered by cotton surgical masks. Only the eyes were visible, wary with fear.

  A week after I returned, the government announced a quarantine—preventative isolation—of part of the Amoy Gardens apartment complex, one of Hong Kong’s many sprawling housing estates, after news broke that hundreds of residents in the building had fallen ill with SARS.8 This was the moment when the fear became real. Until then SARS cases had mostly been confined to hospitals, or to the occasional unlucky traveler. But the Amoy Gardens outbreak seemed to be proof that SARS could spread where we lived. Scientists still didn’t know what caused the disease, and there was no effective treatment regimen yet. (Across the border in Guangdong, speculators were bidding up the cost of vinegar, which was rumored, falsely, to prevent the disease.9) If hundreds of people in one apartment building could contract it, what would stop it from burning through one of the most crowded cities in the world? What would keep us safe?

  The WHO placed an unprecedented travel advisory on Hong Kong and Guangdong, warning people to avoid unnecessary visits to the region—the first time the international health agency had ever taken such a step.10 The city’s gleaming airport, which usually handled hundreds of thousands of passengers a day,11 emptied. Spouses and children of expatriate workers in the city’s financial sector were sent home, or to resort islands like Phuket in Thailand to wait out the outbreak. Five-star hotels went empty and restaurants and bars were deserted. Even the Rolling Stones—whose well-tested immune systems had surely weathered worse—canceled a planned concert in the city. A few Time Asia staffers were chosen to work from home, to ensure the magazine could be put out in case someone in our office got sick and the entire building had to be put into quarantine. We wore masks while working, but the cotton surgical ones grew wet from our breath after a few minutes, making them permeable to germs, while the molded N-95 masks proved too hot and cumbersome to wear for any length of time—and supplies of them were running low in Hong Kong anyway. Every evening around 6 p.m. the Hong Kong government would announce how many new SARS cases had been confirmed that day. At the height of the outbreak fifty people a day were being diagnosed with the disease.12

  As for me, I was staying in a roach-
infested apartment that I was borrowing from another reporter who had left to cover the war in Iraq. I was trapped in a foreign city eight thousand miles away from my family and friends, and if the epidemic worsened, if the disease started spreading without check through Hong Kong, I might die. We all could die.

  And yet that moment is when I discovered what I was meant to do, a discovery that set me on a multiyear journey to writing this book.

  Not long after the Amoy Gardens outbreak began, scientists at the University of Hong Kong (HKU) announced that they had identified the likely cause of SARS: a never-before-seen coronavirus, the same viral family that leads to pneumonia and the common cold. The day after the press conference I visited the lab of the HKU researchers at Queen Mary Hospital. I peered through an electron microscope at the culprit. It looked like a blue circular splotch studded with the halo, or corona, of viral protein spikes that give the coronavirus its name. It was a killer 40 millionths of an inch long.13

  The discovery of the SARS coronavirus marked a turning point in the battle against the disease. SARS could kill—10 percent of the people infected by the virus would eventually perish, a death rate that was high for an infectious disease in the age of antibiotics and antiviral drugs.14 As scary as it was, however, SARS turned out to have its weaknesses. The virus didn’t spread easily—most of the early transmissions were in hospitals, largely because doctors initially hooked up patients to respirators that inadvertently spread viral particles through the air like a biological weapon. Once new infection control methods were put into place, hospital transmissions soon halted. The Amoy Gardens outbreak that alarmed us so much turned out to be a one-off—a single infected resident had diarrhea, an occasional symptom of SARS, and plumbing problems in the apartments resulted in viral particles spreading throughout the building.15 No other wide-scale public outbreaks occurred. On May 23, the WHO finally lifted the travel advisory on Hong Kong, and the following day there were zero new cases in the city for the first time since the beginning of the outbreak. By July 5, SARS—which had infected more than 8,000 people worldwide and killed over 770—was declared contained. By November, even the Rolling Stones had come back to Hong Kong.

  SARS was a twenty-first-century plague. It was a zoonotic disease, meaning it jumped from animals to humans—a pathway it has in common with most emerging diseases, including HIV.16 After years of work, scientists in Hong Kong would eventually conclude that the virus originated in horseshoe bats in southern China. The bats in turn spread the disease to masked palm civets, catlike mammals native to Southeast Asia. Humans entered the picture because civets, along with a menagerie of other wild animals, were kept in the crowded live markets of Guangdong to be sold for food. These markets are unsurpassed viral factories, where wild animals and human beings are in close quarters, close enough for a new pathogen like SARS to jump from one species to the next. Perhaps it spread through a cut or a scratch inflicted on an unwary Guangdong shopper who wanted a freshly killed civet as an ingredient for the exotic “dragon-tiger-phoenix soup,” a wildlife dish popular at the time among wealthy Chinese in the region.17

  The SARS outbreak was the product of a series of accidents and errors, one after the other. First the virus needed to emerge in bats, then spread to an animal more likely to come in contact with people—the civet—and then jump from that intermediate host to a human being. But that wasn’t all. Had this series of viral accidents occurred fifty years before, when mainland China was largely isolated from the rest of the world, SARS might never have gone global. By 2003, however, China had opened up, and thousands of people moved between Guangdong and Hong Kong each day.

  One of them was a doctor in Guangdong named Liu Jianlun. Liu was already infected with SARS when he traveled to Hong Kong in February 2003 for a wedding. Even then, most SARS patients only infected those who had been in very close contact with them, like nurses in a hospital or family members taking care of sick relatives at home. But for reasons that doctors still don’t understand, a handful of SARS patients were “super-spreaders” capable of transmitting the disease to unusually high numbers of people.18 Liu was one. He would infect sixteen people at the Metropole Hotel, and they in turn traveled home by plane to unwittingly seed outbreaks in Canada, Singapore, Taiwan, and Vietnam.

  The last necessary element was government malpractice. SARS spread in Guangdong for months before the Chinese government finally began to admit what was happening, giving the disease time to leak across the border to Hong Kong—which hosts hundreds of international flights each day—and from there to the rest of the world. The secrecy continued even after the disease reached Beijing in March 2003, until a brave doctor named Jiang Yanyong reached out to my Time colleagues in the Chinese capital. Jiang told them that the government was lying to the world about the extent of SARS,19 even going so far as to shuffle dozens of suspected SARS patients between hospitals in an effort to prevent WHO officials from seeing them.20

  SARS demonstrated the difference transparency makes to an outbreak response, when even one sick patient overlooked or hidden can keep an outbreak going. Beijing’s lies made a bad crisis worse. SARS also showed that the connections of a globalized world make us more vulnerable to diseases that can now be spread via the nearly 12 million people who on average travel by air each day.21 The world was primed for the disease.

  Yet those same connections also helped stop the outbreak before it could do even more damage. A network of international labs sharing data over the internet was able to identify the virus that caused SARS barely more than a month after the WHO issued its first global alert.22 Compare that to the two long years that passed between the first signs of AIDS and the discovery of HIV23 in the early 1980s. Once it became clear in March just how dangerous SARS was, the WHO showed admirable spine, placing travel advisories on affected countries despite protests by governments that the moves would cost billions in lost revenue—predictions that turned out to be accurate. Aside from Hong Kong, mainland China, Canada, and Taiwan, most of the outbreaks in the more than thirty affected countries were limited to a handful of cases, thanks to rapid isolation of sick patients and preventative quarantine of those who had come into contact with the infected. Though hundreds ultimately died, SARS could have been far more devastating.24

  We were lucky. There was no vaccine and no antiviral drug for SARS—and there still isn’t—but doctors were able to effectively treat the diseases using the kind of basic supportive methods employed for any severe respiratory illness. Most of the infected recovered. SARS also turned out to be an inefficient transmitter. Diseases are defined by their basic reproductive number, or R0—the number of people one sick person will infect on average. Measles, one of the most contagious diseases on Earth, has an R0 of 12 to 18. SARS, after infection control methods were put in place, had an R0 of 0.4,25 which is why the outbreaks were stopped so swiftly.

  Despite all that, SARS brought East Asia to a near standstill for weeks. It cost the global economy as much as $80 billion,26 which if it were a natural disaster would have made it one of the most expensive in human history. It was the most alarming infectious disease to emerge since AIDS. And yet in the end, my solitary fears in that Hong Kong apartment were wrong. SARS simply lacked the legs to be a truly existential threat.

  This is the paradox of infectious disease as an existential risk. Nothing has killed more human beings through history than the viruses, bacteria, and parasites that cause disease. Not natural disasters like earthquakes or volcanoes. Not even war. By one estimate half of the human beings who ever lived were killed by one disease, malaria,27 which still knocks off nearly half a million people per year.28 Epidemics have been mass killers on a scale we can’t begin to imagine today. The plague of Justinian struck in the sixth century and killed as many as 50 million people, perhaps half the global population at the time,29 while the Black Death of the fourteenth century—likely caused by the same pathogen—may have killed up to 200 million people. Smallpox may have killed as many as
300 million people in the twentieth century alone,30 even though an effective vaccine—the world’s first—had been available since 1796.31 At least 25 million, and perhaps far more, died in the 1918 influenza pandemic32—numbers that dwarf the death toll of World War I, which was being fought at the same time. The 1918 flu virus infected one in every three people on the planet.33 HIV, a pandemic that is still with us and which still lacks a vaccine, has killed 35 million people and infected 77 million, with more added every day.34

  If these numbers surprise, it’s because epidemics are rarely discussed in history classes, and seem to fade more quickly from memory than the catastrophes of war or weather. There are few memorials to the victims of disease. The historian Alfred Crosby was the author of America’s Forgotten Pandemic, one of the great books on the 1918 flu.35 But Crosby was only prompted to begin researching the pandemic when he stumbled on the forgotten fact that American life expectancy had suddenly dropped from 51 years in 1917 to 39 years in 1918, before rebounding the following year.36 That plummet in 1918 was because of the flu.

  Pathogens make such effective mass murderers because they are self-replicating. Most natural disasters are constrained by area, save the very rare planetary catastrophes we covered earlier, which kill globally by changing the climate. An earthquake that strikes in China can’t directly hurt you in the United States. Each bullet that kills in a war must be fired and must find its target. But when a virus—like SARS or the flu—infects a host, that host becomes a cellular factory to manufacture more viruses. (Bacteria, meanwhile, are capable of replicating on their own in the right environment.) The symptoms created by an infectious pathogen—the sneezing, the coughing, the bleeding—put it in a position to spread to the next host, and the next. And because human beings move—while interacting with other human beings in every manner from a handshake to sexual intercourse—they move microbes with them. No wonder that militaries have long tried to harness disease as a tool of war. No wonder that until recently far more soldiers died of disease than died in combat.37 A pathogen is a perfectly economical weapon, turning its victims into its delivery system.