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Scientists agree that a pathogen is likely to cause a global pandemic in the near future. But which one? And how?
Over the past fifty years, more than three hundred infectious diseases have either newly emerged or reemerged, appearing in territories where they’ve never been seen before. Ninety percent of epidemiologists expect that one of them will cause a deadly pandemic sometime in the next two generations. It could be Ebola, avian flu, a drug-resistant superbug, or something completely new. While we can’t know which pathogen will cause the next pandemic, by unraveling the story of how pathogens have caused pandemics in the past, we can make predictions about the future. In Pandemic: Tracking Contagions, from Cholera to Ebola and Beyond, the prizewinning journalist Sonia Shahwhose book on malaria, The Fever, was called a “tour-de-force history” (The New York Times) and “revelatory” (The New Republic)interweaves history, original reportage, and personal narrative to explore the origins of contagions, drawing parallels between cholera, one of history’s most deadly and disruptive pandemic-causing pathogens, and the new diseases that stalk humankind today.
To reveal how a new pandemic might develop, Sonia Shah tracks each stage of cholera’s dramatic journey, from its emergence in the South Asian hinterlands as a harmless microbe to its rapid dispersal across the nineteenth-century world, all the way to its latest beachhead in Haiti. Along the way she reports on the pathogens now following in cholera’s footsteps, from the MRSA bacterium that besieges her own family to the never-before-seen killers coming out of China’s wet markets, the surgical wards of New Delhi, and the suburban backyards of the East Coast.
By delving into the convoluted science, strange politics, and checkered history of one of the world’s deadliest diseases, Pandemic reveals what the next global contagion might look like and what we can do to prevent it.
|Publisher:||Farrar, Straus and Giroux|
|Product dimensions:||6.20(w) x 9.00(h) x 1.10(d)|
About the Author
Sonia Shah is a science journalist and prizewinning author. Her writing on science, politics, and human rights has appeared in The New York Times, The Wall Street Journal, Foreign Affairs, Scientific American, and elsewhere, and she has been featured on Radiolab, Fresh Air, and TED.com, where her talk “Three Reasons We Still Haven’t Gotten Rid of Malaria” has been viewed by more than a million people around the world. Her 2010 book The Fever was long-listed for the Royal Society’s Winton Prize for Science Books.
Read an Excerpt
Tracking Contagions, from Cholera to Ebola and Beyond
By Sonia Shah
Farrar, Straus and GirouxCopyright © 2016 Sonia Shah
All rights reserved.
In search of the birthplace of new pathogens, I set out on a cool rainy day in early 2011 to find a wet market in Guangzhou, the capital of the southern Chinese province of Guangdong.
Wet markets are open-air street markets where vendors sell live animals captured from the wild to consumers to slaughter and consume. They service the Chinese taste for what's called yewei, or "wild," cuisine, in which exotic animals from snakes and turtles to bats are prepared into special dishes.
It was in a wet market in Guangzhou that the virus that nearly caused a pandemic in 2003 was born. This particular virus normally lived inside horseshoe bats. It was a kind of coronavirus, a family of viruses that mostly cause mild respiratory illnesses. (In humans, they're responsible for about 15 percent of all cases of the common cold.) But the virus that was hatched at the wet market in Guangzhou was different.
From the horseshoe bats, it had spread into other wild animals caged nearby, including raccoon dogs, ferret badgers, snakes, and palm civets. As the virus spread, it mutated. And in November 2003, a mutant form of the horseshoe bat virus started infecting people.
Like other coronaviruses, the virus colonized the cells lining the respiratory tract. But unlike its more mild brethren, the new virus tinkered with the human immune system, disrupting infected cells' ability to warn neighboring cells of the viral intruder in the body. As a result, in about a quarter of the infected, what started off seeming like flu rapidly escalated into life-threatening pneumonia as infected lungs filled with fluid and starved the body of oxygen. Over the following months, the virus sickened more than eight thousand with what came to be known as SARS, for severe acute respiratory syndrome. Seven hundred and seventy-four people perished.
The SARS virus vanished after that. Like a brightly burning star, it used up all its available fuel, killing people too quickly to spread any farther. After scientific experts fingered wet markets as the hatcheries that birthed the strange new pathogen, Chinese authorities cracked down on the markets. Many closed. But then a few years passed and wet markets came back, albeit in smaller and more furtive form.
We'd been told there was a wet market somewhere around Zengcha Road, a traffic-clogged four-lane road that runs under a belching highway in Guangzhou. After walking around in circles for a bit, we stopped to ask a uniformed guard for directions. He laughed mirthlessly. The wet market was closed down six years ago, he said, after the SARS epidemic. But then, without pause, he grabbed the hem of a worker passing by and tugged on it, instructing us to reask our question, this time to the worker. We did, and the worker told a different story: go down around the other side of the building, he said, as the guard listened approvingly. We "may" find "some people" selling "some things."
As we turned the corner, the smell hit first, pungent, musky, and damp. The wet market consisted of a series of garage-like stalls lining a cement walkway. Some had been fashioned into office-cum-bedroom-cum-kitchens, in which the animal traders, bundled up for the weather, were passing the time waiting for customers. In one stall, three middle-aged men and a woman played cards on a folding table; in another, a bored-looking teenage girl watched a television bolted to the wall. As we walked in, a man flung the dregs of his soup bowl into the shallow gutter between the stalls and the walkway, a family of eight huddled around steaming bowls of hot pot behind him. A few minutes later, he reappeared to vigorously blow his nose into it.
Ignored entirely were the goods that we'd come to see: the caged wild animals that had been captured and acquired from other traders, in a long supply chain extending deep into China's interior and as far afield as Myanmar and Thailand. A thirty-pound turtle in a white plastic bucket sat desultorily in a puddle of gray water next to cages of wild ducks, ferrets, snakes, and feral cats. Row after row of animals who'd rarely if ever encounter each other in the wild were here, breathing, urinating, defecating, and eating next to each other.
The scene was remarkable in several ways that might explain why SARS had begun there. One was the unusual, ecologically unprecedented conglomeration of wild animals. In a natural setting, horseshoe bats, which live in caves, never rub shoulders with palm civets, a kind of cat that lives in trees. Neither would normally come within spitting distance of people, either. But all three came together in the wet market. The fact that the virus had spread from bats into civet cats had been especially critical to SARS's emergence. The civet cats were, for some reason, especially vulnerable to the virus. This gave the virus the opportunity to amplify its numbers, like a whistle in a tunnel. With increased replication came increased opportunities to mutate and evolve, to the extent that it evolved from a microbe that inhabited horseshoe bats to one that could infect humans. Without that amplification, it's hard to say whether the SARS virus would have ever emerged.
We approached one vendor in a stall lit by a single bare bulb. Behind him, on a sagging shelf, was a smudged, gallon-size glass jar packed with snakes floating in some kind of brine. As my translator Su engaged in small talk with the vendor, two women appeared and flung white cloth sacks on the floor at my feet. Inside one, a tangle of thin brown snakes slithered over each other. In the other, a single, much larger, violently jerking snake hissed. Clearly, this snake was perturbed. Through the sheer fabric I could see that the snake's head had a wide hood, which meant it was a cobra.
While those two facts sank in, the man and the two women, who had thus far not acknowledged my presence, turned to face me with some urgency in their expressions. Su translated their question: Exactly how many people do I plan to feed with this snake?
I stammered "ten" and turned away, flustered. A few minutes later, a woman approached us with another question. She gestured at me and, politely hiding a smirk behind her hand, asked Su whether it was true that foreigners like me ate turkeys. For her, I was the one with the strange eating habits.
* * *
Cholera also started out in the bodies of animals. The creatures that harbored cholera live in the sea. They're a kind of tiny crustacean called copepods. They're about a millimeter long, with teardrop-shaped bodies and a single bright-red eye. Since they can't swim, they're considered a kind of zooplankton, drifting in the water and delaying gravity's pull to the depths with long antennae splayed outward like wings on a glider plane. Though they're not talked about much, they're actually the most abundant multicellular creatures on Earth. A single sea cucumber might be covered with over two thousand copepods, a single hand-size starfish with hundreds. In some places, the copepods are so thick that the water turns opaque, and in a single season each one may produce nearly 4.5 billion offspring.
Vibrio cholerae are their microbial partners. V. cholerae is a microscopic, comma-shaped species of bacteria from the genus Vibrio. Although V. cholerae can live on its own, free-floating in the water, it collects most lushly in and on copepods, sticking to copepods' egg sacs and lining the interior of their guts. Vibrio bacteria performed a valuable ecological function there. Like other crustaceans, copepods encase themselves in crusty exteriors made of a polymer called chitin (pronounced "kite-in"). Several times during their lifetimes, they shed their outgrown skins like snakes, discarding 100 billion tons of carapaces annually. Vibrio bacteria feed on this abundance of chitin, collectively recycling 90 percent of the ocean's excess chitin. Were it not for them, copepods' mountain of exoskeletons would starve the ocean of carbon and nitrogen.
Vibrio bacteria and copepods proliferated in warm, brackish coastal waters, where fresh and salty waters met, such as in the Sundarbans, an expansive wetlands at the mouth of the world's largest bay, the Bay of Bengal. This was a netherworld of land and sea long hostile to human penetration. Every day, the Bay of Bengal's salty tides rushed over the Sundarbans' low-lying mangrove forests and mudflats, pushing seawater as far as five hundred miles inland, creating temporary islands of high ground, called chars, that daily rose and vanished with the tides. Cyclones, poisonous snakes, crocodiles, Javan rhinoceros, wild buffalo, and even Bengal tigers stalked the swamps. The Mughal emperors who ruled the Indian subcontinent up until the seventeenth century prudently left the Sundarbans alone. Nineteenth-century commentators called it "a sort of drowned land, covered with jungle, smitten by malaria, and infested by wild beasts," and possessed of an "evil fertility."
But then, in the 1760s, the East India Company took over Bengal and with it the Sundarbans. English settlers, tiger hunters, and colonists streamed into the wetlands. They recruited thousands of locals to chop down the mangroves, build embankments, and plant rice. Within fifty years, nearly eight hundred square miles of Sundarbans forests had been razed. Over the course of the 1800s, human habitations would sprawl over 90 percent of the once untouched, impenetrable, and copepod-rich Sundarbans.
Contact between human and vibrio-infested copepod had probably never been quite so intense as in these newly conquered tropical wetlands. Sundarbans farmers and fishermen lived in a world semisubmerged in the half-salty water in which vibrio bacteria thrived. It wouldn't have been particularly difficult for the vibrio to penetrate the human body. A fisherman who splashed his face with water by the side of a boat, say, or a villager drinking from a well corroded with a few ounces of floodwaters, could easily ingest a few invisible copepods. Each one might be infested with as many as seven thousand vibrios.
This intimate contact allowed Vibrio cholerae to "spill over" or "jump" into our bodies. The bacteria wouldn't have found a particularly welcoming reception there, at first. Human defenses are designed to repel such intrusions, from the acid environs of our stomachs, which neutralize most bacteria, and the competitive wrath of the microbes that inhabit our gut to the constantly patrolling cells of the immune system. But in time, V. cholerae adapted to the human bodies to which it was repeatedly exposed. It acquired, for example, a long, hairlike filament at its tail that improved its ability to bond to other vibrio cells. Endowed with the filament, the vibrio could form tough microcolonies that could stick to the lining of the human gut like scum on a shower curtain.
Vibrio cholerae became what's known as a zoonosis, from the Greek zoon for "animal" and nosos for "disease." It was an animal microbe that could infect humans. But V. cholerae wasn't a pandemic killer yet.
* * *
As a zoonosis, Vibrio cholerae could infect only people who exposed themselves to their "reservoir" animals, the copepods. It was a pathogen on a leash, unable to infect anyone outside its limited purview. It had no way of infecting anyone who wasn't exposed to copepod-rich waters. While it could cause outbreaks, when multiple people exposed themselves to copepods simultaneously, for example, those outbreaks would always be self-limited. They'd collapse on their own.
For a pathogen to cause a wave of sequential infections — an epidemic or a pandemic, depending on how far the wave traveled — it must be able to spread directly from one human to another. That is to say, its "basic reproductive number" has to be greater than 1. The basic reproductive number (also known as R0, or "R-naught," as the Anglophiles pronounce it) describes the average number of susceptible people who are infected by a single infected person (in the absence of outside interventions). Say you have a cold, and you infect your son and his friend with it. If this hypothetical scenario were typical of the entire population, your cold's basic reproductive number would be 2. If you infect your daughter as well, your cold's basic reproductive number would be 3.
This calculation is a critical one to make in an outbreak, for it immediately predicts its future course. If, on average, each infection results in less than one additional infection — you infect your son and his friend, but each of them infects no one else — then the outbreak will die out on its own, like a population in which each family produces fewer than two children. It doesn't matter how deadly the infection is. But if, on average, each infection results in one more infection, then the outbreaks can theoretically continue indefinitely. If each infection results in more than one additional infection, then the afflicted population is facing an existential threat that requires immediate and urgent attention. It means that, in the absence of interventions, the outbreak will expand exponentially.
The basic reproductive number is, in other words, a mathematical expression of the difference between a zoonotic pathogen and one that has crossed the threshold to become a human one. The basic reproductive number of a zoonotic pathogen, which cannot spread from one infected person into another, is always less than 1. But as it refines its attack on humans, its ability to spread among them improves. Once it tips over the number 1, the pathogen has crossed the threshold and broken free of its reservoir animals. It's a bona fide human pathogen that is self-sustaining in humans.
There are many mechanisms by which zoonotic pathogens can acquire the ability to spread directly between people, severing the cord that binds them to their reservoir animals. Vibrio cholerae did it by acquiring the ability to produce a toxin.
The toxin was the vibrio's pièce de résistance. Normally, the human digestive system sends food, gastric and pancreatic juice, bile, and various intestinal secretions to the intestines, where cells lining the gut extract nutrients and fluid, leaving behind a solid mass of excreta to expel. The vibrio's toxin altered the biochemistry of the human intestines such that the organ's normal function reversed. Instead of extracting fluids to nourish the body's tissues, the vibrio-colonized gut sucked water and electrolytes out of the body's tissues and flushed them away with the waste.
The toxin allowed the vibrio to accomplish two things essential to its success as a human pathogen. First, it helped the vibrio get rid of its competitors: the massive torrent of fluids sloughed off all the other bacteria in the gut, so that the vibrio (clinging to the gut in its tough microcolonies) could colonize the organ undisturbed. Second, it assured the vibrio's passage from one victim to another. Even tiny drops of that excreta, on unwashed hands or contaminated food or water, could carry the vibrio to new victims. Now, so long as the vibrio could get into a single person and cause disease, it could spread to others, whether or not they exposed themselves to copepods or ingested the vibrio-rich waters of the Sundarbans.
The first pandemic caused by the new pathogen began in the Sundarbans town of Jessore in August 1817 after a heavy rainfall. Brackish water from the sea flooded the area, allowing salty copepod-rich waters to seep into people's farms and homes and wells. V. cholerae slipped into the locals' bodies and colonized their guts. Thanks to the toxin, Vibrio cholerae's basic reproductive number, according to modern mathematical models, ranged from 2 to 6. A single infected person could infect as many as half a dozen others. Within hours, cholera's first victims were being drained alive, each expelling more than fifteen quarts of milky-white liquid stool a day, filling the Sundarbans' streams and waste pits with excreta. It leaked into farmers' wells. Droplets clung to people's hands and clothes. And in each drop, vibrio bacteria swarmed, ready to infect a new host.
The Bengalis called the new disease ola, for "the purge." It killed people faster than any other disease known to humankind. Ten thousand perished. Within a matter of months, the new plague held nearly two hundred thousand square miles of Bengal in its grip.
Excerpted from Pandemic by Sonia Shah. Copyright © 2016 Sonia Shah. Excerpted by permission of Farrar, Straus and Giroux.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.
Table of Contents
Introduction: Cholera’s Child
The microbes’ comeback
1. The Jump
Crossing the species barrier at wet markets, pig farms, and South Asian wetlands
The global dissemination of pathogens through canals, steamships, and jet airplanes
The rising tide of feculence, from nineteenth- century New York City to the slums of Port- au- Prince and the factory farms of south China
The amplification of epidemics in the global metropolis
Private interests versus public health, or, how Aaron Burr and the Manhattan Company poisoned New York City with cholera
Cholera riots, AIDS denialism, and vaccine resistance
7. The Cure
The suppression of John Snow and the limits of bio-medicine
8. The Revenge of the Sea
The Cholera Paradigm
9. The Logic of Pandemics
The lost history of ancient pandemics
10. Tracking the Next Contagion
Re-imagining our place in a microbial world
Most Helpful Customer Reviews
Suggest readers read more on the subject to verify and confirm some of the suggestion made by Ms. Shah. Overall, the book makes some good points and some very interesting suggestions. Like any book you read on a particular subject, there is always assertions, conjecture and author bias. Chapters 8 and 9 are interesting and additional reading on the subject is warranted. The connection between the foreclosure crisis and the outbreak of a Dengue Fever in 2009 associated with abandoned pools seems to be a stretch. Aedes egypti is a container breeder and isn't the type of mosquito that would normally be found in overgrown swimming pools with algae. I don't know if Dr. Hribar suggested that or Ms. Shah took it upon herself to link this to support her assertion. The question in my mind is whether these pools were indeed sampled or whether there was perhaps another mosquito species involved. This is the sort of detail I am interested in when examining and exploring a topic like" Pandemic."
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