by Sonia Shah
In the past, livestock excreta were put to good use as fertilizer, in small farms where both animals and crops were raised. That was possible because the amount of animal waste roughly matched the absorptive capacity of nearby cropland. Not anymore. Today, farms produce far more waste than croplands can absorb. Livestock populations have grown much larger. In the United States, the mean size of hog farms grew by more than 2,000 percent between 1959 and 2007; the mean size of farms where chickens are raised for meat grew by over 30,000 percent.54
As a result, livestock produce thirteen times more solid waste than the human population does in the United States.55 To cope with the tens of millions of gallons of excreta they produce, farmers mix it with water and then pump it into untreated, multi-acre cesspools (“manure lagoons”). This wastewater is sprayed on crops, but since local croplands can’t absorb it all, it leaches into the groundwater and runs off into the surface waters. It also creates a plume of odor and a fine mist of polluted water that blankets the drying laundry, cars, and homes of those living downwind of the farms.56 “You don’t plan birthday parties outside,” one resident who lived near a manure lagoon said. “You no longer plan things. You plan around the odor and flies.” (One woman quoted by The New York Times remembers swatting more than one thousand flies in her office in a single day, thanks to a nearby manure lagoon.) Although there are federal regulations aimed at preventing animal waste from entering surface waters, they’re poorly enforced. During storms, the cesspools overflow, spilling their contents into local waterways. In 2013 in Wisconsin, more than one million gallons of manure spilled into the environment. In one of the worst spills, after a 1999 hurricane in North Carolina, 25 million gallons of manure poured into a local river, polluting 9 percent of local drinking-water wells with fecal coliform bacteria and killing millions of fish.57
This widespread fecal pollution creates novel transmission opportunities for a host of new pathogens. Shiga toxin–producing E. coli, or STEC, is one. About half of all cattle on American feedlots are infected with the microbe, which can survive in the environment for weeks or even longer if the weather is cool. In humans, STEC causes bloody diarrhea and life-threatening complications including hemolytic uremic syndrome, in which the kidneys fail. Up to 5 percent perish, and a third of those who survive suffer lifelong kidney problems.
Since the first reported outbreak in 1982, STEC has struck in fifty countries around the world. Despite ongoing efforts to contain it, each year, STEC will infect seventy thousand Americans. Those who live in countries where industrial cattle farming is common, such as in the United States, Canada, Britain, and Japan, are most at risk, and the closer you live to a cattle farm, the higher the risk.58
But the risk extends far beyond farm areas, as feces-contaminated products get shipped and consumed all over the world. In 2011, a batch of fenugreek seeds in Egypt caused an outbreak of disease three thousand miles away in Germany. That outbreak was noteworthy for two reasons. It showed the long reach of fecal-contaminated products and how they pose a risk to everyone along the global food chain. It also showed how pathogens exploit fecally contaminated environments not only for their transmission opportunities but also to become more virulent.
This latter enterprise has to do with how microbes exchange genetic material. Unlike creatures like us, who exchange genes “vertically,” from parents to children, microbes can exchange genes laterally, by bumping up against each other. Scientists call it “horizontal gene transfer.” Since it happens in places where microbes meet, microbe-rich, fecally contaminated environments provide a conducive setting.59
This has allowed many pathogens to become more virulent. Horizontal gene transfer is the process by which cholera turned into a pandemic killer, when a bacteriophage (a virus that infects bacteria) bumped up against the vibrio, endowing it with the ability to secrete toxin. Horizontal gene transfer created MRSA, when Staphylococcus aureus acquired the ability to secrete a toxin called Panton-Valentine leukocidin from another virus, along with genes that allow it to resist antibiotics from related bacterial species. It’s the process by which the NDM-1 plasmid moves between bacterial species, endowing them with its powerful drug-resisting capacities.60
The pathogen that caused the 2011 outbreak in Germany had gained its virulence through two horizontal gene transfers. First, a bacteriophage infected a harmless strain of E. coli, endowing it with the genes to secrete the Shiga toxin, creating STEC. A second horizontal gene transfer endowed the pathogen with the ability to secrete even more toxins and to resist a broad range of antibiotics. The result was an especially virulent strain of STEC called O104:H4, which triggers life-threatening complications in twice as many victims as regular STEC.61
Sometime before 2011, the pathogen spread onto the fenugreek farm in Egypt, migrating deep into the seeds’ interior, where it could hide from the disinfecting solutions that farmers use before planting.62 Fifty different companies in Germany bought sixteen tons of the invisibly contaminated seeds and sold them to gardeners and farmers across the country to grow into sprouts. In the spring of 2011, when people in and around the city of Hamburg ate the sprouts sprinkled on salads and crudités, O104:H4 slid into their bodies.63
Scores started pouring into clinics and hospitals, confused and unable to speak clearly. Their “awareness becomes blurred, they have problems finding words, and they don’t quite know where they are,” said the Hamburg nephrologist Rolf Stahl. The gastroenteritis they suffered included bouts of bloody diarrhea. Children went into seizures and had to be put on dialysis. One woman’s large intestine became gangrenous, and the left side of her colon had to be removed. She had muscle spasms that left her unable to speak. It was a “completely new clinical picture,” Stahl said.
By the end of the outbreak, four thousand people across Europe—primarily in Germany but also a handful in France—had sickened. Close to fifty died. Some survivors developed severe neurological symptoms, including seizures, as a consequence of the infection.64
We haven’t seen the last of this pathogen. After O104:H4 completed its violent passage in people’s bodies, it exited the same way it had in the cows. And it did so for months after the outbreak subsided, as survivors continued to shed the pathogen in their stool, introducing a steady stream of intact pathogens back into the environment, where they will mix and match with the other microbes encountered there.65
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As we grapple with the pathogens this new sanitary crisis imposes on us, we also face the pathogens churned out by the old sanitary crisis, which continues unabated in much of the world where poverty is rampant and governance weak. Fast-forward 178 years after New York City’s first cholera epidemic, to the island of Hispaniola, and the nation of Haiti. The majority of the population used the same waste-management methods as nineteenth-century New Yorkers. As of 2006, only 19 percent of the Haitian population had access to toilets or latrines. “When our children have to take a poop, we put them on a little bowl,” explained a resident of Cité Soleil, Haiti’s biggest slum. “Once they are done, we throw it into an empty lot.” Others used what are euphemistically called “flying toilets.” They defecate “into plastic bags which are then tossed into a mound of garbage or a nearby canal,” as watchdog journalists from the NGO Haiti Grassroots Watch wrote. And the excreta deposited into Haiti’s streets and empty lots aren’t easily moved. The flow of rainwater that might wash it into the sea is regularly blocked by garbage, such as plastic bags, Styrofoam containers, vegetable scraps, and cast-off shoes in various states of decomposition.66
People who live in the slums of South Asia are similarly exposed to human excreta. Nobody pays any mind when little boys, like the one I met at the Ekta Vihar slum in New Delhi, nonchalantly squat over the open gutters that run through the illegal settlement, even as a limber sari-clad woman and her three small children crouching in the dust on the gutter’s banks eat their afternoon meal not twenty yards away. Of more than 5,000 towns in India, only 232 have sewer systems
that carry away human excreta, and even those systems are partial at best. Everyone else must relieve themselves outside, in the open, like 2.6 billion other people around the world. Or they may use dry latrines of some kind or another, which are periodically emptied by India’s 1.2 million “manual scavengers,” who, like New York’s nineteenth-century night scavengers, collect the excreta with their bare hands or a piece of tin. They scrape it into a basket and carry it to a designated dumping ground, such as a nearby body of water.67 Whether collected by scavengers or carried off by sewer systems, the overwhelming majority of human excreta in the developing world ends up in the same streams, rivers, lakes, and seas that people use for domestic purposes, with microbial intensity fully intact.68
For the billions of people who lack adequate sanitation, this problem is a standing public-health catastrophe. Nearly 2 million die every year from diarrhea and scores of others from diseases such as intestinal worms, the helminthic infection schistosomiasis, and blindness-causing trachoma, which sanitary waste disposal systems could prevent. But it’s not a problem only for them. It’s a problem for everyone, because neglected environments contaminated with human filth provide a back channel for pathogens to amplify, spread, and hatch new pandemics that can affect all of us.
In Haiti, it was cholera.
Ten months after a magnitude 7.0 earthquake devastated Haiti in January 2010, a contingent of United Nations peacekeepers arrived direct from Kathmandu, Nepal, which was then in the grip of a cholera epidemic. They were stationed at a camp above the Artibonite River in the mountains north of Port-au-Prince. The facility, nominally a UN camp, had been designed and built by the Nepalese soldiers. Because there was no sewer system in Haiti, they built their own waste disposal system as well. Locals had long known it to be faulty: raw sewage from the camp poured into a stream that flowed into the river. The camp’s neighbors could see it and they could smell it, and reporters later documented it, too.69
This wasn’t the only time that aid workers had seen no option but to deposit human waste into Haiti’s waterways. Earlier in 2010, the Red Cross and other aid agencies had dumped untreated waste from fifteen thousand chemical toilets into an unlined open pit, the size of four football fields, atop the Plaine Cul de Sac aquifer, which supplied the capital city of Port-au-Prince its scarce drinking water.70
While there’s no evidence the contents of those chemical toilets contaminated Haiti’s water supply with pathogens, the Nepalese soldiers’ sewage dumping did. Within days of the soldiers’ arrival, cholera vibrio had been introduced into the Artibonite River. The cholera-contaminated river water washed into the river’s delta, where thousands of Haitian farmers grew rice. The farmers lived knee deep in the delta’s brackish waters, diverting it into their irrigation canals and scooping it up to bathe in and drink. They didn’t stand a chance. Nor did the rest of the Haitian population, which having never been exposed to cholera had no immunological defenses against it. Within a year, there were more cholera victims in Haiti than anywhere else in the world.71
The lack of adequate sanitation in New Delhi similarly allowed NDM-1 bacteria to make their way into local waters. A 2010 study found NDM-1-endowed bacteria in 4 percent of samples collected from drinking-water supplies and 51 of 171 samples collected from puddles in streets and alleys.72 Whether local people have contracted NDM-1 bacteria from contaminated waters in India is unknown, but it’s plausible. Evidence suggests it has happened elsewhere.73
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In a broader context, the real problem lies elsewhere. Waste becomes an issue for management only when the volume of waste grows beyond the space available to dispose of it. That is to say, it’s a direct result of the size and density of human and animal populations. Filth is just a symptom. The real problem is crowding.
FOUR
CROWDS
Were it not for urban growth during the mid-nineteenth century, the 1832 cholera epidemic in New York might have been the city’s last.
The intensity of the epidemic led to its own collapse. By the end of the summer, cholera had rid the city of susceptible victims. Reported cases, which likely comprised just 1 to 30 percent of the total number of cases that occurred (since mild cases generally go unreported), totaled more than 5,800. Reported deaths reached nearly three thousand. Taking into account the extent of unreported cases, cholera had likely infiltrated the entire city. The only people left were survivors of the infection.1 These survivors, as modern experiments have demonstrated, would have been immune to the pathogen. Cholera wouldn’t have been able to cause another epidemic even if post-1832 New Yorkers drank cholera-contaminated water by the gallon.2
And so New York City had gone back to business as usual. “The stores are all open, footwalks lined with bales and Boxes & streets crowded with carts & porter cars,” wrote John Pintard, a prominent merchant, in a letter in mid-August. “What a contrast to the middle of July when this Bazar of our dry-goods [on Pearl Street] had appeared as still & gloomy as the Valley of the Shadow of death … Now all life & bustle, smiling faces, clerks busy in making out Bills, porters in unpacking & repacking Boxes, joy & animation in every countenance.”3
Cholera wasn’t gone, however. The vibrio likely hid unnoticed in the coastal and surface waters around the city. It might even have caused a few easily ignored sporadic and isolated cases. Or it might have retreated into what’s called a “viable but nonculturable” state, a kind of suspended animation in which its cells shrink and stop replicating, biding their time until conditions improve. (Pathogenic bacteria in cow’s milk and bacteria in wastewater retreat into such states when faced with the assault of pasteurization and chlorination, respectively.) Either way, cholera’s presence concealed, the memory of the epidemic of 1832 faded into oblivion.4
Meanwhile, fuel for a new epidemic accumulated.
During the generation that grew up between the cholera epidemic of 1832 and that of 1849, a novel experiment in crowded urban living unfolded. People across Europe and North America were drawn into burgeoning cities like iron fillings to magnets. Between 1800 and 1850, urban populations in France and Germany doubled. During roughly the same period, London’s population tripled. Between 1830 and 1860, urban populations in the United States grew by more than 500 percent, three times faster than the national population.5
Many flocked to the cities for new manufacturing jobs, which offered better pay and more security than the farm work they abandoned. But the economic changes that industrialization unleashed led to large-scale population movements in other, less expected ways, too. The events that brought scores to New York City, for example, began when a steamship carried a peculiar batch of potatoes into Ireland in 1845.6
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Millions of impoverished Irish tenant farmers depended upon the potato—what they called “God’s gift from heaven”—for their sustenance. The average Irish laborer consumed upward of ten pounds of potatoes a day, roughly the amount of potatoes that the typical modern American might eat in a fortnight. He’d burn more potatoes for fuel. This wasn’t the result of any inherent love for the potato, but because it is starchy, calorific, and easy to grow. As a result of discriminatory English policies, Irish tenant farmers had only scarce, marginal lands with which to feed their families. The potato was the only crop they could afford.7
But their overreliance on the tuber made them dangerously vulnerable to any pathogen that might prey upon it. One such pathogen arrived in 1845, in a batch of potatoes infected with a fungal pathogen named after the Greek for “plant destroyer.” Phythophthora infestans originated in the Toluca Valley in Mexico. It had never been seen in Ireland before 1845, because in the days of slow-going sailing vessels, any potatoes infected with it would have turned to mush before hitting shore. But after steam travel shortened the journey, the infested potatoes were able to arrive intact. And once planted, the pathogen within them spread, invisibly broadcasting its deadly spores to nearby plants. Infested plants looked normal enough, but underground, t
heir roots rotted. When farmers rustled in the soil to pull up the potatoes, their hands emerged from the ground covered in smelly goo. They unknowingly ensured the pathogen’s return by discarding the ruined potatoes in heaps, from which the fungus reemerged every spring, ready to destroy the next year’s crop.8
As the potato crop wasted, famine set in. One and a half million perished. Another 1.5 million fled the Phythophthora-devastated countryside, their travel overseas subsidized by their own landlords, who preferred to facilitate their departure rather than contribute more to famine relief efforts, as the Irish government demanded.9
Between 1847 and 1851, nearly 850,000 refugees from Ireland landed in New York City.10 Only the most prosperous continued on into the interior of the country. The rest, unskilled laborers and former servants with nothing to eat and nowhere to live, “with money scarcely sufficient to pay passage for and find food for the voyage,” as a local Irish paper noted in 1847, settled in their port of arrival: Manhattan, which would soon become one of the most crowded places on earth.11
There was no room to sprawl on the island. Nor was there any network of quick transit that could link distant parts of the city with its booming manufacturing and port areas. Locals and newcomers alike needed to live near their work, or at least the possibility of it. Crowds formed around these centers of economic activity like barnacles on piers.
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