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Monday, 17 November 2014

NO-MAN’S-LAND

Posted by mewmew, on 02:52



NO-MAN’S-LAND

FEAR, RACISM, AND THE HISTORICALLY
TROUBLING ATTITUDE OF AMERICAN PIONEERS

Illustration by Tony MillionaireDISCUSSED: Laura Ingalls Wilder, Kansas, Bonnets, “A Great Many Colored People,” Copper Gutters, Martin Luther King Jr., People Who Know Nothing about Gangs, Scalping, South Africa, Unprovoked Stabbing Sprees, Alarming Mass Pathologies, Chicago, Haunted Hot Dog Factories, Gangrene, Creatures from the Black Lagoon, Tree Saws, Headless Torsos, Quilts, Cheerleaders, Pet Grooming Stores, God

ON THE PRAIRIE

“What is it about water that always affects a person?” Laura Ingalls Wilder wrote in her 1894 diary. “I never see a great river or lake but I think how I would like to see a world made and watch it through all its changes.”
Forty years later, she would reflect that she had “seen the whole frontier, the woods, the Indian country of the great plains, the frontier towns, the building of the railroads in wild unsettled country, homesteading and farmers coming in to take possession.” She realized, she said, that she “had seen and lived it all….”
It was a world made and unmade. And it was not without some ambivalence, not without some sense of loss, that the writer watched the Indians, as many as she could see in either direction, ride out of the Kansas of her imagination. Her fictional self, the Laura of Little House on the Prairie, sobbed as they left.
Like my sister, like my cousin, like so many other girls, I was captivated, in my childhood, by that Laura. I was given a bonnet, and I wore it earnestly for quite some time. But when I return to Little House on the Prairie now as an adult, I find that it is not the book I thought it was. It is not the gauzy frontier fantasy I made of it as a child. It is not a naïve celebration of the American pioneer. It is the document of a woman interrogating her legacy. It is, as the scholar Ann Romines has called it, “one of our most disturbing and ambitious narratives about failures and experiments of acculturation in the American West.”
In that place and time where one world was ending and another was beginning, in that borderland between conflicting claims, the fictional Laura, the child of the frontier, struggles through her story. She hides, she cowers, she rages, she cries. She asks, “Will the government make these Indians go west?” and she asks, “Won’t it make the Indians mad to have to—” but then she is cut off and told to go to sleep. She falls ill and wakes from a fever to find a black doctor attending her. She picks up beads at an abandoned Indian camp and strings them for her sister. The real Laura grows up riding back and forth in covered wagons across the Middle West, passing through immigrant towns and towns where she notes in her diary seeing “a great many colored people.” She marries a farmer named Almanzo and settles, finally, in the Ozarks.
Laura Ingalls Wilder loved the land enough to know exactly what had been stolen to make her world. “If I had been the Indians,” she wrote in her 1894 diary, as she looked out over a river and some bluffs in South Dakota, “I would have scalped more white folks before I ever would have left it.”

ON THE BORDER

Shortly after we married, my husband and I moved to a part of Chicago that was once known as “No-Man’s-Land.” At the turn of the century, when Chicago had already burned and been rebuilt again, this was still a sandy forest of birch and oak trees. It was the barely populated place between the city of Chicago and the city of Evanston, the place just north of the boundary that once designated Indian Territory, a place where the streets were unpaved and unlit.
Now this neighborhood is called Rogers Park, and the city blocks of Chicago, all paved and lit, run directly into the city blocks of Evanston, with only a cemetery to mark the boundary between the two municipalities. The Chicago trains end here, and the tracks turn back in a giant loop around the gravel yard where idle trains are docked. Seven blocks to the east of the train station is the shore of Lake Michigan, which rolls and crashes past the horizon, reminding us, with its winds and spray, that we are on the edge of something vast.
There are a dozen empty storefronts on Howard Street between the lake and the train station—a closed Chinese restaurant, a closed dry cleaner, a closed thrift shop, a closed hot dog place. There is an open Jamaican restaurant, a Caribbean American bakery, a liquor store, a shoe store, and several little grocery markets. Women push baby carriages here, little boys eat bags of chips in front of the markets, and men smoke outside the train station while the trains rattle the air.
We moved to Chicago because I was hired to teach at the university in Evanston, which is within walking distance of Rogers Park. Walking to campus along the lakeshore for the first time, I passed the cemetery, and then a block of brick apartment buildings much like the ones on my block, and then I began to pass houses with gables and turrets and stone walls and copper gutters and huge bay windows and manicured lawns and circular drives. I passed beaches where sailboats were pulled up on the sand, where canoes and kayaks were stacked; I passed fountains, I passed parks with willow trees, I passed through one block that was gated at both ends. I passed signs that read PRIVATE ROAD, NO ACCESS, POLICE ENFORCED.
Evanston was still an officially segregated city in 1958 when Martin Luther King Jr. spoke there about the Greek concept of agapē, love for all humanity. On my first visit to Evanston, after my job interview, I experienced a moment of panic during which I stood with the big cool stone buildings of the university and its lawns and trees behind me while I called my sister to tell her that I was afraid this might not be the life for me. I was afraid, I told her, that if I became a professor I would be forever cloistered here, forever insulated from the rest of the world. My sister, who is herself training to be a professor, was not moved. There are, she reminded me, worse fates.
Of the seventy-seven official “community areas” of Chicago, twenty-four are populated by more than 90 percent of one race, and only twelve have no racial majority. Rogers Park is one of those few. It is celebrated as the most diverse neighborhood in a hypersegregated city. By the time I moved to Rogers Park, quite a few people had already warned me about the place. Two of them were my colleagues at the university, who both made mention of gangs. Others were near strangers, like my sister’s roommate’s mother, who asked her daughter to call me on the day I was packing my moving truck to share her suspicion that I might be moving somewhere dangerous. And then there was my mother, who grew up in a western suburb of Chicago but has, for almost twenty years now, lived in an old farmhouse in rural New York. She told me that she had heard from someone that the neighborhood I was moving to might not be safe, that there were gangs there. “Ma,” I said to her, “what do you know about gangs?” And she said, “I know enough—I know that they’re out there.” Which is about as much as I know, and about as much as most white folks who talk about gangs seem to know, which is to say, nothing.

IN THE IMAGINATION

Gangs are real, but they are also conceptual. The word gang is frequently used to avoid using the word black in a way that might be offensive. For instance, by pairing it with a suggestion of fear.
My cousin recently traveled to South Africa, where someone with her background would typically be considered neither white nor black, but colored, a distinct racial group in South Africa. Her skin is light enough so that she was most often taken to be white, which was something she was prepared for, having traveled in other parts of Africa. But she was not prepared for what it meant to be white in South Africa, which was to be reminded, at every possible opportunity, that she was not safe, and that she must be afraid. And she was not prepared for how seductive that fear would become, how omnipresent it would be, so that she spent most of her time there in taxis, and in hotels, and in “safe” places where she was surrounded by white people. When she returned home she told me, “I realized this is what white people do to each other—they cultivate each other’s fear. It’s very violent.”
We are afraid, my husband suggests, because we have guilty consciences. We secretly suspect that we might have more than we deserve. We know that white folks have reaped some ill-gotten gains in this country. And so, privately, quietly, as a result of our own complicated guilt, we believe that we deserve to be hated, to be hurt, and to be killed.
But, for the most part, we are not. Most victims of violent crimes are not white. This is particularly true for “hate” crimes. We are far more likely to be hurt by the food we eat, the cars we drive, or the bicycles we ride than by the people we live among. This may be lost on us in part because we are surrounded by a lot of noise that suggests otherwise. Within the past month, for example, the Chicago Tribune reported an “unprovoked stabbing spree,” a “one-man crime wave,” a boy who was beaten in a park, and a bartender who was beaten behind her bar, the story being, again and again, that none of us are safe in this city.

IN THE CITY

In the spring of 2006, the New York Times published an analysis of all the murders that had been committed in New York City during the previous three years—a total of 1,662 murders. The article revealed one trend: people who were murdered tended to be murdered by other people like them. Most of the killers were men and boys (a disturbing 93 percent—a number that, if we weren’t so accustomed to thinking of men as “naturally” violent, might strike us as the symptom of an alarming mass pathology), and most killed other men and boys. The majority of children were killed by a parent, and in more than half of all the cases, the victim and the killer knew each other. In over three fourths of the killings, the killer and the victim were of the same race, and less than 13 percent of the victims were white or Asian.
Even as it made this point, the article undid its own message by detailing a series of stranger-murders. There was the serial murderer who shot shopkeepers, the KFC customer who stabbed a cashier, the man who offered a ride to a group of strangers and was then murdered for his car. These are the murders we find most compelling, of course, because these are the murders that allow us to be afraid of the people we want to be afraid of.
In a similar layering of popular fantasy with true information, the article went on to mention specific precincts in Brooklyn, the Bronx, and Harlem where murders were concentrated, and then quoted Andrew Karmen, an expert in victimology, who explained, “The problem of crime and violence is rooted in neighborhood conditions—high rates of poverty, family disruption, failing schools, lack of recreational opportunities, active recruitment by street gangs, drug markets. People forced to reside under those conditions are at a greater risk of getting caught up in violence, as victims or as perpetrators.” In other words, particular neighborhoods are not as dangerous as the conditions within those neighborhoods. It’s a fine line, but an important one, because if you don’t live in those conditions, you aren’t very likely to get killed. Not driving through, not walking through, not even renting an apartment.
I worked, during my first year in New York, in some of the city’s most notorious neighborhoods: in Bed-Stuy, in East New York, in East Harlem, in Washington Heights. That was before I knew the language of the city, and the codes, so I had no sense that these places were considered dangerous. I was hired by the Parks Department to inspect community gardens, and I traveled all over the city, on train and on bus and on foot, wearing khaki shorts and hiking boots, carrying a clipboard and a Polaroid camera.
I did not understand then that those city blocks on which most of the lots were empty or full of the rubble of collapsed buildings would be read, by many New Yorkers, as an indication of danger. I understood that these places were poverty stricken, and ripe with ambient desperation, but I did not suspect that they were any more dangerous than anywhere else in the city. I was accustomed to the semirural poverty and postindustrial decay of upstate New York. There, by the highways, yards were piled with broken plastic and rusting metal, tarps were tacked on in place of walls, roof beams were slowly rotting through. And in the small cities, in Troy and Watervliet, in Schenectady and Niskayuna, in Amsterdam and in parts of Albany, old brick buildings crumbled, brownstones stood vacant, and factories with huge windows waited to be gutted and razed.
Beyond the rumor that the old hot-dog factory was haunted, I don’t remember any mythology of danger clinging to the urban landscape of upstate New York. And the only true horror story I had ever heard about New York City before I moved there was the story of my grandmother’s brother, a farm boy who had gone to the city and died of gangrene after cutting his bare foot on some dirty glass. “Please,” my grandmother begged me with tears in her eyes before I moved to New York, “always wear your shoes.”
And I did. But by the time I learned what I was really supposed to be afraid of in New York, I knew better—which isn’t to say that there was nothing to be afraid of, because, as all of us know, there are always dangers, everywhere.
But even now, at a much more wary and guarded age, what I feel when I am told that my neighborhood is dangerous is not fear but anger at the extent to which so many of us have agreed to live within a delusion—namely that we will be spared the dangers that others suffer only if we move within certain very restricted spheres, and that insularity is a fair price to pay for safety.
Fear is isolating for those that fear. And I have come to believe that fear is a cruelty to those who are feared. I once met a man of pro-football-size proportions who saw something in my body language when I shook his hand that inspired him to tell me he was pained by the way small women looked at him when he passed them on the street—pained by the fear in their eyes, pained by the way they drew away—and as he told me this he actually began to cry.
One evening not long after we moved to Rogers Park, my husband and I met a group of black boys riding their bikes on the sidewalk across the street from our apartment building. The boys were weaving down the sidewalk, yelling for the sake of hearing their own voices, and drinking from forty-ounce bottles of beer. As we stepped off the sidewalk and began crossing the street toward our apartment, one boy yelled, “Don’t be afraid of us!” I looked back over my shoulder as I stepped into the street and the boy passed on his bike so that I saw him looking back at me also, and then he yelled again, directly at me, “Don’t be afraid of us!”
I wanted to yell back, “Don’t worry, we aren’t!” but I was, in fact, afraid to engage the boys, afraid to draw attention to my husband and myself, afraid of how my claim not to be afraid might be misunderstood as bravado begging a challenge, so I simply let my eyes meet the boy’s eyes before I turned, disturbed, toward the tall iron gate in front of my apartment building, a gate that gives the appearance of being locked but is in fact always open.

IN THE WATER

My love of swimming in open water, in lakes and oceans, is tempered only by my fear of what I cannot see beneath those waters. My mind imagines into the depths a nightmare landscape of grabbing hands and spinning metal blades and dark sucking voids into which I will be pulled and not return. As a charm against my terror of the unseen I have, for many years now, always entered the water silently repeating to myself this command: Trust the water. And for some time after an incident in which one of my feet brushed the other and I swam for shore frantically in a gasping panic, breathing water in the process and choking painfully, I added: Don’t be afraid of your own feet.
I am accustomed to being warned away from the water, to being told that it is too cold, too deep, too rocky, that the current is too strong and the waves are too powerful. Until recently, what I learned from these warnings was only that I could safely defy them all. But then I was humbled by a rough beach in Northern California where I was slammed to the bottom by the surf and dragged to shore so forcefully that sand was embedded in the skin of my palms and my knees. That beach happened to have had a sign that read how to survive this beach, which made me laugh when I first arrived, the first item in the numbered list being do not go within 500 feet of the water.
It is only since I have discovered that some warnings are legitimate that my fears of open water have become powerful enough to fight my confidence in my own strength. I tend to stay closer to shore now, and I am always vigilant, although for what, exactly, I do not know. It is difficult to know what to be afraid of and how cautious to be when there are so many imagined dangers in the world, so many killer sharks, and so many creatures from the Black Lagoon.
Now that we share a bookshelf, I am in possession of my husband’s dog-eared, underlined copy of Barry Glassner’s The Culture of Fear. Every society is threatened by a nearly infinite number of dangers, Glassner writes, but societies differ in what they choose to fear. Americans, interestingly, tend to be most preoccupied with those dangers that are among the least likely to cause us harm, while we ignore the problems that are hurting the greatest number of people. We suffer from a national confusion between true threats and imagined threats.
And our imagined threats, Glassner argues, very often serve to mask true threats. Quite a bit of noise, for example, is made about the minuscule risk that our children might be molested by strange pedophiles, while in reality most children who are sexually molested are molested by close relatives in their own homes. The greatest risk factor for these children is not the proximity of a pedophile or a pervert but the poverty in which they tend to live. And the sensationalism around our “war” on illegal drugs has obscured the fact that legal drugs, the kind of drugs that are advertised on television, are more widely abused and cause more deaths than illegal drugs. Worse than this, we allow our misplaced, illogical fears to stigmatize our own people. “Fear Mongers,” Glassner writes, “project onto black men precisely what slavery, poverty, educational deprivation, and discrimination have ensured that they do not have—great power and influence.”
Although I do not pretend to understand the full complexity of local economies, I suspect that fear is one of the reasons that I can afford to live where I live, in an apartment across the street from a beach, with a view of the lake and space enough for both my husband and me to have rooms in which to write. “Our lake home,” we sometimes call it, with a wink to the fact that this apartment is far better than we ever believed two writers with student loan debt and one income could hope for. As one Chicago real estate magazine puts it: “For decades, a low rate of owner occupancy, a lack of commercial development… and problems with crime have kept prices lower in East Rogers Park than in many North Side neighborhoods.” And so my feelings about fear are somewhat ambivalent, because fear is why I can afford to swim every day now.
One of the paradoxes of our time is that the War on Terror has served mainly to reinforce a collective belief that maintaining the right amount of fear and suspicion will earn one safety. Fear is promoted by the government as a kind of policy. Fear is accepted, even among the best-educated people in this country, even among the professors with whom I work, as a kind of intelligence. And inspiring fear in others is often seen as neighborly and kindly, instead of being regarded as what my cousin recognized it for—a violence.
On my first day in Rogers Park, my downstairs neighbors, a family of European immigrants whom I met on my way out to swim, warned me that a boy had drowned by the breakwater not too long ago. I was in my bathing suit when they told me this, holding a towel. And, they told me, another neighbor walking his dog on the beach had recently found a human arm. It was part of the body of a boy who had been killed in gang warfare, and then cut up with a tree saw. The torso was found later, they told me, farther up the shore, but the head was never found.
I went for my swim, avoiding the breakwater and pressing back a new terror of heads with open mouths at the bottom of the lake. When I retold the neighbors’ story to my husband later, he laughed. “A tree saw?” he asked, still laughing.

ON THE FRONTIER

When the Irish immigrant Phillip Rogers built a log cabin nine miles north of the Chicago courthouse in 1834, there were still some small Indian villages there. He built his home on the wooded ridges along the north shore after noticing that this is where the Native Americans wintered.
Rogers built just south of the Northern Indian Boundary Line, which was the result of an 1816 treaty designating safe passage for whites within a twenty-mile-wide tract of land that ran from Lake Michigan to the Mississippi River, a treaty that was rendered meaningless by the Indian Removal Act of 1830, which dictated that all of the land east of the Mississippi would be open to white settlement. The Northern Indian Boundary Line, which was originally an Indian trail, would eventually become Rogers Avenue. And my apartment building would be built on the north corner of Rogers Avenue, just within the former Indian Territory.
During my first weeks in Rogers Park, I was surprised by how often I heard the word pioneer. I heard it first from the white owner of an antiques shop with signs in the windows that read WARNING, YOU ARE BEING WATCHED AND RECORDED. When I stopped off in his shop, he welcomed me to the neighborhood warmly and delivered an introductory speech dense with code. This was a “pioneering neighborhood,” he told me, and it needed “more people like you.” He and other “people like us” were gradually “lifting it up.”
And then there was the neighbor across the street, a white man whom my husband met while I was swimming. He told my husband that he had lived here for twenty years, and asked how we liked it. “Oh, we love it,” my husband said. “We’ve been enjoying Clark Street.” The tone of the conversation shifted with the mention of Clark Street, our closest shopping street, which is lined with taquerias and Mexican groceries. “Well,” the man said, in obvious disapproval, “we’re pioneers here.”
The word pioneer betrays a disturbing willingness to repeat the worst mistake of the pioneers of the American West—the mistake of considering an inhabited place uninhabited. To imagine oneself as a pioneer in a place as densely populated as Chicago is either to deny the existence of your neighbors or to cast them as natives who must be displaced. Either way, it is a hostile fantasy.
My landlord, who grew up in this apartment building, the building his grandfather built, is a tattooed Harley-riding man who fought in Vietnam and has a string of plastic skulls decorating the entrance to his apartment. When I ask him about the history of this neighborhood he speaks so evasively that I don’t learn anything except that he once felt much safer here than he does now. “We never used to have any of this,” he says, gesturing toward the back gate and the newly bricked wall that now protects the courtyard of this building from the alley. “We never even used to lock our doors even—I used to come home from school and let myself in without a key.”
For some time, the front door of the little house that Laura’s pa built on the prairie was covered with only a quilt, but when Pa built a door, he designed it so that the latch-string could be pulled in at night and no one could enter the house from outside. Pa padlocked the stable as soon as it was built, and then, after some Indians stopped by and asked Ma to give them her cornmeal, Pa padlocked the cupboards in the kitchen. These padlocks now strike me as quite remarkable, considering that Pa did not even have nails with which to construct the little house, but used wooden pegs instead.
In one scene of Little House, the house is ringed by howling wolves; in another, a roaring prairie fire sweeps around the house; in another a panther screams an eerie scream and the girls are kept inside. And then there are the Indians. The Indians who ride by silently, the Indians who occasionally come to the door of the house and demand food or tobacco, the Indians who are rumored—falsely, as Pa reveals—to have started the prairie fire to drive out the settlers. Toward the end of the book, the Indians hold a “jamboree,” singing and chanting all night so that the family cannot sleep. Pa stays up late making bullets, and Laura wakes to see Pa sitting on a chair by the door with his gun across his knees.
This is our inheritance, those of us who imagine ourselves as pioneers. We don’t seem to have retained the frugality of the original pioneers, or their resourcefulness, but we have inherited a ring of wolves around a door covered only by a quilt. And we have inherited padlocks on our pantries. That we carry with us a residue of the pioneer experience is my best explanation for the fact that my white neighbors seem to feel besieged in this neighborhood. Because that feeling cannot be explained by anything else that I know to be true about our lives here.
The adult characters in Little House, all of them except for Pa, are fond of saying, “The only good Indian is a dead Indian.” And for this reason some people don’t want their children reading the book. It may be true that Little House is not, after all, a children’s book, but it is a book that does not fail to interrogate racism. And although Laura is guilty of fearing the Indians, she is among the chief interrogators:
“Why don’t you like Indians, Ma?” Laura asked, and she caught a drip of molasses with her tongue.
“I just don’t like them; and don’t lick your fingers, Laura,” said Ma.
“This is Indian country, isn’t it?” Laura said. “What did we come to their country for, if you don’t like them?”
With the benefit of sixty years of hindsight, Laura Ingalls Wilder knew, by the time she wrote Little House, that the pioneers who had so feared Native Americans had been afraid of a people whom they were in the process of nearly exterminating. And so as a writer she took care, for instance, to point out that the ribs of the Indians were showing, a reminder that they came, frighteningly, into the house for food not because they were thieves but because they were starving. They were starving because the pioneers were killing all their game. If anyone had a claim on fear, on terror, in the American frontier, it was obviously the Indians, who could not legally own or buy the land they lived on, and so were gradually being driven out of their lives.
Near the very end of Little House, after the nights of whooping and chanting that had been terrifying the Ingalls family, and after many repetitions of the phrase “the only good Indian is a dead Indian,” Pa meets an Indian in the woods, the first Indian he has met who speaks English, and he learns from him that the tall Indian who recently came into the house and ate some food and smoked silently with Pa has saved their lives. Several tribes came together for a conference and decided to kill the settlers, but this tall Indian refused, thus destroying a federation of tribes and saving the settlers. On reporting the news to his family, Pa declares, “That’s one good Indian.”
This turn of events has the advantage of offering a lesson and also of being a fairly accurate account of what took place in Kansas in 1869. Because Laura Ingalls Wilder was actually only a toddler during the time her family lived in Kansas, she did quite a bit of research for Little House, traveling back to Kansas with her daughter and writing to historians, in the process discovering the story of the tall Indian, Soldat du Chene.
And so Wilder, the writer and the researcher, knows that the land the Ingalls have made their home on in Little House is part of the Osage Diminished Reserve. It is unclear whether Pa knows this, but it is clear that he knows he is in Indian Territory. He goes into Indian Territory on speculation, because he has heard that the government is about to open it up to settlers. At the end of the book, he gets word from his neighbors that the government has decided to uphold its treaty with the Indians, and soldiers will be coming to move the settlers off the land.
“If some blasted politicians in Washington hadn’t sent out word it would be all right to settle here, I’d never have been three miles over the line into Indian Territory,” Pa admits, in a rare moment of anger and frustration. “But I’ll not wait for the soldiers to take us out. We’re going now!”
The Ingalls family did indeed leave their home in Kansas under these circumstances. But the possibility the book suggests, by ending where it does, is that the settlers left Indian Territory to the Indians. “It’s a great country, Caroline,” Pa says, as they ride off in their covered wagon. “But there will be wild Indians and wolves here for many a long day.”
This is how it could have been, Laura Ingalls Wilder seems to be proposing. The government could have enforced a fair policy. The settlers could have left and stayed away. But, as it happened, the government revoked its treaty with the Plains tribes within what one historian estimates was a few weeks after the Ingalls family abandoned their house in Kansas.
Laura Ingalls Wilder does not tell us this. She tells us, instead, that Pa digs up the potatoes he just planted and they eat them for dinner. The next day they get back into their covered wagon, leaving the plow in the field and leaving their new glass windows, leaving their house and their stable, and leaving the crop they have just planted. This is the end of the book, and this, I believe, is the moral of the story.

ON THE LAKE

Leaving my apartment one morning, I found a piece of paper on the sidewalk that read, “Help! We have no hot water.” This message was printed in pink ink above an address that I recognized as nearby, but farther inland from the lake. The paper was carried by the wind to the water’s edge, I imagined, as a reminder of the everyday inconveniences, the absent landlords and the delayed buses and the check-cashing fees, of the world beyond.
“Everyone who lives in a neighborhood belongs to it, is part of it,” Geoff Dyer writes in Out of Sheer Rage. “The only way to opt out of a neighborhood is to move out….” But this does not seem to hold true of the thin sliver of Rogers Park bordering the lake, which many of our white neighbors drive in and out of without ever touching the rest of the neighborhood. They do not walk down Howard to the train station, do not visit the corner store for milk or beer, do not buy vegetables in the little markets, do not, as one neighbor admitted to me, even park farther inland than one block from the lake, no matter how long it takes to find a spot.
Between my apartment building and the lake there is a small park with a stony beach and some cracked tennis courts where people like to let their dogs run loose. In the winter, the only people in the park are people with dogs, people who stand in the tennis courts holding bags of shit while their dogs run around in circles and sniff each other. In the summer, the park fills with people. Spanish-speaking families make picnics on the grass and Indian families have games of cricket and fathers dip their babies in the lake and groups of black teenagers sit on the benches and young men play volleyball in great clouds of dust until dusk. “The warm weather,” my landlord observed to me not long after I moved in, “brings out the riffraff.”
When my landlord said this, I was standing on the sidewalk in front of our building in my bathing suit, still dripping from the lake, and a boy leaving the park asked if I had a quarter. I laughed and told the boy that I don’t typically carry change in my bathing suit, but he remained blank-faced, as uninterested as a toll collector. His request, I suspect, had very little to do with any money I may have had, or any money he may have needed. The exchange was intended to be, like so many of my exchanges with my neighbors, a ritual offering. When I walk from my apartment to the train I am asked for money by all variety of people—old men and young boys and women with babies. Their manner of request is always different, but they are always black and I am always white. Sometimes I give money and sometimes I do not, but I do not feel good about it either way, and the transaction never fails to be complicated. I do not know whether my neighbors believe, like I do, that I am paying paltry reparations, but I understand that the quarters and dollars I am asked for are a kind of tax on my presence here. A tax that, although I resent it, is more than fair.
One day in the late summer after we moved to Rogers Park, my husband came home from the fruit market with a bag of tomatoes and a large watermelon he had carried the half mile from the market to our house, stopping once to let some children feel how heavy it was. He was flushed from the sun and as he split the melon, still warm, my husband mused, “I hope more white people don’t move here.” My husband isn’t prone to sentimentality of any kind, or to worrying about white people, so I asked him why and he said, “Because kids were playing basketball by the school, and they had cheerleaders cheering them on, and black men say hello to me on the street, and I love our little fruit market, and I don’t want this place to change.”
But this place probably will change, if only because this is not a city where integrated neighborhoods last very long. And we are the people for whom the new coffee shop has opened. And the pet grooming store. “You know your neighborhood is gentrifying,” my sister observes, “when the pet grooming store arrives.” Gentrification is a word that agitates my husband. It bothers him because he thinks that the people who tend to use the word negatively, white artists and academics, people like me, are exactly the people who benefit from the process of gentrification. “I think you should define the word gentrification,” my husband tells me now. I ask him what he would say it means and he pauses for a long moment. “It means that an area is generally improved,” he says finally, “but in such a way that everything worthwhile about it is destroyed.”
My dictionary defines gentrification as meaning “to renovate or improve (esp. a house or district) so that it conforms to middle-class taste.” There is definitely the sense among the middle-class people in this neighborhood that they are improving the place. New condos fly banners that read luxury! The coffee shop and pet grooming store have been billed as a “revitalization.” And if some people lose their neighborhood in the process, there is bound to be someone like Mrs. Scott of Little House who will say, “Land knows, they’d never do anything with this country themselves. All they do is roam around over it like wild animals. Treaties or no treaties, the land belongs to folk that’ll farm it. That’s only common sense and justice.”
Meanwhile, when I walk home from the train station at night, I watch unmarked cars pull up in front of black teenagers who are patted down quickly and wordlessly. Some of the teenagers, my husband observes, carry their IDs in clear cases hanging from their belts for easy access. One evening, I watch the police interrogate two boys who have set a large bottle of Tide down on the sidewalk next to them, and I cannot forget this detail, the bottle of Tide, and the mundane tasks of living that it evokes. I consider going to one of the monthly beat meetings the police hold for each neighborhood and making some kind of complaint, but month after month I do not go.
Walking down Clark Street, I pass a poster on an empty storefront inviting entrepreneurs to start businesses in Rogers Park, “Chicago’s most diverse neighborhood.”
It takes me some time, standing in front of this poster, to understand why the word diverse strikes me as so false in this context, so disingenuous. It is not because this neighborhood is not full of many different kinds of people, but because that word implies some easy version of this difficult reality, some version that is not full of sparks and averted eyes and police cars. But still, I’d like to believe in the promise of that word. Not the sun-shininess of it, or the quota-making politics of it, but the real complexity of it.

ON THE COAST

There are three of us here on the beach, with Lake Michigan stretching out in front of us. We are strangers, but we have the kind of intimacy that can exist between people who are lying on the same deserted beach. Aisha, a young black woman, sits on one side of me, and Andre, a middle-aged Polish immigrant, sits on the other.
We bury our feet in the sand and talk of the places we have lived. Aisha is from Chicago, and she has never, in her twenty-one years, lived anywhere else. Andre left Poland when he was seventeen, looking for more opportunities. Now, he says, he isn’t entirely sure that he didn’t make a mistake. We all fall silent after this confession.
This beach is a kind of no-man’s-land. To the south are the last city blocks of Chicago, where the beaches are free but rocky and plagued with chunks of concrete. To the north are the first city blocks of Evanston, where the beaches are expansive and sandy but require a fee of seven dollars. To the west, beyond the wall of rocks directly behind us, is the cemetery that separates Chicago from Evanston, and a sign that forbids entry to this stretch of beach. To the east is an endless prairie of water.
When I mention that yesterday a lifeguard from Evanston came down in a boat while I was swimming and informed me that it was illegal to be here and that I had to leave because this land belongs to Evanston, Aisha rolls her eyes and says, gesturing back toward the cemetery, “This land belongs to the dead people.” Andre, the immigrant, the pioneer, looks out across the water and says, “This land belongs to God.”
Eula Biss is the author of The Balloonists. She teaches nonfiction writing at Northwestern University and is coeditor of Essay Press. “No-Man’s-Land” will be included in a collection of her essays forthcoming from Graywolf Press in 2009.

The Arrow of Disease

Posted by mewmew, on 02:44

The Arrow of Disease

When Columbus and his successors invaded the Americas, the most potent weapon they carried was their germs. But why didn't deadly disease flow in the other direction, from the New World to the Old?

 The three people talking in the hospital room were already stressed out from having to cope with a mysterious illness, and it didn’t help at all that they were having trouble communicating. One of them was the patient, a small, timid man, sick with pneumonia caused by an unidentified microbe and with only a limited command of the English language. The second, acting as translator, was his wife, worried about her husband’s condition and frightened by the hospital environment. The third person in the trio was an inexperienced young doctor, trying to figure out what might have brought on the strange illness. Under the stress, the doctor was forgetting everything he had been taught about patient confidentiality. He committed the awful blunder of requesting the woman to ask her husband whether he’d had any sexual experiences that might have caused the infection.

As the young doctor watched, the husband turned red, pulled himself together so that he seemed even smaller, tried to disappear under his bed sheets, and stammered in a barely audible voice. His wife suddenly screamed in rage and drew herself up to tower over him. Before the doctor could stop her, she grabbed a heavy metal bottle, slammed it onto her husband’s head, and stormed out of the room. It took a while for the doctor to elicit, through the man’s broken English, what he had said to so enrage his wife. The answer slowly emerged: he had admitted to repeated intercourse with sheep on a recent visit to the family farm; perhaps that was how he had contracted the mysterious microbe.

This episode, related to me by a physician friend involved in the case, sounds so bizarrely one of a kind as to be of no possible broader significance. But in fact it illustrates a subject of great importance: human diseases of animal origins. Very few of us may love sheep in the carnal sense. But most of us platonically love our pet animals, like our dogs and cats; and as a society, we certainly appear to have an inordinate fondness for sheep and other livestock, to judge from the vast numbers of them that we keep.

Some of us--most often our children--pick up infectious diseases from our pets. Usually these illnesses remain no more than a nuisance, but a few have evolved into far more. The major killers of humanity throughout our recent history--smallpox, flu, tuberculosis, malaria, plague, measles, and cholera--are all infectious diseases that arose from diseases of animals. Until World War II more victims of war died of microbes than of gunshot or sword wounds. All those military histories glorifying Alexander the Great and Napoleon ignore the ego-deflating truth: the winners of past wars were not necessarily those armies with the best generals and weapons, but those bearing the worst germs with which to smite their enemies.

The grimmest example of the role of germs in history is much on our minds this month, as we recall the European conquest of the Americas that began with Columbus’s voyage of 1492. Numerous as the Indian victims of the murderous Spanish conquistadores were, they were dwarfed in number by the victims of murderous Spanish microbes. These formidable conquerors killed an estimated 95 percent of the New World’s pre-Columbian Indian population.

Why was the exchange of nasty germs between the Americas and Europe so unequal? Why didn’t the reverse happen instead, with Indian diseases decimating the Spanish invaders, spreading back across the Atlantic, and causing a 95 percent decline in Europe’s human population? Similar questions arise regarding the decimation of many other native peoples by European germs, and regarding the decimation of would-be European conquistadores in the tropics of Africa and Asia.

Naturally, we’re disposed to think about diseases from our own point of view: What can we do to save ourselves and to kill the microbes? Let’s stamp out the scoundrels, and never mind what their motives are!

In life, though, one has to understand the enemy to beat him. So for a moment, let’s consider disease from the microbes’ point of view. Let’s look beyond our anger at their making us sick in bizarre ways, like giving us genital sores or diarrhea, and ask why it is that they do such things. After all, microbes are as much a product of natural selection as we are, and so their actions must have come about because they confer some evolutionary benefit.

Basically, of course, evolution selects those individuals that are most effective at producing babies and at helping those babies find suitable places to live. Microbes are marvels at this latter requirement. They have evolved diverse ways of spreading from one person to another, and from animals to people. Many of our symptoms of disease actually represent ways in which some clever bug modifies our bodies or our behavior such that we become enlisted to spread bugs.

The most effortless way a bug can spread is by just waiting to be transmitted passively to the next victim. That’s the strategy practiced by microbes that wait for one host to be eaten by the next--salmonella bacteria, for example, which we contract by eating already-infected eggs or meat; or the worm responsible for trichinosis, which waits for us to kill a pig and eat it without properly cooking it.

As a slight modification of this strategy, some microbes don’t wait for the old host to die but instead hitchhike in the saliva of an insect that bites the old host and then flies to a new one. The free ride may be provided by mosquitoes, fleas, lice, or tsetse flies, which spread malaria, plague, typhus, and sleeping sickness, respectively. The dirtiest of all passive-carriage tricks is perpetrated by microbes that pass from a woman to her fetus--microbes such as the ones responsible for syphilis, rubella (German measles), and AIDS. By their cunning these microbes can already be infecting an infant before the moment of its birth.

Other bugs take matters into their own hands, figuratively speaking. They actively modify the anatomy or habits of their host to accelerate their transmission. From our perspective, the open genital sores caused by venereal diseases such as syphilis are a vile indignity. From the microbes’ point of view, however, they’re just a useful device to enlist a host’s help in inoculating the body cavity of another host with microbes. The skin lesions caused by smallpox similarly spread microbes by direct or indirect body contact (occasionally very indirect, as when U.S. and Australian whites bent on wiping out belligerent native peoples sent them gifts of blankets previously used by smallpox patients).

More vigorous yet is the strategy practiced by the influenza, common cold, and pertussis (whooping cough) microbes, which induce the victim to cough or sneeze, thereby broadcasting the bugs toward prospective new hosts. Similarly the cholera bacterium induces a massive diarrhea that spreads bacteria into the water supplies of potential new victims. For modification of a host’s behavior, though, nothing matches the rabies virus, which not only gets into the saliva of an infected dog but drives the dog into a frenzy of biting and thereby infects many new victims.

Thus, from our viewpoint, genital sores, diarrhea, and coughing are symptoms of disease. From a bug’s viewpoint, they’re clever evolutionary strategies to broadcast the bug. That’s why it’s in the bug’s interests to make us sick. But what does it gain by killing us? That seems self-defeating, since a microbe that kills its host kills itself.

Though you may well think it’s of little consolation, our death is really just an unintended by-product of host symptoms that promote the efficient transmission of microbes. Yes, an untreated cholera patient may eventually die from producing diarrheal fluid at a rate of several gallons a day. While the patient lasts, though, the cholera bacterium profits from being massively disseminated into the water supplies of its next victims. As long as each victim thereby infects, on average, more than one new victim, the bacteria will spread, even though the first host happens to die.

So much for the dispassionate examination of the bug’s interests. Now let’s get back to considering our own selfish interests: to stay alive and healthy, best done by killing the damned bugs. One common response to infection is to develop a fever. Again, we consider fever a symptom of disease, as if it developed inevitably without serving any function. But regulation of body temperature is under our genetic control, and a fever doesn’t just happen by accident. Because some microbes are more sensitive to heat than our own bodies are, by raising our body temperature we in effect try to bake the bugs to death before we get baked ourselves.

Another common response is to mobilize our immune system. White blood cells and other cells actively seek out and kill foreign microbes. The specific antibodies we gradually build up against a particular microbe make us less likely to get reinfected once we are cured. As we all know, there are some illnesses, such as flu and the common cold, to which our resistance is only temporary; we can eventually contract the illness again. Against other illnesses, though--including measles, mumps, rubella, pertussis, and the now-defeated menace of smallpox--antibodies stimulated by one infection confer lifelong immunity. That’s the principle behind vaccination--to stimulate our antibody production without our having to go through the actual experience of the disease.

Alas, some clever bugs don’t just cave in to our immune defenses. Some have learned to trick us by changing their antigens, those molecular pieces of the microbe that our antibodies recognize. The constant evolution or recycling of new strains of flu, with differing antigens, explains why the flu you got two years ago didn’t protect you against the different strain that arrived this year. Sleeping sickness is an even more slippery customer in its ability to change its antigens rapidly. Among the slipperiest of all is the virus that causes AIDS, which evolves new antigens even as it sits within an individual patient, until it eventually overwhelms the immune system.

Our slowest defensive response is through natural selection, which changes the relative frequency with which a gene appears from generation to generation. For almost any disease some people prove to be genetically more resistant than others. In an epidemic, those people with genes for resistance to that particular microbe are more likely to survive than are people lacking such genes. As a result, over the course of history human populations repeatedly exposed to a particular pathogen tend to be made up of individuals with genes that resist the appropriate microbe--just because unfortunate individuals without those genes were less likely to survive to pass their genes on to their children.

Fat consolation, you may be thinking. This evolutionary response is not one that does the genetically susceptible dying individual any good. It does mean, though, that a human population as a whole becomes better protected.

In short, many bugs have had to evolve tricks to let them spread among potential victims. We’ve evolved countertricks, to which the bugs have responded by evolving counter-countertricks. We and our pathogens are now locked in an escalating evolutionary contest, with the death of one contestant the price of defeat, and with natural selection playing the role of umpire.

The form that this deadly contest takes varies with the pathogens: for some it is like a guerrilla war, while for others it is a blitzkrieg. With certain diseases, like malaria or hookworm, there’s a more or less steady trickle of new cases in an affected area, and they will appear in any month of any year. Epidemic diseases, though, are different: they produce no cases for a long time, then a whole wave of cases, then no more cases again for a while.

Among such epidemic diseases, influenza is the most familiar to Americans, this year having been a particularly bad one for us (but a great year for the influenza virus). Cholera epidemics come at longer intervals, the 1991 Peruvian epidemic being the first one to reach the New World during the twentieth century. Frightening as today’s influenza and cholera epidemics are, though, they pale beside the far more terrifying epidemics of the past, before the rise of modern medicine. The greatest single epidemic in human history was the influenza wave that killed 21 million people at the end of the First World War. The black death, or bubonic plague, killed one-quarter of Europe’s population between 1346 and 1352, with death tolls up to 70 percent in some cities.

The infectious diseases that visit us as epidemics share several characteristics. First, they spread quickly and efficiently from an infected person to nearby healthy people, with the result that the whole population gets exposed within a short time. Second, they’re acute illnesses: within a short time, you either die or recover completely. Third, the fortunate ones of us who do recover develop antibodies that leave us immune against a recurrence of the disease for a long time, possibly our entire lives. Finally, these diseases tend to be restricted to humans; the bugs causing them tend not to live in the soil or in other animals. All four of these characteristics apply to what Americans think of as the once more-familiar acute epidemic diseases of childhood, including measles, rubella, mumps, pertussis, and smallpox.

It is easy to understand why the combination of those four characteristics tends to make a disease run in epidemics. The rapid spread of microbes and the rapid course of symptoms mean that everybody in a local human population is soon infected, and thereafter either dead or else recovered and immune. No one is left alive who could still be infected. But since the microbe can’t survive except in the bodies of living people, the disease dies out until a new crop of babies reaches the susceptible age-- and until an infectious person arrives from the outside to start a new epidemic.

A classic illustration of the process is given by the history of measles on the isolated Faeroe Islands in the North Atlantic. A severe epidemic of the disease reached the Faeroes in 1781, then died out, leaving the islands measles-free until an infected carpenter arrived on a ship from Denmark in 1846. Within three months almost the whole Faeroes population-- 7,782 people--had gotten measles and then either died or recovered, leaving the measles virus to disappear once again until the next epidemic. Studies show that measles is likely to die out in any human population numbering less than half a million people. Only in larger populations can measles shift from one local area to another, thereby persisting until enough babies have been born in the originally infected area to permit the disease’s return.

Rubella in Australia provides a similar example, on a much larger scale. As of 1917 Australia’s population was still only 5 million, with most people living in scattered rural areas. The sea voyage to Britain took two months, and land transport within Australia itself was slow. In effect, Australia didn’t even consist of a population of 5 million, but of hundreds of much smaller populations. As a result, rubella hit Australia only as occasional epidemics, when an infected person happened to arrive from overseas and stayed in a densely populated area. By 1938, though, the city of Sydney alone had a population of over one million, and people moved frequently and quickly by air between London, Sydney, and other Australian cities. Around then, rubella for the first time was able to establish itself permanently in Australia.

What’s true for rubella in Australia is true for most familiar acute infectious diseases throughout the world. To sustain themselves, they need a human population that is sufficiently numerous and densely packed that a new crop of susceptible children is available for infection by the time the disease would otherwise be waning. Hence measles and other such diseases are also known as crowd diseases.

Crowd diseases could not sustain themselves in small bands of hunter-gatherers and slash-and-burn farmers. As tragic recent experience with Amazonian Indians and Pacific Islanders confirms, almost an entire tribelet may be wiped out by an epidemic brought by an outside visitor, because no one in the tribelet has any antibodies against the microbe. In addition, measles and some other childhood diseases are more likely to kill infected adults than children, and all adults in the tribelet are susceptible. Having killed most of the tribelet, the epidemic then disappears. The small population size explains why tribelets can’t sustain epidemics introduced from the outside; at the same time it explains why they could never evolve epidemic diseases of their own to give back to the visitors.

That’s not to say that small human populations are free from all infectious diseases. Some of their infections are caused by microbes capable of maintaining themselves in animals or in soil, so the disease remains constantly available to infect people. For example, the yellow fever virus is carried by African wild monkeys and is constantly available to infect rural human populations of Africa. It was also available to be carried to New World monkeys and people by the transatlantic slave trade.

Other infections of small human populations are chronic diseases, such as leprosy and yaws, that may take a very long time to kill a victim. The victim thus remains alive as a reservoir of microbes to infect other members of the tribelet. Finally, small human populations are susceptible to nonfatal infections against which we don’t develop immunity, with the result that the same person can become reinfected after recovering. That’s the case with hookworm and many other parasites.

All these types of diseases, characteristic of small, isolated populations, must be the oldest diseases of humanity. They were the ones that we could evolve and sustain through the early millions of years of our evolutionary history, when the total human population was tiny and fragmented. They are also shared with, or are similar to the diseases of, our closest wild relatives, the African great apes. In contrast, the evolution of our crowd diseases could only have occurred with the buildup of large, dense human populations, first made possible by the rise of agriculture about 10,000 years ago, then by the rise of cities several thousand years ago. Indeed, the first attested dates for many familiar infectious diseases are surprisingly recent: around 1600 B.C. for smallpox (as deduced from pockmarks on an Egyptian mummy), 400 b.c. for mumps, 1840 for polio, and 1959 for AIDS.

Agriculture sustains much higher human population densities than does hunting and gathering--on average, 10 to 100 times higher. In addition, hunter-gatherers frequently shift camp, leaving behind their piles of feces with their accumulated microbes and worm larvae. But farmers are sedentary and live amid their own sewage, providing microbes with a quick path from one person’s body into another person’s drinking water. Farmers also become surrounded by disease-transmitting rodents attracted by stored food.

Some human populations make it even easier for their own bacteria and worms to infect new victims, by intentionally gathering their feces and urine and spreading it as fertilizer on the fields where people work. Irrigation agriculture and fish farming provide ideal living conditions for the snails carrying schistosomes, and for other flukes that burrow through our skin as we wade through the feces-laden water.

If the rise of farming was a boon for our microbes, the rise of cities was a veritable bonanza, as still more densely packed human populations festered under even worse sanitation conditions. (Not until the beginning of the twentieth century did urban populations finally become self-sustaining; until then, constant immigration of healthy peasants from the countryside was necessary to make good the constant deaths of city dwellers from crowd diseases.) Another bonanza was the development of world trade routes, which by late Roman times effectively joined the populations of Europe, Asia, and North Africa into one giant breeding ground for microbes. That’s when smallpox finally reached Rome as the plague of Antonius, which killed millions of Roman citizens between a.d. 165 and 180.

Similarly, bubonic plague first appeared in Europe as the plague of Justinian (a.d. 542-543). But plague didn’t begin to hit Europe with full force, as the black death epidemics, until 1346, when new overland trading with China provided rapid transit for flea-infested furs from plague-ridden areas of Central Asia. Today our jet planes have made even the longest intercontinental flights briefer than the duration of any human infectious disease. That’s how an Aerolíneas Argentinas airplane, stopping in Lima, Peru, earlier this year, managed to deliver dozens of cholera- infected people the same day to my city of Los Angeles, over 3,000 miles away. The explosive increase in world travel by Americans, and in immigration to the United States, is turning us into another melting pot-- this time of microbes that we previously dismissed as just causing exotic diseases in far-off countries.

When the human population became sufficiently large and concentrated, we reached the stage in our history when we could at last sustain crowd diseases confined to our species. But that presents a paradox: such diseases could never have existed before. Instead they had to evolve as new diseases. Where did those new diseases come from?

Evidence emerges from studies of the disease-causing microbes themselves. In many cases molecular biologists have identified the microbe’s closest relative. Those relatives also prove to be agents of infectious crowd diseases--but ones confined to various species of domestic animals and pets! Among animals too, epidemic diseases require dense populations, and they’re mainly confined to social animals that provide the necessary large populations. Hence when we domesticated social animals such as cows and pigs, they were already afflicted by epidemic diseases just waiting to be transferred to us.

For example, the measles virus is most closely related to the virus causing rinderpest, a nasty epidemic disease of cattle and many wild cud-chewing mammals. Rinderpest doesn’t affect humans. Measles, in turn, doesn’t affect cattle. The close similarity of the measles and rinderpest viruses suggests that the rinderpest virus transferred from cattle to humans, then became the measles virus by changing its properties to adapt to us. That transfer isn’t surprising, considering how closely many peasant farmers live and sleep next to cows and their accompanying feces, urine, breath, sores, and blood. Our intimacy with cattle has been going on for the 8,000 years since we domesticated them--ample time for the rinderpest virus to discover us nearby. Other familiar infectious diseases can similarly be traced back to diseases of our animal friends.

Given our proximity to the animals we love, we must constantly be getting bombarded by animal microbes. Those invaders get winnowed by natural selection, and only a few succeed in establishing themselves as human diseases. A quick survey of current diseases lets us trace four stages in the evolution of a specialized human disease from an animal precursor.

In the first stage, we pick up animal-borne microbes that are still at an early stage in their evolution into specialized human pathogens. They don’t get transmitted directly from one person to another, and even their transfer from animals to us remains uncommon. There are dozens of diseases like this that we get directly from pets and domestic animals. They include cat scratch fever from cats, leptospirosis from dogs, psittacosis from chickens and parrots, and brucellosis from cattle. We’re similarly susceptible to picking up diseases from wild animals, such as the tularemia that hunters occasionally get from skinning wild rabbits.

In the second stage, a former animal pathogen evolves to the point where it does get transmitted directly between people and causes epidemics. However, the epidemic dies out for several reasons--being cured by modern medicine, stopping when everybody has been infected and died, or stopping when everybody has been infected and become immune. For example, a previously unknown disease termed o’nyong-nyong fever appeared in East Africa in 1959 and infected several million Africans. It probably arose from a virus of monkeys and was transmitted to humans by mosquitoes. The fact that patients recovered quickly and became immune to further attack helped cause the new disease to die out quickly.

The annals of medicine are full of diseases that sound like no known disease today but that once caused terrifying epidemics before disappearing as mysteriously as they had come. Who alive today remembers the English sweating sickness that swept and terrified Europe between 1485 and 1578, or the Picardy sweats of eighteenth- and nineteenth- century France?

A third stage in the evolution of our major diseases is represented by former animal pathogens that establish themselves in humans and that do not die out; until they do, the question of whether they will become major killers of humanity remains up for grabs. The future is still very uncertain for Lassa fever, first observed in 1969 in Nigeria and caused by a virus probably derived from rodents. Better established is Lyme disease, caused by a spirochete that we get from the bite of a tick. Although the first known human cases in the United States appeared only as recently as 1962, Lyme disease is already reaching epidemic proportions in the Northeast, on the West Coast, and in the upper Midwest. The future of AIDS, derived from monkey viruses, is even more secure, from the virus’s perspective.

The final stage of this evolution is represented by the major, long-established epidemic diseases confined to humans. These diseases must have been the evolutionary survivors of far more pathogens that tried to make the jump to us from animals--and mostly failed.

Diseases represent evolution in progress, as microbes adapt by natural selection to new hosts. Compared with cows’ bodies, though, our bodies offer different immune defenses and different chemistry. In that new environment, a microbe must evolve new ways to live and propagate itself.

The best-studied example of microbes evolving these new ways involves myxomatosis, which hit Australian rabbits in 1950. The myxoma virus, native to a wild species of Brazilian rabbit, was known to cause a lethal epidemic in European domestic rabbits, which are a different species. The virus was intentionally introduced to Australia in the hopes of ridding the continent of its plague of European rabbits, foolishly introduced in the nineteenth century. In the first year, myxoma produced a gratifying (to Australian farmers) 99.8 percent mortality in infected rabbits. Fortunately for the rabbits and unfortunately for the farmers, the death rate then dropped in the second year to 90 percent and eventually to 25 percent, frustrating hopes of eradicating rabbits completely from Australia. The problem was that the myxoma virus evolved to serve its own interests, which differed from the farmers’ interests and those of the rabbits. The virus changed to kill fewer rabbits and to permit lethally infected ones to live longer before dying. The result was bad for Australian farmers but good for the virus: a less lethal myxoma virus spreads baby viruses to more rabbits than did the original, highly virulent myxoma.

For a similar example in humans, consider the surprising evolution of syphilis. Today we associate syphilis with genital sores and a very slowly developing disease, leading to the death of untreated victims only after many years. However, when syphilis was first definitely recorded in Europe in 1495, its pustules often covered the body from the head to the knees, caused flesh to fall off people’s faces, and led to death within a few months. By 1546 syphilis had evolved into the disease with the symptoms known to us today. Apparently, just as with myxomatosis, those syphilis spirochetes evolved to keep their victims alive longer in order to transmit their spirochete offspring into more victims.

How, then, does all this explain the outcome of 1492--that Europeans conquered and depopulated the New World, instead of Native Americans conquering and depopulating Europe?

Part of the answer, of course, goes back to the invaders’ technological advantages. European guns and steel swords were more effective weapons than Native American stone axes and wooden clubs. Only Europeans had ships capable of crossing the ocean and horses that could provide a decisive advantage in battle. But that’s not the whole answer. Far more Native Americans died in bed than on the battlefield--the victims of germs, not of guns and swords. Those germs undermined Indian resistance by killing most Indians and their leaders and by demoralizing the survivors.

The role of disease in the Spanish conquests of the Aztec and Inca empires is especially well documented. In 1519 Cortés landed on the coast of Mexico with 600 Spaniards to conquer the fiercely militaristic Aztec Empire, which at the time had a population of many millions. That Cortés reached the Aztec capital of Tenochtitlán, escaped with the loss of only two-thirds of his force, and managed to fight his way back to the coast demonstrates both Spanish military advantages and the initial naïveté of the Aztecs. But when Cortés’s next onslaught came, in 1521, the Aztecs were no longer naive; they fought street by street with the utmost tenacity.

What gave the Spaniards a decisive advantage this time was smallpox, which reached Mexico in 1520 with the arrival of one infected slave from Spanish Cuba. The resulting epidemic proceeded to kill nearly half the Aztecs. The survivors were demoralized by the mysterious illness that killed Indians and spared Spaniards, as if advertising the Spaniards’ invincibility. By 1618 Mexico’s initial population of 20 million had plummeted to about 1.6 million.

Pizarro had similarly grim luck when he landed on the coast of Peru in 1531 with about 200 men to conquer the Inca Empire. Fortunately for Pizarro, and unfortunately for the Incas, smallpox had arrived overland around 1524, killing much of the Inca population, including both Emperor Huayna Capac and his son and designated successor, Ninan Cuyoche. Because of the vacant throne, two other sons of Huayna Capac, Atahuallpa and Huáscar, became embroiled in a civil war that Pizarro exploited to conquer the divided Incas.

When we in the United States think of the most populous New World societies existing in 1492, only the Aztecs and Incas come to mind. We forget that North America also supported populous Indian societies in the Mississippi Valley. Sadly, these societies too would disappear. But in this case conquistadores contributed nothing directly to the societies’ destruction; the conquistadores’ germs, spreading in advance, did everything. When De Soto marched through the Southeast in 1540, he came across Indian towns abandoned two years previously because nearly all the inhabitants had died in epidemics. However, he was still able to see some of the densely populated towns lining the lower Mississippi. By a century and a half later, though, when French settlers returned to the lower Mississippi, almost all those towns had vanished. Their relics are the great mound sites of the Mississippi Valley. Only recently have we come to realize that the mound-building societies were still largely intact when Columbus arrived, and that they collapsed between 1492 and the systematic European exploration of the Mississippi.

When I was a child in school, we were taught that North America had originally been occupied by about one million Indians. That low number helped justify the white conquest of what could then be viewed as an almost empty continent. However, archeological excavations and descriptions left by the first European explorers on our coasts now suggest an initial number of around 20 million. In the century or two following Columbus’s arrival in the New World, the Indian population is estimated to have declined by about 95 percent.

The main killers were European germs, to which the Indians had never been exposed and against which they therefore had neither immunologic nor genetic resistance. Smallpox, measles, influenza, and typhus competed for top rank among the killers. As if those were not enough, pertussis, plague, tuberculosis, diphtheria, mumps, malaria, and yellow fever came close behind. In countless cases Europeans were actually there to witness the decimation that occurred when the germs arrived. For example, in 1837 the Mandan Indian tribe, with one of the most elaborate cultures in the Great Plains, contracted smallpox thanks to a steamboat traveling up the Missouri River from St. Louis. The population of one Mandan village crashed from 2,000 to less than 40 within a few weeks.

The one-sided exchange of lethal germs between the Old and New worlds is among the most striking and consequence-laden facts of recent history. Whereas over a dozen major infectious diseases of Old World origins became established in the New World, not a single major killer reached Europe from the Americas. The sole possible exception is syphilis, whose area of origin still remains controversial.

That one-sidedness is more striking with the knowledge that large, dense human populations are a prerequisite for the evolution of crowd diseases. If recent reappraisals of the pre-Columbian New World population are correct, that population was not far below the contemporaneous population of Eurasia. Some New World cities, like Tenochtitlán, were among the world’s most populous cities at the time. Yet Tenochtitlán didn’t have awful germs waiting in store for the Spaniards. Why not?

One possible factor is that the rise of dense human populations began somewhat later in the New World than in the Old. Another is that the three most populous American centers--the Andes, Mexico, and the Mississippi Valley--were never connected by regular fast trade into one gigantic breeding ground for microbes, in the way that Europe, North Africa, India, and China became connected in late Roman times.

The main reason becomes clear, however, if we ask a simple question: From what microbes could any crowd diseases of the Americas have evolved? We’ve seen that Eurasian crowd diseases evolved from diseases of domesticated herd animals. Significantly, there were many such animals in Eurasia. But there were only five animals that became domesticated in the Americas: the turkey in Mexico and parts of North America, the guinea pig and llama/alpaca (probably derived from the same original wild species) in the

Andes, the Muscovy duck in tropical South America, and the dog throughout the Americas.

That extreme paucity of New World domestic animals reflects the paucity of wild starting material. About 80 percent of the big wild mammals of the Americas became extinct at the end of the last ice age, around 11,000 years ago, at approximately the same time that the first well- attested wave of Indian hunters spread over the Americas. Among the species that disappeared were ones that would have yielded useful domesticates, such as American horses and camels. Debate still rages as to whether those extinctions were due to climate changes or to the impact of Indian hunters on prey that had never seen humans. Whatever the reason, the extinctions removed most of the basis for Native American animal domestication--and for crowd diseases.

The few domesticates that remained were not likely sources of such diseases. Muscovy ducks and turkeys don’t live in enormous flocks, and they’re not naturally endearing species (like young lambs) with which we have much physical contact. Guinea pigs may have contributed a trypanosome infection like Chagas’ disease or leishmaniasis to our catalog of woes, but that’s uncertain. Initially the most surprising absence is of any human disease derived from llamas (or alpacas), which are tempting to consider as the Andean equivalent of Eurasian livestock. However, llamas had three strikes against them as a source of human pathogens: their wild relatives don’t occur in big herds as do wild sheep, goats, and pigs; their total numbers were never remotely as large as the Eurasian populations of domestic livestock, since llamas never spread beyond the Andes; and llamas aren’t as cuddly as piglets and lambs and aren’t kept in such close association with people. (You may not think of piglets as cuddly, but human mothers in the New Guinea highlands often nurse them, and they frequently live right in the huts of peasant farmers.)

The importance of animal-derived diseases for human history extends far beyond the Americas. Eurasian germs played a key role in decimating native peoples in many other parts of the world as well, including the Pacific islands, Australia, and southern Africa. Racist Europeans used to attribute those conquests to their supposedly better brains. But no evidence for such better brains has been forthcoming. Instead, the conquests were made possible by Europeans’ nastier germs, and by the technological advances and denser populations that Europeans ultimately acquired by means of their domesticated plants and animals.

So on this 500th anniversary of Columbus’s discovery, let’s try to regain our sense of perspective about his hotly debated achievements. There’s no doubt that Columbus was a great visionary, seaman, and leader. There’s also no doubt that he and his successors often behaved as bestial murderers. But those facts alone don’t fully explain why it took so few European immigrants to initially conquer and ultimately supplant so much of the native population of the Americas. Without the germs Europeans brought with them--germs that were derived from their animals--such conquests might have been impossible. 
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