Feature

No Easy Way Out

HUMAN HEALTH, WILDLIFE DISEASE, AND CONSERVATION are inextricably linked. Yet modern medicine has fostered the profoundly dangerous illusion that we are above or apart from the natural world.

In December 2003,the chickens at the Umsung-gun poultry facility, 70 kilometers south ofSeoul, Korea, did not come home to roost. Twenty thousand had died of avianinfluenza.

So began the catastrophic outbreakof “bird flu” that recently swept across Asia. Although the virus affectedmostly poultry, the staid British journal The Lancet voiced widespreadconcern in the medical community that the bird virus could evolve to becomecontagious among humans and called the episode “massively frightening.” Wasthe world on the brink of another historic influenza pandemic like theSpanish Flu of 1918-1919, which killed an estimated 20 million people?

Avian influenza is just one of a host of recently emerging diseases, including HIV/AIDS, West Nile virus, hantavirus, Lyme disease, and mad cow disease. Some are new to medicine; others are old diseases appearing in new and more deadly forms or springing up in totally new areas throughout the world.

These diseases might appear to emergeunpredictably from nowhere. But research over the past decade stronglysuggests that people, far from being innocent victims of new plagues, havecaused most of them by radically changing the natural environment. So closelyis their emergence tied to ecological change that they might well be called “ecodemics.” Theecological whole of these diseases is far greater than the sum of theirindividual parts, and their significance is far greater than the relativelyfew people who have become sick. The global ecological changes precipitatingthese new epidemics usually fall into several sometimes-overlapping categories:intensive agriculture, global climate change, and alteration and fragmentationof forests. Increasing global trade and travel have exacerbated the emergenceand spread of the epidemics.

It is no coincidencethat the recent bird flu outbreak started in Asia. In fact, nearly allflu strains can be traced to southern China, known for its sprawling agriculturalsystems that integrate many species. The deadly, pandemic Hong Kong andAsian flus as well as the annual garden varieties of flu are almost certainlytied to the kind of intensive, close-quartered agriculture practiced bytens of millions of farmers across southern China and elsewhere in Asia.What’s more, the roots of the problem may stretch back over 4,000 years.

The Chinese began domesticating wildducks—the natural reservoir of influenza genes—around 2500 B.C. By theearly part of the Ch’ing Dynasty, in the mid-1600s, rice farmers were usingducks to control pests in the rice paddies. Ducks not only ate crabs thatinvaded rice paddies in some river-delta regions but also devoured locusts,flying lice, leafhoppers, shield bugs, and army worms. Domesticated ducksalso plucked aquatic weeds from the paddies. Farmers removed the duckswhen the rice paddies bloomed. At harvest, the fowl were set loose againto fatten themselves on rice grains that had escaped collection. Duck droppingsin turn fertilized the paddies for the next planting. In some regions,five duck crops a year could be raised in this beautifully efficient system.Farmers appeared to win on all accounts: ridding their paddies of pests,fertilizing their crops, and fattening their ducks.

By the late 1600s, many farmers beganto raise fish in their rice paddies. Typically, a bamboo duck house stoodon one side of a pond, a vegetable garden on another, and the family dwellingon an open side. The ducks—they are called manure machines for good reason—defecatedinto the ponds and supplied fertilizer. The fish in turn fattened themselveson both the manure and the plants. The farmers often fed molasses, ricebran, and other kitchen wastes to the ducks, whose swimming, splashing,and diving aerated the water for the fish. The farmer collected duck eggsfor eating and selling, and he slaughtered the older ducks for food ortook them to market. Periodically, he harvested the fish. In time, swinealso became a part of these artificial, integrated systems.

The convergence of so many specieswithin a seemingly self-contained ecological system was a man-made agriculturalwonder for which the Chinese are justifiably famous. But profound ecologicalupsets often belie the manipulations we deem useful by shallow, short-term,human measures. The seemingly idyllic mixed-agriculture system perfectedby the Chinese became an ideal breeding ground for new influenza viruses.Each animal species offers another “laboratory” in which the virus replicates,mixes with other strains, acquires new genes, and potentially transformsitself from an ordinary flu virus into a deadly pandemic strain that canquickly spread around the world.

Nearly six months would pass beforethe most recent Asian bird flu epidemic was contained. More than 100 millionpoultry had been slaughtered to prevent further spread. Millions of already-poorfarmers had been pushed further into poverty. More than 30 people caughtthe deadly virus from their poultry, and 23 died.

Unfortunately, avian influenza willnot be the last disastrous recipe concocted in the kitchen of intensiveagriculture. The heavy use of antibiotics to make feedlot cattle grow morequickly has given rise to severe forms of food poisoning in humans (salmonellaand campylobacter) that no longer respond to most antibiotics. And it was throughinfected beef that people contracted mad cow disease in the late 1980s. Thehigh density of animals, close proximity of different species, and unnatural feeding and management schemes have opened a barn door to new agriculturallyrelated diseases.

In the spring of1993, a mysterious wave of fatal respiratory illness swept across the ColoradoPlateau in the southwestern U.S., sickening a dozen people and killingnearly half of them—including Merrill Bahe, 20, and his fiancée, FlorenaWoody, 21, who lived on the Navajo Indian Reservation in New Mexico.

Both probably came into contact withinfected mice secretions either in their home or in one of the nearby outbuildingsin their village. Florena was stricken within days of inhaling the virusand was rushed with breathing difficulty to a medical clinic. She diedbefore a helicopter could airlift her to a hospital.

Merrill’s symptoms began to show afew days after his fiancée’s death. While being driven to her funeral inthe city of Gallup, New Mexico, Merrill’s lungs began to fill with fluid,his lips turned purple, and he collapsed at a roadside convenience store.He died hours before Florena was to be buried. Their deaths would soonbecome a haunting example of how the fates of a vibrant young couple inStillwater, New Mexico, were influenced—if not sealed—by fluctuating oceantemperatures off the coast of Peru, thousands of miles away.

The Colorado Plateau has seen morerain and snow during the past 25 years than in any other comparable periodduring the past 200 years, which have been the wettest on the Plateau duringthe previous two millennia—a shift that many climatologists attribute todramatic rises in ocean temperature near the western coast of South America,a phenomenon known as El Niño.

If El Niño is a natural phenomenon,the extremes and duration of the heated Pacific appear to be new—made worseby a warmer global climate, some scientists argue. And that, much evidencesuggests, results from the present scale and character of human activity.

When scientists from the U.S. Centersfor Disease Control (CDC) first showed up in the Four Corners area to investigatethe deaths of Merrill and Florena, they were apparently clueless aboutthe ecological roots of the illness—that is, until several of them attendeda meeting of Navajo healers held in response to the outbreak. Elder afterelder stood up at the meeting and spoke of times past, when a similar diseasestruck. The elders referred to the illness as the “mouse disease” (CDClater identified it specifically as a hantavirus) and said that the diseaseinvariably followed periods of unusually heavy rain.

At the time of the outbreak, RobertParmenter, a professor of ecology at the University of New Mexico in Albuquerqueand director of the university’s long-term ecology research program at SevilletaResearch Field Station, didn’t put much stock in Navajo claims to know somuch about the disease. But he did put a lot of stock in modern science andits conclusions about the ecological origins of hantavirus.

He and other researchers soon confirmedthat rains induced by El Niño had been unusually heavy during the winterand spring before the disease outbreak—just as the elders had claimed.What’s more, Parmenter and his colleagues had been collecting data on mousepopulations in the region for several years prior to the epidemic.

“The spring of 1993 saw a huge explosionin mouse populations,” he said—nearly a 75 percent increase in some areas.And this explosion, like mouse population explosions in the past, had followedseasons of heavy rain. The wetter soil fed the unusual bounty of energy-richwildflowers, nuts, juniper berries, and cones that led to an increasednumber of mice, whose reproductive cycles were triggered by a chemicalin the abundant green vegetation.

But the picture turned out to be ecologicallyeven more complex than Parmenter or other ecologists at first believed.In 2000, researchers from Johns Hopkins University analyzed precipitationdata from the El Niño years more precisely and found that, although rainfallwas above normal in some areas on the Plateau, it was in fact normal aroundthe homes where the victims had become infected. This posed a mystery:how could increased rainfall account for the appearance of hantavirus?

It turned out not to be simple cause-and-effectbut to be an ecological cascade: after the deer mouse populations had explodedin areas with unusually heavy rain, the mice spilled out of canyons andtraveled into secondary habitats near houses, trailers, and outhouses—thevery places where people became infected.

In 1998 one of the strongest El Niñoson record sent winter storms blasting across the Colorado Plateau, at onepoint prompting the federal government to declare disaster areas in partsof New Mexico. Parmenter worried that the increased precipitation couldpresage “fierce years” ahead for hantavirus. Indeed, studies showed thatprior to the 1997-1998 El Niño cycle, less than ten percent of the micehe sampled showed evidence of hantavirus infection. Following the El Niñowinter, nearly half of the mice showed evidence of infection. True to predictions,1999 also saw an upsurge of human cases of hantavirus on the Plateau.

While some climate models suggestthat El Niño will reappear in 2004, no one is certain. But at some pointit will return. The subsequent lush flowering of the arid landscape willlikely reveal a darker side of the ecology of infectious disease: morepeople will die of hantavirus pulmonary syndrome.

Because this ecological cascade isso complex, predicting the incidence of hantavirus pulmonary syndrome isimpossible. But our inability to make pinpoint predictions should not obscurethe fundamental truth that is emerging.

In early October2001 John Beckley, Hunterdon County’s director of public health, and hiswife Linda were driving home from a weekend in Cape Cod, Massachusetts,when Linda started feeling stiffness in her spine. “All my muscles hurt.I lost my appetite and got very agitated. I got a fever, and shivers camein spasms,” she explained. The night after a nurse practitioner diagnosedher illness as flu, John noticed the telltale bull’s-eye rash on his wife’sright shoulder blade. She had Lyme disease, he felt certain. A visit withher doctor and a three-week course of antibiotics cured her symptoms. Shewas lucky to have been diagnosed quickly.

The intervals of Linda’s illness havebeen shrunk, in a sense. Her doctors compressed the definition of her Lymedisease into the interval between being bitten and successfully completingher course of antibiotics. But this clinical definition excludes the largerecological implications of her illness and hence its full meaning. Herillness was not just about a bacterium that entered her body. It was anextension of the unfortunate history of the eastern U.S. forests, and itwas connected to autumn oaks and hickories, an absence of predators, andan overabundance of deer and mice. Her illness was not exclusively hers.

Linda wasn’t sure where she pickedup the tick, but she believed it happened while she was walking their dogWillie near the South Branch of the Raritan River, not far from home. “WhenI moved here three years ago, all this used to be a big farm, and beyondthe farm was all woods. Now it’s all new houses,” she said. With the housescame legions of people suddenly thrust within an arm’s length of deer thatcame to feed on the lawns. Along new clearings, leafy browse flourished.Rock walls were built at the perimeters of properties, and wood piles appeared at the edges of driveways,creating a paradise for the carriers of Lyme disease ticks.

Like much of the Raritan River Valley,Hunterdon County, New Jersey, has seen some of the most rapid developmentin the eastern U.S. Drained by three graceful rivers, cloaked by beautifulif young forests, and situated within commuting distance of New York City,Hunterdon has been transformed over several decades from countryside toa suburbanized hub with more than 120,000 people. As with so many otherplaces, the intervals between major changes seem to shrink day by day:neighbors moving to new jobs in other cities, a newly constructed mallhere, a farm giving way to a new housing development there. Linda Beckley’sillness was an intimate part of a picture almost too big to see.

Perhaps no one understands this bigpicture better than Richard Ostfeld, an ecologist with the Institute ofEcosystem Studies in Millbrook, New York. Ostfeld suspected he might actuallybe able to predict people’s risk of contracting Lyme disease by observing,of all things, the abundance of acorns in the region in a given year. Acornscome in bursts, or “masts,” with almost none produced in some years andbumper crops produced in others.

Ostfeld’s reasoning went like this:the more mice there were in an area, the more likely it would be that activelyfeeding ticks in that area would become infected. And since more mice wouldbe drawn to the acorn-rich plots, a higher percentage of infected tickswould be found there. Acorns attract deer and mice, mice infect ticks,and infected ticks give people Lyme disease. People’s health was linkedto acorn production.

The year 1997 saw one of the mostprolific acorn crops in the mid-Atlantic states in years. If Ostfeld’stheory was correct, the rate of infection should rise among people therein the second year after the mast. Indeed, 1999 saw the third-highest annualnumber of Lyme disease cases ever reported in the mid-Atlantic region.

Ostfeld has also postulated that agreater diversity of species native to many healthy forests could helpdecrease the rate of Lyme disease in people. Ticks are born without theLyme disease bacterium. They pick it up from feeding on other forest animals.Mice transmit the Lyme disease bacterium to the ticks much more efficientlythan most of these other animals. Since ticks will feed on a wide varietyof forest animals, including birds, a greater diversity of species wouldproportionately reduce the chance of the tick feeding on a high-risk mouse.Ostfeld calls this the “dilution effect” of high biological diversity.

Ostfeld’s current research, whichemploys mathematical modeling as well as continuing field research, suggeststhat the dilution effect may apply to more than just Lyme disease. It wouldnot be totally surprising if it worked in the case of other similar tick-bornediseases, he said, but “It is interesting that the dilution effect seems to apply to diseases like hantavirus pulmonary syndrome, which are not vector-transmitted.”

If proven, Ostfeld’s theory will haveyielded a broad and intriguing principle: high biological diversity mayhelp protect people against many infectious diseases.

Current studies are underway, forexample, to determine whether a greater variety of birds in a region couldreduce the human cases of West Nile virus. The reservoir of West Nile

virus is birds, from whom it is transmitted to people by mosquitos. Underlyingthe theory is the notion that if mosquitos had a greater variety of birdspecies to feed upon—and some bird species served as more fertile reservoirsfor the virus than others—then the diversity could dilute the presence and spread of West Nile virus in the same way that a greater diversity of small forest animals seemsto dilute the transmission of Lyme disease bacteria.

Ostfeld, like manyother scientists, acknowledges that the links between emerging diseasesand ecological change are often so complex that they cannot always be proven.Nevertheless, taken together, many new and emerging epidemics offer profoundinsights into the way we live and how we think, and into the assumptionswe embrace as children of the age of medical miracles.

For all that modern medicine has prolongedlife and relieved suffering, it has also fostered the profoundly dangerousillusion that we are above or apart from the natural world with its weather, forests, other species, and cycles of life and death. Thesediseases are reminding us otherwise.

About the Author

Mark Jerome Walters has been a visiting lecturer at HarvardMedical School for the past two years and is a professor of journalismat the University of South Florida St. Petersburg.