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.
By Mark Jerome Walters
In December 2003,the chickens at the Umsung-gun poultry facility, 70 kilometers south of Seoul, Korea, did not come home to roost. Twenty thousand had died of avian influenza.
So began the catastrophic outbreak of “bird flu” that recently swept across Asia. Although the virus affected mostly poultry, the staid British journal The Lancet voiced widespread concern in the medical community that the bird virus could evolve to become contagious among humans and called the episode “massively frightening.” Was the world on the brink of another historic influenza pandemic like the Spanish 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, hanta virus, 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 emerge unpredictably from nowhere. But research over the past decade strongly suggests that people, far from being innocent victims of new plagues, have caused most of them by radically changing the natural environment. So closely is their emergence tied to ecological change that they might well be called “ecodemics.” The ecological whole of these diseases is far greater than the sum of their individual parts, and their significance is far greater than the relatively few people who have become sick. The global ecological changes precipitating these new epidemics usually fall into several sometimes-overlapping categories:intensive agriculture, global climate change, and alteration and fragmentation of forests. Increasing global trade and travel have exacerbated the emergence and spread of the epidemics.
It is no coincidence that the recent bird flu outbreak started in Asia. In fact, nearly all flu strains can be traced to southern China, known for its sprawling agricultural systems that integrate many species. The deadly, pandemic Hong Kong and Asian flus as well as the annual garden varieties of flu are almost certainly tied to the kind of intensive, close-quartered agriculture practiced by tens 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 wild ducks—the natural reservoir of influenza genes—around 2500 B.C. By the early part of the Ch’ing Dynasty, in the mid-1600s, rice farmers were using ducks to control pests in the rice paddies. Ducks not only ate crabs that invaded rice paddies in some river-delta regions but also devoured locusts, flying lice, leaf hoppers, shield bugs, and army worms. Domesticated ducks also plucked aquatic weeds from the paddies. Farmers removed the ducks when the rice paddies bloomed. At harvest, the fowl were set loose again to fatten themselves on rice grains that had escaped collection. Duck dropping in 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 began to raise fish in their rice paddies. Typically, a bamboo duck house stood on one side of a pond, a vegetable garden on another, and the family dwelling on an open side. The ducks—they are called manure machines for good reason—defecated into the ponds and supplied fertilizer. The fish in turn fattened themselves on both the manure and the plants. The farmers often fed molasses, rice bran, and other kitchen wastes to the ducks, whose swimming, splashing,and diving aerated the water for the fish. The farmer collected duck eggs for eating and selling, and he slaughtered the older ducks for food or took them to market. Periodically, he harvested the fish. In time, swine also became a part of these artificial, integrated systems.
The convergence of so many species within a seemingly self-contained ecological system was a man-made agricultural wonder for which the Chinese are justifiably famous. But profound ecological upsets often belie the manipulations we deem useful by shallow, short-term,human measures. The seemingly idyllic mixed-agriculture system perfected by 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 transforms itself from an ordinary flu virus into a deadly pandemic strain that can quickly spread around the world.
Nearly six months would pass before the most recent Asian bird flu epidemic was contained. More than 100 million poultry had been slaughtered to prevent further spread. Millions of already-poor farmers had been pushed further into poverty. More than 30 people caught the deadly virus from their poultry, and 23 died.
Unfortunately, avian influenza will not be the last disastrous recipe concocted in the kitchen of intensive agriculture. The heavy use of antibiotics to make feedlot cattle grow more quickly has given rise to severe forms of food poisoning in humans (salmonella and campylobacter) that no longer respond to most antibiotics. And it was through infected beef that people contracted mad cow disease in the late 1980s. The high density of animals, close proximity of different species, and unnatural feeding and management schemes have opened a barn door to new agriculturally related diseases.
In the spring of1993, a mysterious wave of fatal respiratory illness swept across the Colorado Plateau in the southwestern U.S., sickening a dozen people and killing nearly half of them—including Merrill Bahe, 20, and his fiancée, Florena Woody, 21, who lived on the Navajo Indian Reservation in New Mexico.
Both probably came into contact with infected mice secretions either in their home or in one of the nearby outbuildings in their village. Florena was stricken within days of inhaling the virus and was rushed with breathing difficulty to a medical clinic. She died before a helicopter could airlift her to a hospital.
Merrill’s symptoms began to show a few days after his fiancée’s death. While being driven to her funeral in the 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 soon become a haunting example of how the fates of a vibrant young couple in Stillwater, New Mexico, were influenced—if not sealed—by fluctuating ocean temperatures off the coast of Peru, thousands of miles away.
The Colorado Plateau has seen more rain and snow during the past 25 years than in any other comparable period during the past 200 years, which have been the wettest on the Plateau during the previous two millennia—a shift that many climatologists attribute too dramatic 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 worse by a warmer global climate, some scientists argue. And that, much evidence suggests, results from the present scale and character of human activity.
When scientists from the U.S. Centers for Disease Control (CDC) first showed up in the Four Corners area to investigate the deaths of Merrill and Florena, they were apparently clueless about the ecological roots of the illness—that is, until several of them attended a meeting of Navajo healers held in response to the outbreak. Elder after elder stood up at the meeting and spoke of times past, when a similar disease struck. The elders referred to the illness as the “mouse disease” (CDC later identified it specifically as a hantavirus) and said that the disease invariably followed periods of unusually heavy rain.
At the time of the outbreak, Robert Parmenter, a professor of ecology at the University of New Mexico in Albuquerque and director of the university’s long-term ecology research program at Sevilleta Research Field Station, didn’t put much stock in Navajo claims to know so much about the disease. But he did put a lot of stock in modern science and its conclusions about the ecological origins of hantavirus.
He and other researchers soon confirmed that rains induced by El Niño had been unusually heavy during the winter and spring before the disease outbreak—just as the elders had claimed.What’s more, Parmenter and his colleagues had been collecting data on mouse populations in the region for several years prior to the epidemic.
“The spring of 1993 saw a huge explosion in mouse populations,” he said—nearly a 75 percent increase in some areas.And this explosion, like mouse population explosions in the past, had followed seasons of heavy rain. The wetter soil fed the unusual bounty of energy-rich wildflowers, nuts, juniper berries, and cones that led to an increased number of mice, whose reproductive cycles were triggered by a chemical in the abundant green vegetation.
But the picture turned out to be ecologically even more complex than Parmenter or other ecologists at first believed.In 2000, researchers from Johns Hopkins University analyzed precipitation data from the El Niño years more precisely and found that, although rainfall was above normal in some areas on the Plateau, it was in fact normal around the 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-effect but to be an ecological cascade: after the deer mouse populations had exploded in areas with unusually heavy rain, the mice spilled out of canyons and traveled into secondary habitats near houses, trailers, and outhouses—the very places where people became infected.
In 1998 one of the strongest El Niños on record sent winter storms blasting across the Colorado Plateau, at one point prompting the federal government to declare disaster areas in parts of New Mexico. Parmenter worried that the increased precipitation could presage “fierce years” ahead for hantavirus. Indeed, studies showed that prior to the 1997-1998 El Niño cycle, less than ten percent of the mice he sampled showed evidence of hantavirus infection. Following the El Niño winter, 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 suggest that El Niño will reappear in 2004, no one is certain. But at some point it will return. The subsequent lush flowering of the arid landscape will likely reveal a darker side of the ecology of infectious disease: more people will die of hantavirus pulmonary syndrome.
Because this ecological cascade is so complex, predicting the incidence of hantavirus pulmonary syndrome is impossible. But our inability to make pinpoint predictions should not obscure the fundamental truth that is emerging.
In early October 2001 John Beckley, Hunterdon County’s director of public health, and his wife 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 came in spasms,” she explained. The night after a nurse practitioner diagnosed her illness as flu, John noticed the telltale bull’s-eye rash on his wife’s right shoulder blade. She had Lyme disease, he felt certain. A visit with her doctor and a three-week course of antibiotics cured her symptoms. She was lucky to have been diagnosed quickly.
The intervals of Linda’s illness have been shrunk, in a sense. Her doctors compressed the definition of her Lyme disease into the interval between being bitten and successfully completing her course of antibiotics. But this clinical definition excludes the larger ecological implications of her illness and hence its full meaning. Her illness was not just about a bacterium that entered her body. It was an extension of the unfortunate history of the eastern U.S. forests, and it was connected to autumn oaks and hickories, an absence of predators, and an overabundance of deer and mice. Her illness was not exclusively hers.
Linda wasn’t sure where she picked up the tick, but she believed it happened while she was walking their dog Willie near the South Branch of the Raritan River, not far from home. “When I moved here three years ago, all this used to be a big farm, and beyond the farm was all woods. Now it’s all new houses,” she said. With the houses came legions of people suddenly thrust within an arm’s length of deer that came 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 development in the eastern U.S. Drained by three graceful rivers, cloaked by beautiful if young forests, and situated within commuting distance of New York City, Hunterdon has been transformed over several decades from countryside to a suburbanized hub with more than 120,000 people. As with so many other places, the intervals between major changes seem to shrink day by day: neighbors moving to new jobs in other cities, a newly constructed mall here, a farm giving way to a new housing development there. Linda Beckley’s illness was an intimate part of a picture almost too big to see.
Perhaps no one understands this big picture better than Richard Ostfeld, an ecologist with the Institute of Ecosystem Studies in Millbrook, New York. Ostfeld suspected he might actually be 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. Acorns come in bursts, or “masts,” with almost none produced in some years and bumper 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 actively feeding ticks in that area would become infected. And since more mice would be drawn to the acorn-rich plots, a higher percentage of infected ticks would be found there. Acorns attract deer and mice, mice infect ticks, and infected ticks give people Lyme disease. People’s health was linked to acorn production.
The year 1997 saw one of the most prolific acorn crops in the mid-Atlantic states in years. If Ostfeld’s theory was correct, the rate of infection should rise among people there in the second year after the mast. Indeed, 1999 saw the third-highest annual number of Lyme
disease cases ever reported in the mid-Atlantic region.
Ostfeld has also postulated that a greater diversity of species native to many healthy forests could help decrease the rate of Lyme disease in people. Ticks are born without the Lyme disease bacterium. They pick it up from feeding on other forest animals. Mice transmit the Lyme disease bacterium to the ticks much more efficiently than most of these other animals. Since ticks will feed on a wide variety of forest animals, including birds, a greater diversity of species would proportionately 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, which employs mathematical modeling as well as continuing field research, suggests that the dilution effect may apply to more than just Lyme disease. It would not be totally surprising if it worked in the case of other similar tick-borne diseases, 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 have yielded a broad and intriguing principle: high biological diversity may help protect people against many infectious diseases.
Current studies are underway, for example, to determine whether a greater variety of birds in a region could reduce the human cases of West Nile virus. The reservoir of West Nile virus is birds, from whom it is transmitted to people by mosquitos. Underlying the theory is the notion that if mosquitos had a greater variety of bird species to feed upon—and some bird species served as more fertile reservoirs for 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 seems to dilute the transmission of Lyme disease bacteria.
Ostfeld, like many other scientists, acknowledges that the links between emerging diseases and ecological change are often so complex that they cannot always be proven. Nevertheless, taken together, many new and emerging epidemics offer profound insights into the way we live and how we think, and into the assumptions we embrace as children of the age of medical miracles.
For all that modern medicine has prolonged life and relieved suffering, it has also fostered the profoundly dangerous illusion that we are above or apart from the natural world with
its weather, forests, other species, and cycles of life and death. These diseases are reminding us otherwise.
About the Author
Mark Jerome Walters has been a visiting lecturer at Harvard Medical School for the past two years and is a professor of journalismat the University of South Florida St. Petersburg.
Illustration by James Marsh/illoart.com
