The Coming Plague (98 page)

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Authors: Laurie Garrett

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Given how recently, on a scale of evolutionary time, these rodents have spread around the world, it should come as no surprise that they carry viruses which, whether found on the Volga steppes or in the deserts of Arizona, bear remarkable resemblances. And if the origins of these hantaviruses can be traced back to the earliest periods of mouse and rat evolution, it would seem logical to assume that careful inspection of
Rattus, Peromyscus
, and
Mus
cousins all over the world would reveal still more hanta strains.
The Four Corners outbreak prompted scientists to rethink diseases once labeled as “unknown etiology” and consider the possibility that millions of people worldwide may needlessly suffer ailments and death caused by the rodent-carried viruses.
Kidney expert Dr. Guy Neild of Middlesex Hospital in London was moved to ask during the Four Corners investigation whether the long-mysterious “trench nephritis” that claimed the lives of hundreds of soldiers hunkered down in trenches during the American Civil War and World War I may not have been due to hantaviruses carried by co-entrenched rats or mice.
20
German physicians from the University of Würzburg reported that a surge in European hantavirus cases occurred during the spring of 1993, leading to hemorrhagic fever with kidney complications. They noted that rodent control efforts had slowed a bit since German unification, and wondered whether the surge in the German rat population could have been prevented.
21
German records indicated that a first, fairly small hantavirus epidemic surfaced in that country during mid-1990, causing no fatalities, but 88 confirmed renal illnesses. A second German hantavirus epidemic ran its course from September 1992 to October 1993: some 183 illnesses, no deaths. Researchers were certain that the outbreaks were the result of local surges in the rodent and vole populations, and that illnesses in the 1993 outbreak were more severe. They were also certain that hanta cases were underreported by German physicians.
22
Similar surges in Puumala infection were noted in France, Belgium, and the Netherlands in 1993.
23
Though the Four Corners type of respiratory hantavirus had never been
seen in Russia, classic kidney disease-producing forms were seen between 1985 and 1992 in twenty-three regions of the country, afflicting 68,796 people. The ailments were caused by more than seventy different hantavirus strains that were carried by sixty-three different species of birds and small mammals, including all common rodents.
“These rodents and their viruses have been here for millennia,” McDade concluded. “There may have originally been a common ancestor virus infecting a single rodent species, which may have mutated and spread to other rodents over time. But these viruses have almost certainly been among us for centuries.”
McDade paused, examined his hands for a moment, and added, “I often wonder with Legionnaires' Disease, if there had not been an association with a particular hotel, a drama, if you will. If there had just continued to be sporadic, scattered, inexplicable pneumonia deaths, would we have ever recognized Legionnaires' as a distinct disease?
“And I now wonder the same thing about Four Corners. If there hadn't been that one cluster of four cases among healthy Navajos, would we have ever recognized the virus among us?” McDade asked, noting that there were many other diseases for which no clear cause is known.
“We should continue to allow for the possibility that they are all due to infectious agents,” he said.
24
 
Inside the CDC's P4 laboratory Dr. Luanne Elliott was toiling around the clock during the summer and fall of 1993 trying to find a way to grow the Louisiana and Four Corners viruses in test tubes. For four months the slow-growing viruses stubbornly resisted her expert efforts. In the last week of September she finally succeeded in experimentally infecting laboratory mice, and a month later was able to cultivate live virus.
At USAMRIID similar efforts to grow the Four Corners virus in the laboratory, isolate it, and further elaborate its genetic makeup were underway. The two federal laboratories raced to complete the jobs first, eventually reaching a dead heat with both groups declaring victory at the annual meeting of the American Society of Tropical Medicine and Hygiene in Atlanta on November 3, 1993, and at a University of New Mexico hantavirus conference on November 20. Jahrling succeeded in growing virus that came from a New Mexico patient, and University of New Mexico collaborator Kurt Nolte made electron microscope photographs of the Four Corners virus budding from the membranes of monkey cells.
25
At the same time, Schmaljohn succeeded in growing Four Corners virus that was extracted from a deer mouse trapped near the California mountain cabin of hantavirus victim Jeanne Messier. As was the case with Jahrling's isolate, the Schmaljohn virus grew on monkey Vero cells.
And the CDC team isolated the virus from a New Mexico deer mouse, also successfully growing the microbe on monkey cells.
Unfortunately, each group jostled for credit as “the first,” and considerable
tensions existed between the CDC and USAMRIID. Eventually they agreed to simultaneous publication of their work, sharing credit for the isolation and identification of the Four Corners virus.
Successful isolation of the virus opened up the next obvious phases of the effort: development of a vaccine and an easy screening test that could be used in rural medical clinics. Schmaljohn's team had already developed an experimental vaccine for the Seoul virus,
26
so there were reasonable grounds for optimism that a similar Four Corners vaccine could be created quickly.
Perhaps more important than an eventual vaccine or diagnostic test was the actual process whereby the collective scientific enterprise identified the cause of the mysterious disease and swiftly brought the epidemic to a halt. Though there were unfortunate tensions between the CDC and USAMRIID, and Navajos felt the sting of discrimination, the overall effort was noteworthy as a demonstration of two old principles of epidemic investigation and as an illustration of an exciting new principle.
The old, but often overlooked principles were simple. All “new” diseases must first be noticed by someone who has the insight and courage to sound an alarm and set in motion a thorough investigation. And once in place, investigations are best conducted in an atmosphere of candor and collectivity, rather than the secrecy, backbiting, rivalry, and mutual contempt that had unfortunately characterized many other scientific pursuits of emerging microbes.
The novel discovery—one that is sure to permanently change the course of emerging microbe and epidemic research—was the utility of molecular biology and, in particular, PCR. Just as police work was forever changed by the discovery that all human beings have unique fingerprints that can be “lifted” from weapons and other objects found at the scene of a crime, so PCR provided a revolutionary tool that, for the first time, put the laboratory scientists in the driver's seat in an epidemic investigation. Before the CDC animal catchers even set foot in the Four Corners area, Stuart Nichol had been able to use USAMRIID genetic primers for various hantaviruses to rapidly screen human samples shipped to Atlanta by the New Mexico authorities. That would have been impossible twelve years earlier, when the AIDS virus made its appearance.
The hantavirus investigation of 1993 proved that things could be done right, that humanity could comprehend and control the microbes, if there was the political and scientific will.
At the beginning of 1994, the CDC reported that a total of fifty-five hantavirus ARDS cases had been confirmed in sixteen of the United States. Thirty-two of the infected individuals had died. And one of the newly confirmed cases occurred in Florida—an area that was definitely bereft of
P. maniculatus
deer mice.
27
Days later the CDC and the states of Rhode Island and New York announced the death of David Rosenberg, a twenty-year-old student at the Rhode Island School of Design in Providence.
Though Rosenberg died of ARDS in a Providence hospital, he had spent the weeks prior to taking ill with his parents on Long Island, and making a student film in his father's abandoned warehouse in Queens. Investigations revealed that one worker in the Rosenberg family electrical supplies factory, located near the warehouse, had developed antibodies to hantaviruses, and Rosenberg was infected with a virus that closely resembled the Four Corners strain. No infected animals were retrieved, but investigations were hampered by an unusually harsh winter that brought seventeen major snowstorms in New York, driving rodents into hiding.
28
In January 1994 the strange new microbe was officially named Muerto Canyon, after the valley inside the Navajo Nation in which the Four Corners virus first appeared.
Muerto Canyon—Valley of Death.
Nature and Homo sapiens
SEAL PLAGUE, CHOLERA, GLOBAL WARMING, BIODIVERSITY, AND THE MICROBIAL SOUP
 
It is hard to gain historical perspective on an event that is completely unlike any other we have seen before.
—Al Gore,
Earth in the Balance,
1992
 
 
That humanity had grossly underestimated the microbes was no longer, as the world approached the twenty-first century, a matter of doubt. The microbes were winning. The debate centered not on whether
Homo sapiens
was increasingly challenged by microscopic competitors for domination of the planet; rather, arguments among scientists focused on the whys, hows, and whens of an acknowledged threat.
It was the virologists, and one exceptional bacteriologist, who started the debate in 1989, but they were quickly joined by scientists and physicians representing fields as diverse as entomology, pediatric infectious disease, marine mammal biology, atmospheric chemistry, and nucleic genetics. Separated by enormous linguistic and perceptual gulfs, the researchers sought a common language and lens through which they could collectively analyze and interpret microbial events.
There had never really been a discipline of medical microbial ecology, though some exceptional scientists had, over the years, tried to frame disease and environmental issues in a manner that embraced the full range of events at the microscopic level. It was far less difficult to study ecology at the level of human interaction—the plainly visible.
There were certainly lessons to be drawn from the study of classical ecology and environmental science. Experts in those fields had, by the 1980s, declared that a crisis was afoot spanning virtually all tiers of earth's macroenvironment, from the naked mole rats that foraged beneath the earth to the planet's protective ozone layer. The extraordinary, rapid growth of the
Homo sapiens
population, coupled with its voracious appetite for planetary dominance and resource consumption, had put every measurable biological and chemical system on earth in a state of imbalance.
Extinctions, toxic chemicals, greater background levels of nuclear and
ionizing radiation, ultraviolet-light penetration of the atmosphere, global warming, wholesale devastations of ecospheres—these were the changes of which ecologists spoke as the world approached the twenty-first century. With nearly 6 billion human beings already crowded onto a planet in 1994 that had been occupied by fewer than 1.5 billion a century earlier, something had to give. That “something” was Nature—all observable biological systems other than
Homo sapiens
and their domesticated fellow animals. So rapid and seemingly unchallenged was human population growth, the World Bank predicted that nearly three times more
Homo sapiens
, on the order of 11 to 14.5 billion, would be crowded onto the planet's surface by 2050. Some high-end United Nations estimates forecast that more than 9 billion human beings would be crammed together on earth as early as 2025.
The United Nations Population Fund spoke of an “optimistic” forecast in which the planet's
Homo sapiens
population “stabilized” at 9 billion by the middle of the twenty-first century.
1
But it was hard to imagine what kind of stability—or, more likely,
instability
—the world would then face, particularly given that the bulk of that human population growth would be in the poorest nations on earth. By the 1990s it was already obvious that the countries that were experiencing the most radical population growths were also those confronting the most rapid environmental degradations and worst scales of human suffering.
2
Biologists were appalled. Like archivists frantic to salvage documents for the sake of history, ecologists scrambled madly through the planet's most obscure ecospheres to discover, name, and catalogue as much flora and fauna as possible—before it ceased to exist. All over the world humans, driven by needs that ranged from the search for wood with which to heat their stoves to the desire for exotic locales for golf courses, were encroaching into ecological niches that hadn't previously been significant parts of the
Homo sapiens
habitat. No place, by 1994, was too remote, exotic, or severe for intrepid adventurers, tourists, and developers.
At Harvard University, Dr. E. O. Wilson was one of the leaders of a worldwide effort to catalogue the world's species and protect as much of the planet's biodiversity as possible. He estimated that there were 1.4 million known species of terrestrial flora, fauna, and microorganisms on earth in 1992, and perhaps as many as 98.6 million yet to be identified. The vast majority of those unknown plants and creatures, he argued, were living in the world's rain forests.
3
There the plentiful supply of rain, tropical sunlight, and nutrient-rich soil bred such striking diversity that Wilson found 43 different
species
of ants living on a single tree in the Amazon.
4
Devoted biologists were literally risking their lives in a mad rush to identify the missing 10 to 98.6 million species, some 50 percent of which were thought to reside in the rain forests of Amazonia, Central Africa, and South Asia.
The pace of the loss was staggering—on the order, by UN estimates, of 4.75 million acres annually.
5
Whether supplying the highly profitable heroin and cocaine markets, which in the Andes was responsible for devastation of upward of 90 percent of the Colombian forest and only slightly less alarming percentages of the forests of Ecuador, Peru, and Bolivia, the fast-food beef consumption habits, or the coffee needs of the wealthy world, entrepreneurs of the developing nations were responding to all too present economic incentives when they destroyed their natural ecologies.
6
Without competing economic incentives for protecting the ecospheres it seemed unrealistic to expect that local human beings would take meaningful steps to reverse or slow the pell-mell pace of deforestation.
7
Using Landsat satellite imagery that was enhanced to reflect geographic features that might be hidden in flat photographs, David Skole and Compton Tucker, of the University of New Hampshire and NASA's Goddard Space Flight Center, made computer estimates of destruction in the Amazon between 1978 and 1988. Six percent of the Amazon's upper canopy and 15 percent of its total forest mass had, they concluded, effectively been destroyed.
Though it was well known to biologists that tiny isolated pockets of dense vegetation surrounded by devastation couldn't support a diverse range of species, none of the prior ecosphere calculations had factored for such islets of forestry. When Skole and Tucker studied the Amazon, however, they realized that many areas looked like a checkerboard, with slashes and zigs and zags of devastation slicing the rain forest into ever-thinner islets bordered by constantly thickening swaths of desertification or development. Humanity didn't nibble into the forest from its edges; it built huge superhighways that plunged into the pristine center and side roads that bisected one subsection after another.
So, the two scientists concluded, about 15,000 square kilometers of Amazonia were being directly destroyed by human beings every year, but another 38,000 square kilometers were indirectly destroyed annually by the isolation and fragmentation process.
8
That combined effect represented an annual forest loss of an area larger than the United Kingdom of Great Britain and Northern Ireland. It also implied that between 1978 and 1988 Amazonia effectively lost 15 percent of its productive forest.
When ecospheres were so severely stressed, certain species of flora and fauna that were best suited to adapt to the changed conditions would quickly dominate, often at the expense of less flexible competitors. The net result would be a marked decline in diversity. This could clearly be visualized when, for example, a tropical area was cut to make way for a golf course. Though the golf course was comprised of flora and fauna, its range of diversity was strictly controlled by human beings. At the course's periphery Nature would constantly try to push its way back in, but the aggressive species were usually limited to the healthiest plants and animals. If humans ceased trying to control the golf course, those sturdy aggressor species
would swiftly move in, but it would be years before the original scope of diversity would be restored—if ever.
Both deforestation and reforestation could, therefore, give rise to microbial emergence. If an ecology had been entirely devastated, and its eventual replacement species were of inadequate diversity to ensure a proper balance among the flora, fauna, and microbes, new disease phenomena might emerge.
Such was the case in 1975–76 in the Atlantic seaside town of Lyme, Connecticut. Like many New England coastal communities that dated back to the colonial era, Lyme was a quaint town of two-hundred-year-old buildings, birch trees, and homes interspersed with pockets of picturesque pastoral scenery.
During the mid-1970s fifty-one residents of the town came down with what looked like rheumatoid arthritis. The ailment, dubbed Lyme disease, would by 1990 have surfaced in all 50 states and parts of Western Europe. Though scattered reports of Lyme would emanate from states with ecologies as disparate as those of Alaska and Hawaii, more than 90 percent of all cases were reported out of coastal and rural areas between Long Island, New York, and Maine. New York would, by 1988, lead the world in Lyme diagnoses with 6.09 cases per 100,000 adults, and reported cases from the northeastern states would double every year between 1982 and 1990.
9
The typical Lyme disease patient suffered localized skin reddenings that were indicative of insect bites, followed days to months later by skin lesions, meningitis, progressive muscular and joint pain, and arthritic symptoms. Untreated, the ailment could be lifelong, leading to a range of neurological disorders, amnesia, behavioral changes, serious pain syndromes in the bones and muscles, even fatal heart disease or respiratory failure.
10
Once physicians learned of Lyme, the disease was undoubtedly overdiagnosed in endemic areas of the Northeast,
11
but there remained a clear upward trend in the United States in bona fide cases, and by 1992 Lyme was the most reported vector-borne disease in the country.
Most Lyme sufferers lived in wooded areas that were inhabited by common North American feral animals: deer, squirrels, chipmunks, and the like. Notably absent in these untroubled, quiet woods were the ancient predators, such as wolves, cougars, and coyotes. Keeping deer and small mammal populations in check had, in fact, become a major headache for affluent wooded communities all over North America.
In 1982, Dr. Allen Steere of Tufts University in Boston discovered that Lyme patients were infected with a previously little-studied spirochete bacterium,
Borrelia burgdorferi
.
12
Subsequently he and other physicians showed that many of the dreadful symptoms of the disease were the result of the immune system's protracted battles with the microbe.
13
Scientists soon determined that the
Borrelia
bacteria were transmitted to people by a tick,
Ixodes dammini.
While the tick was happy to feed on
Homo sapiens
, its preferred lunch was deer blood, specifically that of the white-tailed deer then common to the North American woods. About 80 percent of all North American cases were linked to either residing in a deer habitat or hiking through such an area.
14
Harvard's Andy Spielman showed, however, that getting rid of the deer in a region didn't eliminate Lyme disease. While the incidence of the disease among human beings might decline, it didn't go away. Further, there was a seasonal periodicity to Lyme outbreaks that coincided with the life cycle of the
I. dammini
tick, but not necessarily with that of the deer.
15
Spielman and his lab staff figured out that the ubiquitous northeastern mouse
Peromyscus leucopus
was the natural reservoir for the
B. burgdorferi
bacterium that caused Lyme disease. The immature ticks lived on the mice and fed on the rodents' blood. The mice, which were harmlessly infected with the bacteria, passed their
B. burgdorferi
on to the ticks. As spring approached, the winter thaw each year witnessed surges in the populations of both the
P. leucopus
mice and their tick passengers. The two species, rodent and insect, shared the ecology of low scrub brush that grew along the sand-duned shores and woodlands of the American Northeast. The deer grazed through these areas, picking up
I. dammini
ticks, which, while feeding on deer blood, passed on the bacteria.

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