The Coming Plague

by Laurie Garrett

  The lesson of macroecology was that no species, stream, air space, or bit of soil was insignificant; all life forms and chemical systems on earth were intertwined in complex, often invisible ways. The loss of any “rivet”—even a seemingly obscure one—might imperil the physical integrity of the entire “plane.”

  The “plane,” in the Ehrlichs’ scenario, was destined to crash. What hadn’t been anticipated was that the plane would first get sick, heavily encumbered by emerging pathogenic microbes.

  In 1987, Siberian fishermen and hunters working around Lake Baikal noticed large numbers of dead seals (Phoca sibirica) washing up along the shores of the huge Central Asian lake. By year’s end, the seal death toll would top 20,000, or nearly 70 percent of the entire population. The world’s deepest lake—a mile deep—was a unique 12,000-square-mile ecosphere inhabited by a number of species of flora and fauna found nowhere else in the world, including the dark gray freshwater seals. Because the Soviet government had long used the country’s lakes as waste dumps, it was first assumed that the seals were victims of some toxic chemicals.

  But with the spring thaw of 1988 came an apparent epidemic of miscarriages among female harbor seals (P. vitulina) in the North Sea along the coasts of Sweden and Denmark. Some 100 spontaneously aborted seal pups were recovered, a few of which survived long enough for scientists to study their symptoms: lethargy, breathing difficulties, nasal congestion.23 A quick-and-dirty analysis of the pups’ blood revealed that the dying and dead seals had antibodies that reacted weakly in laboratory tests against canine distemper viruses.

  With the arrival of summer 1988 came hundreds of dead adult seals in the North Sea area. They washed up upon shores separated by huge expanses of land and sea, from the western Baltic Sea area of Sweden and Denmark to the far west coast of Scotland. By August dead seals were even found scattered along the beaches of northern Ireland.

  In laboratories in the Netherlands, Ireland, Russia, and the United States, scientists swiftly determined that the seals were dying from a morbillivirus—the same class that included human measles, cattle rinderpest virus, and canine distemper. The die-offs continued well into 1990, eventually claiming more than 17,000 North Sea harbor seals, or more than 60 percent of the entire population.

  Scientists working in laboratories from Atlanta to Irkutsk swiftly determined that two different viruses were responsible for what seemed to be separate seal epidemics in Lake Baikal and the North Sea. The virus isolated from the massively infected lungs of Lake Baikal’s seals was dubbed phocine distemper virus-2 (PDV-2), and it proved virtually identical to canine distemper virus.

  The North Sea seals, however, were suffering from something never before seen. Their microbial assailant, named phocine distemper virus-1 (PDV-1), was distinct from any other known morbillivirus. It appeared to be something new, and the extraordinary death rates among harbor seals indicated that their immune systems had never previously encountered such a virus.

  While the seal experts worked on that puzzle, veterinarians in Spain were examining dolphins that were beaching themselves along the Mediterranean coast of Catalonia, Spain. By July 1990 more than 400 Mediterranean dolphins had washed onto the shores of North Africa, Spain, and France, clearly suffering respiratory distress. Autopsies of the animals revealed startling brain damage and acute immunodeficiencies. Similar signs of immune deficiency had already been documented in the North Sea seals, and accounts in the popular Spanish press were soon calling the mysterious marine mammal ailment “dolphin AIDS.”

  But it wasn’t AIDS—it was more like measles. Dolphins were also coming down with a deadly morbillivirus. By 1991 common dolphins (Delphinus delphis), striped dolphins (Stenella coeruleoalba), white-beaked dolphins (Lagenorhymchus albirostris), and porpoises (Phocoena phocoena) all over the Mediterranean and Ionian seas were dying.

  Dutch scientists determined that at least four newly discovered viruses were attacking Europe’s and Central Asia’s marine mammals: PDV-1, which was similar to human measles; PDV-2, which appeared to be identical to the virus that caused distemper in dogs; and PMV or porpoise morbillivirus, and DMV, or dolphin morbillivirus.

  Russian scientists discovered a possible explanation for the Lake Baikal epidemic of PDV-2. It seemed that an epidemic of distemper swept through the Siberian sled dog population in 1986; local people threw their dead dogs into the lake. Curious seals that investigated the large corpses became infected. In the Siberian case, then, the virus was not new to the world, though it was new to the freshwater seal species. The extraordinary death toll was the result of a microbe jumping from an ancient host species into a new, immunologically vulnerable species.

  While the PDV-2 puzzle appeared to have been solved, mystery continued to shroud the origins of PDV-1, DMV, and PMV. Where did the viruses come from? How did they spread so rapidly over such a broad geographic area? Were they old viruses with newfound mutant virulence? Or were the animals particularly vulnerable because of other factors?

  Spanish researchers were convinced that PCB pollution of European seas played a key role. All the dolphins they autopsied had high levels of PCBs stored in their body fat; some showed signs of PCB-induced tumors. So one hypothesis was that seals and dolphins that inhabited particularly contaminated waters were already immune-deficient when the virus appeared, making them uniquely vulnerable. Such an explanation might resolve questions about why Canadian seals, though infected with PDV-1, apparently hadn’t fallen ill, while their cousins living in polluted North Sea and Baltic waters, had. But still unanswered was the origin of the viruses.

  By 1993 the dolphin and porpoise die-offs had slowed considerably, and many scientists felt that the epidemic might be over. But why?

  A key difference between 1988–90 and 1993 was the severity of Europe’s winter. In the Mediterranean, in particular, the earlier winters were remarkably mild, which meant that small fish populations in the region were unusually low. Spanish researchers examined some 500 dolphin corpses, and concluded that all the animals were unusually skinny and their livers were severely damaged. The scientists decided that PCBs, which are normally stored in human and animal body fat, had flooded the dolphins’ livers as the starving animals burned up stored body fat. That, in turn, led to high blood levels of the toxic chemicals and mild immune deficiency. The virus subsequently exploited the dolphins’ vulnerability.

  By the close of 1990 at least 1,000 Mediterranean and Ionian dolphins had succumbed.

  The morbillivirus mystery deepened still further when bottlenose dolphins, beluga whales, Atlantic harbor seals, and porpoises were washed ashore on beaches stretching from the Gulf of Mexico to Quebec’s St. Lawrence Seaway. Those that were discovered alive often appeared dazed and distressed, as if suffering brain damage or high fevers.

  Again, scientists looked for viral and pollution explanations, finding a confluence of factors at play. As had been the case with European sea mammals, the North American die-offs came during unusual weather. An El Niño weather pattern gave rise to extraordinary rainfall in the Midwest, which led to high levels of pesticide, pollutant, and human and livestock fecal waste runoff into the Mississippi and other major arteries. That waste made its way to the Gulf of Mexico, where some of the first bottlenose die-offs occurred. The polluted waters moved through the Gulf, up the Florida coastline to the Carolinas, where more marine mammal die-offs ensued. From there, the water mass wended its way along the coasts of New Jersey, New York’s Long Island, Massachusetts, Maine, the St. Lawrence Seaway, and Nova Scotia, everywhere claiming a toll.

  Debates about what factors in that water led to the die-offs raged well into 1993. PCBs and other chlorinated hydrocarbon toxic chemicals were in the river runoff water, but few scientists believed the chemicals were directly responsible; many accepted the notion that chemically induced immunodeficiency served to aggr
avate some other underlying cause of disease in the dolphins, seals, whales, and porpoises.24

  Off the Carolinas scientists discovered massive colonies of algae of the species Ptychodiscus brevis that secreted a powerful neurotoxin called brevetoxin. They hypothesized that the unusual weather, coupled with high levels of nitrogen-rich human and livestock fecal matter, had led to the formation of huge “red tides,” or algal blooms, that contained such toxic algae.

  It was a tempting explanation, not only for the situation in the Americas but also for the European epidemic. Whether the animals were killed directly by some species of algae or indirectly by morbilliviruses that were spread around the world by hiding inside such algae, it would no longer appear terribly mysterious that seals in the Ionian Sea, Mediterranean, Baltic, North Sea, Gulf of Mexico, and off the shores of Long Island should all experience lethal epidemics at roughly the same time and under similar climatic conditions.25

  For more than two decades biologist Rita Colwell of the University of Maryland had been amassing evidence that bacteria and viruses lurked inside algae, and by the late 1980s other scientists were not only acknowledging the tremendous body of evidence but also correlating her algal findings with disease outbreaks in marine life and humans. Colwell knew that hundreds—perhaps thousands—of species of predatory algae were capable of secreting toxins designed to kill or paralyze their larger marine prey, allowing groups of the microscopic beings time to consume their conquest at leisure.

  Algae were the oldest living species on earth, thought to have developed out of the planet’s primordial soup more than three billion years ago. As creatures they resembled protozoa, but their use of chlorophyll to convert the sun’s energy into useful chemicals made them, technically, plants. Algae clustered in both fresh and salt water, sometimes forming visible discolorations and “tides” on the surface. Three broad categories of algae were designated on the basis of their colors, which, in turn, reflected the nature of their internal chemistry: blue-green, red, and brown.

  Algae could, during times of environmental stress or food shortages, encyst themselves in a protective coating, go dormant, and drop into hiding for extended periods. Once activated, however, algae needed sunlight and plenty of nitrogen. Most species preferred warmer waters, and under ideal conditions could multiply rapidly, drifting about in massive colonies that, in the case of oceanic red or brown tides, could span surface distances larger than Greater Los Angeles.

  Just as E. O. Wilson speculated about the tremendous numbers of terrestrial species of all sizes that had yet to be discovered in the earth’s rain forests, Colwell was concerned about the mysteries of the planet’s marine world.

  “Of the some 5,000 species of viruses known to exist in the world, we’ve characterized less than four percent of them,” Colwell said. “We’ve only characterized 2,000 bacterial species, most of them terrestrial. That’s about 2,000 of an estimated 300,000 to one million thought to exist. Less than one percent of all ocean bacteria have been characterized.”26

  Colwell had devoted years to the study of microorganisms living in Maryland’s Chesapeake Bay, where she discovered that viruses were seasonal: they reached their nadir in population during the icy months of January, when there were about ten thousand viruses per milliliter of water, and increased steadily in numbers as the bay warmed. By October, after three hot summer months, there were as many as a billion per milliliter, and the viruses outnumbered algae and bacteria. Even more profound variation in viral populations was seen in the waters of Norway’s fjords, and Norwegian researchers were convinced that viruses passed genetic material on to algae to assist in their adaptation to change.27

  In Colwell’s Chesapeake some of the swollen summer viral population was indigenous to the bay, having simply multiplied in number as the water warmed. But increasingly over her more than thirty years of studying the Chesapeake, Colwell saw viral intrusion occurring, as human and animal waste washed into the bay, carrying with it a variety of pathogens. The greatest density of intrusion was around dump and sewage sites, where Colwell found veritable stews of viruses, plasmids, transposons, and bacteria intermingling.

  “The probability of genetic exchange is very great,” Colwell said. Indeed, lab studies had shown that some ocean bacteria possessed antibiotic-resistance genes, presumably acquired under just such conditions. Those newly antibiotic-resistant bacteria were, in turn, ingested by various mollusks and then eaten by sea mammals and humans. The mollusks and crustaceans—from scallops to lobsters—readily ingested all manner of microorganisms found along the world’s polluted coastlines, including a host of enteric human pathogens.28

  “We have very few places left on earth where we can get pathogen-free mollusks,” Colwell said.

  Hepatitis, Norwalk virus, polio, and a host of other microbes were turning up in shellfish caught in the world’s coastal waters, particularly around waste dump sites. And strange microbes appeared that burned through the shells of mollusks, killed off salmon, and made lobsters lose their sense of direction.

  By one calculation a single gram of typical human feces contained one billion viruses. And in a liter of raw human waste there were more than 100,000 infectious viruses—none of which were vulnerable to mere chlorine treatment. Chlorine might eliminate the bacteria—though increasing chlorine resistance in bacterial populations was rendering such chemical sanitation insufficient—but viral elimination required more extensive filtration and tertiary treatment.29

  Ocean pollution due to raw sewage, fertilizers, pesticides, and other chemical waste was increasing steadily, producing tremendous changes in coastal marine ecospheres. Though the World Bank and the United Nations had designated sewage and sanitation systems a top priority for development during the 1980s, it was estimated that at least two billion Homo sapiens had no access to a sanitary fecal waste disposal system, most of them residents of Africa and southern Asia.30 Their fecal waste, as well as that of their domestic animals, ended up in nearby rivers, streams, and seas.

  Algal blooms, as a result, increased in frequency and size worldwide throughout the four post-World War II decades. The nutrient supply provided by steady flows of fecal matter, garbage, fertilizers, silt, and agricultural runoff gave the algae plenty of food. Many scientists thought that the thinning ozone layer warmed the sea surfaces to temperatures suitable for microbial growth and reproduction. Algal blooms grew so rapidly on the surface of lakes, ponds, and the open sea that they actually blocked all oxygen and sunlight for the creatures swimming below, literally suffocating fish, marine plants, and mollusks. And some scientists believed there was evidence that the additional load of ultraviolet light making its way through the ozone layer was driving a higher mutation rate in sea surface organisms, possibly allowing for more rapid rates of adaptive evolution. If such a mechanism were in effect, it would favor microorganisms, which, on a population basis, were well positioned to make use of helpful mutations and tolerate individual die-offs due to disastrous mutations. The reverse would be the case for more complex marine creatures, such as fish, whales, and dolphins.

  “The oceans have become nothing but giant cesspools,” declared oceanographer Patricia Tester, “and you know what happens when you heat up a cesspool.”31

  Jan Post, a marine biologist at the World Bank, used a similar metaphor when announcing the release of the Bank’s 1993 report on the condition of the seas: “The ocean today has become an overexploited resource and mankind’s ultimate cesspool, the last destination for all pollution.”32

  Tester, who worked for the U.S. National Marine Fisheries Service in Beaufort, North Carolina, had been monitoring weather patterns and algal blooms. She was one of many oceanographers who noted that the die-offs of dolphins, seals, porpoises, and whales during 1987–92 coincided with massive algal-induced bleaching of coral r
eefs worldwide and enormous red tides. She felt that there was compelling evidence for not only increased frequency and size of algal blooms but also their territorial expansion into latitudes of the seas formerly considered too cold for such algal growth. Using satellites to track the algal blooms, scientists documented increases—in some cases doublings—in size and scope of algal blooms during the 1980s and early 1990s.33

  Meanwhile, the overall diversity of the marine ecosphere was declining at a dramatic rate. With more than 95 percent of all marine life adapted to coastal regions, their susceptibility was high: human interference in the form of coastal development, sewage, and fishing was claiming a huge toll. U.S. Fish and Wildlife Service biologist Kenneth Sherman calculated that biomass production off the shores of New England, for example, had declined by more than 50 percent between 1940 and 1990 due, primarily, to overfishing.34

  A feedback loop of oceanic imbalance was thus in place. As the populations of plankton/algae eaters—whales, for example—declined, only the viruses remained to keep blooms in check. But raising the sizes of viral populations in the world’s saline soup held out other dangers to marine and, ultimately, human health.

  Rita Colwell was convinced that the entire oceanic crisis was already directly imperiling human health by permitting the emergences of cholera epidemics. During the 1970s she showed that the tiny resilient cholera vibrio could live inside of algae, resting encysted in a dormant state for weeks, months, perhaps even years. Colwell, a gritty, energetic woman, fought hard for years to convince the world’s public health establishment that the key to forecasting emergence of cholera lay in tracking algal blooms that drifted from the shores of Bangladesh and India, key endemic sites for the microbe.

  “But the bloody stupid physicians have this idée fixe that cholera is only directly transmitted, from person to person,” Colwell said. “They just couldn’t wrap their minds around the concept of microbial ecology. They fight me tooth and nail at every turn.”