The Next Species: The Future of Evolution in the Aftermath of Man

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The Next Species: The Future of Evolution in the Aftermath of Man Page 10

by Michael Tennesen


  The risk of disease outbreak grows when we disturb natural habitats and reduce the biodiversity of the land. “Bushmeat hunting is clearly responsible for the initial outbreaks of HIV/AIDS, Ebola, and many other viruses,” Ostfeld told me. As animal numbers go down, the animals that are left harbor the most disease. “The principles seem the same: the best wildlife reservoirs for the pathogen are also the species that thrive when biodiversity is lost.”

  The risk of a number of these horrible killer diseases, including Ebola, severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and others, are linked to environmental destruction. Ostfeld studies Lyme disease, for which New England rodent populations are a critical part of the disease cycle, just as they are in monkey pox, hantavirus, and tick-borne encephalitis.

  “Thirty years ago, these diseases were absent from our landscape,” said Ostfeld. “Now they are established and spreading. When humans fragment the habitat and reduce species diversity, the probability of catching these diseases increases.” He believes that studying the ecosystem of these diseases can give us better insights to the ecosystems of others.

  A broader range of different animal species means that the effects of the disease are spread out and diluted. With more animal species there are more hosts for the disease, and some of the hosts are going to be less effective at passing the disease on, thus diluting its total effect. Biodiversity also allows for more predators, and that can reduce disease host populations.

  With respect to controlling critical outbreaks, Ostfeld thinks that scientists sometimes rush to judgment and make inappropriate decisions. He cites the response to SARS, a serious form of pneumonia, as a typical misguided counterattack against an infectious disease. In 2003, WHO physician Carlo Urbani first identified SARS in a forty-eight-year-old businessman who had traveled from China to Vietnam by way of Hong Kong. The disease had started in China’s Guangdong Province and spread from there. The businessman was admitted to the French hospital in Hanoi, worsened, and died. Dr. Urbani died from the disease just weeks after he helped to identify it and warned the world of its dangers. SARS infected more than eight thousand people and killed 774 around the world before it was brought under control.

  When SARS first broke out, scientists quickly identified it as a virus probably transmitted to humans through an animal. Researchers from the University of Hong Kong examined twenty-five animals from eight species in a live animal market in southern China, and found a SARS-like virus in all six civets they sampled, as well as in a badger and a raccoon. A civet is a small, catlike animal native to the tropical forests of Asia and Africa. It has a pointed snout like an otter. The term “civet” applies to over a dozen different mammal species.

  Authorities quickly rounded up and destroyed all the civets sold in these markets. Ostfeld told me, “Civets weren’t the real culprit; it was fruit bats. The bats may have contaminated an area used by civets with bat urine and feces, much like a dog would, but it is highly unlikely the civets were the source of transmission to humans.” Two different studies of SARS confirm that bats were the real reservoir of the disease.

  Another example of misidentification occurred when health authorities went after bovine tuberculosis, an illness that affects cattle and is a tremendous financial risk to meat and milk producers. Health authorities found that one of the ways for cattle to get exposed is through contact with badgers. In Europe and the UK, studies show that badgers are the natural reservoir. So officials started killing badgers. “Only they found that badgers are an intensely social animal that stay together,” says Ostfeld. “But if you disrupt their environment, they will disperse, start to run around more, and in the long run increase exposure to cows.”

  According to Ostfeld, when a disease outbreak hits, first responders at government agencies are good at mobilizing quickly and figuring out what the pathogen is. But when they try to figure out where the disease comes from, they aren’t as capable. He thinks that it’s not enough to identify the most obvious players—the pathogen and a host or two. These may be only parts of a greater cast of characters. Without an understanding of the complete ecology of the disease, some health responses may enable a wider spread of the disease. Fruit bats are reservoirs of Hendra virus, an acute respiratory and neurologic disease found in horses and humans in Hendra, a suburb of Brisbane, Australia. And the response has been to go in and cut down the trees to drive out or kill the bats. But when bats don’t have enough to eat or are disturbed, their immune response lowers and they tend to shed a lot more virus. This is an example of the consequences we face when we change the natural landscape to fulfill a purpose different from the one for which it originally evolved.

  CRITICAL MASS AND CROWD DISEASES

  The advent of agriculture has disrupted the natural processes of evolution. As we discussed before, it changed life for man by increasing food production, but it also increased the presence of infectious disease. As man grew more food, he was able to have larger families, and with more people came more garbage and sewage. The increase in farm animals drew more rats and mice, creatures that brought a number of serious diseases, including typhus and the bubonic plague.

  It is widely understood that you need a certain number of people in close proximity for disease to spread. The critical mass—the point at which the disease achieves optimal virulence and transmissibility—for measles is a half million. Measles could not have raged in the days before agriculture, when man lived in small groups and hunted for a living. Chicken pox had an easier time making the transition from hunter to farmer, since its critical mass is only about a hundred.

  At first, infectious diseases were a much bigger problem for farmers than for hunter-gatherers. But slowly evolution selected for the farmers who had better immune responses to these outbreaks. These Old World immune responses were also passed on to city dwellers when the farmers went to more densely populated areas to sell their goods. All the while hunter-gatherers in the Americas and Africa developed fewer immune responses to what were basically crowd diseases; they didn’t have as many crowds.

  Some people in Africa even managed to develop immunities that protected them from malaria, which is not a crowd disease. It is transmitted among humans by female mosquitoes of the genus Anopheles during the blood meal they must take to produce eggs. While this may seem a blessing for people in Africa, immunity to malaria can come at great cost. One of the best known is sickle-cell anemia, which can itself be a very serious disease. About 250,000 children are born each year with this disease. Sickle-cell anemia is an inherited disorder in which red blood cells are abnormally shaped and may get stuck in blood vessels, making the delivery of oxygen throughout the body difficult. It is a chronic disease, though it can be treated. It strikes Africans more than others, though the trade-off is their immunity to falciparum malaria, a response that scientists have been trying to accomplish for hundreds of years. According to the World Health Organization, malaria in 2012 caused an estimated 627,000 deaths, mostly among African children.

  There were no vaccines available when Columbus and other explorers brought the Old and New Worlds together, and it was the New World that was the least prepared. American Indians as well as Australian aborigines, Polynesians, and many island populations had never encountered the strange crowd diseases that arrived with the Old World invaders, and against which the natives had few natural defenses.

  American Indians had migrated from Northeast Asia to the Americas about fifteen thousand years ago, before the advent of agriculture and crowd diseases. Thus they had no resistance, and the place they went to, the Americas, was so sparsely populated that they couldn’t grow immune to crowd diseases. These first American travelers had to pass through Siberia and Alaska to get to their destination, and they left behind tropical insect-borne diseases such as malaria.

  Michael Greger, MD, author of Bird Flu: A Virus of Our Own Hatching, believes that the real reason Old World diseases like smallpox never developed in the
Americas prior to the conquistadors was that there were far fewer domesticated animals in the New World. The last ice age and its hunters had knocked off most of the easily domesticated animals like American camels and horses, leaving the indigenous population to raise for food species such as llamas and guinea pigs, none of which were good carriers of lethal human diseases.

  The dramatic differences that these selection pressures brought to the table was evident when Old World explorers started coming into regular contact with New World natives. European diseases such as smallpox, whooping cough, measles, diphtheria, leprosy, and bubonic plague attacked the unprepared immune systems of American Indians, with devastating results.

  In the tropics, malaria and yellow fever joined the list of infectious agents, and native populations dropped by 90 percent or more, according to some estimates, in just a few centuries. Hernán Cortés conquered the Aztecs, and Francisco Pizarro conquered the Incas, aided by the introduction of Old World diseases.

  FOLLOWING THE EUROPEANS

  Disease followed Western Europeans into the Amazon as well. In 1542, Spanish explorer Francisco de Orellana and his men headed down the east face of the Andes and on to the Amazon River looking for El Dorado, the mythic “City of Gold.” His expedition found villages, towns, and well-developed societies with agriculture, ceremonies, and elaborate wooden structures. They reported passing twenty villages in one day, and one settlement that “stretched for five leagues”—a league being the distance a person or a horse could walk in one hour.

  Still, the lack of gold, the hostility of the tribes (who often greeted the Spanish boats with fusillades of poison arrows), and the treachery of the Amazon River itself left Orellana’s expedition in rags. By the time further explorations were mounted, the dense populations Orellana had witnessed were gone. Some five million people may have lived in the Amazon region in 1500, but by 1900 the population had fallen to one million and by the early 1980s it was less than two hundred thousand. Recent archaeological evidence supports Orellana’s accounts of dense populations. Scientists believe that disease, perhaps even arriving with Orellana’s expedition, spread throughout the Amazon, devastating ancient cultures as it had elsewhere.

  If American Indians had not succumbed to Old World epidemics, they would have been better able to adapt to European military strategies, and the going would have been far more difficult for the conquerors.

  This tendency to be felled by Old World diseases upon initial introduction continued in South America even into modern times. In 1967, a missionary’s two-year-old daughter came down with measles in a village of predominantly Yanomami Indians in Brazil near the northern border with Venezuela. Almost all of the 150 Indians, young and old, caught the disease and one in ten died, despite the desperate efforts of the missionaries.

  First contacts were often the most deadly, killing one-third to one-half of the native New World population in the first five years. In Brazil, of eight hundred Suruí Indians who were contacted in 1980, six hundred died by 1986, mostly from tuberculosis. As Charles Darwin said, “Wherever the European has trod, death seems to pursue the aborigine.”

  ON TO AFRICA

  However, when Western Europeans tried to conquer sub-Saharan Africa, disease went after the explorers, not the aborigines. Europe didn’t make serious attempts to explore Africa until the fifteenth century, about the same time they discovered America. The king of Portugal sent eight men, one of the first expeditions, up the Gambia River around 1500 but only one came back alive.

  Europeans bought slaves at coastal outposts or on offshore islands. Going deeper into the jungle posed too many dangers from native ambushes, poisonous snakes, and disease. British soldiers stationed on the Gold Coast might lose half their men in as little as a year. Arab or part-African slave traders seemed to be less susceptible. Mungo Park, a Scottish explorer, made his second attempt to explore Africa in 1805 with a party of forty-five Europeans. Only eleven still stood when they reached the Niger. Dr. David Livingstone, the famous Scottish medical missionary, lasted for a while but eventually fell to malaria, as did his wife.

  In the early twentieth century, quinine, a drug developed from the cinchona shrub of South America, became available as an antidote for malaria. At the same time efforts to control mosquitoes helped prevent the spread of this disease and yellow fever, as did efforts to control the tsetse fly, which caused sleeping sickness. With these potential killers held at bay, European countries ventured into Africa and quickly conquered almost the entire continent.

  Africa did not become another America. Europeans did not displace Africans. It seemed that in order for Europeans to take command, the locals had to die off, and Africans did not die off as American Indians did. Tropical diseases bested anything the Europeans brought with them. The Africans had some selective resistance to these diseases, whereas the Europeans had none.

  Resistance is particularly unreliable with new diseases. Back at the Cary Institute, biologist Rick Ostfeld stood in a New England forest with a white-footed mouse in his hand. Both Ostfeld and I were dressed in white coveralls with latex gloves. A very-much-alive mouse had been collected from a trap the previous night. Ostfeld ran his index finger through the mouse’s back fur, spotting several ticks attached to its skin. It was spring and the forest around us was thick with tall trees, bright green leaves, and lots of ticks. The biologist carefully pulled one of the ticks off the mouse and showed it to me. “If that tick bit you, you would have a 40 to 45 percent chance of catching Lyme disease,” he said. I stepped back.

  Ostfeld, a senior scientist at the institute—a calm, meticulous man whose broad shoulders attest to his weight lifting—has been studying Lyme disease here for twenty-four years. Dutchess County and four other mid–Hudson Valley counties have the nation’s highest rates of Lyme disease.

  Ostfeld and others at the Cary Institute are investigating the ecosystem surrounding Lyme disease, the West Nile virus, and similar diseases recently proliferating in the US that are transmitted by ticks and insects through their animal hosts. Recently they discovered that the black-legged ticks that spread Lyme disease could also infect people with Powassan virus encephalitis, which can cause central nervous system disruption, meningitis, and even death in 10 to 15 percent of reported cases. Adding to the problem is the fact that unlike Lyme disease and other ailments carried by black-legged ticks that take hours to transmit once a tick is attached to its victim, Powassan virus encephalitis and its variants can be transmitted in just fifteen minutes. This leaves very little “grace period” for removing ticks, and underscores the importance of vigilance when in tick habitats.

  Tick removal has become a critical activity of late for Northeastern outdoorsmen. Lyme disease was first reported in the United States in the town of Lyme, Connecticut, in 1975. “It reached a high of 30,841 reported cases in 2012,” says Ostfeld. “But the CDC [Centers for Disease Control] has recently estimated that reported cases represent only 10 percent of the actual number of cases, so it is likely that Lyme disease exceeds 300,000 cases per year.” Such statistics keep some hikers at home on the couch on weekends, a not-too-healthy alternative.

  Most cases occur in the Northeast and upper Midwest, but there have been many reported along the Pacific Coast and elsewhere. If diagnosed in the early stages, Lyme disease can be cured with antibiotics. It may start out feeling just like the flu, which is sometimes ignored by patients, but the results can be severe. Without treatment, the CDC claims it can affect joints, the heart, and the nervous system—causing pain, paralyzed facial muscles, and nerve damage in the arms and legs.

  In his laboratory at the Cary Institute, Ostfeld showed me a slide of the slender spiral-shaped bodies of Borrelia burgdorferi, the bacterium that causes Lyme disease and all its symptoms. Certain ticks carry the bacterium, though they aren’t born with it. They acquire it when they bite an infected mouse or chipmunk. Man acquires the disease when bitten by an infected tick.

  The black-legged tick (Ixodes sc
apularis) carries Lyme disease bacteria in these woods. It goes through three stages in its short two-year life span—as larvae, nymph, and then adult—with each period requiring at least one good blood meal before moving on to the next. It is during these blood meals that the ticks acquire the disease and pass it on.

  Ostfeld came to the Cary Institute in 1990 with a background in the behavior and evolutionary ecology of small mammals like voles, which undergo periodic, dramatic population swings. The biologist studied the disease, black-legged ticks, the ticks’ animal hosts, and the forest that surrounded them to see how all the players in this disease drama functioned together. Ostfeld and his colleagues soon realized that the booms and busts he witnessed in small mammals and in forests themselves could play an important role in the spread of infectious disease.

  The cycle may begin with an abundant crop of oak acorns in any year. Because acorns are a highly nutritious and long-lasting food source, they create an explosion of white-footed mice and eastern chipmunks in the following year. These small mammals are the preferred hosts of black-legged ticks. Still, the ticks must go through several phases before they start transmitting the disease to man, meaning the risk of Lyme disease is highest two years after plentiful acorns. It’s a complex system.

 

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