BITING FLIES, KISSING BUGS, AND SLEEPING SICKNESS
NOT ALL arthropods have cast their lots with the rodents. Some of them, the biting flies that carry parasites that cause sleeping sickness and kala-azar (leishmaniasis) among them, have gone upscale on the evolutionary ladder.
One of a family of diseases caused by a genus of slinky, willow-leaf-like blood parasites called trypanosomes, sleeping sickness is one of those African diseases that have perplexed and frightened people for many centuries. The parasites, members of a class of living things called Euglenozoa, are descended from some of the oldest living things with nuclei (eukaryotes). They are thought to be about 300 million years old, which takes us back to the Paleozoic era (roughly 543 to 248 million years ago), a world of swamps, explosions of a brilliant, exuberant diversity of all forms of animal life, and wandering supercontinents, when Africa and South America were still joined at the hip. The era ended catastrophically (at least in the unimaginably long lifetime of earth) with a breaking up and drifting apart of the continents and, one might suggest, an incontinent flood of species extinctions (as high as 90 percent). This early birth of the trypanosome species explains why there are different genuses, with different ecologies, but similar ancestries, in South America and Africa. I’ll come back to the South American one a bit later.
Tsetse flies, which (in Africa) now transmit the parasites from one tropically warm bloodstream to another, go back about 200 million years, to Mesozoic times (some 2 48 to 6 5 million years ago). That era gave us ferns, cycads, ginkgophytes, bennettitaleans, and other unusual plants, as well as conifers and angiosperms (a curious name, with etymological scents of blood vessels [angio] and male reproduction). Some with a more prosaic turn of phrase would call them flowering plants, which provide us with pretty well all the foods and many of the drugs we rely on. The era also gave us Jurassic Park and the oil deposits of the North Sea. Sadly, it also ended with a mass extinction, which took down not only the dinosaurs but also the ammonites, who I once fondly dreamed might have been the forebears to Mennonites, who begat me. Alas, not so. According to some sources, these marine mollusks succumbed on the Maastrichtian stage in, one would imagine, a dramatic fashion. The stage is named after the site in the Netherlands where chalk rocks typical of this era are found and where the Treaty on European Union was staged and signed in 1992, although it would be stretching credibility to argue for some sort of evolutionary connection here.
So both the parasites and the flies are survivors. We humans are newcomers on the scene, a mere 5 million or so years ago, and probably just picked up the parasite when we started farming and herding cattle in risky landscapes. For thousands of years, people and parasites lived in a kind of loose truce, people tending to avoid tsetse fly habitats and clearing brush from around their houses. Our written records of the flies (probably) go back to the Jewish prophet Isaiah of the early to mid-700s BC, who wrote: “In that day, the Lord will whistle for flies from the distant streams of Egypt . . . They will come and settle in the steep ravines and in the crevices in the rocks, on all the thorn bushes and at all the water holes” (Is. 7:18–19, New International Version). The image of this Old Testament YHWH whistling for flies, evoking, for me at least, a picture of an old, white-haired field biologist surrounded by a cloud of small insects, is not the one I was offered as a child.
The historian Ibn Khaldoun in 1406 reported not just on the annoying flies but also on the disease itself. There were reports from Mali that a king suffered two years of profound sleep on the throne (did no one notice?) before he finally died of the disease. Khaldoun apparently picked up this information from traders crossing the Sahara. Certain tribes in western Africa apparently had about fifty names for the disease, which, if one might draw a parallel to the many names for “snow” northerners are said to have, or names for “sand” among desert dwellers, indicates either very close familiarity with the disease or a culture where people have much idle time on their hands. Our scientific knowledge of the parasite increased rapidly in the nineteenth and early twentieth centuries, when it began to interfere with the slave trade and hindered European pillaging of Africa.
As one might imagine, the trypanosome ancestors probably evolved, much as people have, from free-living swimmers to parasites of non-human animals (about 5 million years ago).
Some subspecies only affect wildlife and domestic cattle. The Zulus named the animal disease “nagana,” meaning “a state of depressed spirits,” which pretty well sums it up. Two members of the species Trypanosoma brucei, however, can be shared between other animals and people. T. brucei gambiense generally lives in western Africa, and the disease it causes unfolds slowly and inexorably, a bit, perhaps, like nagana. This species of the parasite is fully adapted to, living in, and spreading between people and has shown no interest in returning to the wild. Other species only infect animals, which are of interest to veterinarians and as historical artifacts but not as zoonoses. For those interested in genealogy, the earliest trypanosomes were probably adapted to wildlife, in which many of them, to this day, seem to cause few problems. The zoonotic form (T. brucei rhodesiense) emerged later, probably in the Ionian (also known as the Middle Pleistocene) epoch, tens to hundreds of thousands of years ago. Still later (say, ten thousand years ago), the human-adapted form, T. brucei gambiense, emerged.
One member of this family of blood parasites, particularly relevant to our understanding of disease emergence, ecology, and our stumbling attempts to define a convivial niche for ourselves on the planet, is T. brucei rhodesiense. This one lives mostly in eastern and central Africa and causes acute fever, aches and pains, and general miserableness. The body’s immune system attacks the parasites, but these little guerrillas have complicated, multi‑ and mini-circles of DNA, including one thousand genes (which also mutate, creating more) coding for different surface coats. Just when the body thinks it has defeated them, they come back in different uniforms, and the battle starts again; the immune system is at first very active and later exhausted. Toward the end, the parasites slink their way across the blood-brain barrier into the king’s castle and start messing with people’s minds.
Classically, human sleeping sickness starts with a flu-like illness and proceeds through disrupted sleep patterns to the final sleep of an irreversible coma—hence the name—but psychoses and aggression are not unheard of, and patients have inadvertently ended up in prisons and mental hospitals. WHO has estimated that there are upward of 300,000 cases in people a year. In the region in eastern Uganda that I visited as part of a research team in 2001, about twelve thousand people had died since 1986.
This “Rhodesian” sleeping sickness can be carried around by a lot of different animals, including cattle, where it may stay cryptic or cause nagana. These trypanosomes are carried from animal to animal and to people by tsetse flies, which, like many sensible animals in the tropics, prefer to live in shady places, especially near waterways. The female fly, perhaps having been schooled by thrifty Scottish Presbyterians, breeds once and then, with almost obsessive thrift, saves the sperm and uses it as she needs it. I have no information about what must surely be the onanistic, lonely habits of the males. The female fly lays an egg every nine days in moist, loose ground, and the new flies emerge about three weeks later. This reproductive frugality flies in the face of the “reputed logic” of reckless child production systems, which have allowed humanity to fill and dominate the earth but are now threatening the whole wonderful biospheric experiment. The flies have been around for a lot longer than us, and we might reconsider our strategies.
Context, of course, is everything.
On May 28, 2000, the day before my fifty-second birthday, I was sitting on the deck at the home of Catherine Kenyatta, gregarious, gracious, cheerful granddaughter of Jomo Kenyatta, founder of modern Kenya, and her husband, Sean. We were in Mbale, eastern Uganda. A motley crew of researchers from Kenya, Canada, Zambia, England, Scotland, and Uganda, we were there to work with the Ugandans to try to understand, and control, the re-emergence of sleeping sickness in eastern Africa.
The view from where I nursed my beer was across the darkening shadow of the town to the foothills of Mount Elgon. I would say it was evening, but readers in temperate zones might confuse this with the slow draining of color that occurs at dusk. There, I could already sense the black pixels gathering under leaves, in the shadows of huts and palms. When they reached some critical point, the whole landscape would suddenly cascade into darkness. I wondered if this difference in the experience of diurnal change might explain the faith among many temperate zone scientists in gradually changing ecosystems (global warming degree by degree, increments of pollution, slowly rising chronic disease epidemics) and blinding them to the critical points, collapses, and sudden changes that characterize pretty well all the world’s ecosystems and may give us clues as to the behavior of twenty-first-century pandemics.
From a distance, the nearest hill rose up in red-gray-black cliffs to a plateau, waterfalls spraying down crevices, shaggy green tatters like carpets stuck precariously to the cliff faces. But views from a distance should not be confused with “broader views” and may be misleading; sometimes distance gives not perspective but fuzzy thinking.
That afternoon, veterinary epidemiologist John McDermott, geographer Barry Smit, and I had clambered up one of those steep slopes. Up close, every fold and wrinkle of the hillside was inhabited by villages and farms, kids, goats, men and women washing carrots in a stream. The green patches on the cliff faces were farmers’ fields. Barry, a Kiwi-cum-Canadian, aspiring sheep farmer, co-author of reports from the Intergovernmental Panel on Climate Change, does not suffer fools or idle activities gladly. Unlike me, he dislikes activities without a clear purpose. He therefore gave our walk a purpose, identifying an end (some caves high up on the slopes), and things to learn on the way (asking our guides all about the crops being grown).
I was at first annoyed at this intrusion into my non-doing, thoughtless, mind-clearing activity. I was soon captivated, however, as Barry asked again and again: What is this? Why are they growing that? In those scant, thin soils clinging to the rocks, farmers were growing: Irish potatoes (three kinds); yams (four kinds); sweet potatoes; cabbage; carrots; cassava; bananas (one kind for eating; another kind where the fruit was inedible but the sap from the stem was used for treating measles); plants to treat malaria and gonorrhea; peas; beans; pumpkins; leguminous trees; napier grass for erosion control, cattle feed, and mulching; eucalyptus for fuel and soil control; onions; coffee; and at least two kinds of trees near houses to serve as lightning rods. I was in awe of this managed complexity and the possibility for hope for our species that this human-modified landscape embodied.
Members of the Resilience Alliance use a lazy-eight, or infinity-sign, model to interrogate and explore the world. In this model, linked social-ecological systems move through natural phases of growth, conservation, creative destruction, and reorganization. According to the Resilience Alliance researchers, the systems we live in and are part of can recover from destruction such as fires and disease outbreaks if that destruction is localized, embedded in a larger, resilient system. The whole complex model has been called a “panarchy.” Through a variety of networks and feedback loops, the larger landscape within which the local areas are nested provides nutrients, genetic material, and energy for renewal. The larger system “learns” from the smaller outbreaks and in turn uses this learning to respond to other local outbreaks and fires elsewhere in the larger system. This learning is embodied not just in biological and genetic diversity but also in social and cultural diversity and in the links and communications that exist among these diverse elements. This idea of many small catastrophes embedded in a larger resilient set of systems is sometimes referred to as a shifting steady-state mosaic. Individuals die and families suffer, but the biosphere continues to make a home for our descendants. In a sense, the nature of which we are a part is a kind of flexible, responsive, diverse welfare state.
For farmers in the tropics, maintaining various diverse crops means that they can more easily adapt to changing market, social, and climate conditions around them. If some parts of the system crash (prices of certain crops, the crops themselves), there is enough redundancy of function in their collective agroecosystems that some of them will be okay most of the time, they can take care of each other, and, collectively, they can ride out the crash, learn from it, and keep going. Also, diverse ecosystems provide some protection against disease epidemics; if a variety of crops serving similar functions (providing food, healing, material for building) are grown, and a variety of animals, including those that eat insects, inhabit that agro-ecosystem, then bacteria, viruses, and parasites don’t have the equivalent of one of those all-you-can-eat “trough” restaurants that are so beloved by many Americans and that monocultures freely provide.
Although diversity protects against the spread of epidemics and pandemics, however, it can, in some circumstances (when people invade new territories, for instance), foster the emergence of new troublemaking microbes, as the stories of avian influenza, SARS-COV, and SARS-COV-2 demonstrate. The challenge is to find ways to foster diversity-related resilience without promoting diversity-related disease. It is possible, but it will require us to go well beyond the ecologically simplistic thinking embedded in the either-or mindsets of “progressive, scientific economies of scale” versus “old-fashioned, subsistence poverty.”
When we reached the end of our walk, up near the ridge of the mountain, we stepped into a cool, dank cave, once used by rebels during the time of Idi Amin. For a moment we stood there—John, Barry, the two guides, and I—bent over in the low dusk of the cave. Then, Barry’s clear tenor voice echoed around us, singing the haunting Righteous Brothers song “Unchained Melody.” We stood in silence, as if this were some kind of religious ritual, which, I supposed later, it was. Then we walked back down the mountain.
That night, I lay on my back and pondered the options available to the Ugandans—available to us, if I am to count myself as a fellow human being—for dealing with zoonotic sleeping sickness. Barry Smit, myself, and the others were here because John McDermott had put together an international research team to answer the question: “Links between sleeping sickness and natural resource endowments and use: what can communities do?” What indeed? I thought.
We could wait until people were sick and then treat them. But finding sick people early and treating them aggressively with toxic drugs is not a program with a high chance of success in central and eastern Africa. For one thing, this was not the plague, and the drug of choice was not some benign antibiotic, as it still is, in many places, for Yersinia pestis. Some suggested that the treatment for sleeping sickness felt like having an infusion of red-hot chili peppers. Médecins sans Frontières had enough trouble getting pharmaceutical companies to produce and provide the drugs and then putting them to use, against the much simpler problem of human-adapted gambiense sleeping sickness.
We could try to get rid of all the animals that are carrying the parasite. This had been tried before, both by people (as in game destruction) and by the unpredictable gods of history. In 1896, an epidemic of rinderpest, caused by a virus that is probably the ancestor of measles in people and distemper in dogs, swept through southern and eastern Africa, killing millions of cattle and big game. The parasites, in a small-is-beautiful move that presaged the economic philosophy of E.F. Schumacher, survived in the small, numerous, adaptable bushpigs and bushbucks, as well as spending more time among people.
We could spray massive amounts of pesticides to kill the flies or cut down all the shady places where the flies like to breed, but those strategies had already been tried. In the 1950s, before there were subjects like biology in school, both knapsack sprayers and airplanes were used. And clearing all the brush along streams is also a non-starter. Poor communities who live near rivers and depend on cattle and wildlife for food are not usually keen on destroying the places where they live in order to get rid of a disease.
The big outbreaks of sleeping sickness in the twentieth century happened during periods of social upheaval—the early and late years of Idi Amin’s terrible reign, for instance. In these times there was breakdown of health and agricultural infrastructure, along with widespread violence. During the fighting, people fled their homes; after the fighting, they returned, bringing with them cattle from southern, infected territories. When raiders from Sudan in the north rustled those cattle away, the people brought in more infected cattle.
Now, in the post-Amin years, Eric Fèvre, Lea Berrang Ford, and other members of our research team found that new areas were becoming infected as cattle were moved into them from the south. After entering a new area, the parasites and tsetse flies spread out along waterways and other fly-friendly habitats. Our big concern was that the rhodesiense parasite was moving into territory normally inhabited by the human-adapted gambiense, with complicated consequences for diagnoses and control. Could the epidemic be stopped? The diversity of the farms we had seen on the hillside reflected a newfound optimism among Ugandans, which was also expressed in a vibrant local democracy. This optimism, coupled with civic engagement, offered some hope for finally coming to terms with the old parasite.
Still, the disease presented itself as what is sometimes called a “smoldering” epidemic: the infection spread inexorably through the countryside, but clinical cases were always at a level low enough to stay just under the radar. On the one hand, a low number of cases seemed to offer an opportunity to eradicate the disease, at least from certain areas. On the other hand, for people resettling land and struggling to get past decades of war and destruction, a few cases here and there hardly provided motivation to mount major control programs. The old top-down approaches of technocrats telling locals what to do didn’t have much support; the people at the top didn’t have the money to sustain such a program, and the people on the ground had other things on their minds, and had had enough of others telling them what to do.
The day after our trek up the mountain, we piled into our vehicles and headed out past open fields north toward Soroti, catching glimpses of Lake Kyoga, and over rutted, dusty roads where weather-beaten villagers huddled next to burlap sacks of charcoal, to a group of mud and thatch huts gathered in the shade of a grove of trees. This was to be our medical research post for the day. We set up tables with centrifuges and blood collection tubes. Some of us interviewed farmers under a tree. Men from the village, joined by researchers, wrestled with the cows, checking ears and testicles for ticks (lots of them), taking tubes of blood from the jugular and sucking up a tiny bit from the ear into a glass capillary tube.
Women, men, children lined up under the trees, forming a winding line around the village, all to be questioned, examined by a nurse or doctor, and have blood taken. Cattle milled about in the shade of various trees in the vicinity. Children cried, cattle in heat clambered on to each other and tried to breed. One young cow chased a dog around and around, trying with its nose and tongue to determine the nature of this shy creature. Children stood in a circle around me as I did a second reading on hemoglobin color tests for the medical technologist. They were most fascinated when she injected blood from cows, suspected of being infected, into mice, where it could be kept alive for later molecular studies. The mice, held by the loose skin on their necks, looked open-mouthed with surprise.
Near lunch, in the heat of the day, I went out with three other fellows to hang traps for tsetse flies. We wandered down a sun-beaten path to the swampy area near the river, one of the spidery fingers of water draining into Lake Kyoga. The soft ground was crisscrossed with deep ruts, paths from people and animals looking for water. I wished I had my Tilley hat, and I carried the traps over my head for protection from the blistering sun. The traps are like tents, with white mesh at the peak and blue and black cloth at the base, since tsetse flies are attracted to black and dark shades of blue. Thus, there was some poignancy is seeing schoolkids wearing blue and black shorts and tops clearly made from fly-attracting traps, which underlined the urgency of engaging local populations in the enterprise, combining education with action.
When the flies reach the colored lower part of the trap, they fly up toward the light, through small holes, and into the top part, where they are trapped. We hung the traps from trees in shady areas, often near water. I didn’t pay much attention to the first water hole we came to, thinking it to be a dugout for cattle.
At the second or third dugout we visited, there were several women, bent over, letting the brown liquid burble into their bright canary-yellow jerry cans. I asked about the coffee-latte-colored water in the hole. Was this for drinking?
“Yes,” said the ten-year-old kid who was showing us around.
“Without boiling?”
He cleared away the flotsam and insects at the surface, scooped some water into his hand, and drank it. “But not for you,” he grinned. “You will get sick.”
The two other men with us, who were from outside the area, also said they would be sick if they drank that water. I thought of the people in Walkerton, Ontario, where thousands had been sickened in May 2000 by drinking “clear” tap water; several died. Pausing beside a termite mound six feet or more high, the boy grinned at me as he dug away with a stick, pointing out the big, angry termite guards that came out to challenge his intrusions. When fried, he assured me, they were excellent with sesame paste.
This is why I am here, I mused. A sense not so much of home, or of saving the world (although we would all like to do that, I suppose), but of camaraderie, of being on an incredible journey together, of being part of something wonderful, bigger than all of us, of trying to make a not-too-uncomfortable place for ourselves in the midst of the messy, complex, amazing world we live in. Of promoting health, defined by the late, great microbiologist René Dubos as “modus vivendi enabling imperfect [people] to achieve a rewarding and not too painful existence while they cope with an imperfect world.”
Returning from hanging the traps, we found that the others had already eaten lunch. I stood under a tree, wiping the sweat from my forehead, and drank a Coke. I recalled the Coca-Cola sign at the equator, when we had driven over from Kenya the previous week. I had thought then, and I thought now, that one of my motivations for being here was to provide a counterweight, to help people find an alternative story, to that of the ubiquitous Coca-Cola-type McEmpires. But out there in the sun, damn, was I thirsty.
On the evening of May 29, 2000, at the Sunrise Restaurant in Mbale, I looked around the table at our sunburned, disheveled group and reflected once more on the web of narratives and motives that had drawn us there. We looked over the menu, and someone asked what a White Russian was. I did not, then, recount my entire family history, the revolution, the civil war, the fleeing of wealthy farmers from Stalin’s bureaucratic utopia, that ultimate in top-down scientific technocratic solutions. But I did think then that my own personal story was part of this larger story, that every researcher is part of what he or she does research on, that sustainable health and development are all about finding a common journey and a Chaucerian story we can tell each other on the way. What passed my lips was something like, “Did you know that my parents fled from the Soviet Union in 1926? And now here I am in Uganda, on my birthday.”
The British epidemiologist Paul Coleman’s response to this statement was to order a round of White Russians, with the rule that I would have to finish the drinks of all those who didn’t. As a benediction, somewhat inebriated, fresh from a day in the field and beers at Catherine and Sean’s, emotional (I hesitate to call it maudlin, but perhaps it was), scrounging through my topsy-turvy mind for a succinct summing-up of this out-of-the-lab-and-into-the-world science, my mental and physical transports from Canada to Mbale, I could think of no better response to the complex history of sleeping sickness, and our challenge to come to some convivial, ecologically negotiated truce with it, than to recite the poem “Wild Geese,” by Mary Oliver, a wonderful evocation of wild geese flying overhead and their “harsh and exciting” message to us that we are all part of the same family.
TRYPANOSOMES IN THE Western Hemisphere took a somewhat different path to finding a home. Chagas disease, named after Carlos Chagas, one of the world’s great biomedical investigators, is a kind of distant cousin to African sleeping sickness. Caused by the parasite Trypanosoma cruzi, the disease is sometimes called American sleeping sickness, but that is a misnomer, since the disease it causes is nothing like African sleeping sickness. Technically, one could simply call it American trypanosomiasis. As you can imagine, after a few hundred million years of separation, the family resemblance has been somewhat diluted. Unlike its African cousins, this parasite does not cross the blood-brain barrier, so the disease has none of the manifestations associated with infection of the brain. Many people get infected, but not many become ill. In those who do succumb, the heart grows large and flabby, and it can’t effectively pump blood anymore. In another form of the disease, the intestines get large and flabby and food pools in the gut. In either case, the victim dies, slowly, painfully, over many years.
One Brazilian researcher, the late Philip Davis Marsden, described the disease as “retribution for colonizing the New World.” From Mexico south to Chile and Argentina, some 8 million people are thought to be infected. The CDC estimates that there are about 300,000 people infected with T. cruzi in the United States. Evidence from dried-out human mummies suggests that the parasite was already cycling among animals and bugs in southern Peru and northern Chile nine thousand years ago, waiting for more humans to come intruding. They did.
Although they behave differently, T. cruzi don’t look much different from other trypanosomes once they are in the human bloodstream. Swimming along like delicate tropical fish, the parasites undulate their way into various body cells, where they lose their tails and, like many new human home-owners, wreak their damage locally. Actual clinical disease associated with these parasites, though not common, may be acute or chronic and involve a wide range of organs, from the heart to the brain to the intestines. Until research-based control programs were instituted in the late twentieth and early twenty-first century, it was an important cause of sudden death from cardiomyopathy (pathology of the heart muscles) throughout Latin America, as well as causing a chronic ballooning of the intestines called megacolon.
From a medical-ecological point of view, there are various cycles of transmission, some restricted to non-human mammals (over a hundred species infected), some crossing into human populations, and some passing from person to person. The traditional means of transport for the trypanosomes is through what have been called “kissing bugs” of the triatomine family. These blood-feeding insects might be tens of millions of years old, but they have adapted well to human invasion of their territories. At night, they quietly emerge from the cracks and crevices where they live and “kiss” people, soundlessly, painlessly, looking for a blood meal, at the corners of their victims’ eyes or in small wounds or scratches. The bugs’ eyes are bigger than their stomachs, as my mother would have said, and they have to urinate a lot just to keep sucking in the blood. These bugs, not being hygienically fastidious, defecate where they eat. The parasite lives in the triatomine’s feces. Rubbing their eyes when they feel the tickle of the bug, people also rub the parasite into their blood. More than fifty species of triatomines can carry the parasite.
From a broader cultural point of view, this is a disease of global politics and power struggles between empires, from the Europeans and Incas several hundred years ago to the United States and Latin America today. Triatomine bugs originally lived (happily?) in free-living forest mammals in South and Central America. With deforestation, some bugs that were originally sylvatic (“wild,” as in Sylvester the cartoon cat) seem to have adapted to more open types of vegetation and have also developed a penchant for certain kinds of human dwellings, thus increasing the frequency of transmission of T. cruzi to humans.
These types of poorly constructed (for people, not bugs) dwellings, frequently found crowded into shantytowns, did not occur by mere chance. During the height of the cold war, the United States and the former Soviet Union fought their battles in many poor countries. While the Soviets were subjugating parts of Europe, in Latin America, the U.S. overthrew democratic governments and fought pitched and dirty battles against popular uprisings. These wars drove many people from the countryside to slums around major cities. In recent years, the move from the countryside to the city has been accelerated by neoliberal economic policies, which have tended to favor large, wealthy landowners and to drive peasants into forest areas (and the T. cruzi sylvatic cycles) or into the slums (the T. cruzi urban cycles). The slums that have resulted from this combination of military and economic battles are an ideal breeding ground for the triatomine bugs that carry the parasites.
Now, in a new twist on the retribution theme and another warning of how small organisms can adapt more quickly to cultural change than the people who initiated the changes, the parasites recently discovered a new superhighway created by people: blood-bank systems in Latin America in the 1980s were infested with the parasites at rates from 6 percent (Buenos Aires) to 63 percent (Santa Cruz, Bolivia). These blood banks are likely to provide a pathway for the disease to spread from the poor to the wealthy. If they had the brains to anticipate, the parasites would no doubt look forward to a globalized blood supply.
Going to an even larger picture, it seems that changes in climate may have already begun to increase the distribution of one of the insect vectors of Chagas, T. nigromaculata, which has been found for the first time at altitudes above 2,600 feet in Venezuela. Infected vectors were first found at 2,600 feet in 1939, but an uninfected colony was found more recently in a modern dwelling at an altitude of more than 3,600 feet in the Venezuelan Andes. So fossil fuel use, which contributes to global warming, can also be considered a cause of the spread of Chagas disease.
In some ways, if the conundrums of diseases such as these can be solved, there is hope that many other difficult global problems can be resolved. Indeed, we may need to resolve just about everything in order to solve anything in particular. This is both a good thing and a bad thing. It means that the solutions to disease and food and energy and community may all be part of the same, much larger, more complex solution. If only we can find them.
THE PARASITES THAT cause American and African sleeping sickness are not the only troublemakers in this family of parasites.
From the mid-1980s to the mid-1990s, a couple of hundred thousand people in the southern Sudanese state of Western Upper Nile (also called Unity State by the government in Khartoum) died of what was described as an “AIDS-like” disease. The disease, kala-azar, or visceral leishmaniasis, was being carried by sand flies in acacia forests along flooded rivers. Investigators think soldiers took the infection into an area that had been reforested after destructive floods in the 1960s.
The leishmania are one-celled parasites from the same family as the trypanosomes and thus go back hundreds of millions of years. According to one (well-grounded) story, at least one of the major forms of the parasite has its ancestral home in what is now southern Sudan and spread out with early human migrations into the wider world of central Asia and southern Europe. It was probably living in our faithful hangers-on, domestic dogs.
In the early nineteenth century, there may have been a second African exodus, some parasite-infected animals hitchhiking on the slave trade boats to head east across the Red Sea and into India. A British army physician, William Leishman, discovered the parasite associated with Dum-Dum fever at a military camp at Dum-Dum, outside Calcutta (and where the airport is today). Later, as the creation of tea plantations allowed the disease to spread into Assam State, it was called British government disease. But other forms of the parasite emerged elsewhere. In eighteenth-century Turkey, it was called Aleppo boil. Among the Incas, it (or something like it) was called valley sickness and, paradoxically, Andean sickness. There is evidence that the disease was present in the Americas as far back as the first century AD.
Unlike true (African) sleeping sickness, which is found only in Africa, and Chagas disease, which occurs in the Western Hemisphere, leishmaniasis is a global citizen. Leishmaniasis is one of the world’s top ten most important infectious diseases (along with both African and American trypanosomiasis). WHO’s Tropical Disease Research Programme reports that leishmaniasis is endemic in almost a hundred countries and territories, including sixteen European nations. There are probably more than a million people infected every year. WHO estimates that almost sixty thousand people die from it every year and that it costs the world more than 2 million disability-adjusted life years annually.
Until World War II and the introduction of DDT, serious infections in children were common in Mediterranean Europe. The drop in numbers of people affected was attributed to the use of pesticides, but the infection remained in dogs, which means the parasite was still around and reproducing. More likely, the disease in kids disappeared because of better nutrition and improved immunity, the same things that staved off a lot of other diseases (without necessarily stopping infection). HIV, which allows latent infections to become active for many diseases, gave leishmaniasis, like tuberculosis, a new lease on life.
These little blood parasites live quite happily, not causing any major problems, in a variety of marsupials, two‑ and three-toed sloths, armadillos, and forest rodents (in Central and South America), rock hyraxes and African grass rats (in Africa), fat sand rats (in Saudi Arabia), and great gerbils (in Russia, Mongolia, and central Asia). In many countries, domestic dogs carry it, but they get sick enough to suggest that they aren’t the natural host animal. In 2000, foxhounds in eighteen U.S. states and two Canadian provinces were sick with leishmaniasis, but that strain appeared to be transferred only between dogs directly, and no human cases were reported. In some parts of India and Africa, there appears to be one form that is adapted just to people, but that could be because we haven’t looked at the right animal host yet.
Usually—the epidemic in foxhounds notwithstanding—blood-sucking sand flies (of which there are about seventy important disease-transmitting species) pick up the parasites from one animal and carry them to another. People often get the parasite, via the sand flies, from dogs, after the dogs get it from nosing around in the woods. The types of sand flies and the habitats they prefer vary from place to place. The flies seem to prefer dry areas in the Old World and tropical forests and savannas in the New. In some areas, they prefer large cities with slums and lots of poor people.
A couple of weeks after the female sand fly lays her five or six dozen eggs, they hatch, and the larvae nose around to feed on any kind of organic stuff they can find. They pupate and emerge as adults in darkness, just before the birds’ morning song. Indeed, the wiggling larvae may just be the reason why the birds are singing. Male flies encourage females to mate by flapping their wings and giving off odors (what else is new?); both feed on sugary secretions of plants, but only the females suck blood. When not breeding or sucking on things, the flies rest in cool, shady, humid places. If the females suck blood from an infected animal, they get infected.
In sand flies, the parasites are slinky things, each with a flagellum (tail), which allows them to move around and hang on to the fly’s gut cells. The parasites need to hang on tightly until about the third day after a blood meal, which is when the fly defecates. Once the fly has had a good dump, the parasites let go, relax, and multiply as fast as they can. They reproduce by dividing down the middle, which seems considerably less pleasurable, but more efficient, than some other means. The newly “born” parasites then swim around anxiously waiting for the fly to take another meal; when that happens, they are off to the big blood meal in the sky: a mammal.
In animals, including people, the parasite invades white blood cells of the immune system, where it loses its tail, rounds itself into a ball and multiplies. Once in an animal, it can do a variety of things, depending on the immune state of the animal, the particular species of Leishmania, and a lot of things that aren’t yet very well understood. Much of the time, it appears that nothing particularly bad happens.
In other cases, very bad things indeed happen. Sometimes, if the parasite stays on the skin, it causes a reddish, insect-bite-like sore, which can expand into an open, wet sore called an Oriental sore, which looks a bit like a volcano. In some people, especially with one species of parasite in Brazil, the mucous membranes of the mouth or nose may be completely eaten away, sometimes years after the initial invasion. This condition is called espundia. The worst form of the disease is visceral leishmaniasis, in which the little stinkers invade the spleen and liver and cause a wasting-away-until-death-do-us-part scenario.
How do we begin to get a handle on these complicated parasitic diseases? There are the old diagnosis-treatment-vaccination tricks, of course. They are handy, but they depend on good diagnostic laboratories, vaccines, and drugs—in other words, on money and trained people. These are in short supply in those parts of the world where these parasitic diseases are most common.
In those places where dogs are a major source of the parasites for flies and people, they may offer some opportunities for control. In the late 1980s, one of my graduate students went to investigate an epidemic of leishmaniasis in a town in Central America. She wanted to explore the role of dogs. When she arrived, she found that local authorities had already killed all the dogs, and new ones were being brought in. The Chinese apparently were effective in getting rid of the disease in some places by getting rid of dogs. Dogs, however, are not just carriers of disease or even just human companions. In some countries, they are food. And, as we discovered in our work in Nepal, they may have other jobs, for example as night guards and community police. Even removing rodents or rodent habitats may pose unexpected problems, such as those we encountered with the plague in Africa.
How, then, can these diseases be prevented? The answers go beyond the community engagement and setting of fly traps that might have a chance for controlling sleeping sickness in Uganda. The biomedical approach would include treating sick people, spraying for bugs, testing people at risk, and screening blood supplies. This might help control the disease; it would also bring large benefits to certain chemical and technical industries in wealthy countries. But any sustainable health program to prevent these diseases would surely quickly become a social activist program. An ecosystemic and socially holistic approach to health will not, contrary to expectations, always create win-win situations. We still have to make moral choices.
Any programs to prevent these diseases caused by blood parasites must include a political agenda to create more egalitarian societies and a more just global distribution of wealth. With better nutrition, fewer people get sick, even if they are infected. With better-built houses, biting flies and bugs can be more easily be kept outside. If people do get sick, good medical care can stop the cycle of reinfection more quickly. It is just such a combination of medical and socio-political programs that seems to be bringing down the incidence of Chagas disease in the southern cone countries (Argentina, Bolivia, Brazil, Chile, Paraguay, and Uruguay).
It remains to be seen whether similar programs can be mounted for leishmaniasis and sleeping sickness, which have a more complex ecology. Given the general ecology of these diseases, we are unlikely ever to be rid of them completely, and the need for supportive medical programs to deal with inevitable tragedies in an overcrowded world is not going to disappear. We are left with a need for both ecological awareness and global solidarity.