THE THOUGHT OF ALL THOSE plastic bags that Aufderheide had filled with brittle flesh remained with me when I left Dahkleh. I wondered just what would come of them. In our conversations in the desert, Aufderheide had frequently talked about the scientific value of such tissue samples, and I believed him. Mummified human tissue, even just a few fractions of an ounce, was becoming a scarce commodity for medical researchers. In some parts of the world, museum curators had taken to refusing all requests from aspiring researchers for scraps of ancient flesh, complaining bitterly about the deluge of letters of solicitation. At the rate things were going, they said, there soon would be nothing left of the preserved bodies in their care, not even a lock of hair.
The situation reminded me uncomfortably of stories I’d read of the infamous Resurrection Men. During the eighteenth and early nineteenth centuries, British and American anatomists faced a serious shortfall of something essential to their profession: human cadavers. As researchers, they needed fresh bodies in order to investigate the intricate arrangements of human muscles, tendons, sinews, bones, and internal organs. As teachers, they required corpses for their students to dissect. Without such firsthand experience of anatomy, young doctors and surgeons risked grave malpractice. In one notorious case, described in The Lancet in 1823, a confused British physician mistook a dislocated shoulder for a sprained muscle. His ignorance was not terribly surprising: there were simply not enough corpses to go around in anatomy classes. According to the British laws of the day, medical schools could only dissect the bodies of executed criminals, and the gallows could scarcely keep up with demand. In 1826, 701 English medical students had to make do with fewer than 600 cadavers.
But what the law prohibited, the spade and shovel nimbly provided. Professional body-snatchers stole into city cemeteries at night, digging up recently buried coffins by the light of a shaded lantern. Sliding the bodies into burlap sacks and tea chests, these Resurrection Men, as they were known, sold their ill-gotten merchandise by the inch to anatomists. News of this practice scandalized England. To save their kin from dissectionists, wealthy citizens began burying their relatives in costly guarded cemeteries. Middle-class families kept bodies until putrefaction clearly set in; no self-respecting Resurrectionist wanted such spoiled goods. Eventually, European and American legislators came to their senses, relaxing laws governing the dissection of cadavers. But as a result of this grim history, many people came to view medicine’s hunger for human bodies and tissues with considerable distrust.
Such misgivings linger even today and extend to ancient bodies and ancient flesh. I certainly share these qualms. But those researchers who collect mummified tissue for their studies do their best to set these doubts to rest. They have very high hopes for their work. Aufderheide and a small group of his colleagues are struggling to advance scientific knowledge of some of the world’s most serious plagues by tracing their history and origins through distant time. Reflecting on this, I wondered how much we could expect from such investigations. Could the flesh of mummies supply us with clues to cures or drug treatments for an ancient scourge? Could it help researchers develop something as complex as a vaccine? Could the ancient dead somehow reach out from the stillness of their tombs and give life to the living? The answers, I discovered, lay in places such as the Chihuahuan Desert of North America and along the lush Nile Valley of Egypt, with hundreds of mummies ravaged by tiny, microscopic parasites.
RESEARCHERS HAVE DISCOVERED more than one hundred kinds of creatures that parasitize human beings, quite apart from bacteria, fungi, and viruses. Most of these organisms dwell in tropical parts of the planet, where they assume a stunning variety of shapes and forms, from simple-looking protozoa to more fantastic life-forms, such as the tiny cactuslike organisms known as thorny-headed worms. Some of their invasions produce nothing worse than a bad case of itching or a fleeting bout of intestinal cramps. But at the more serious end of the spectrum, their incursions lead to mutilation and hideous disfigurement, chronic illness and death. The microscopic protozoan Leishmania braziliensis, for example, so ulcerates human mucous membranes in the mouth and throat that it corrodes away the lower half of the face, turning its victims into mute ghouls, while the tiny tapeworm Echinococcus granulosus so entrenches itself in the brain and other human organs that it forms immense growing cysts of poisonous fluid: the slightest rupture can bring rapid death. By such means, obscure parasites spread misery, infecting an estimated 4.5 billion people.
To protect human beings from these creatures, medical researchers have long sought to learn more about them. As early as the turn of the last century, this quest for knowledge led science to mummified human tissue. In 1909, Marc Armand Ruffer, the son of a French baron and a former student of Louis Pasteur, detected dozens of minute calcified eggs, each equipped with a tiny spine, in the kidney tissue of Egyptian mummies. Ruffer had gone to Egypt to convalesce from a nearly fatal bout of diphtheria that he had contracted in London. He found Egypt to his liking and he stayed, taking a post as professor of bacteriology at the Cairo Medical School. When surveyors began turning up mummies by the cartload during preparations for raising the Aswan Dam in 1907, Ruffer recognized the value of these finds for medical science. He took tissue samples and began scouring them for traces of infectious disease. The three-thousand-year-old calcified eggs he detected belonged to a parasitic worm, Schistosoma haematobium, that damaged its victims’ bladders and kidneys to such a degree that their urine turned bright bloody red.
Other researchers followed this lead, eventually identifying dozens of serious parasites in the withered organs of the ancient dead. But it wasn’t until the late 1990s that mummy researchers began to envision something grander and more ambitious. At the mummy congress in Arica, they talked about ways of charting the waxing and waning of devastating parasites in ancient populations over hundreds or thousands of years. They were eager to study the epidemiology of the ancient past. An infectious disease, after all, is a delicate minuet danced over time by three parties: a parasite, the environment, and human behavior. Changes affecting any one of these dance partners can trigger or quell an epidemic. When the Aswan High Dam was built in Egypt during the 1960s, for example, economists hoped that construction would bring a new prosperity for farmers along the Nile. The dam would help irrigate more desert lands and, with a perennial source of water, farmers could sow four crops a year. The future looked very bright. What the economists did not take into account, however, was the parasitic worm S. haematobium. All the new, perennially filled water canals created prime habitat for snails that harbored S. haematobium during part of its life cycle. Four years after the dam was built, the incidence of schistosomiasis, the debilitating and often fatal disease caused by the parasite, rose sevenfold among farmers from Aswan to Cairo.
Aufderheide and a small group of other mummy experts were intent on examining the rise and fall of such parasites in the distant past. This was not an academic exercise. With a clearer understanding of these ancient scourges, they hoped to discern clues to new weapons against the most serious parasites. Medicine was desperate for treatments, vaccines, and cures. Aufderheide and his colleagues didn’t want to waste time. So they turned their attention to three of the world’s most destructive parasites. The first was a protozoan known as Trypanosoma cruzi, which causes Chagas’ disease. More widespread in Latin America than HIV, T. cruzi infects an estimated 16 to 18 million people. It kills 43,000 of them annually.
KARL REINHARD DOESN’T look like someone who has spent most of his career squinting over the dregs of human intestines. He is an energetic and enthusiastic man with a passion for all things Brazilian. In his mid-forties, he has a beard, curly black hair and a thinning pate, and looks extremely fit, the consequence of a passion for both cycling and running. When he isn’t teaching or lecturing, he favors wraparound sunglasses, T-shirts, and bicycle shorts and wears a Brazilian good-luck charm—a thin, faded-blue piece of cotton printed with the word Bahia—tied to his wrist. He has a teenager’s breezy, casual way of talking and it makes him sound decades younger than he is. He still calls his wife, Debbie, of nearly twenty years “his bride” and uses expressions like “kind of groovy” to describe human organs that resist putrefaction. Instead of saying good-bye on the phone to friends, he often closes with, “See you on the flip side.”
With interests scattered all over the scientific map, Reinhard has variously taught physical anthropology, palynology, and parasitology at the University of Nebraska in Lincoln. He is also on call to identify the bones of local murder victims, work he loathes. Lincoln, it seems, is still a small town at times: on one occasion, he was called in to piece together the remains of one of his own students who had been murdered. But Reinhard has a striking gift at times for turning sows’ ears into silk purses. At the morgue, he infused a local forensic pathologist with his enthusiasm for studying disease in mummies. After that, the friendly Nigerian helped him get CT-scan time and collaborated with him on papers. “We became very good friends over red wine and dead bodies,” observed Reinhard with a grin. “Not necessarily together.”
Reinhard’s speciality, however, is the study of ancient parasites. There are not many people in this esoteric field; Reinhard has the only accredited paleoparasitology lab in North America, work that he gravitated to naturally. His father was an epidemiologist who studied disease in remote Inuit communities in Alaska, his mother a nurse. At universities in Arizona and later at Texas A&M University, Reinhard combined archaeology with parasitology, becoming an expert on the strange parasitic worms that colonize the human gastrointestinal tract. This entailed becoming an expert on everything that came out of this tract—parasite eggs, parasite larvae, bits of adult worms, pollen, partly digested food, and other wastes. He is an expert in the poop end of things, as some of his mummy colleagues like to put it.
It is a great discipline for someone who likes attention and who remains an overgrown kid. Reinhard is fond of livening up lectures by describing in plain language the grotesque biology of the creatures he studies, such as the female pinworm, which slithers out of the anus of an infected human at night and explodes shortly after, showering her eggs into the darkness like a cloud of spores. Audiences, he knows, love the graphic details. Moreover, Reinhard is constantly astonished by his subjects’ endless hunger for life. “I once watched hookworms mate in a petri dish after we had removed them from puppy intestines,” he recalled. “The puppies had been dead for eight hours, but the parasites were still alive and happy as can be, to the point of copulating blindly in a petri dish after we had taken them out. They just didn’t care.”
Reinhard came across his first case of ancient Chagas’ disease in 1986 while visiting a rancher along the Texas-Mexico border. The man possessed a mummy that his father had casually exhumed during a Sunday afternoon outing in 1937. The preserved bodies of ancient Native Americans were once relatively common in caves overlooking the Rio Grande and its tributaries. Indeed, archaeologists had discovered several hundred of them in the remote region, which lay along the northern fringes of the Chihuahuan Desert. These mummies were the work of nature. Dry sand in the cave floors had wicked moisture away from their bodies, naturally dessicating their flesh.
When the rancher first uncovered the mummy, it wore a rabbit-fur robe and bore a painted red deer-hide strap about its waist. The rancher brought the body home and laid it out on the spare bed in his son’s room. He and his son treated it like a family member, even building a special shed to house it. As Reinhard looked at it for the first time, he asked one of his companions, a prominent Texas archaeologist, what she thought the likely cause of death was. She pointed to a badly abcessed tooth. Reinhard, however, had his doubts. The skin and tissue covering the abdomen had rotted away. Inside, the large intestine was clearly visible. It was so packed with food that it literally filled the entire pelvic girdle. It looked as if its owner hadn’t relieved himself for months before his death. “That mass of food haunted me for years after,” said Reinhard. “I couldn’t put it out of my mind.”
Reinhard knew that Aufderheide and another American pathologist, Marvin Allison, had found several mummies in Chile with similarly distended intestines. In a paper Allison published on the subject, he suggested that these ancient Chileans had perished from Chagas’ disease. Now Reinhard had turned up a similar-looking case along the Texas-Mexico border, five thousand miles to the north. If the unfortunate man in the rancher’s house had died from Chagas’, the case raised some interesting questions. Where had the ancient plague begun and how quickly had it spread across Latin America? Reinhard decided to go back to the Rio Grande in the spring of 1998 to take a better look. He got permission from the ranch owner and headed south.
He spent several days photographing, measuring, and visually examining the mummy, meticulously studying the various organs exposed by decay. He couldn’t get over the state of the body. An average mummified human has a large intestine just a bit over an inch in diameter. It generally holds about an ounce of fecal matter. The Rio Grande mummy had a terribly distended intestine. It was four inches wide and bulged with thirty-eight ounces of food. This included half-digested fish, rodents, bats, grasshoppers, plant fibers, seeds, and grass pollen. All this food occupied nearly a cubic foot of space. “The volume was so incredible I calculated it three times to make sure,” said Reinhard. Crammed with food, the intestine crowded out the kidneys and the bladder and jammed up against the spine. “There was actually an indentation in the colon from the bones of the spine. And this man must not have been able to urinate, either, at the end. He had no body functions. What an awful way to die.”
Medical researchers have a polite name for this condition: megacolon. There are two main causes. Children can inherit megacolon as part of a rare congenital disorder, Hirschsprung’s disease, which affects the nerves in the large intestine. Without any form of treatment they die. Adults, on the other hand, develop megacolon as a result of a massive infection from a tiny flagellate protozoan, T. cruzi.
T. CRUZI LOOKS A little like a microscopic wisp of egg white in water. It has a pointed posterior and a long whip behind that propels it. Stretched out end to end, T. cruzi measures no more than the width of two red blood cells. Its tiny size, however, is no measure of its destructive capability. It has a great affinity for mammalian muscle and nerve cells, particularly those in the intestines, esophagus, and heart. “When it attacks the nerves of the colon,” observed Reinhard, “what happens is that peristalsis, the normal contractions of the intestines, becomes disrupted and after a while it stops. Then the intestine fills with food. The muscles of the intestinal wall lose their tone and the intestine becomes incredibly enlarged.” The colon ends up looking like a knee sock that has wearily sprung its elastic. “The individual who is infected eventually dies, usually of blood poisoning, after several months of not being able to defecate.”
In the Rio Grande Valley that separates Mexico from Texas, there is no shortage of suitable vectors for the disease. T. cruzi is carried by several different insect species that all belong to the Reduviidae family. Collectively known as assassin bugs or kissing bugs in English, or vinchuchas in Spanish, the reduviids are nocturnal winged creatures that vary in color from a dark brown to an ugly, viscous-looking amber. They range from Patagonia in South America to the northern forests of Canada. They are relatively small creatures, measuring about half an inch in length, and they suck blood with a long conelike beak. There is nothing pretty about them, and they are not the kind of company humans like to have around. But in poor communities in Latin America, families seldom have much choice.
Most assassin bugs live in the wild, hiding out by day in prickly pear thickets or under the bark of mesquite trees. But a few species—the worst kind, from a human point of view—prefer the walls of thatched mud-brick houses. Often families are blissfully unaware of the extent of the infestation in their homes because assassin bugs have the eerie trick of melting away during daylight into tiny cracks around windows and doors. Even entomologists have a hard time trapping them. To gauge their numbers in poor South American houses, researchers have experimentally taken apart buildings mud brick by mud brick. In one small house, they gathered up nearly ten thousand assassin bugs.
At night, the insects emerge from their hiding places like an army of tiny vampires. What they crave is a blood meal, a prerequisite for molting. Almost any mammal will do, from guinea pigs and dogs to humans. Lured by the carbon dioxide in exhaled breath, they crawl onto sleepers’ faces and quench their thirst, defecating as they drink. If the insects are infected with T. cruzi, they excrete the miniature parasites along with their wastes, and humans who absently scratch or rub a bite risk sweeping the protozoa into their mouths or eyes. Once inside the human body, T. cruzi gravitates swiftly to local lymph nodes and begins multiplying. This often triggers an acute infection, which can be lethal in young children. The most serious trouble, however, generally follows much later. Two decades or more can pass before an infected person realizes something is seriously wrong. By then the tiny invaders have stormed nerve cells in the central and peripheral nervous systems and muscle cells throughout the body. Nearly one in four of the infected develop severe and often fatal cardiac problems. One in seventeen present more gruesome symptoms—megacolon or megaesophagus.
The rancher’s mummy, a man in his late thirties or early forties, had been just that unlucky 1,100 years ago. In all likelihood, said Reinhard, he was sleeping in a cave when he picked up T. cruzi from an assassin bug. Archaeologists in the region have found ancient grass beds in caves, which show that the early desert dwellers slept there. Such beds would have been ideal homes for vegetation-loving species of assassin bugs. But the infected man did not know this. Nor would he have known that anything was seriously wrong with him for a very long time, until one day he lost the ability to defecate and his abdomen began growing. Before long, he would have found it painful to move about, which is why he wrapped the deer-hide strap around his abdomen. This helped brace the ponderous mass of food. But it gave only temporary relief. With every meal he ate, his abdomen grew larger and harder until finally it could expand no more. His death was a misery. His intestines likely ruptured, spilling bacteria and partially decayed food into his bloodstream.
IN MANY WAYS, Reinhard had been very lucky. Researchers didn’t often encounter such textbook cases of advanced Chagas’ in mummies—for two good reasons. First of all, the ancient inhabitants of Latin America seldom lived to a ripe middle age. Most perished of malnutrition, pneumonia, diarrheal diseases, abcessed teeth, infestations of intestinal worms, complications from childbirth, swimming and hunting accidents, and the like before they ever reached their forties. This meant that many ancient Americans infected with T. cruzi succumbed to other things before the wispy protozoa could wipe out a major organ. The second problem related to the visibility of the disease. Three out of every four people infected with T. cruzi failed to develop any obvious anatomical signs of the disease. Their organs looked perfectly normal to the naked eye.
Both problems have long stood in the way of researchers interested in tracing the ancient epidemiology of T. cruzi. They bothered Art Aufderheide. As a pathologist, he had spent decades helping physician colleagues make difficult diagnoses and, through his studies of mummies, he had seen for himself the suffering that T. cruzi caused. So Aufderheide decided to apply all of his medical experience to solving the problem of detecting the microscopic parasite in mummies. The best way to find the minute protozoa in hundreds or even thousands of ancient bodies, he realized, would be to look for them on a molecular level. The best target would be the distinctive pattern of proteins that made up the DNA of T. cruzi. “If we could find the DNA of the bug,” he explained, sitting in his Duluth laboratory one early spring morning after his return from Egypt, “then we’d be able to identify Chagas’ even if there were no anatomical marks at all.”
Aufderheide knew that this approach could work. A few years earlier he and a biochemist colleague had spearheaded similar research on a test for Mycobacterium tuberculosis in mummies. But he also knew the work would be complicated. Human geneticists were accustomed to analyzing tissue samples taken from living or recently dead human beings. Their tests targeted relatively long strands of DNA that had undergone little or no decay at all. “The problem with ancient DNA,” said Aufderheide, “is that it’s usually broken up into smaller pieces. Most people would never bother trying to chase down DNA unless it was more than two hundred base-pairs long.” With mummified tissue, Aufderheide didn’t have that luxury. The double helix strands in the cells of an ancient cadaver often look as if they had been run through an office shredding machine.
For assistance, Aufderheide contacted Felipe Guhl, a Colombian biologist he had met at the mummy congress in Cartagena. Guhl was the head of a DNA lab in Colombia and had a strong interest in Chagas’. Intrigued by the project, Guhl agreed to start by looking for longer segments of ancient T. cruzi DNA, just to see if it could be done. Aufderheide sent the Colombian researcher a small box containing tiny bits of heart, esophagus, colon, rectum, ileum, and lung tissue he’d collected over the years from his dissections of South American mummies. The two researchers worked together closely. By the spring of 1997, they registered their first success. They identified a small but telltale segment of T. cruzi DNA in one-third of the heart samples and in all of the esophageal samples.
It was a solid beginning, but this form of testing wasn’t nearly sensitive enough. It would almost certainly miss the really tiny snippets of T. cruzi DNA, all that remained in many mummies. Aufderheide wanted a test that could pick them up. As it happened, a medical lab at the University of Minnesota, where he worked, was experimenting with modern DNA. The lab’s director offered to look for an 85-base-pairs segment of ancient T. cruzi DNA. After considerable trial and error, the team finally found it. Still Aufderheide wasn’t satisfied—he knew the test was too cumbersome to be of much practical value. Mummy researchers needed something much simpler and swifter—a molecular probe for the tiny targeted segment. With this, they could test a batch of twenty mummy tissue samples in just a few hours. This would make an ancient epidemiological study possible.
So Aufderheide discussed the matter with biochemist Wilmar Salo, who agreed to make the probe. In his lab, Salo split a tiny targeted segment of DNA up the middle with an enzyme, creating two molecules. Repeating this reaction twenty times, he obtained a million-fold amplification of the DNA snippet, which became the probe. To test it, Salo coated a glass slide with nitrocellulose, a compound formed by the treatment of cellulose with nitric and sulphuric acids. Then he added a drop containing DNA from a mummy already diagnosed with Chagas’. The probe worked beautifully.
DOCTORS IN THE developed world usually think of T. cruzi as a Latin American problem, but this isn’t true. During decades of civil wars, death squads, and unrelenting poverty in Latin America, millions of migrants have fled to the United States and other safe havens. Many carry T. cruzi. According to estimates based upon contagion rates in their countries of origin, nearly 370,000 Latin American immigrants in the United States alone are infected with the parasite. Worse still, few are aware of it. Physicians in the developed world, for example, seldom consider Chagas’ as a possible diagnosis. Cardiologists rarely order blood tests for T. cruzi when they detect cardiac muscle degeneration in their patients. Instead they assume they are looking at coronary artery disease and other heart muscle ailments.
Moreover, migrants aren’t the only infected ones. In the American South, assassin bugs also carry T. cruzi, occasionally transmitting it to humans. During the 1970s, researchers drew blood samples from five hundred longtime residents of the Rio Grande Valley in Texas, testing them for antibodies to T. cruzi. A positive result meant that the donor had come into direct contact with the protozoan. One in every forty of the Texans tested positive. Since then, health authorities in Texas have recorded nearly half a dozen home-grown cases of Chagas’. Some researchers now worry that this represents only a small fraction of the real number of infections in the region. They also suspect that the incidence of the disease is silently growing. Among new transient communities, known as colonias, just north of the Mexico border, houses are simple and assassin bugs are free to nestle in makeshift walls riddled with cracks and crevices.
Undiagnosed, the infected pose a threat to the safety of blood banks, for T. cruzi is perfectly capable of inveigling its way into a transfusion bag. Latin American studies have shown that one in every six people who receive blood tainted with the protozoa becomes infected—a risk factor that American and European blood banks have been slow to recognize and screen for. Medical researchers have reported four cases of transfusion-transmitted Chagas’ disease in North America. In one of these, a seventeen-year-old boy died from an inflammation of the heart muscle after receiving tainted blood.
What makes this plague even more worrisome is the fact that medicine has few ways of battling it. Physicians possess just two drugs, benznidazole and nifurtimox, for combating the parasite. Both are toxic and of dubious value for established infections. In South America, where the death toll from Chagas’ is highest, health experts have pinned their hopes on schemes to break the chain of T. cruzi infection. Their main tactic is to wipe out the assassin bug from mud-brick and thatch homes. Since 1991, teams have sprayed more than two million rural dwellings with insecticides, but no one really knows how effective this will be in the long term. Almost a half century ago, the World Health Organization launched a similar campaign against malaria-carrying mosquitoes. Health workers sprayed houses and mosquito-breeding grounds in the tropics with DDT, wiping out most of the insects. But the few that survived bred offspring resistant to DDT and other insecticides, creating an even worse problem. Further complicating the campaign against Chagas’ are sweeping changes in places such as Brazil. As settlers slash and burn the forests of the Amazon, pushing into previously uninhabited areas, they create new frontiers for assassin bugs and T. cruzi.
As a result, medicine urgently needs to know everything it can about the parasite. So Aufderheide and his colleagues have gone to work, testing South American mummies with their new DNA probe. The new data, they believe, will tell science a great deal about where Chagas’ came from. Reinhard and others have theorized that the plague was born during an ancient agricultural revolution in the South American Andes. Some four to five thousand years ago, wandering bands in the region began sowing corn along the banks of winding rivers. To tend fields and store the harvest, families had built houses and settled in villages, raising guinea pigs for meat. All these conditions—the new houses with their cracks and crevices, the veritable shopping market of hosts—would have attracted hordes of assassin bugs infected with T. cruzi. Under the circumstances, it would have been only a matter of time, said Reinhard, before the parasite made its way into the human bloodstream. “I would guess that Chagas’ was an almost inevitable consequence of settling the New World.”
In addition to tracing the origins of Chagas’, Aufderheide wants to find clues to controlling the devastating parasite. By charting the prevalence of T. cruzi infections over time and space, he and others hope to study the ancient waxing and waning of the epidemic. A sharp decline in infection rates in some part of T. cruzi’s range could point to a previously unrecognized biological, chemical, or environmental agent effective against the protozoa, something that medical researchers could develop into a weapon.
It would not be the first time, noted Aufderheide, that ancient epidemiology had supplied clues to a new vaccine. English researcher Keith Manchester had turned up something important while investigating the ancient relationship between two parasitic diseases, leprosy and tuberculosis. Through written records from the Middle Ages and the Renaissance, Manchester had charted prevalence rates of the two diseases over time. What he discovered was a neat inverse relationship. Leprosy sharply declined in England in the fifteenth century just as tuberculosis began to rage. It turned out that the human immune response to tuberculosis had a suppressive effect on leprosy, reducing infection rates in a community. Earlier researchers had suspected this, but Manchester demonstrated the relationship superbly. And as a result of this, physicians in India and elsewhere are now employing a weakened strain of tuberculosis as a dual weapon against tuberculosis and leprosy. “So that was the payoff,” concluded Aufderheide. “Once we recognized what caused the changes in the relative frequencies in these diseases, we found a way to exploit that by modern methods.”
Aufderheide has only begun testing the mummified tissues in his private collection, but he firmly believes that such ancient samples might hold similar revelations. He is not alone in this conviction. At the Mummy Congress in Arica, I had met another leading researcher tracking ancient disease. With a team of American and Egyptian medical researchers, Rosalie David is testing the tissues of Egyptian mummies for residues of two other deadly parasites, Schistosoma haematobium and Schistosoma mansoni. David seemed excited about the research. She gave me her card and encouraged me to call. Curious to learn more, I decided to take her up on the offer.
IN A SMALL restaurant on the University of Manchester campus, David briskly brushed the crumbs from her suit, irritation mounting. After weeks of unanswered e-mails and unreturned phone calls, I had finally succeeded in arranging a meeting with the prominent Egyptologist and had flown to Manchester with a notebook full of questions. But once she had speedily downed lunch and a dish of sticky toffee pudding, her favorite dessert, David had begun wrapping things up, pleading other engagements. I had, it seemed, just crossed an entire continent and the Atlantic Ocean for a one-hour lunch. It was maddening, but then David’s brush-offs were well known to some of her colleagues. Desperate to stretch out lunch another five minutes, I offered the harried waitress a credit card for the bill. David wasn’t amused. Across the table, her pale-blue eyes followed the waitress’s every movement. She looked like a fox ready to pounce.
David is the keeper of Egyptology at the Manchester Museum and director of the famous Manchester Egyptian Mummy Research Project. Less officially, however, she is the grande dame of mummy studies in England and like grande dames everywhere, she doesn’t seem to care much what others think of her. She favors sensible floral frocks and sturdy navy suits and wears her long graying brown hair in a bun on the top of her head, a style she hasn’t changed a whit in almost thirty years. She wears no makeup. She sports no jewelry, other than a wedding ring. She seldom smiles or laughs. In all likelihood, she wouldn’t draw a second look in a crowd.
But this seeming ordinariness camouflages one of the shrewdest minds in Egyptology. The author of more than twenty books on ancient Egypt and its mummies, David first recognized her calling at the age of six, when a teacher held up a photograph of the famous line of pyramids at Abu Sir. At home, David devoured books on Egypt, and eventually she applied to the prestigious Egyptology program at University College London. The university took only one student in Egyptology every few years, and in the 1960s they picked David, the daughter of a sea captain from South Wales, as their student. Delighted, David immersed herself in the study of hieroglyphics and Egyptian history.
When a position for an Egyptologist finally came open at the Manchester Museum, David took it. With its dour gray stone and Gothic atmosphere, the museum looks more like a set for the Addams Family than a serious research institution, but its galleries hold a superb collection of Egyptian antiquities. David decided to study its mummies. One of her heroes, Margaret Murray, had autopsied two mummies from the museum in 1908, aided by an interdisciplinary scientific team. Since then, few English researchers had been daring enough to bring science into the shuttered confines of Egyptology. David thought it time to try again. She picked a team of medical specialists and chose a mummy from the Manchester collections. The autopsy she conducted on it in 1975 became a media frenzy, something that appalled many of her colleagues. “They thought I was just trying to get on television,” huffed David. She ignored the gibes, however, and the new data she gleaned from that autopsy and from later explorations of mummies through medical imaging and endoscopic sampling convinced many of her colleagues to take up similar projects.
Since then, David has published widely on mummies and, six years ago, she came in contact with George Contis. Contis is the president of Medical Service Corporation International, an American health services firm that helps governments in developing countries control their deadliest parasites. At the time, Contis had an idea for a new project. His firm had just completed an epidemiological study of schistosomiasis in Egypt, and he wanted to extend investigations of S. haematobium and S. mansoni into the distant past there. The schistosomes are the source of much human suffering, infecting nearly 200 million people globally and killing 20,000 annually. Contis was keen on seeing the past geographical range of S. haematobium and S. mansoni and studying the differences in infection rates between men and women and adults and children. Such studies could give clues to a new vaccine.
David was fascinated. She loved the idea that research on the ancient Egyptian dead could yield tangible benefits for the living. “It was one way our studies could help the modern day, apart from being extremely interesting,” she said. She was also keen to see whether parasitic infections such as schistosomiasis, also known as bilharzia, increased during periods of turmoil in ancient Egyptian history. Moreover, she suspected there would be sound financial benefits to combining Egyptology with medicine. Public enthusiasm for mummies rarely translates into funding for research. Medical studies do.
David was optimistic that ancient mummies along the Nile could reveal much about schistosomiasis, for the Egyptians themselves had frequently recorded its symptoms. In the famous Ebers papyrus, ancient physicans described a condition that turned men’s urine red, one of the principal early symptoms of schistosomiasis. So common was this condition that many Egyptians believed that boys came of age when blood appeared in their urine, rather like a woman’s menstruation. It was not until the modern era that parasitologists in Egypt managed to tease out the real cause. In 1851, a young researcher at Cairo’s Kasr-el Aini hospital, Theodore Bilharz, found a strange white worm in the blood of the portal vein of a human cadaver. It was the first time that science had taken note of S. haematobium and Bilharz was enthralled. As he pored over his find, he observed its peculiar biology, describing it in wonderfully detailed letters to his mentor, the famed German zoologist Karl Theodor von Siebold. The pale worm, it transpired, was not one creature but two. The long flat-bodied organism was the male of the species; the female was a gray thread that lay in a groove bisecting the length of his body. From this strange quirk of biology came the name schistosome, or split body.
Modern studies have revealed much about the destructive lives of the schistosomes. As the males copulate with their respective females, they migrate into smaller and smaller veins in the human intestine or bladder. Raising and lowering their posterior suckers, the females release a cloud of tiny eggs at each stop along the way, laying as many as two thousand a day over a five-year period. Nearly half these eggs are swept into the gut or the bladder, where they are safely shed into the outside world, but the others are trapped. They lodge in gut and bladder walls by the thousands and calcify, causing serious damage. Schistosome eggs in the urinary system can trigger bladder cancer, kidney disease, or liver failure. Those embedded in the intestines can lead to lethal complications of the liver and spleen.
Infected humans who seek out irrigation canals and rivers as toilets release the eggs into water. In this new medium, the schistosomes hatch into juveniles and immediately begin searching for their next hosts, freshwater snails from three different genera. Inside the bodies of the snails, the schistosomes undergo further development. Each produces as many as four thousand more juveniles, and a month later this parasitic armada takes to the water again, this time in pursuit of mammalian hosts. Humans who bathe, swim, fish, or work in contaminated waters are prime targets. Schistosomes are attracted to humans by the secretions on their skin, and the microscopic worms creep about the hair follicles until they are finally able to penetrate the epidermis. Shedding their tails, they worm their way to the nearest vein, where they are swept into the liver, launching the whole cycle again.
After decades of concerted effort, medical researchers have found few effective defenses against the schistosomes. There is no safe effective vaccine and no cure. The most effective treatment is chemotherapy with a drug called praziquantel, but it seldom gives long-term relief. When patients return to working on irrigation canals or fishing boats, they often become reinfected. Moreover, physicians have recently noticed something alarming: the schistosomes are beginning to develop resistance to the chemotherapy. “So if we could see what had actually happened to the parasite over a long period of time,” observed David, “it might be possible to see where it was going in the future, or what it was likely to do, because it’s a very clever parasite. You’ve got to try to find methods to treat it while it’s changing and developing.”
An important first step was to devise a sensitive and cheap technique for detecting the parasites in mummified human tissue. David’s medical collaborators chose to home in on the chemistry of the ancient human immune system. When schistosomes invade the human bloodstream they produce distinctive proteins known as antigens, which circulate freely in the blood and produce an immune response. By developing a kind of litmus test for these antigens, team members could check any type of ancient tissue available—whether skin, brain, or lung—rather than just the urinary or intestinal tracts where the parasites thrived. “You don’t have to have the parasite, because the reaction against it will be present throughout the body,” observed David.
At the Mummy Congress in Arica, David had described the team’s first major success. After months of work, her colleagues had finally succeeded in detecting schistosome antigens in the ancient Egyptian mummies they had tested. One of the most encouraging results came from the liver sample from a four-thousand-year-old mummy. “It’s the first time, as far as I’m aware, that this technique has been developed for this purpose,” observed David with pride in her voice. But before the team could proceed with wide-scale testing for the parasite, they needed something enormously difficult to obtain: tissue samples, thousands of them, from mummies of every time period in ancient Egypt.
For nearly anyone other than England’s doyenne of mummy research, this would have been a tall order. But David and colleague Patricia Lambert-Zazulak had devised a sound plan. They had compiled lists of all the world’s collections of Egyptian mummies. Then Lambert-Zazulak canvassed each by letter, asking curators and private collectors to donate tiny bits of ancient tissues. Such donations, obtained by careful endoscopy and gleaned from already exposed organs, would be housed in a new tissue bank at the University of Manchester and shared by researchers worldwide. “The point of taking the samples,” observed David, “is that you only have to do it once, so you’re not having to go back and intrude on the mummies time and time again. The sample is there for future study.”
David was pleased with the replies the team had received. “Many of the major Egyptian collections have responded favorably, and I think we’ll end up with several hundred institutions and multiple samples from each one. So we’ll probably have in the region of several thousand samples.” With such a tissue bank at the University of Manchester, David believes that she and her colleagues will be able to trace the ancient history of the schistosomes back nearly five thousand years in Egypt, a record that will help answer many of the questions that Contis had first posed to her. Further down the road, David said, similar studies could explore many other diseases. She is personally very interested in charting the ancient history of malaria, the world’s most devastating tropical disease. Each year, malaria kills one million people, and with global warming many experts fear that this toll will rise.
As I later thought about our conversation, I began to see the stunning range of possibilities that people like David and Aufderheide envisioned. In years to come, medical researchers struggling to outwit all manner of deadly parasites—from viruses to bacteria, rickettsia to amoeba, fungi to protozoa—could turn to the mummified dead in search of new weapons. Sealed in their preserved cells is an astonishing molecular archive of disease, a record of misery and malady far more ancient and far more complete than any noted on rice paper, papyri, clay tablets, or stone. Humanity, after all, discovered its knack for writing just five thousand years ago, and the written history of disease is woefully incomplete.
In decades to come, as we remake our world with technology, as we log entire rain forests, drain seas, dump our wastes in rivers and oceans, and warm the world with our greenhouse gases, we will have great need of such an archive. Transforming the world beyond recognition, we will blindly tip the balance of disease, freeing ancient parasites held in check for millennia, and we will succumb to a host of their new plagues. That is the essence of life and parasites hungry for life. Their diseases are inevitable. And the more the world around us changes and evolves, the more help we will need from the mummified dead who lie unchanged in their tombs.