In the dermatology lab, a photographer arrived with a Canon digital camera. He affixed a little ruler just below the ulcer on my arm and took dozens of photographs. I was ushered into an examination room where the lesion was inspected by a gaggle of earnest medical students, who took turns peering, palpating, and asking questions. Next, in the biopsy lab, a nurse cut two wormlike plugs of flesh out of the lesion, and the holes were stitched up.

When the biopsy came back it would offer no surprise: Like Dave and everyone else, I had Leishmania braziliensis. Or at least that’s what the doctors initially believed.

Our primary doctor, Theodore Nash, was seventy-one years old. He did his rounds in a white lab coat with a roll of papers precariously shoved into a side pocket. He had curly salt-and-pepper hair brushed back from a domed forehead, steel-rimmed spectacles, and the kindly, distracted air of a professor. Even though, like most doctors, he was fantastically busy, his manner was unhurried and relaxed, and he was gregarious and happy to answer questions at length. I said I wanted to hear the straight story without any window dressing. He said that was how he preferred to work with all his patients. He was refreshingly, even alarmingly, direct.

The National Institutes of Health has been conducting clinical studies on leishmaniasis since the early 1970s, treating recent immigrants and people who had picked up the disease while traveling. Many of the patients were Peace Corps volunteers. Dr. Nash participated in the treatment of most of them. He had written the upgraded leishmaniasis treatment protocol for the NIH in 2001, and it is still in use today. He shifted treatment away from the antimonial drug, which he thought was too toxic, to amphotericin and other drugs, depending on the parasite species and the geographic variety. Nash knew as much about leish treatment as any doctor in the United States. This is not a simple disease, and treatment is more an art than a science. The clinical data aren’t deep enough to give doctors a precise formula, and there are too many forms of leish and many unknowns.

Dr. Nash had spent almost his entire medical career in the parasitology section of the NIH—forty-five years—going back, he said, to the time when parasitology was “the backwater of science, no one was interested, and no one would work with you.” Because most people who get parasites are poor, and because infectious-disease medicine is not usually fee-based, parasitology is one of the lower-paying of all the medical specialties. To go into the field, you have to truly care about helping people. Your extremely expensive, ten-year medical education gives you the privilege of working long hours for modest pay among the poorest and most vulnerable people in the world, encountering a staggering amount of misery and death. Your reward is to relieve a small bit of that suffering. It takes a rare kind of human being to become a parasitologist.*

Nash’s early research focused on schistosomiasis and then giardia, a common, worldwide, waterborne parasite. Today the main focus of his work is a parasitic disease called neurocysticercosis, in which the brain is invaded by tapeworm larvae that originate in undercooked pork. The larvae circulate in the bloodstream and some get stuck in the tiny vessels in the brain, where they form cysts, leaving the brain peppered with grape-sized, fluid-filled holes. The brain becomes inflamed and the victim suffers seizures, hallucinations, memory failure, and death. Neurocysticercosis affects millions of people and is the world’s leading cause of acquired epileptic seizures. “If only we had the smallest fraction of the money that is devoted to malaria,” he declared to me in anguish, “we could do so much to stop this disease!”

In our first meeting, Nash sat me down and explained why he thought our team had become infected, how leishmaniasis works, what its life cycle is, and what I had to expect from treatment. The disease requires two animals: a “reservoir host”—an infected mammal whose blood is teeming with the parasite—and a “vector,” which is the female sand fly. When the sand fly bites a host and sucks its blood, it also draws in parasites. Those parasites proliferate in the sand fly’s gut until it bites another host. The parasites are then injected into the new host, where they complete their life cycle.

Each host animal lives out its life as a Typhoid Mary, infecting the sand flies that drink its blood. The parasite, while it can devastate a human being, generally does not “cost” the host animal very much, although some host mammals get lesions on their noses. A good guest does not burn down the house he’s staying in; leishmania wants its host animal to live long and prosper, spreading as much disease as possible.

In the isolated valley of T1, far removed from human habitation, sand flies and an as-yet-unknown mammalian host—it could be mice, rats, capybaras, tapirs, peccaries, or even monkeys—had been locked in a cycle of infection and reinfection going on for centuries. “And then,” said Nash, “you intruded. You were a mistake.” By invading the valley, we were like clueless civilians wandering onto a battlefield and getting shot to pieces in the crossfire.

When an infected sand fly bites a person, the fly unleashes hundreds to thousands of parasites into the person’s tissue. These tiny single-celled animals have flagella so they can swim around. They are small; it would take about thirty to span a human hair. But they are positively gargantuan compared to bacteria and viruses that cause disease. Almost a billion cold viruses, for example, could be packed into a single leishmania parasite.

Because it is a complex, single-celled animal, its methods are more subtle and devious than a virus or bacterium. When a sand fly injects leishmania, the human body, sensing the intrusion, sends an army of white blood cells to hunt down, swallow, and destroy the parasites. White blood cells, which come in many types, usually deal with bacteria and other foreign bodies by engulfing and digesting them. Unfortunately, this is exactly what the leishmania parasite wants—to be swallowed. Once inside the white blood cell, the parasite drops its flagellum, becomes egg-shaped, and starts to multiply. Soon the white blood cell is bulging with parasites like an overstuffed beanbag, and it bursts, releasing the parasites into the victim’s tissues. More white blood cells rush to attack and engulf the loose parasites, and they are in turn hijacked into producing more parasites.