CHAPTER 23

Four members of the expedition have become ill with the same symptoms.

In the weeks after our return from the jungle in February 2015, I and the other members of the expedition settled back into our everyday lives. The power of the experience stayed with us; I felt humbled and awed by the glimpse we’d had of a place completely outside the twenty-first century. We all shared a sense of relief, too, that we had emerged from the jungle unscathed.

A few days after our return from Honduras, Woody sent everyone a broadcast e-mail. It was part of his standard follow-up to any expedition he leads into the jungle, and it included this excerpt:

All, if you find anything at all, feel slightly unwell, develop a slight fever that goes away or any of your multitude of bites appear not to be healing I would advise seeking medical advice as soon as possible, explaining where you have been etc. Better safe than sorry.

At the time, I was completely covered, like everyone else, with bug bites that itched awfully, but that gradually began to fade. A month later, in March, I took a vacation with my wife to France, where we went skiing in the French Alps and visited friends in Paris. While walking around Paris, I began to feel a stiffness in my legs, as if they were sore from excessive exercise. At first I attributed it to the skiing, but over several days the stiffness grew worse, until I could hardly walk without becoming exhausted. When I developed a fever of 103, I went online to the website of the Centers for Disease Control, to check the incubation period for various tropical diseases I might have been exposed to. Thankfully, I was beyond the normal incubation period for chikungunya, Chagas’ disease, and dengue fever. But I was smack in the middle of it for malaria, and my symptoms matched those described at the CDC website. I was furious at myself for prematurely stopping my malaria medication. What the hell had I been thinking? But then I wondered how I could have gotten malaria, a disease transmitted between humans via mosquitoes, when the valley of T1 was uninhabited. Mosquitoes do not usually travel more than a few hundred yards in their entire lifetime, and the nearest humans potentially with malaria were many miles away.

My Parisian friends made some phone calls and found a hospital a short metro ride away with an infectious-disease lab that could test for malaria. I went that evening, they drew blood, and ninety minutes later I had the results: no malaria. The doctor thought I had a common virus, unrelated to the Honduran trip, and assured me it was nothing to worry about. My fever had vanished even while I awaited my test results. Two days later I had fully recovered.

Another month passed. The bug bites on my legs eventually faded away, along with the itching. But one bite did not go away. It was on my upper left arm, midway between elbow and shoulder, and it seemed to be getting redder and bigger. I didn’t worry about it at first because, unlike the other bites, it didn’t itch or bother me.

In April I had an outbreak of sores in my mouth and on my tongue, accompanied by another sudden fever. I went to the local emergency room in Santa Fe. The doctor who examined me thought it was herpes and gave me a prescription for an antiviral medication. I showed him the bug bite on my arm, which was getting uglier. He suggested I treat it with antibiotic ointment. That fever went away quickly and the mouth sores disappeared soon after. The antibiotic cream, however, did nothing for my arm.

Over the next few weeks, the bug bite expanded and developed a vile crust. I discussed it with Steve Elkins, and he said that Dave Yoder and Chris Fisher reported having similar bites that wouldn’t heal. Steve suggested that we all photograph our bites and e-mail the pictures around, to compare. Dave, who lived in Rome, sent me a picture of his bite, which was on the back of his leg. It looked like mine, only worse. Dave was frustrated: He had gone to the ER in Rome three times, and the doctors kept diagnosing it as an infection and giving him antibiotics, which didn’t work. “It doesn’t look like a normal infection,” he told me. “It looks like a miniature volcanic crater. It just won’t heal.”

Dave began researching what he might have. “I try not to Google images of disease on the web,” he said. “I’ve given myself two health scares caused by Googling. But this time I did, because I knew my doctors were wrong.”

The pictures that popped up made him think he might have the tropical disease leishmaniasis.

He e-mailed pictures of his bug bite to two fellow photographers at National Geographic who had gotten leishmaniasis while on assignment. One was Joel Sartore, who contracted the disease while shooting in the Bolivian rainforest and who almost lost his leg as a result. Both photographers told Dave that what he had “sure looked like leish.”

Dave sent me an e-mail:

Have you considered the possibility of leishmaniasis? It can be a serious thing. I’m pretty sure that’s what I have, at this point. I’m investigating the situation right now.

I immediately Googled the disease and read about it with fascination and disgust. The images of leish in the early stages did indeed look like my bug bite. The pictures also showed me what it could develop into, and that was a perfect horror. Leishmaniasis is the second deadliest parasitic disease in the world, behind only malaria, and it affects twelve million people worldwide, with around one or two million new cases every year. It kills sixty thousand people a year. Of the leading “neglected tropical diseases” (NTDs) in the world leishmaniasis is one of the most prominent, if not number one. But because it almost always affects poor people in rural areas of the tropics, there is little economic incentive for pharmaceutical companies to develop vaccines or treatments.

Meanwhile, Bill Benenson and Steve began circulating e-mails to the entire group, asking if anyone else had bug bites that weren’t going away. Mark Adams, the sound engineer, reported he had a lesion on his knee. Tom Weinberg had a suspicious ulcer on his knuckle. Mark Plotkin had an unexplained rash. Sully and Woody both had bug bites that were turning into sores.

A few days later—this was in late April 2015—fed up with his local doctors and the Italian ER, Dave went to the largest hospital in Rome and demanded to see a tropical disease specialist there. At the beginning of the examination, when Dave opined that it was leish, the doctor snapped, “No it isn’t.” But by the end of the examination, the doctor agreed that he did indeed appear to have the disease. He suggested Dave return to the States for a more precise diagnosis, since leish is notoriously difficult to identify; it is not a single disease but a suite of diseases caused by some thirty different parasitic species carried by several dozen kinds of sand flies.

On May 2, 2015, Dave sent an e-mail to the group in which he reported on his visit to the tropical disease doctor in Rome and offered some advice:

Brothers in the leish:

Despite the fact nobody from the group has been diagnosed with anything, I’m going to perhaps jump the gun and address one elephant in the room directly. There may be cause to explore the possibility of leishmaniasis in my case, and as I understand the situation, possibly others from the group.

He said he had decided to return to the States for a firm diagnosis and treatment.

This set off a minor panic. Dozens of messages circulated among the expedition members discussing symptoms, real and imagined. Even those without evident signs of leish rushed to their doctors, worried about various complaints—rashes, fevers, headaches, and other ailments. Stomach-turning photographs of everyone’s expanding ulcers were circulated, and circulated again.

Steve Elkins remained exasperatingly healthy, but Bill Benenson had discovered two jungle ticks on himself when he returned to California. While that had not led to anything serious, he was shaken up, and he was very concerned about what was happening to others. He sent out an e-mail:

I feel we should all share our relevant medical information together, if possible and comfortable, to help ourselves and for all future Explorers as well. Let’s remember, we’ve not only made history together in February but that we’re still discovering a great deal that’s new and exciting, about a lost place in a very threatened environment.

I was now thoroughly alarmed about my own sore. Steve Elkins dug up the name of a tropical disease specialist in New Mexico who might be able to help me: Dr. Ravi Durvasula at the Veterans Affairs Medical Center in Albuquerque. Dr. Durvasula was a specialist in “Old World” leishmaniasis. I called the VA hospital hoping to speak to him. An hour later, after multiple phone calls and a mind-boggling number of transfers from one wrong office to another, after being told that no such doctor existed, that the doctor worked there but didn’t take patients, that I wasn’t allowed to speak to his office without a referral, and that the doctor did not take referrals, I gave up. (I can’t imagine how our wounded soldiers negotiate this same telephone system.)

“Forget calling the VA,” Steve said to me. “Send him an e-mail. Be sure to play up the whole expedition thing, the lost city, National Geographic, all that sexy stuff.”

So I did:

Dear Dr. Durvasula,

I am a journalist for National Geographic magazine and The New Yorker… I recently returned from an expedition into an extremely remote area in the La Mosquitia rainforest, exploring a large, unknown pre-Columbian ruin. We were in the jungle from February 17-26. Since that time, four members of the expedition have become ill with the same symptoms… I live in New Mexico and I had heard you were a specialist in leishmaniasis and that is why I’m contacting you to see if you might be willing to take my case.

Dr. Durvasula e-mailed me back immediately. He couldn’t have been more helpful and concerned—in contrast to the VA staff. We arranged a phone call, and he asked me some questions.

“Does the area have a whitish, pearlescent appearance, surrounded by red?”

“Yes.”

“Does it itch?”

“No.”

“Does it hurt or feel sore at all?”

“No.”

“No discomfort?”

“None at all.”

“Ah, well. I am afraid those are the classic signs of leishmaniasis.”

He asked me to e-mail him a photo. When he got it, he confirmed it certainly appeared to be leish. He suggested I seek help at the National Institutes of Health (NIH), the best place in the world, he said, for leishmaniasis study and treatment.

In the meantime, Dave Yoder explored treatment options in the States. He, too, zeroed in on the National Institutes of Health and contacted them. At the NIH, Dave reached Dr. Thomas Nutman, deputy chief of the Laboratory of Parasitic Diseases. Nutman was fascinated by the story of the expedition to the lost city and the mass outbreak of disease. He wrote Dave:

Dear Dave,

I think there is a very high likelihood that this is Leishmania and because of the strains in Honduras there is a small but real chance that this could turn into mucocutaneous disease depending on the strain… The big issue is defining which strain of Leishmania you have and tailoring treatment to that particular strain… We have taken care of a number of National Geographic folks in the past.

The National Institutes of Health’s overall mission is to “seek fundamental knowledge about the nature and behavior of living systems,” and then leverage that knowledge to “enhance health, lengthen life, and reduce illness and disability.” It is strictly a research institution, and anyone admitted for treatment must be part of a research study. Each of its projects has a set of rules that outline who can be treated, why, and how their treatment will contribute to medical knowledge. If a potential patient meets the criteria and is enrolled, the care is free. It even includes financial help with transportation and lodging. In return, the patient agrees to follow the rules and donate to medical research any tissue samples, cells, blood, parasites, and so forth. A participant can withdraw at any time, for any reason.

The NIH doctors were keenly interested in our situation. The mass outbreak of disease was unusual, the valley of T1 seemed extraordinarily “hot,” and the region was unknown medically, all of which made the expedition an enticing medical study. The doctors offered to treat us all for free. It was nice to be wanted.

In late May, Dave flew from Rome to Washington for a firm diagnosis. “Hopefully,” he joked, “we’ll all turn up negative, and it’ll turn out to be a minor staph infection from Woody’s jungle stew that is easily treated with an application of cayenne sauce.”

The doctor in charge of the project, who would be treating Dave, me, and the other potential “brothers in the leish,” was Theodore Nash, principal investigator in the Clinical Parasitology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases. Nash was one of the country’s leading experts in leishmaniasis treatment, having worked under Dr. Frank Neva, a pioneer in leishmaniasis treatment who came to the NIH from Harvard. After Neva’s retirement, Nash became the chief clinical researcher into leish at the NIH, and over the past decades he advanced its treatment with new drugs and formulations.

At NIH, doctors took a biopsy of Dave’s lesion, looked at it under a microscope, and saw it was teeming with round, microscopic leishmania parasites. But Dave’s treatment would depend on what kind of leish it was. A special lab at NIH began the process of sequencing the parasites’ DNA.

Leishmaniasis has a long and terrible history with human beings, stretching back as far as human records exist and causing suffering and death for thousands of years.

A few years ago, a hundred-million-year-old piece of Burmese amber was found to have trapped a sand fly that had sucked the blood of a reptile, most likely a dinosaur. Inside this sand fly, scientists discovered leishmania parasites, and in its proboscis, or sucking tube, they found reptilian blood cells mingled with the same parasites.

Even dinosaurs got leishmaniasis.

Leishmania has probably been around since the final breakup of the primordial continent known as Pangaea. As these ancient landmasses eventually drifted apart to become the Old and New Worlds, the populations of that sand fly ancestor were separated and continued to evolve independently, eventually giving rise to the two basic strains of the disease in the Old World and the New. At some point the disease made the leap from reptiles to mammals. (Modern reptiles still get leish, and there has been a medical debate over whether reptilian leish can be transmitted to humans; the answer is probably not.)

Unlike many diseases that afflict human beings, leish was global from the very outset, and it was dreaded by our ancient ancestors in both hemispheres. Archaeologists have found leish parasites in Egyptian mummies dating back five thousand years, and in Peruvian mummies going back three thousand years. A description of leish appears in one of the earliest written human documents: the cuneiform tablets of King Ashurbanipal, who ruled the Assyrian Empire 2,700 years ago.

Leishmaniasis comes in three main varieties, each with distinct symptoms.

The most common form is cutaneous (i.e., skin) leishmaniasis, which is found in many parts of the Old World, especially Africa, India, and the Middle East. It is also widespread in Mexico and Central and South America, and it recently popped up in Texas and Oklahoma. Some US troops returning from Iraq and Afghanistan contracted cutaneous leish during their deployments and nicknamed it the Baghdad boil. This kind of leish starts as a sore at the location of the bite, which grows into a weeping lesion. If left alone, it usually goes away, leaving only an ugly scar. It can usually be treated by burning, freezing, or surgically removing the ulcer.

In visceral leishmaniasis, the second type—also from the Old World—the parasite invades the body’s internal organs, particularly the liver, spleen, and bone marrow. It is sometimes known as black fever, because it often turns its victim’s skin black. This variety is deadly; without treatment it is always fatal. But treatment of visceral leish is quick and reliable, requiring a single infusion of an antibiotic drug that yields a cure rate of about 95 percent. Most of the deaths in the world from leish are caused by the visceral form, among poor children who don’t have access to treatment.

The final form of leish is the mucocutaneous or mucosal variety, the major New World form of the disease. It starts as a skin sore like the cutaneous kind. Months or years later, the sores can reappear in the mucous membranes of the nose and mouth. (The sores I had in my mouth, however, were probably unrelated.) When leish moves to your face, the disease gets serious. The ulcers grow, eating away the nose and lips from the inside and eventually causing them to slough off, leaving the face horrifically disfigured. The parasite continues to devour the bones of the face, the upper jaw, and teeth. This form of leish, while not always lethal, is the most difficult to treat, and the treatment itself involves a drug that has toxic—and sometimes fatal—side effects.

The pre-Columbian inhabitants of South America were plagued by mucosal leish, which they called uta. The grotesque disfigurement of the face terrified the Moche, Inca, and other ancient cultures. They may have considered it a punishment or a curse from the gods. Archaeologists have uncovered burials in Peru and elsewhere of people whose disease was so advanced that they had a caved-in hole where the face used to be—the disease had eaten away everything, including the facial bones. Ancient Peruvian pots so faithfully record the disfigurations that researchers can identify in them the actual clinical stages of the disease, from the early soft-tissue destruction of the nose, to the general destruction of the nose and lips, and finally to the disintegration of the hard palate, nasal septum, upper jaw, and teeth. The Peruvian custom of punishing people by mutilating the nose and lips may have been intended to imitate the facial deformities caused by the disease, perhaps to mimic what they believed was divine retribution.

Acute fear of the disease may have even driven human settlement patterns in South America. The archaeologist James Kus, a retired professor at California State University, Fresno, believes that the Inca site of Machu Picchu may have been chosen, in part, because of the prevalence of mucosal leish. “The Incas were paranoid about leishmaniasis,” he told me. The sand fly that transmits leish can’t live at higher altitudes, but it is widespread in the lowland areas where the Inca grew coca, a sacred crop. Machu Picchu lies at just the right altitude: too high for leish, but not too high for coca; at Machu Picchu the king and his court could rule from a place of safety and preside over the rituals associated with coca cultivation, without the risk of getting this most dreaded disease.

When the Spanish conquistadors arrived in South America in the sixteenth century, they were horrified at the facial deformities they saw among native people in the lowlands of the Andes, especially among the coca growers. The Spanish thought they were looking at a form of leprosy and called the disease lepra blanca, “white leprosy.” Over the years, mucosal leish has acquired many nicknames in Latin America: tapir nose, hoarse voice, spongy wound, big canker.

Mucosal leish didn’t exist in the Old World. But the even deadlier visceral form, the kind that invades the internal organs, had long plagued the Indian subcontinent. It first gained the attention of Western medicine as the British extended their empire into India. Eighteenth-century writers described it as “kala-azar” or “black fever.” Visceral leish easily spreads from person to person via the bite of sand flies, using human beings as its primary reservoir host. It was so deadly and spread so fast that in certain regions of India in the nineteenth century, leishmaniasis would sweep through an area, killing everyone and leaving a landscape of empty villages, entirely bereft of human life.

The British also noted the cutaneous form of the disease in India and the Near East and gave it various names: Aleppo evil, Jericho button, Delhi boil, Oriental sore. But doctors did not recognize a connection between the two strains until 1901. William Boog Leishman, a doctor from Glasgow who was a general in the British Army, was posted in the town of Dum Dum, near Calcutta, where one of his soldiers fell ill with a fever and a swollen spleen. After the man died, Leishman looked at thin sections of the man’s spleen under the microscope and, using a new staining method, discovered tiny round bodies in the cells—the leishmania parasite. Leishman called it Dum Dum fever. A few weeks after Leisham published his discovery, another British doctor, named Charles Donovan, also stationed in India, independently reported the results of his own research. He, too, had spied the offending parasite, and between the two of them the disease “leishmaniasis” was identified. Leishman got the dubious honor of having the disease named after him, while Donovan was gifted with the species’ name: Leishmania donovani. Doctors figured out in 1911 that it was transmitted by the sand fly, and later they realized that a bewildering number of mammals could be reservoir hosts for the disease, including dogs, cats, rats, mice, gerbils, hamsters, jackals, opossums, foxes, monk seals, and, of course, humans. This astonishingly broad range of host animals makes it one of the most successful diseases on the planet.

I was still trying to decide whether I should go to NIH or not when the DNA analysis of Dave’s parasites came back. It showed he was infected with a species of leish parasite known as Leishmania braziliensis. This was bad news for Dave and the rest of us, because L. braziliensis causes the third, mucosal variety of the disease, and is considered to be one of the most difficult of all to cure.

Dr. Nash decided to begin Dave’s treatment immediately. He would use a drug called amphotericin B, administered by slow infusion. Doctors have nicknamed the drug “amphoterrible” because of its nasty side effects. It is considered a last resort, most commonly given to patients with fungal infections of the blood when other drugs have failed; most of these patients are extremely ill with AIDS.

Dr. Nash would give Dave and the rest of us a formulation of the drug called liposomal amphotericin. In this form, the toxic drug is encapsulated in microscopic spherules made of lipids (fats). This makes the drug safer, reducing some of the most dangerous side effects. But the lipid droplets can cause disturbing side effects of their own.

The length of treatment depends on how well the patient tolerates the drug and how quickly the ulcer begins to heal. The ideal course, which Dr. Nash had determined over many years of experience, was seven days—long enough to halt the disease but not so long as to harm the patient.

Shortly after Dave was diagnosed with leish, Tom Weinberg learned from the CDC that he, too, had the disease. Chris Fisher, Mark Adams, and Juan Carlos Fernández went to the NIH and were also diagnosed with it. All were treated except Juan Carlos; Dr. Nash recognized that his immune system appeared to be fighting it off and decided to delay treatment. It was the right decision, and Juan Carlos ended up leish-free without going through the rigors of amphotericin B.

From the UK we heard that Woody had contracted leish, as had Sully, despite bundling themselves up so scrupulously every evening. Sully was going to be treated at the Royal Centre for Defence Medicine at Birmingham Heartlands Hospital, while Woody was starting treatment at the Hospital for Tropical Diseases in London. Both would get a new drug, miltefosine. Word soon came back from Honduras that many Honduran members of the expedition had also fallen ill with leishmaniasis. These included Oscar Neil, the archaeologist; the commanding officer of the military contingent, Lt. Col. Oseguera; and nine soldiers.

When the news of our mini-epidemic began to spread among members of the expedition, accompanied by gruesome photos of weeping ulcers, it was hard not to think about the centuries-old legend and its oft-cited “curse of the monkey god.” All those flowers we chopped down! Gallows humor aside, though, many of us were privately aghast at having walked so blithely into that hot zone, and then having congratulated ourselves, prematurely, for emerging from the jungle unscathed. The jokes petered out quickly in the face of this dramatic disease, which had the potential to alter the course of each of our lives. This was deadly serious.

Because amphotericin is expensive and not available in Honduras, the Honduran members of the expedition were being treated with an older drug, a pentavalent antimonial compound. Antimony, a heavy metal, is directly below arsenic in the periodic table of elements and is similarly poisonous. This drug kills the parasite while sparing (one hopes) the patient. As bad as ampho B is, this one is worse: Even in the best scenarios it has dreadful side effects. We heard from Virgilio that Oscar, who had been bitten on the right side of his face, had almost died of the treatment and was recovering in seclusion in Mexico. He would have a nasty scar for life; he later grew a beard to cover it up and declined to speak of his experience or do any further work at T1.

After Dave was diagnosed with mucosal leish, I finally understood that I had to stop procrastinating and get treated. As bad as the treatment sounded, I wasn’t willing to take a chance with the disease itself, or with my face.

So finally, at the end of May, I called the NIH and set up an appointment for early June to get a biopsy and diagnosis. By this time my bug bite had turned into an oozing crater the size of a quarter, fiery red and disgusting to look at. It didn’t bother me; I’d had no more fevers and I felt fine. Dr. Nash said he doubted my fevers had been caused by the leish anyway; they were, he thought, coincidental viral infections, perhaps opportunistic because my immune system had been shaken up by leish, which hijacks white blood cells.

As my date approached, I heard that Dave’s treatment with liposomal amphotericin had gone very badly. He had suffered serious kidney damage and Dr. Nash had halted it after only two infusions. He remained hospitalized at the NIH under observation while the doctors debated what to do next.