The ulcer that forms around the infected area isn’t caused by the parasite per se, but by the body’s immune system attacking it. The inflammation, not the parasite, is what eats away the person’s skin and (in the mucosal form) destroys the face. The immune system goes nuts trying to get rid of the parasite that is blowing up its white blood cells, and this fight trashes the battlefield, inflaming and killing the tissues in the bite area. As the parasite slowly spreads, the lesion expands, destroying the skin and leaving a crater exposing the raw flesh below. The ulcer is usually painless—nobody knows why—unless it occurs over joints, when the pain can be intense. Most deaths from mucosal leish occur from infections invading the body through this unprotected doorway.

Nash then talked about the drug that I would be taking, amphotericin. He said it was the gold standard, the drug of choice, for this kind of leish. While miltefosine was a newer drug and could be taken in pill form, he didn’t want to use it. And besides, there was none available.* There had been too few clinical trials to make him comfortable with it, and in one trial in Colombia it seemed to be ineffective against L. braziliensis. He also said you never really knew what kind of side effects might pop up until at least ten thousand people had taken a drug, and miltefosine had not reached that benchmark. He had had long experience with amphotericin B, and it produced an approximately 85 percent remission rate, which was about “as good as it gets” in any drug treatment. The drug works by binding to the parasite’s cell membrane and tearing open a tiny hole in it, causing the organism to leak and die.

Nash told me what I might experience in taking the drug. He didn’t sugarcoat his comments. The side effects of liposomal amphotericin, he said, can be dramatic and “are almost too numerous to mention.” There are acute reactions that occur instantly upon receiving the drug, and there are dangerous long-term side effects that occur days later. Many of these side effects are complex and poorly understood. When he started using it around fifteen years ago, things went well at first, and then, all of a sudden, his patients began to experience acute reactions when the drug went into the body. It turns out that some people tolerate the drug and some don’t. These reactions, he said, initially panicked him because they mimicked symptoms of an acute infection—fever, chills, pain, soaring heart rate, chest pressure, and difficulty breathing. On top of that, the drug had a mysterious psychological effect on a few patients. Within seconds of receiving the drug they became overwhelmed by a feeling of impending doom that, in the worst cases, made them believe they were actually dying. In those, he had to halt the infusion and sometimes administer a narcotic to calm down or knock out the patient. That acute reaction, however, usually went away quickly, and Nash emphasized that many patients experienced no reaction at all. I might be one of the lucky ones.

He reeled off other common side effects: nausea, vomiting, anorexia, dizziness, headache, insomnia, skin rash, fever, shaking, chills, and mental confusion; other physical effects include electrolyte imbalances, decreases in white blood cell count, and liver function abnormalities. These outcomes were so frequent, he explained, that I could expect to get at least some of them. But the most common and dangerous side effect is that the drug damages the kidneys, degrading renal function. The harm tends to be worse the older you are; old people, he said, lose renal function naturally as they age. I asked Nash if I was, at fifty-eight, in the “old” category, and he thought that was funny. “Oh, ho!” he cried. “So you’re still telling yourself you’re middle-aged? Yes, we all go through that period of denial.” As a general rule of thumb, he would stop administering the drug when kidney function had dropped to 40 percent of baseline.

The whole process, he said, is “stressful for the patient and stressful for the doctor.”

When I asked him if the disease was curable, he hemmed and hawed a bit. It’s curable in the sense that the symptoms go away. But it’s not curable in the sense that the body is completely rid of the parasite—what doctors call a “sterile cure.” Like chicken pox, which can come back years later as shingles, the parasite hides in the body. The point of the treatment is to beat down the parasite enough to allow the body’s immune system to take over and keep it in check. Rather than mounting a frontal attack on the body, a Pickett’s Charge, the parasite hides and shifts about, sniping from cover. But white blood cells talk to each other using chemicals called cytokines. The cytokines tweak how white blood cells respond to a leishmania attack, eventually “training” them to mount a better defense.

But the mucosal and visceral forms of the disease can come roaring back if your immune system goes downhill. That can happen, for example, if you get HIV or undergo cancer treatment or an organ transplant. In L. braziliensis, recurrences of the disease are not uncommon in people with good immune systems. But even in the best-case scenario your body must engage in low-level warfare with the parasite for the rest of your life.

While I was in the hospital for my biopsy, I visited Dave, who was recovering from his aborted treatment. He was installed in a large private room with a fine view of rooftops, trees, and lawns. Eager to see him for the first time since we left the jungle, I found him sitting on the side of the bed, dressed in a hospital gown. Even though I knew he’d been through hell, his appearance was a shock: Dave looked shattered, a far cry from the robust, sardonic professional who, festooned with cameras and cracking jokes, had a few months earlier tramped around the jungle in the pouring rain shoving lenses in our faces. But he managed to greet me with a wan smile and a sweaty handshake, not rising from the bed, and told me what had happened.