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sick
with
malaria. The typical Malawian kid might suffer a dozen episodes of malaria within the first two years of life and think nothing of it. Which is why if you asked a local if he’d ever had malaria, as I foolishly once did, his reactions would be similar to how a New Yorker or Londoner might respond if a reporter asked if he’d ever had a cold. “Yeeessss,” he’d say, eyebrows raised. As in: “And what of it, pray tell?”
    Thanks to their acquired immunity, only a fraction of Malawians with the malaria parasite living in their blood get seriously sick from it, suffering the fever and chills of “clinical” malaria. Most of them are the “uncomplicated” cases, which resolve themselves on their own. But sometimes, out of nowhere, an otherwise routine falciparum infection will turn vicious. After suffering through the usual few days of fever, instead of slowly recovering, the victim will start convulsing and fall into a coma. Older victims suffer kidney failure, and their lungs collapse or fill with fluid. If they are not treated rapidly, they will almost surely die. Even if they are treated with the very best and most effective therapies, 20 percent will die. Nobody knows why.
    Some contributory mechanisms are understood, at least in outline. Blood cells infected with falciparum parasites became sticky and get clogged in the small blood vessels. This is likely a survival tactic for the parasite. Stuck inside the vessels, it avoids being washed into the bloodstream and neutralized by the pathogen-killing spleen. There it can grow and develop undisturbed. 55 But the clogged vessels deprive the victim’s tissues of oxygen, and clogged microvessels in the brain can starve the brain and bring on coma. 56
    Malarial coma doesn’t always result in death; four times out of five the comatose patient wakes up, gets out of bed, and is able to walk home (albeit with subtle cognitive deficits, for some). Perhaps such patients are blessed with some as-yet-unknown genetic endowment. Another theory is that those who die are infected by some especially virulent tribe of falciparum parasite. Often malaria patientsare infected by several different, genetically distinct strains of
P. falciparum
. Taylor has seen, under the microscrope, three different parasites gorging upon the same blood cell. Perhaps the winning parasite in such struggles is the most aggressive one, which somehow triggers the kind of malaria that kills. Or perhaps mortality in these cases is a result of the multiple infection itself. 57 But then again, says Taylor, there’s no real evidence that the distinctions observed between parasite strains have any significance at all. They could be as meaningless as different-size spots on a dog.
    What we do know is this: this rare and precipitous complication of falciparum infection—called simply severe malaria—develops in perhaps 2 percent of all clinical malaria cases 58 and accounts for nearly 90 percent of all the deaths from malaria worldwide. 59
    On Duke’s second day on the ward, the antimalarial drugs and blood transfusion his doctors gave him started to work. The drugs starved the parasite in his cells, and its numbers started to fall. His blood thickened with healthy red blood cells. He stopped posturing and convulsing, and his fever dropped. His gaze steadied. Taylor and her team were thrilled, jubilant.
    By the afternoon, even as the population of parasites in Duke’s body continued to ebb, the speckling of his eyeballs multiplied. That evening, suddenly, Duke stopped breathing. Taylor’s team rushed to his side. His heart thrummed an even, loud rhythm. But one by one his organs failed. His heartbeat kept going. “So strong!” remembers Taylor. “You just can’t stop trying!” They tried to resuscitate him for two hours.
    A few days later, I stand in the clinic’s lab examining the boy’s cauliflowered brain, which Taylor has had excised and pickled in a small Tupperware container after the