by Sonia Shah
Duke and the other comatose children who appear in Taylor’s ward are surely sick, and they are often clearly carrying the malaria parasite, but this isn’t enough for doctors to know that they are 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 patients are 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 cases58 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 boy died. Since 1996, Taylor and her colleagues have been conducting an extraordinary study in which the bodies of children who died of malaria are autopsied and scrutinized for clues to the series of events that led to their deaths. Duke’s brain is riddled with tiny spots, signs of some epic battle with the falciparum parasite. “Is that what killed him?” I ask. Taylor isn’t sure, even holding the boy’s brain in her hands. “I have no idea,” she says softly, swishing the container.
Before I leave, Taylor insists I see the miscreant itself. “Show her how pretty the parasites are in red cells!” she instructs the lab tech. Peering into a microscope focused on a drop of infected blood, falciparum parasites are clearly visible. For Taylor it is an image fraught with mystery and power. “They’re beautiful!” she blurts.
I go to find my bicycle, locked outside. The rain has started, and as I hurry through the halls, earthy odors rise through the moist air. Soon the rain is pounding on the corrugated tin roof, and I must wait. An orange dog similarly takes cover under the eaves in the gulley, trying not to get wet.
There’s a tiny room in the hospital, at the end of a hall filled with desultory waiting patients, where the facility’s medical records are kept. Despite the caprice of the pathogens that stalk its patients, the enduring mystery of how they kill, each piece of paper describing the carnage finds its way there and is collected into eight-inch piles, carefully tied with string. Part of Duke’s story, like that of thousands of others like him, certainly rests in those pages, a final whisper of his short life after his distraught family trekked back home to their village. Researchers such as Terrie Taylor extract bits into computerized databases in hopes of one day deciphering those yellowing stacks. For now, they line the walls of the tiny room from floor to ceiling. The rain ends as abruptly as it started. The door is ajar as I pass by on my way to the exit, and I glimpse the shelves, buckling under the weight.
3. SWEPT IN MALARIA’S CURRENT
When historians consider how infectious diseases have shaped human history, they don’t generally make much of malaria. Other pathogens—smallpox, measles, plague—have made a much bigger splash, by piling up the bodies, fast. But malaria’s tide also has sculpted our landscape, in more subtle but equally long-lasting ways, from refashioning the ethnic makeup of sub-Saharan Africa to determining settlement patterns in the Americas and even influencing the creation of Great Britain.
There was a strange moment at the Multilateral Initiative on Malaria’s international scientific meeting held in Yaoundé, Cameroon, in 2005. Malariologists from Europe and North America and a sprinkling of African scientists had descended upon the sweltering city to deliver earnest presentations on the latest techniques in the fight against malaria.
One afternoon early on in the conference, a local television journalist took the stage; how he’d gotten on the program is unclear. In a tailored suit, he had far outdressed the scruffy scientists assembled in the audience. His address was brief—which was probably for the best, as he quickly overturned the central premise of the meeting. He began by recounting his own malarial fevers, but not in the hushed stentorian tones of the others. For him, malaria was more like the annoying cousin who comes to visit over the holidays. And then he implied that malaria wasn’t Africa’s scourge, and that the malariologists present weren’t Africa’s saviors. Au contraire: malaria, he said, had saved Africa; it was the scientists who were the invaders.
Channeling the nineteenth-century king of Madagascar who famously boasted that no invader could take on his country’s hazo (impenetrable forests) or tazo (its malignant malarial fevers), he extolled “General Anopheles” for thwarting the armies that would have attacked Africa.1 And now, “you scientists,” the journalist said, smiling and gesturing at the crowd, “are trying to take him on again!”2
His speech, with its somewhat ungracious equation of malaria scientists with imperialist intruders, passed without comment, and the conference continued as before, focusing on malaria’s undeniable burden upon its local victims. There were slide shows. There were tours of malaria clinics. There were pleas for more funding, for better statistics, for more public atten
tion. But through it all resonated the message behind the journalist’s words: Not everyone living under P. falciparum’s spell considers their situation an unmitigated misfortune. It isn’t easy to live with malaria, but those who survive the gauntlet of a falciparum-infested childhood gain a powerful immunological advantage over others. P. falciparum, deadly for outsiders, can no longer kill them.
The Bantu-speaking farmers who spread from western Africa and throughout the interior of southern Africa were among the first peoples whose relative immunity to P. falciparum likely vanquished potential rivals. Linguistic evidence shows that the three hundred or so different language groups found in the wide expanse of southern Africa diverged from a shared proto-Bantu language three thousand to four thousand years ago. There was, at one time, a greater diversity of linguistic groups on the continent. Remnants of these hunter-gatherer populations remain, speaking non-Bantu-derived languages, living mostly on more marginal lands, and often in positions of political subordination.
Somehow, over a few thousand years, the Bantu-speaking farmers spread across the entire continent, pushing nomadic hunter-gatherers to the edges. How did they achieve this rapid hegemony? Some say the Bantu enjoyed better diets or were more fearsome warriors. But neither of these theories fully accounts for their swift dominance.
From what we know about the early Bantu peoples, they would have had far greater tolerance to falciparum malaria than the hunter-gatherers. Here’s why: Living in fixed agricultural communities where Anopheles gambiae roosted would have subjected the Bantu to year-round falciparum infection. Endemic falciparum malaria would have regularly killed their babies, children, and first-time mothers. But those who survived pregnancy and infancy would have enjoyed an advantage that no outsider could have claimed. P. falciparum— at least the local strain to which their immune systems had been primed—could no longer kill them. It would have weakened them and made them sick on occasion, but no adult from an endemic region would have died from falciparum malaria.
Nomadic hunter-gatherers did not create or live around A. gambiae habitat as the Bantu did. Wandering across dry areas, where A. gambiae were scarce, meant that their exposure to P. falciparum would have been minimal. On occasion, and more often as the malarious farmers multipled and spread, these falciparum-naïve bands of hunter-gatherers would have happened upon an infested settlement, and P. falciparum would have rampaged unfettered in their virgin bodies.
Over time, the accumulation of such encounters would have decimated once wide-ranging African communities such as the Khoisan, Pygmy, Cushite, and those speaking Mande and Atlantic languages, and pushed their bedraggled survivors to the periphery of the continent, where they remain to this day. The immunological fence that P. falciparum built around the Bantu repelled incursions by outsiders as effectively as a standing army. The Bantu villagers didn’t have to be bigger or stronger to beat back the nomads: a couple of bites from their mosquitoes did the trick.3
• • •
Diminished to the point of vanishing in Africa some ten thousand years ago, P. vivax reemerged some five thousand years later in ancient Egypt, Greece, India, and China. Antigens to Plasmodium in five-thousand-year-old Egyptian and Nubian mummies and references to malaria in four-thousand-year-old Sumerian and Egyptian texts testify to the parasite’s arrival.4 Also, the ancients described the disease in vivid enough terms for historians to confirm its identity. Ancient Greeks understood malaria as a seasonal scourge that arrived during harvest time. The physician Hippocrates described it as a disease common around swamps, while the poet Homer referred to malaria when he decried Sirius as an “evil star” that was the “harbinger of fevers.”5 The ancient Chinese called malaria the “mother of fevers,” while in India thirty-five hundred years ago it became known as the “king of diseases,”6 personified by the fever demon Takman. The Vedic sages accurately described malaria’s signature chills and fever. “To the cold Takman,” they wrote, “to the shaking one, and to the deliriously hot, the glowing, do I render homage. To him that returns on the morrow, to him that returns for two successive days, to the Takman that returns on the third day, shall homage be.”7
By the time of Christ, P. vivax had swept over temperate Europe, and it entered northern Europe during the early Middle Ages. By the sixteenth century, P. vivax was deeply ensconced in Europe and Asia, P. falciparum held Africa in its thrall, and the Americas teemed with mosquitoes with pristine, parasite-free guts. As human populations and the Plasmodium parasites in their veins collided during the age of exploration and conquest, malaria’s differential killing power shuddered through the continents, altering the fate of nations.
On the continent of Africa, the falciparum malaria to which locals had become partially immune violently repelled unexposed European explorers and would-be conquerors. When European armies attempted to capture African gold mines in the 1570s, P. falciparum felled their soldiers, sleeping sickness took down their horses, and the Africans’ iron weapons vanquished the rest.8 P. falciparum killed the majority of the party of Portuguese missionaries and soldiers sent up the Zambezi River in 1569; in 1841, it sickened 80 percent of Thomas Fowell Buxton’s party of 159, sailing up the Niger.9 Fevers killed 88 out of 108 Europeans on an 1825 expedition into the Gambia.10
For centuries, Europeans could sustain little more than lightly manned trading posts in Africa.11 Malaria and other African diseases to which the Europeans had no immunity usually killed half of any group within a year of their arrival on the continent. That mortality rate, writes historian Philip Curtin, was “simply too high” for more intensive occupation.12 The British wouldn’t even risk exiling their convicts there. After the loss of its American colonies, British Parliament debated the notion of sending convicts to Gambia, but noting that such an exile amounted to a death sentence, they decided against it. They sent them to the terra incognita of New South Wales, Australia, instead.13
Most scientists agree that the Americas were malaria-free for thousands of years before Europeans arrived. The first human settlers may have had malaria parasites in their blood and livers when they crossed the Bering Strait eleven thousand years ago, but the parasites would have withered and died during the slow, frigid, mosquito-free journey.
When colonists from England arrived in the early 1600s, they had parasites roosting in their veins, and they encountered a land teeming with mosquitoes and wetlands, much more so than today. Swamp, bog, wetland, and marsh covered more than 220 million acres of the region that would become the United States.14 A beaver population roughly forty times that of today’s flooded even more land every year.15 And this temperate mosquito wonderland was connected by a narrow isthmus to the tropical South American continent, which was dripping with dense mosquito-friendly rain forest.
The New World’s mosquitoes included an array of Anopheles species. Anopheles crucians spread its wings in the Floridian cypress swamps. Clouds of Anopheles punctipennis swarmed the continent’s great temperate forests, and Anopheles quadrimaculatus16 gathered at the edges of sun-dappled lakes. In Europe, malaria parasites had rendered such watery environs uninhabitable, but Native Americans were able to exploit the lush and abundant wetlands to the fullest.
In the spring of 1607, the English sailed gingerly into the Chesapeake Bay and up the James River. Wary of attack from the local Algonquins—as well as from the Spanish, farther south—they denied themselves the dry, fertile ground farther inland in favor of a small island in the river, separated from the mainland by a narrow channel. Whatever they gained in strategic security, though, the Jamestown colonists lost in vulnerability to the local Anopheles, for marshes covered the low-lying island, and the mosquitoes that hatched from them likely started biting the colonists not long after their arrival.17
The English called vivax malaria the ague (the word rhymes with “plague you”), and we know that at least one of the Jamestown settlers was probably infected with it when he arrived. Shortly before his departure for Jamestown, Nathaniel Powell descr
ibed his malarial state in a letter: “I have not yet lost my quartane Ague,” he wrote, “but as I had him yesterday so I expect him on Thursday next.”18 Given the relatively quick transit time across the Atlantic (compared, at least, with the earlier traverse of the Bering land bridge), infected colonists such as Powell almost certainly ferried viable vivax parasites to Jamestown.
Malaria’s arrival wouldn’t have emerged as a major force to be reckoned with at first. Measles and smallpox destroyed the local native peoples with cruel efficiency, while diseases of filth—typhoid, dysentery—ransacked the Jamestown settlers.19 But those pathogens don’t have much staying power. Measles and smallpox burned through all the virgin blood available to them and then receded to near oblivion. And as soon as conditions in new settlements improved even marginally, dysentery and typhoid started to recede, too. What the settlers had to live with, in the long term, was malaria, cresting like a shark on the undertow.
By the mid-1600s, the surviving Virginia settlers took over the local Native Americans’ drier, more fertile lands, but in an age of water travel they could never stray too far from the mosquito-ridden lowlands by the rivers and bays, and by the late 1600s, vivax malaria had become endemic. Living in Virginia required suffering what residents called a “seasoning”—that is, “two or three small fits of a feaver and ague,” as one settler wrote in 1687.20
The penalty of “seasoning” and the subsequent debility of chronic malaria infection reduced Jamestown and the other Chesapeake colonies to a sorry state. Chroniclers of the day described the survivors’ dirt-floored, windowless houses riven with cracks, and their farms littered with rotting stumps.21 They’d be lucky to pull in three pounds sterling in annual profit.22 Those who did prosper—such as Powell, who joined the governor’s council in 1619—enjoyed a modicum of immunity to P. vivax. Like Powell, many had grown up in low-lying Kent and Essex, two of the most malarious counties in England.23