1493: Uncovering the New World Columbus Created

by Charles C. Mann

  Because I am interested in Colón, I bought a copy of the translation when I spotted it in a used-book store. Part of a series the Italian state published to honor the five hundredth anniversary of his first voyage to the Americas, the book is a big, lush, cream-colored object that doesn’t fit on a standard bookshelf. Disappointing to readers like me, Gil and Varela announced in the introduction that “these previously unknown texts do not present any spectacular revelations” about Colón’s life and character. But halfway through the newly revealed chronicle of the admiral’s second voyage I came across a curious detail—one that wasn’t in the fine biographies by Samuel Eliot Morison and Felipe Fernández-Armesto.

  In the translation, Colón explains that after the expedition arrived at La Isabela “all my people went ashore to settle, and everyone realized it rained a lot. They became gravely ill from tertian fever.” Tertian fever, an old-fashioned term, refers to bouts of fever and chills that occur in a regular forty-eight-hour pattern—a day of sickness followed by a day of quiet, then a day of sickness as the pattern repeats (tertian, taken from the Latin for “three days,” derives from the Roman custom of counting time from the beginning of one period to the beginning of the next). Tertian fever is the fingerprint of the most important types of malaria, one of humankind’s most intractable scourges. Taken literally, Colón seemed to be saying that at La Isabela his men contracted malaria. No wonder the colonists didn’t want to work, I thought, and marked the passage with a pencil.

  In 2002 Noble David Cook, a historian at Florida International University, in Miami, published an article entitled, alarmingly, “Sickness, Starvation, and Death in Early Hispaniola,” which detailed the island’s catastrophic history after Colón’s landing. Researchers generally agree that human malaria did not exist in the Americas before 1492 (some believe a kind of monkey malaria was present). If Colón’s men contracted malaria, Cook explained, they must have brought the disease with them from Spain, which like much of Europe then was rife with the disease. It was a textbook case of the Columbian Exchange, recorded by its progenitor himself.

  Remembering the cream-colored book, I hauled it from my bookshelf and turned to the relevant passage. The original Spanish, printed on the facing page, didn’t use the Spanish words for malaria or tertian fever. Instead Colón wrote that his men had contracted something called çiçiones, a term I had never encountered. Why did Cook and the translator of Colón’s letter think this meant malaria?

  Çiçiones is hard to find in modern Spanish dictionaries—I consulted the dozen or so in my local library without success. Google, too, was no help. Nor was Colón himself. He provided no description of the symptoms of çiçiones, perhaps because he believed they were familiar to his readers. All he said about the disease, in fact, was to guess that it was spread by the native women around La Isabela, “who are abundant there; and since they [that is, the women] were immodest and disheveled, it is no wonder that they [that is, the men] had trouble.” To me, this sounded like the admiral thought çiçiones was some kind of venereal disease.

  But that doesn’t jibe with other sources, as I learned when I contacted an expert in sixteenth-century Spanish, Scott Sessions of Amherst College. The first dictionary of the Spanish language appeared in 1611, Sessions told me. In it is an entry for çiçiones: “the fever that comes with chills, which is attributed to the cierzo [mistral wind], because it is the most acute, cold and penetrating.” The next authoritative Spanish dictionary, issued in multiple volumes by the Royal Spanish Academy between 1726 and 1739, similarly defines çiçiones as “the fever that starts with chills, which from being acute and penetrating like the mistral wind, as [the first dictionary] says, one derives the word: but it more likely refers to tertian fever”—malaria. Cook and the translator, in other words, were correct: Colón may well have been describing malaria.

  The scenario isn’t implausible. Malaria can lie dormant in the body for months, only to reemerge at full strength. The disease is transmitted by mosquitoes, which take in microscopic malaria parasites when they drink blood from infected people and pass them on to the next people they bite. Colón left on his second voyage in September 1493. If one of his crew had a malaria relapse after landing in La Isabela, only one bite from the right type of mosquito would be necessary to spread the disease—and those mosquitoes are abundant on Hispaniola.

  All of this is highly speculative, to say the least. Today we know that many different diseases cause chills and fevers, including influenza and pneumonia. But for centuries people couldn’t distinguish one from another; they didn’t understand that malaria was a specific disease. Sessions, the Amherst historian, told me that paludismo, the Spanish word for malaria, didn’t appear in Royal Spanish Academy dictionaries until 1914. Even then, few realized that it was caused by a mosquito-borne parasite—the 1914 dictionary defined paludismo as a “group of deadly phenomena produced by marshy emanations.” (The English word “malaria” comes from the Italian mal aria, evil or bad air.) Colón was using a word that probably indicates malaria, in other words, but he could well have been describing ordinary chills and fever. A single word is not enough to make a diagnosis.

  Yet the impossibility of finding definitive answers does not mean historians should stop seeking them—the question is too important. Despite a global eradication program that began in the 1950s, malaria is still responsible for unimaginable suffering: more than three-quarters of a million deaths per annum, the great majority of them children under the age of five. Every year about 225 million people contract the disease, which even with modern medical care can incapacitate for months. In Africa it afflicts so many people so often that economists believe it is a major drag on development; since 1965, according to one widely cited calculation, countries with high rates of malaria have had annual per capita growth rates 1.3 percent less than countries without malaria, enough to ensure that many of the former lost ground to the latter.

  As it does today, malaria played a huge role in the past—a role unlike that of other diseases, and arguably larger. When Europeans brought smallpox and influenza to the Americas, they set off epidemics: sudden outbursts that shot through Indian towns and villages, then faded. Malaria, by contrast, became endemic, an ever-present, debilitating presence in the landscape. Socially speaking, malaria—along with another mosquito-borne disease, yellow fever—turned the Americas upside down. Before these maladies arrived, the most thickly inhabited terrain north of Mexico was what is now the southeastern United States, and the wet forests of Mesoamerica and Amazonia held millions of people. After malaria and yellow fever, these previously salubrious areas became inhospitable. Their former inhabitants fled to safer lands; Europeans who moved into the emptied real estate often did not survive a year.

  The high European mortality rates had long-lasting impacts, the Harvard and Massachusetts Institute of Technology economists Daron Acemoglu, Simon Johnson, and James A. Robinson have argued. Even today, the places where European colonists couldn’t survive are much poorer than places that Europeans found more healthful. The reason, the researchers said, is that the conquering newcomers established different institutions in disease zones than they did in healthier areas. Unable to create stable, populous colonies in malarial areas, Europeans founded what Acemoglu, Johnson, and Robinson called “extractive states,” the emblematic example being the ghastly Belgian Congo in Joseph Conrad’s Heart of Darkness, where a tiny cohort of high-collared Europeans forces a mass of chained, naked slaves, “shadows of disease and starvation,” to build a railroad to ship ivory from the interior.

  Tobacco brought malaria to Virginia, indirectly but ineluctably, and from there it went north, south, and west, until much of North America was in its grip. Sugarcane, another overseas import, similarly brought the disease into the Caribbean and Latin America, along with its companion, yellow fever. Because both diseases killed European workers in American tobacco and sugar plantations, colonists imported labor in the form of captive Africans—the
human wing of the Columbian Exchange. In sum: ecological introductions shaped an economic exchange, which in turn had political consequences that have endured to the present.

  It would be an exaggeration to say that malaria and yellow fever were responsible for the slave trade, just as it would be an exaggeration to say that they explain why much of Latin America is still poor, or why the antebellum cotton plantations in Gone with the Wind sat atop great, sweeping lawns, or why Scotland joined England to form the United Kingdom, or why the weak, divided thirteen colonies won independence from mighty Great Britain in the Revolutionary War. But it would not be completely wrong, either.

  SEASONING

  Malaria is caused by the two hundred or so species in the genus Plasmodium, ancient microscopic parasites that plague countless types of reptile, bird, and mammal. Four of those two hundred species target humankind. They are dishearteningly good at their jobs.

  Although the parasite consists of but a single cell, its life story is wildly complex; it changes outward appearance with the alacrity of characters in a Shakespearean comedy. From the human point of view, though, the critical fact is that it is injected into our flesh by mosquitoes. Once in the body, the parasite pries open red blood cells and climbs inside. (I am here skipping several intermediate steps.) Floating about the circulatory system like passengers in so many submarines, the parasites reproduce in huge numbers inside the cell. Eventually the burgeoning offspring burst out of the cell and pour into the bloodstream. Most of the new parasites subvert other red blood cells, but a few drift in the blood, waiting to be sucked up by a biting mosquito. When a mosquito takes in Plasmodium, it reproduces yet again inside the insect, taking on a different form. The new parasites squirm into the mosquito’s salivary glands. From there the insect injects them into its next victim, beginning the cycle anew.

  In the body, Plasmodium apparently uses biochemical signaling to synchronize its actions: most of the infected red blood cells release their parasites at about the same time. Victims experience these eruptions as huge, coordinated assaults—a single infection can generate ten billion new parasites. Overwhelmed by the deluge, the immune system sets off paroxysms of intense chills and fever. Eventually it beats back the attack, but within days a new assault occurs; some of the previous wave of parasites, which have hidden themselves inside red blood cells, have produced a new generation of Plasmodium, billions strong. The cycle repeats until the immune system at last fights off the parasite. Or seems to—Plasmodium cells can secret themselves in other corners of the body, from which they emerge a few weeks later. Half a dozen episodes of chills and fever, a bit of respite, then another wave of attacks: the badge of full-blown malaria.

  Single-celled Plasmodium parasites burst out of dying red blood cells, beginning the assault on the body that leads to full-blown malaria. (Photo credit 3.1)

  If the suffering caused by malaria today is difficult to grasp, it is almost impossible to imagine what it was like when its cause was unknown and no effective treatments existed. One can get a hint by reading the accounts of victims like Samuel Jeake, a seventeenth-century merchant in southeast England, who doggedly recorded every skirmish in his decades-long war with what we now recognize as malaria. To pick an example almost at random, here is Jeake on February 6, 1692, near the end of one six-month bout, stoically recording that he had been “taken ill the Seventh time: with a Tertian Ague [fever]; about 3h p.m. it began, & was of the same nature with my last which I had all January, but this was the worst.”

  Feb. 8: A 2d fit which took me earlier & was worse.

  Feb. 10: About noon a 3d fit. which shook me about 3h p.m. a very bad fit & violent feaver.…

  Feb. 12: Before noon, a 4th fit. with which I shook about 3h p.m. & then went to bed: where had a very violent Feaver; this being the worst fit of all: my breath very short; & delirious.…

  Feb. 14: About noon, a 5th fit.…

  Feb. 16: About 2h. p.m. a 6th fit, very little, or scarce sensible, but sweat much in the night. And it pleased God that this was the last fit.

  The respite lasted just fifteen days.

  Mar. 3: About 4h. p.m. Taken ill the Eighth time: of a Tertian ague, succeeded by a Feaver & sweat in the night.…

  Mar. 5: About 3h p.m. A 2d fit; worse than the former.

  The attacks stopped nine weeks later. But malaria was not done with Jeake. The parasite, a superbly canny creature, can hide in the liver for as long as five years, periodically emerging to produce full-blown malarial relapses. Six months later, Plasmodium again massed in his blood.

  Tertian fever of the sort experienced by Jeake is the signature of Plasmodium vivax and dium falciparum, which cause the two most widespread types of malaria. Despite the similarity of the symptoms, the two Plasmodium species have different effects on the body. After inserting itself inside red blood cells, falciparum, unlike vivax, manages to alter them so that they stick to the walls of the tiny capillaries inside the kidneys, lungs, brain, and other organs. This hides the infected cells from the immune system but slowly cuts off circulation as the cells build up on the capillary walls like layers of paint on an old building. Untreated, the circulation stoppage leads to organ failure, which kills as many as one out of ten falciparum sufferers. Vivax doesn’t destroy organs, and thus is less deadly. But during its attacks sufferers are weak, stuporous, and anemic: ready prey for other diseases. With both species, sufferers are infectious while sick—mosquitoes that bite them can acquire the parasite—and can be sick for months.

  dium, a tropical beast, is exquisitely sensitive to temperature. The speed at which the parasite reproduces and develops in the mosquito depends on the temperature of the mosquito, which in turn depends on the temperature outside (unlike mammals, insects cannot control their own internal temperature). As the days get colder, the parasite needs more and more time to develop, until it takes longer than the mosquito’s lifespan. Falciparum, the most deadly variety of malaria, is also the most temperature sensitive. Around 72°F it hits a threshold; the parasite needs three weeks at this temperature to reproduce, which approaches the life expectancy of its mosquito host; below about 66°F it effectively cannot survive. Vivax, less fussy, has a threshold of about 59°F.

  Unsurprisingly, falciparum thrives in most of Africa but gained a foothold only in the warmest precincts of Europe: Greece, Italy, southern Spain, and Portugal. Vivax, by contrast, became endemic in much of Europe, including cooler places like the Netherlands, lower Scandinavia, and England. From the American point of view, falciparum came from Africa, and was spread by Africans, whereas vivax came from Europe, and was spread by Europeans—a difference with historic consequences.

  Human malaria is transmitted solely by the Anopheles mosquito genus. In Jeake’s part of England the principal “vector,” as the transmitting organism is known, is a clutch of tightly related mosquito species known jointly as Anopheles maculipennis. The mosquito’s habitat centers on the coastal wetlands of the east and southeast: Lincolnshire, Norfolk, Suffolk, Essex, Kent, and Sussex counties. A. maculipennis—and the dium vivax it carries—seem to have been uncommon in England until the late sixteenth century, when Queen Elizabeth I began encouraging landlords to drain fens, marshes, and moors to create farmland. Much of this low, foggy terrain had been flooded regularly by the North Sea tides, which washed away mosquito larvae. Draining blocked the sea but left the land dotted with pockets of brackish water—perfect habitat for A. maculipennis. Farmers moved into the former marsh, still soggy but now usable. Their homes and barns, heated during cold weather, provided space for the mosquito—and the vivax parasites inside its body—to survive the cold weather, ready to breed and spread in the following spring.

  As the British medical historian Mary Dobson has documented, draining the marshes set off an inferno of vivax malaria. Visitors to maculipennis habitat recoiled at the wretchedness they encountered. An all-too-typical sight, lamented the Kent writer Edward Hasted in 1798, was “a poor man, his wife, and whole family of f
ive or six children, hovering over the fire in their hovel, shaking with an ague [fever], all at the same time.” Curates died in such numbers after being sent to coastal Essex, the writer John Aubrey remarked, that the area was known as “Killpriest.” Natives fared no better; babies born in the marshland, Hasted wrote, seldom “lived to the age of twenty-one.” Dobson recorded baptisms and burials in twenty-four wetland parishes. In the 1570s, before Queen Elizabeth drained the swamps, baptisms exceeded burials by 20 percent—the population was rising. Two decades later draining was in full swing, and burials outnumbered baptisms by almost a factor of two. Population boomed elsewhere in England, but these parishes didn’t return to their earlier growth rates for two centuries.1

  “The marshes would have these bursts of mortality,” Dobson told me. “About every ten years they’d have a year in which 10 or 20 percent of the population would die. A few miles away, in higher ground, were some of the healthiest parts of England.” Inured to the cavalcade of suffering, residents viewed their circumstances with fatalistic cheer. (Readers of Charles Dickens will recall the stoicism of the fen-dwelling Gargerys in Great Expectations, raising the child Pip within a short walk of the “five little stone lozenges” that marked the resting places of his “five little brothers.”) Traveling in feverish Essex County, writer Daniel Defoe met men who claimed to have “from five or six, to fourteen or fifteen wives.” Explaining how this was possible, one “merry fellow” told Defoe that men thereabouts brought in wives from healthier inland precincts.

  [W]hen they took the young lasses out of the wholesome and fresh air, they were healthy, fresh and clear, and well; but when they came out of their native air into the marshes among the fogs and damps, there they presently changed their complexion, got an ague or two, and seldom held it above half a year, or a year at the most; and then, said he, we go to the uplands again, and fetch another.