1493: Uncovering the New World Columbus Created (15 page)

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 five 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.

The marshman laughed as he spoke, Defoe wrote, “but the fact, for all that, is certainly true.”

In 1625 the bubonic plague engulfed England. More than fifty thousand people died in London alone. Many of the urban wealthy fled into the malarial eastern marshes, with results later described by the satirical poet George Wither:

In Kent, and (all along) on Essex side
A Troupe of cruell Fevers did reside:…
And, most of them, who had this place [London] forsooke,
Were either slaine by them, or Pris’ners tooke…

As this nineteenth-century copy of a now-lost earlier drawing suggests, malaria was long a constant fear in England’s southeastern marshlands. (
Photo credit 3.2
)

In the end, Wither explained, “poorest beggers found more pitty here [London], / And lesser griefe, then richer men had there.” The implication is mind-boggling: people who fled to vivax country would have been better off staying home with the bubonic plague.

Data are sketchy and incomplete, but according to the Brandeis University historian David Hackett Fischer about 60 percent of the first wave of English emigrants came from nine eastern and southeastern counties—the nation’s
Plasmodium
belt. One example was the hundred-plus colonists who began Jamestown. Fifty-nine of their birthplaces are known, according to Preservation Virginia, the organization that backs Jamestown archaeology; thirty-seven were in malaria-ridden Essex, Huntingdonshire, Kent, Lincolnshire, Suffolk, Sussex, and London. Most of these men, one assumes, set off from higher, inland areas that were less malarial than the coastal wetlands. But many would have come from the marshes. Even those who didn’t come from the malaria zone usually passed through it just before departure, their ships waiting for weeks or months at Sheerness, a Kent harbor town near the mouth of the Thames that was a malaria center. Other ships waited at the almost equally pestilential Blackwall, east of London on the same river.

People in malarial paroxysms would have been unlikely candidates for an arduous sea voyage. But
Plasmodium vivax
, one recalls, can hide itself inside the apparently healthy. Colonists could board a ship without symptoms, land in Chesapeake Bay tobacco country, and then be struck by the teeth-chattering chills and sweat-bursting fevers of malaria. At which point, alas, they could unknowingly pass the parasite to every mosquito that bit them.

“In theory, one person could have established the parasite in the entire continent,” said Andrew Spielman, a malaria researcher at the Harvard School of Public Health. Almost certainly many of the
tassantassas
at Jamestown were infectious. At some point one of them was bitten by
Anopheles quadrimaculatus
, a cluster of five closely related mosquitoes that is the East Coast’s primary malaria vector. “It’s a bit like throwing darts,” Spielman told me before his death in 2006. “Bring enough sick people in contact with enough mosquitoes in suitable conditions, and sooner or later you’ll hit the bull’s-eye—you’ll establish malaria.”

By 1657 the governor of Connecticut colony, John Winthrop, was recording cases of tertian fever in his medical journal. Winthrop, a member of the Royal Society, was one of the most careful scientific observers in New England. “If he said he saw tertian fever, he probably was seeing tertian fever,” said Robert C. Anderson, the genealogist who is transcribing Winthrop’s medical journal. More than that, Anderson told me, the existence of malaria in the 1650s suggests a date of introduction before 1640—after that year, political convulsions in England shut down emigration to New England for decades. “There were few colonists to bring it over,” Anderson said. If
Plasmodium vivax
had come to Connecticut by, say, 1635, I asked Spielman, could one make any inferences about Virginia? “New England is
cold
,” he said. “It’s hard to believe that malaria would have established itself there before Virginia.” Could the parasite have invaded Chesapeake Bay as early as the 1620s? “Given that hundreds or thousands of people from malaria zones came into the area, I wouldn’t have trouble believing that,” he said. “Once malaria has a chance to get into a place, it usually gets in fast.”