1493_ Uncovering the New World Columbus Created - Charles C. Mann [60]
The worst problem, though, was something else. As in Virginia, malaria came to Carolina. At first the English had extolled the colony’s salubrious climate. Carolina, one visitor wrote, has “no Distempers either Epidemical or Mortal”; colonists’ children had “Sound Constitutions, and fresh ruddy Complexions.” The colonists decided to use the warm climate to grow rice, then scarce in England. Soon after came reports of “fevar and ague”—rice paddies are notorious mosquito havens. Falciparum had entered the scene, accompanied a few years later by yellow fever. Cemeteries quickly filled. In some parishes, more than three out of four colonists’ children perished before the age of twenty. As in Virginia, almost half of the deaths occurred in the fall. (One German visitor’s summary: “in the spring a paradise, in the summer a hell, and in the autumn a hospital.”)
Unfortunately, Indians were just as prone to malaria as English indentured servants—and more vulnerable to other diseases. Native people died in ghastly numbers across the entire Southeast. Struck doubly by disease and slave raids, the Chickasaw lost almost half their population between 1685 and 1715. The Quapaw (Arkansas) fell from thousands to fewer than two hundred in about the same period. Other groups vanished completely—the last few dozen Chakchiuma were absorbed by the Choctaw. The Creek grew to power by becoming, in the phrase of one writer, “the receptacle for all distressed tribes.” It was God’s will, Carolina’s former governor observed in 1707, “to send unusual Sicknesses” to the Westo Indians, “to lessen their numbers; so that the English, in comparison to the Spaniard, have but little Indian Blood to answer for.”
Naturally, the colonists looked for a different solution to their labor needs—one less vulnerable to disease than European servants or Indian slaves.
VILLA PLASMODIA
Like other cells, red blood cells are covered by a surface membrane made up of proteins, the long, chain-like molecules that are the principal constituents of our bodies. One of these proteins is the Duffy antigen. (The name comes from the patient on whose blood cells the protein was first discovered; an “antigen” is a substance recognized by the immune system.) The Duffy antigen’s main function is to serve as a “receptor” for several small chemical compounds that direct the actions of the cell. The compounds plug into the receptor—think of a spaceship docking at a space station, scientists say—and use it as a portal to enter the cell.
The Duffy antigen is not especially important to red blood cells. Nonetheless, researchers have written hundreds of papers about it. The reason is that Plasmodium vivax also uses the Duffy antigen as a receptor. Like a burglar with a copy of the front-door key, it inserts itself into the Duffy antigen, fooling the blood cell into thinking it is one of the intended compounds and thereby gaining entrance.
Duffy’s role was discovered in the early 1970s by Louis H. Miller and his collaborators at the National Institutes of Health’s Laboratory of Parasitic Disease. To nail down the proof, Miller and his collaborators asked seventeen men, all volunteers, to put their arms into boxes full of mosquitoes. The insects were chockablock with Plasmodium vivax. Each man was bitten dozens of times—enough to catch malaria many times over. Twelve of the men came down with the disease. (The researchers quickly treated them.) The other five had not a trace of the parasite in their blood. Their red blood cells lacked the Duffy antigen—they were “Duffy negative,” in the jargon—and the parasite couldn’t find its way inside.
The volunteers were Caucasian and African American. Every Caucasian came down with malaria. Every man who didn’t get malaria was a Duffy-negative