1493_ Uncovering the New World Columbus Created - Charles C. Mann [61]
Duffy negativity is an example of inherited immunity, available only to people with particular genetic makeups. Another, more famous example is sickle-cell anemia, in which a small genetic change ends up deforming the red blood cell, making it unusable to the parasite but also less functional as a blood cell. Sickle-cell is less effective as a preventive than Duffy negativity—it provides partial immunity from falciparum malaria, the deadlier of the two main malaria types, but its disabling of red blood cells also leads many of its carriers to an early grave.
Both types of inherited immunity differ from acquired immunity, which is granted to anyone who survives a bout of malaria, in much the way that children who contract chicken pox or measles are thereafter protected against it. Unlike the acquired immunity to chicken pox, though, acquired malaria immunity is partial; people who survive vivax or falciparum acquire immunity only to a particular strain of vivax or falciparum; another strain can readily lay them low. The only way to gain widespread immunity is to get sick repeatedly with different strains.
Inherited malaria resistance occurs in many parts of the world, but the peoples of West and Central Africa have more than anyone else—they are almost completely immune to vivax, and (speaking crudely) about half-resistant to falciparum. Add in high levels of acquired resistance from repeated childhood exposure, and adult West and Central Africans were and are less susceptible to malaria than anyone else on earth. Biology enters history when one realizes that almost all of the slaves ferried to the Americas came from West and Central Africa. In vivax-ridden Virginia and Carolina, they were more likely to survive and produce children than English colonists. Biologically speaking, they were fitter, which is another way of saying that in these places they were—loaded words!—genetically superior.
Racial theorists of the last century claimed that genetic superiority led to social superiority. What happened to Africans illustrates, if nothing else, the pitfalls of this glib argument. Rather than gaining an edge from their biological assets, West Africans saw them converted through greed and callousness into social deficits. Their immunity became a wellspring for their enslavement.
How did this happen? Recall that vivax, covertly transported in English bodies, crossed the Atlantic early, as I said; certainly by the 1650s, given the many descriptions of tertian fever, quite possibly before. Recall, too, that by the 1670s Virginia colonists had learned how to improve the odds of survival; seasoning deaths had fallen to 10 percent or lower. But in the next decade the death rate went up again—a sign, according to the historians Darrett and Anita Rutman, of the arrival of falciparum. Falciparum, more temperature-sensitive than vivax, never thrived in England and thus almost certainly was ferried over the ocean inside the first African slaves.
Falciparum created a distinctive pattern. Africans in Chesapeake Bay tended to die more often than Europeans in winter and spring—the result, the Rutmans suggested, of bad nutrition and shelter, as well as unfamiliarity with ice and snow. But the African and European mortality curves crossed between August and November, when malaria, contracted during the high mosquito season of early summer, reaches its apex. During those months masters were much more likely to perish than slaves—so much more that the overall death rate for Europeans was much higher than that for Africans. Much the same occurred in the Carolinas. Africans there, too, died at high rates, battered by tuberculosis, influenza, dysentery, and human brutality. Many fell to malaria, as their fellows brought Plasmodium strains they had not previously encountered. But they did not die as fast as Europeans.
Because no colonies kept accurate records, exact comparative death rates