MALARIA

Both European and African immigrants introduced malaria, a mosquito-borne parasitical illness that produces alternating cycles of fevers and chills, to North America. From the British Isles, the early colonists brought vivax malaria, the great debilitator, that was known as "the ague." It became established in the British North American colonies, although outbreaks were only sporadic in the more northern territories, where human populations were low and adult mosquitoes died during the winter. The African captives brought falciparum malaria, the great killer. Falciparum became established in regions of the southern and middle colonies, alongside vivax malaria.

Both forms of malaria were prevalent in tidewater, marshy, riverine, and low-lying regions of the British North American colonies and are best considered as endemic. In the middle colonies, most malarial infections seem to have been vivax, with its low (characteristically, 1 to 2 percent) rate of mortality. In the southern colonies, both falciparum and vivax infections were common, particularly during the summer months.

The patterns of infection varied greatly, however, between Africans and Europeans. Almost all Africans were unable to contract vivax malaria, owing to a genetic mutation of a hemoglobin antigen known as red blood cell Duffy negativity. Europeans, on the other hand, were fully susceptible to vivax malaria, and because the vivax parasite could lie dormant in the liver, Europeans were subject to malarial relapses even without additional infection. Africans and Europeans also had differential responses to falciparum infections. Many Africans carried a genetic hemoglobin mutation known as hemoglobin S or sickle-cell that afforded considerable protection against the great killer. Europeans had no such genetic defense, and mortality during the first year of falciparum infections could run as high as 50 percent. The differential response to both vivax and falciparum underwrote European American convictions that the European and African "races" were biologically different and thus helped to rationalize the institution of racial slavery.

Malaria was, however, not only a disease of the eastern seaboard. As European American migrants opened up new territories beyond the Appalachian Mountains and began the great deforestations of the Ohio and Mississippi Valleys, malaria insinuated itself into the newly converted biomes. On soils broken by the plow, hoof, and wheel, rainfall puddled and produced ideal conditions for mosquito breeding. A frontier of malaria moved with the migrants, pushing westward a zone of endemic malarial infection.

The only effective cure during the eighteenth century was to ingest powdered bark from the cinchona tree, which grew high in the Andes. In 1820 pharmacists in France succeeded in isolating the antimalarial alkaloids from cinchona bark, and within a few years their techniques became known in the United States. In the early 1820s a new quinine industry took root in Philadelphia, and a national market developed. Quinine relieved suffering, but until the late nineteenth century the alkaloid remained expensive and its use was never sufficiently universal to break the chains of infection. Malaria continued to plague the nation into the late nineteenth century and, in some southern regions, the first half of the twentieth century.

See alsoEpidemics; Health and Disease; Medicine .

bibliography

Ackerknecht, Erwin H. Malaria in the Upper Mississippi Valley, 1760–1900. Baltimore: Johns Hopkins University Press, 1945. Reprint, New York: Arno Press, 1977.

Kiple, Kenneth F., and Virginia H. King. Another Dimension to the Black Diaspora: Diet, Disease, and Racism. New York: Cambridge University Press, 1981.

James L. A. Webb Jr.