Response To Sheldon Watts, "Yellow Fever Immunities In West Africa And The Americas In The Age Of Slavery And Beyond: A Reappraisal" - in this journal page 955

Journal of Social History, Summer, 2001 by Kenneth F. Kiple

In a review of Sheldon Watts Epidemics and History (which he cites in note 6) I complained, among other things, about words and phrases that were employed such as "guerilla terrorists" to describe Spanish conquistadors, as well as other unwarranted epithets to denigrate medical researchers of the past like Ronald Ross or Walter Reed. At the time I assumed that such deliberately offensive writing stemmed from the author's passion in blaming the West for the epidemiological and medical imperialism it had (often inadvertently) unleashed on the rest of the world. Now, however, I am wondering if this kind of reckless rhetoric could be a style.

The review in question was generally favorable, although apparently not favorable enough. I also objected to Watts dismissing "out of hand and with no discussion of the evidence" (p.105) our demonstration of a black resistance to yellow fever that could not be explained by acquired immunity. And Professor Watts writes (between notes 14 and 15) that in the aftermath of the publication of The Cambridge World History of Human Disease (which I edited) that I (and my followers???) "felt at liberty to criticize younger scholars who refused to accept the Kiple yellow fever orthodoxy."

The notion of an "old-guy" conspiracy guarding a non-existent orthodoxy is comical; less so is the contention that it is wrongheaded as well as racist and dangerous to point out that populations from areas of endemic yellow fever may have developed a tolerance for the disease that others without the benefit of such residence did not possess. Professor Watts is correct that I have puzzled over the question for the last quarter of a century or so. And during this time to my knowledge no one has ever spied evil or racist intent in that exploration, even though it dealt with sensitive issues and must have made a tempting target. Now that those days are obviously over, I am glad of a chance to restate my reasoning with the hope that it will never again be so misread, misunderstood, and especially misrepresented in the future.

Before looking directly at yellow fever immunities it might be useful to glance at the historical experience of human groups with a couple of other illnesses to remind ourselves of the ways, other than acquiring immunity by surviving diseases, that peoples have mustered some measure of resistance to them. Tuberculosis makes a good example. Historically, populations having a long experience with it have suffered significantly less from its ravages than those with only abbreviated exposure. The reasons for this differential experience are obscure. Immunity to tuberculosis cannot really be acquired; indeed prior exposure may make development of active disease much more likely. To be sure there is a high correlation between tuberculosis and poor nutrition and overcrowding, both functions of poverty. But it is difficult to study rampant tuberculosis among native- Americans, Afro-Americans and native Hawaiians during the latter decades of the nineteenth century and the early decades of the twentieth without also c rediting an extraordinary susceptibility to the disease. Conversely it is difficult to view the comparatively low morbidity and mortality rates of white counterparts and not credit some growing "natural" resistance to tuberculosis. And it would seem neither racist nor dangerous to emphasize the differential treatment that tuberculosis meted out, even though many questions of tuberculosis susceptibilities and immunities have, to date, eluded satisfactory explanations and thus, remain mysterious.

Another disease worth taking a look at is malaria, and especially falciparum malaria--the most lethal of the malaria types. Immunity to it can be acquired but it requires repeated infection to become effective and then is only a strain specific resistance. Probably because of such immunological imperfection, peoples with long residence in endemic malarial regions developed genetic defenses to supplement acquired immunity. But although such protective mechanisms have been present for millennia--and certainly helped to create in the minds of whites the conviction that blacks in the Americas were impervious to the disease, it was only in 1954 (not so long ago for some of us) that A.C. Allison correlated sickle trait with endemic areas of falciparum malaria. This study, in turn, confirmed hypotheses which had postulated that sickle trait offered malaria protection, and triggered research campaigns which turned up more sickling anomalies, along with thalassemia traits and blood anomalies--mostly, but not exclusive ly, among Africans or those of African descent--that conferred protection against falciparum malaria. Moreover, during the war in Viet Nam it was noticed that black soldiers were far more resistant to vivax malaria than white counterparts; subsequent research confirmed that blacks were almost completely refractory to this malaria type.

Since vivax malaria is not (not now at least) an especially lethal illness, nor is it any longer very prevalent in Africa, the question of why such protection developed in the first place is intriguing, with one plausible explanation being that this too confers resistance against falciparum malaria. But, as in the case of tuberculosis immunology, numerous obscure parameters stand between researchers and the answers to immunological questions.