RESPONSE TO SHELDON WATTS, "YELLOW FEVER IMMUNITIES IN WEST AFRICA AND THE AMERICAS IN THE AGE OF SLAVERY AND BEYOND: A REAPPRAISAL".

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.

The same may be true in the case of yellow fever. The lecture by Professor Watts, notwithstanding, I (as well as everybody else I have read who has written about the disease since its etiology and epidemiology were unraveled) have repeatedly pointed out the importance of immunity to yellow fever that is acquired by hosting the virus and surviving it--a feat most readily accomplished by the young whose form of the disease is generally mild. Consequently, most adults put aboard slave ships to the Americas from African endemic yellow fever regions would doubtless have already acquired an immunity to the disease as children that made their experience in the New World with epidemic yellow fever dramatically different from that of Europeans (or native Americans for that matter) who were facing the disease for the first time as adults.

Presumably, however, the children of the arrivals with yellow fever immunity would have had to earn their own immunity just like everybody else, and it is true that both whites and blacks from Rio de Janeiro to Cartagena, from Bricigetown to Kingston, and from New Orleans to Charleston did acquire yellow fever immunity to the extent that they came to regard the disease as "strangers fever" and nothing for them to worry about. It is also true that these cities (and others in yellow fever's path where there was economic opportunity) were frequently filled with "strangers" who monopolized the death rolls generated by the disease. And finally it is true that until the end of the slave trade thousands upon thousands of immune individuals from Africa continued to be delivered to the Americas annually to reinforce the idea that black people were somehow impervious to yellow fever.

Yet, despite this, in epidemic after epidemic, my reading of contemporary reports suggests that blacks seemed to enjoy some sort of special protection that went beyond acquired immunity, and such "special protection" is visible in those few instances where acquired immunity could not have played much of a role. One of these occurred during what is generally acknowledged to be the beginning of yellow fever's Caribbean career. The official debut of yellow fever in the New World took place in 1647 in Barbados. And according to data provided by Jorge Leroy y Cassa (La primera epidemia de fiebre amarilla en la Habana, en 1649. Habana 1930, 39-40) the disease reached Havana in 1649 to elevate the mortality level as follows:

Deaths in Havana 1646-1650
Year  Deaths  Estimated death rates per 1,000
1646    87                   19
1647   106                   23
1648   134                   29
1649   562                  122
1650   148                   32
That mortality, however, was restricted mostly to the white population:
Havana Deaths by Month and Race, 1649
Month      Whites  Blacks
January       7       1
February     10      --
March         3      --
April         3      --
May           4      --
June          2       2
July          7       5
August      208       4
September   235       8
October      24       3
November     20      --
December     13       3
Totals      536      26

Unlike Barbados at the time (which was the first of the Caribbean Islands to undergo a sugar revolution and import African slaves to fuel that revolution) Cuba was a sparsely settled Spanish outpost and an economic backwater hardly in need of a slave trade. Many of the estimated 4,600 individuals in Havana were there to defend the city, and victual Spanish ships, with an estimated 600 of these of African descent, but mostly Creole-born meaning that, like the whites, they had had no opportunity to acquire immunity in a heretofore yellow fever free New World.

The next example comes long after the British had abolished their slave trade (1807) and thus long after the waves of arriving Africans armed with yellow fever immunity acquired in their homeland had ceased. K.H. Uttley ("The Mortality of Yellow Fever in Antigua, West Indies, Since 1857," West Indian Medical Journal, 9:1960, 185-88) has presented data on yellow fever mortality in Antigua during the years 1857 to 1895 (presumably both blacks and whites would have had equal opportunity to acquire immunity during this period) which reveals that 84 percent of the Island's yellow fever deaths were among whites even though 96 percent of the population was black.

In both the Havana example and that of Antigua blacks did not escape the disease entirely, and they probably suffered considerably more than the death records indicate. As the nineteenth century advanced and the slave trades to the New World began to wither and finally die, physicians and other observers started to notice that black people did get yellow fever after all. They just did not die of it like whites did. In Port Royal in the South Carolina Sea Islands, for example, of the 137 blacks that did not flee in the face of its 1877 yellow fever epidemic 87 contracted the disease. But only one died. By contrast of the 100 or so whites who remained most contracted the disease and one-quarter of those died.

A final example lies in the 1878 yellow fever outbreak in Memphis Tennessee where practically everybody--both black and white--should have been without acquired immunity to the disease because yellow fever was both a relatively new and an infrequent visitor that far up the Mississippi. And they clearly were. Fully 11,000 of the city's black population of around 14,000 were infected with the yellow fever virus, as were practically all of the 6000 whites that did not leave the city. But according to the death records only 9 percent of the blacks died as opposed to 70 percent of the whites.

Of course none of these mortality data is precisely accurate--not those from the first outbreak in Havana, nor those from the mortality rolls of Antigua, and certainly not those from Memphis. But what they do indicate, even if imperfectly, is the magnitude of the difference with which yellow fever treated blacks and whites. Clearly those of African descent were not immune to the disease. But they were far more likely to survive it than those of European descent.

This, then, is the "special protection" I referred to earlier. But it was not a racial protection any more than sickle trait is racial protection against falciparum malaria. Rather, just as sickle trait was selected for as a defense against endemic falciparum malaria to supplement acquired immunity (probably by helping the individual stay alive long enough to acquire an effective resistance) it seems likely that the ability we can discern to survive yellow fever infection would have developed in areas of endemic yellow fever to also help the individual acquire immunity by surviving the disease.

Thus, the heavy mortality suffered by blacks in the Nuba mountains of Sudan (1940) and in the Omo Valley of Ethiopia (1960-62) is exactly what one might expect to happen to peoples, black or white, whose roots were in areas that lay on the edge or beyond the zone of endemic yellow fever, and consequently were immunologically defenseless. But beginning toward the end of the nineteenth century colonialism helped to create similar conditions of susceptibility even within yellow fever zones by shuffling people about, and moving many outside their traditional disease environment. Civil wars, in turn, have accomplished much the same thing in the aftermath of colonialism. This may help to explain the reemergence of epidemic yellow fever in Nigeria in 1968, which continues to trouble the country to this day. But reports of the disease have characterized it as both extremely virulent and relatively mild, and these reports, along with serious difficulties in correctly diagnosing the illness (it is frequently confused w ith malaria, hepatitis and other maladies), all serve to underscore the complexity of what beginning in the 1980s has seemed to be a new sort of yellow fever (T.F. Tsai et al. "Investigation of a possible yellow fever epidemic and serosurvey for flavivirus infections in northern Cameroon, 1984," Bulletin of the World Health Organization 65: 1987, 855-60). Wilbur G. Downs et al. "Yellow Fever," chapter 38 in John A. Spittell, Jr. (ed) Clinical Medicine, Philadelphia, 1981; K.M. De Cock et al., "Epidemic Yellow Fever in Eastern Nigeria, 1986, The Lancet, March 19,1986,630-632; and Wilbur Downs, "The known and the unknown in yellow fever ecology and epidemiology," Ecology of Disease 1: 1982, 103-110).

Among the confounding variables discussed in the above essays is the replacement of the Aedes aegypti mosquito as the major yellow fever vector in tropical Africa by a large number of other mosquito species. Another is that the virulence of yellow fever, a flavivirus, may depend on the activity of other flaviviruses, such as the dengues, to which antibodies are also developed. And yet another possibility is that some yellow fever strains have increased in virulence with or without the help of new vectors and quite apart from the activity of other flaviviruses. In awaiting epidemiological explanation we might speculate that the recent African yellow fever epidemics may turn out to constitute still another chapter in the history of yellow fever--and one that will not shed as much light as we would like on earlier chapters.

I will close by touching on two more difficulties that I have with the present arguments of Professor Watts--but two difficulties which may help to buttress charges I also made in the review, namely that he does not always seem to have read the sources he cites, and that, at times, his grip on epidemiological history seems a bit shaky. In the first instance perhaps Professor Watts was just swinging wildly when he resurrected the question of the continent of yellow fever's origin. The Mayan writings he mentions, and other scant evidence of an American origin for yellow fever were discounted and the entire argument laid to rest by experts in tropical medicine decades ago. It was only before the fundamentals of the etiology and epidemiology of the disease were grasped that an argument for an American origin could be plausibly advanced. Important in discounting notions of an American origin were the discoveries that Native Americans, including the Mayans, had no acquired immunity to yellow fever, nor did other Am erican primates, unlike their African cousins.

A similar venture into scholarly quicksand takes place after text note 39, where Professor Watts claims that he has "demonstrated elsewhere" that yellow fever could have lurked about slave quarters in the American south to produce acquired immunities on a year round basis. The "elsewhere" is his recent book (his endnotes point the way), where he speculates that the yellow fever virus could have overwintered in the southern states providing that temperatures remained above freezing or that the mosquitoes found warmth indoors, and thus the disease could have achieved endemic status. But of course temperatures in the south do not remain above freezing, and, in fact, even when the thermometer dips below 62 degrees Fahrenheit the female Aedes (which spreads yellow fever) will not bite and extended cold temperatures send her into hibernation. This is the reason why yellow fever was invariably an epidemic disease of the hot months in North America and the virus always had to be imported again for new epidemics to oc cur. And when such importation did occur the disease was epidemic urban yellow fever, which, although it may have been carried to remote areas at times, remained an urban phenomenon.

Yet Professor Watts is hypothesizing an endemic (or jungle) form of the disease in the American south, as in South America or Africa where there are monkey populations to keep the virus alive. To my knowledge, no one has ever made such an argument--not even before the disease was understood. Ante-bellum physicians then may not have known much about their "summer scourge" but they did know that its visitations ended with the first frost. And that mosquitoes could have remained active as hosts in the slave quarters from year to year is fanciful precisely because cold temperatures drive them into hibernation. Otherwise why not have yellow fever-infected mosquitoes buzzing about year-round in dwellings throughout the south, with cases reported every winter and a rash of epidemics routinely breaking out with the first warm days of spring?

Staying with the slave cabins, however, the argument becomes even more absurd. The "hickory" fires which the author discusses enthusiastically in his book were, during cold weather, actually hard pressed to warm those directly in front of a fireplace let alone absent minded mosquitoes in remote cabin corners who had forgotten to hibernate and, in addition to warmth, required water and blood meals from obliging humans (who would not swat them) for survival.

I have supplied little in the way of documentation because I am mostly rehashing what I have already written. However, for the appropriate citations and for the very same arguments about yellow fever immunities that I have just repeated here please see Kenneth F. Kiple, The Caribbean Slave: A Biological History (1984), 18-20, and 161-176; Kenneth F. Kiple and Virginia H. King, Another Dimension to the Black Diaspora: Diet, Disease, and Racism (1978), 29-49; and Donald B. Cooper and Kenneth F. Kiple "Yellow Fever," in The Cambridge World History of Human Disease (1993) 1100-1107. All of these were published at New York and Cambridge by Cambridge University Press.

Abstract: Kenneth F. Kiple, "Response to Sheldon Watts, 'Yellow Fever Immunities in West Africa and the Americas in the Age of Slavery and Beyond: A Reappraisal'"

Yellow fever immunities are generally acquired, but individuals whose roots lie in areas of endemic yellow fever may also have been equipped with some sort of innate resistance as indicated by historical data from seventeenth-century Cuba, and Antigua and the United States during the nineteenth-century. Those that seem to have possessed this ability were of African descent but born in the New World where, for a variety of reasons, they would not have had any more opportunity than white counterparts to acquire immunity to yellow fever. Nonetheless, they fared much better with the disease. Professor Watts professes to spy racism in this, as yet, inexplicable differential resistance to yellow fever. Although a student of epidemics, he does not seem to understand that different peoples have historically reacted differently to disease exposure because of the physical environments that forged them.