YELLOW FEVER IMMUNITIES IN WEST AFRICA AND THE AMERICAS IN THE AGE OF SLAVERY AND BEYOND: A REAPPRAISAL.

Lawrence Stone, one of the most respected members of the history profession, conducted a vigorous campaign against "extreme" post modernism, particularly as exemplified by the later works of Simon Schama of Harvard. [1] In the same spirit I would like to call attention to another problem.

In the last twenty five years historians have begun to turn their attention to the history of medicine and disease. [2] Among the illnesses that have captured their attention is yellow fever, one of the most lethal diseases in the Atlantic World. Commenting on human responses, William Coleman, the senior medically-trained historian at the University of Wisconsin, had this to say in 1987:

Africans do not possess an innate immunity [to yellow fever] but those populations living in infected areas first touched by European seafarers surely enjoyed a high level of protection, presumably an immunity acquired during childhood when the disease is relatively less severe. (Childhood mortality due to yellow fever might, nevertheless, have been high.) The Europeans possessed no such immunity and the result was usually disastrous. [3]

Specialists in the field may (or may not) have inferred that Coleman's cautiously worded statement (with its use of the word "Africans") was intended to refute quite different claims about "Africans" and yellow fever which were being regularly made in and after the year 1977 by Kenneth Kiple of Bowling Green State University. [4] In any case, the two historians seem to have been talking past each other. In his "survey of recent literature" published in 1988, Kiple makes no mention of Coleman's major contribution. [5] However in 1999, Kiple did make a direct attack on an historian of medicine who strongly supported Coleman's position. [6] In light of this development, it is appropriate to re-examine and re-assess Kiple's yellow fever thesis.

Since 1977, Kenneth Kiple has been claiming that the indigenous inhabitants of pre-modern West Africa, together their enslaved descendants in the New World and their present-day heirs, [7] have displayed a peculiar ability to resist the worst ravages of yellow fever and that "white men" never shared this immunity. [8] According to Kiple, "blacks" (he generally uses this term rather than referring to any specific ethnic group, such as Yoruba or Ibo) [9], have a "genetic immunity, (which he sometimes terms "inherited" community and sometimes "refractoriness" or resistance to the disease). Building on this concept, he claims that the present ethnic composition of those islands in the New World in which Afro-Caribbean people form the majority is the result of the inability of 17th, 18th and 19th century whites to keep themselves alive in the face of yellow fever, which left "blacks" all but untouched. Other than his use of disease determinism as an all-purpose explanatory device, perhaps of more direct concern t o historians in their professional capacities is Kiple's claim that "history makes a very compelling case for ... innate Black yellow fever resistance" [10]

Kiple bases these assertions on the findings of what he terms "biological history", a field which he and his several followers consider to be well-established and respectable. Yet among modern research scientists, for reasons Kiple can not understand (quoting his words):

... yellow fever has failed to stimulate genetic research, even though historically the black has revealed an incredible agility in sidestepping that plague's lethal scythe, a scythe which invariably chopped a wide swath through whites. [11]

Kiple is convinced that:

But, in fact, the black did possess innate yellow fever immunities, immunities that medical science has yet to acknowledge let alone explain, but immunities that nevertheless are discernible within the history of black, white and red men and the yellow plague. [12]

Both comments were written in the 1980s: one must allow for the possibility that Kiple later modified his position. This did not happen. At the tail end of the twentieth century, Kiple continued to insist that he and his team had fully demonstrated "a yet to be explained ability of slaves to resist yellow fever in the Americas...." [13]

By the early 1990s Kiple had already won recognition within the profession; his books had been published by mainstream university presses and institutions such as the Smithsonian. Following on from this, the Cambridge University Press appointed him editor of the Cambridge World History of Human Disease. Contributors to this 1176 page volume, which was published in 1993, included practicing research scientists, medically trained historians and historians (like Kiple and his co-author on the article on yellow fever) with special interests in disease. With the publication of this massive work, Kiple's world-wide reputation seemed assured. [14] Thereafter he and his followers felt at liberty to criticize younger scholars who refused to accept the Kiple yellow fever orthodoxy. [15]

My critical assessment of this orthodoxy is organized around several points. My first point is that insider reports by tropical medicine specialists such as Dr. Thomas Monath on yellow fever epidemics and yellow fever research in the last forty years, together with current World Health Organization bulletins on yellow fever, articles in the Lancet and the like clearly show that indigenous people in sub-Saharan Africa (including West Africa and west-central Africa-Angola) have no innate, or inherited, or genetic resistance to the disease. The present day medically-informed position is that the yellow fever immunity some people do possess is acquired in one of two ways: either through vaccination (introduced in French African colonies in the 1930s) or by having a barely noticeable case of the disease as a little child or surviving a case as an adult. When yellow fever attacks the very young (new-comers to their society) it might either kill them or pass over lightly and by so doing give them partial immunity t o the next attack. [16]

The importance of acquired immunity to explain the difference in morbidity and mortality rates between long-time residents in yellow fever-prone localities in West Africa on the one hand and, on the other, among adolescent and adult strangers coming in (who had not been in a position to acquire immunity as little children) was insisted upon as early as 1910/11 by the then head of the Liverpool University Yellow Fever Bureau, Sir Rubert Boyce. [17] Seventeen years later at an international conference on tropical medicine held in Cairo (in 1928), Cuban experts on their island's yellow fever problems came out strongly in support of the same conclusion. All agreed that immunity is not inherited or genetic: instead all immunity is acquired. [18]

Building on these understandings, in 1933 the (U.S.A. based) International Health Division of the Rockefeller Foundation at work in British-occupied Sudan devised a simple test, using human blood and a mouse, to detect immune bodies to yellow fever in a human's blood which had been the result of natural infection, in most cases in early childhood. Using the mouse test, the Rockefeller team discovered the fault line running between previously exposed Sudanese (who had thus become immune), and those who had not been able to acquire immunity in this way. Though the team had warned British authority in 1940 that a yellow fever epidemic threatened in areas in which the population had no acquired immunity, no program of vaccinations was initiated, In the resulting (preventable) epidemic in the Nuba mountains, 40,000 Sudanese came down sick with the disease, with a mortality rate of nearly l0%. [19]

More recently, there have been major yellow fever epidemics in West Africa, the very region from which a high percentage of the slaves who were shipped off to the Caribbean and the United States had originated. In 1986, an epidemic broke out among a widely scattered population in eastern Nigeria. Some 10,000 people, out of an estimated regional population of 200,000, suffered "clinical" (unmistakable, readily-apparent) illness, with more than 5000 deaths. In 1987 soon after I had left the area, another major epidemic broke out in western Nigeria, near the city of Oshogbo: there were 120,000 cases and 24,000 deaths. In 1995, yellow fever re-emerged in epidemic form in Senegal with a case fatality rate of 18.9%. [20]

These tragic events, witnessed by Western and African specialists in tropical diseases, clearly demonstrated that the ability to resist yellow fever is NOT genetically transferred over the centuries from one generation of West Africans to the next. One of Kiple's responses to this argument exemplifies his apparent understanding of basic human reproductive processes. As he put it:

This method of accounting for black yellow fever refractoriness, however, has the appearance rather than the essence of a satisfactory explanation, for it contains a fundamental contradiction; if endemic yellow fever had produced a largely immune population of West African peoples, then the virus itself, with no host, should have disappeared.... This in turn would have meant that following generations would not have had the opportunity to experience the disease as children, and consequently should have been ripe for yellow fever in epidemic proportion. Yet, whites in Africa reported no such epidemics.... [21]

Kiple here fails to recognize that in any human society, there are always a sizable grouping of newcomers and strangers--newborn babies, infants and young Children--and that, in areas where yellow fever is locally endemic (and where no vaccination program has intervened), the yellow fever virus almost always has access to youthful human hosts.

This brings me to the second part of my critical assessment of the Kiple thesis: the question of the Continent of origin. In order to give credibility to his claim that "Africans" were genetically immune to yellow fever when they involuntarily found themselves in the New World, Kiple must prove that yellow fever had been present in Africa "for millenia." [22] This requirement forces him to be rather selective in his use of sources. He all but ignores early twentieth century experts in tropical diseases such as General W. C. Gorges (Gorges successfully stamped out yellow fever in the Panama Canal Zone preparatory to the completion of the canal) who held that yellow fever had originated in south and central America. Specialists now have access to pre-Columbian records written in a Mayan language that can be interpreted as saying that epidemic yellow fever had occurred in that region before 1492.23 Kiple also ignores Sir Rubert Boyce's well reasoned conclusion that yellow fever (which in endemic form, Boyce fou nd in some local areas, but not in others) may only have come to West Africa in the 1760s or '70s. [24] Though Kiple knew that the first European-language text attesting to what can only have been yellow fever in coastal West Africa (rather than some other "fever") only dates from 1778, [25] and that the first Western-documented appearance of yellow fever in the New World was in 1647 (more than a century and a quarter earlier), he credits the time lag to a "conspiracy" of silence among white slavers and merchants working the West African coast. He adds that: "given that conspiracy, had such epidemics occurred, knowledge of it would probably have been suppressed." This point established , he states: "the early reporting of the disease in the New World becomes paradoxically additional testimony to its African origins. ..." [26] Yet writing in 1992, Kiple claimed that:

Immunologically, both humans and non-human primates in West Africa have historically demonstrated steadfast resistance to the disease, indicating a long and intimate relationship. [27]

In view of his claim that conspiracies of silence had obliterated all knowledge of epidemics of yellow fever in West Africa before 1778, it is legitimate to ask about the nature of the sources he used to support his phrases "historically demonstrated" and "a long and intimate relationship."

Writing in the early 1860s, Dr. William Budd, a British specialist in infectious diseases, made a useful distinction between "Sentiment" and "Science". Budd pointed out that in discussion of disease causation it was dangerous to allow "Sentiment" to intrude into the domain of "Science". Yet as he had found from long experience, many experts were extremely stubborn: accordingly "to attempt the refutation of such sentiment by argument is impossible." [28] Dr. Budd's stricture is of general relevance, but here it applies particularly to Kenneth Kiple's reliance on the posthumous, book-length study of yellow fever written by Henry Rose Carter (1852-1925). At this point some biographical details are relevant.

Carter had been born in Virginia shortly before the U.S. Civil War (1861-65). Thus during the impressionable years of his early youth he would have heard accounts of battles fought a few miles from his home between Northern forces and Confederate defenders of Black African slavery. Later, Carter received a degree in medicine and joined the US Army Medical Corps. In that capacity he carried out yellow fever research in the Mississippi Delta where the Klu Klux Klan was instrumental in maintaining the hegemony of whites over freed slaves. Later, during the Spanish American War (when the USA saw itself as picking up the "white man's burden") he was involved in the assault on yellow fever in Havana.

During his spare time, and later in retirement, Carter wrote a book on the disease in which he claimed that: "the negro ... has a true racial resistance [to yellow fever] which is not dependent upon prior infection or exposure." [29] Another phrase found a few pages on in Carter's book is quoted with approval by Kiple:

In the words of Henry Rose Carter, one of yellow fever's conquerors, the blacks' "reaction to yellow fever is just what one would expect to have been evolved in a race for many generations in Africa subject to that infection." [30]

So on the question of the continent of origin, Kiple firmly states: "Henry Rose Carter published posthumously the best and most though examination of the question of yellow fever's origin and concluded unequivocally that the answer was Africa." [31]

Convinced that West Africa is "the home of man's most dangerous diseases" (forgetting that bubonic plague and cholera are not native to Africa), [32] Kiple holds that in the early centuries of the slave trade, it was likely that "blacks probably did host the disease in the holds of ships but escaped the notice of their white captors.... " [33] However, it should be borne in mind that it is equally possible that non-immune white crew members might instead have served as the human host who first brought the disease to West Africa from the port cities of Brazil or southern Mexico.

Kiple's West Africa origin-of-yellow-fever hypothesis depends heavily on what was perhaps respectable scientific opinion in 1925, the year of H. R. Carter's death. However, research findings made since then have overturned many of the old certainties. In Dr. Budd's typology, the "Science" of yesteryear has been relegated to the category of "Sentiment."

Thus, for example, H. R. Carter had found it unnecessary to explore the hypothesis that the yellow fever virus might be able to survive in the eggs of the principal host mosquito type in West Africa (Aedes aegypti). Working on the assumptions which had been in fashion when he was a student in medical school (which of course did not take mosquito eggs into account), Carter, and more recent historians who depend on his insights, supposed that it was essential that living virus-infected female Aedes aegypti mosquitoes bring yellow fever from Africa to the New World. Given the life expectancies of the virus and of the mosquito and other time constraints, this would have meant that in the course of a four to six months' sea voyage between coastal Africa and the Caribbean islands, several generations of mosquito would have had to infect a series of human hosts (each of whom would only remain infective to an incoming mosquito for a few days). Only with the completion of this complex series of processes would some infective Aedes aegypti mosquitoes have been around at the end of the voyage to infect fresh human hosts on shore. In Kiple's words: "So the female Aedes mosquito was a must for the journey". [34]

However, the posited complex of interchanges between virus, successive generations of mosquitoes and a series of humans lost its explanatory value twenty-five years ago. In 1977 (this was some time before Kiple's book-length studies were published), it was confirmed that the eggs of the Aedes egypti mosquito could host the living yellow fever virus for a considerable length of time (the process known as lateral transmission). Later in the '70s lateral transmission was confirmed for the indigenous New World mosquito host, Haemagogus equinus. In the light of these discoveries it was no longer necessary to posit the existence of human carrier hosts or of living mosquito hosts on a sailing ship crossing the Atlantic from east to west (Africa to the New World) or from the New World to Africa.

This then brings us to the third and last part of this critical assessment of the Kiple interpretation of yellow fever. This concerns the question of why, in the USA during an outbreak of epidemic yellow fever, there was perceived to be a sharp contrast between the response of whites (with a very high death rare) and the response of people of African descent (who according to white men s sources, very seldom died). The answer to this question requires inquiry into several specialized fields of research.

Firstly, as the Rockefeller commission working in the Sudan in 1933 fully recognized, only a very small percentage of people undergoing an attack of yellow fever, particularly in its low-level endemic forms, exhibit the full range of clinical symptoms. In the 1930s, British doctors who had spent years in the Sudan swore they had never seen or heard of cases of yellow fever, yet application of the Rockefeller mouse test proved that thousands of Sudanese had acquired immunity by suffering a light case of the disease in early childhood. These African people (with their acquired immunity) were nor among those killed when epidemic yellow fever swept through central Sudan in 1940. [35]

More recent information from the WHO suggests that only one yellow fever sufferer in several hundred or a thousand will demonstrate the unmistakable symptoms of the disease. [36] Knowledge of this relatively recent medical research-finding should alert historians to the danger of relying on medical reports dating from the early and mid- and late nineteenth century, the pre-clinical era, when "Sentiment" was generally the guiding force in what locally, in the American South, passed as "Science".

My second point follows on from this. An important part of Kiple's thesis about genetic resistance to yellow fever among American slaves and their descendants after 1865 hinges on his insistence that yellow fever is an urban disease which only breaks out in epidemic form when large numbers of non-immune people put themselves in the way of infectious mosquitoes. To buttress his argument, he specifically states that the plantations in which the great majority of slaves were found before 1865 were not visited by yellow fever. On this point, his own words bear quotation. He writes of slaves "quarantined" on their plantations" [37] and "Thus the yellow fever which made incursions into the antebellum South was strictly an urban disease and hardly the scourge of plantations it is occasionally represented to have been." [38]

Yet as I have demonstrated elsewhere [39] it was quite likely that endemic yellow fever could keep itself in being for several years near the slave quarters of a large plantation. In that venue there were numerous little children who would have the opportunity to acquire immunity to the disease through suffering a light case of what no white authority would recognize as yellow fever. Fortuitously for his critics, Kiple inadvertently provided a clue as to why little African-American slave children and their Klu Klux Klan-disciplined successors after 1865 were rather more likely to acquire immunity in this way than were white children. According to his source, doctor J. D. Ramph writing in 1854, well-brought up white children were pampered and made to sleep indoors away from the imagined and real dangers of the night. On the other hand, during the hot summer months, black children and adults commonly slept outdoors. Of course black field hands of all ages spent most of their waking hours outdoors as well. [40] Thus, because of differing behavioral patterns, blacks of all ages were far more exposed to the bites of infective mosquitoes than were whites.

Other behavioral patterns of African-American slaves and free persons of color would also repay close study. Even today there is a certain degree of misunderstanding between African-Americans and Euro-Americans. Mutual distrust was even deeper in the nineteenth century and in the first three-quarters of the twentieth century before the power of local white vigilante squads was broken. Accordingly, among black slaves and free persons of color in time of serious illness and death there was a tendency to keep themselves apart from whites, so that the appropriate rituals could be observed. This was certainly one reason why black victims of yellow fever were invisible as far as white record keepers were concerned.

This then brings me to my next area of investigation: the nature of the source material Kiple used, and the way in which he choose to interpret this material. The fact that medical doctors in the American South before and after the Civil War had low social status and that their livelihood depended on the patronage and good will of the local landed and political elite must be taken into account when assessing the value of their claims that blacks were not much troubled by yellow fever. As Kiple makes abundantly clear, the Sentiment among most laymen and white physicians before and after the Civil War was that blacks were less than fully human: draft animals--horses and oxen--did not die of yellow fever; neither did blacks. [41]

For whatever reason, Kiple consistently overlooks the many opportunities offered to him in the course of his analysis to put deep water between himself and the "antebellum physicians" whose opinions he liberally quotes. For example, he writes: "Few would have disagreed with Dr. Samuel Cartwright of New Orleans when he pronounced Africans 'perfect non-conductors of yellow fever'." [42] Building on the mid-nineteenth notion that Cod had created black Africans (immune to yellow fever) with the intent that they should be slaves to whites in the plantations in the American South, Kiple writes: "It can be said then, with little fear of exaggeration, that black related disease immunities played a crucial role in the wholesale enslavement of the West African, while black disease susceptibilities played a similarly crucial role in rationalizing that enslavement." [43] Kiple goes on to claim that black disease immunities "virtually guaranteed that the black, by the deadly process of elimination, was the chief European instrument for colonizing the vastness of Plantation America." [44] This contention, so central to much of Kiple's work, will not bear close examination.

Instead, the fact that most of the islands in the Caribbean have a predominantly black population today can be quite adequately explained without resorting to disease determinism. Robin Blackburn's recent study of the origins of slavery in the New World is a case in point. With the exception of a brief reference to smallpox in a footnote, [45] Blackburn manages to explain the rise and perpetuation of New World slavery with no mention of diseases or of culturally-perceived disease immunities.

In examining the push and pull factors governing population mobility in times past, one can follow the lead of historical geographers and examine the full range of possible alternatives. As I have explained at length elsewhere, during the crucial years 1680-1720 when migration patterns to the sugar-rich Caribbean islands and the American mainlands North and South were still in flux, West Europe was undergoing population stasis. Accompanying the near absence of population growth, was the new phenomenon known as proto-industry. Protoindusty took hundreds of forms (including knitting stockings as one walked along a village street) and provided ordinary men and women with new opportunities to earn a discretionary income so that they could become consumers of new exotic imported products like tea and sugar.

Thanks to the conjunction of proto-industry and population stasis, many young people found it possible to make an adequate living in their homeland and saw no particular reason why they should emigrate to the sugar plantations of the New World. This despite the fact that the plantation owners-themselves European transplants-much preferred ethnic European workers to any other kind of workers. [46] Only when they eventually realized (this took forty or fifty years) that most of the Native American population were either dead or unavailable for service, and that the response they got from labor recruitment agents in Europe was completely inadequate, did Caribbean plantation owners reluctantly turn to the third alternative, the use of enslaved West African and West Central Africans (Angola) sold to them by profiteering slavers.

During this critical period when the die for future labor recruitment patterns was being cast, Caribbean agents were not aware of any meaningful differential disease response among the ethnic groups. Reporting on the yellow fever epidemic which ran through the sugar-rich island of Barbados in 1691, the contemporary historian, John Oldmixon, reported that it had swept away great numbers of "masters, servants and slaves." 47 This then brings me around to my final point: Kiple's use and abuse of statistics.

Throughout his many studies, Kiple repeatedly quotes statistics generated by southern medical doctors, coroners and public health workers which, on the face of it, support his contention that whites died of yellow fever at a higher rate than did blacks: as he puts it: "the impressionistic evidence of differential black and white treatment by yellow fever has been confirmed statistically." [48] Yet Kiple is unwilling to fully acknowledge that in assessing "differential black and white fever mortality in nineteenth century United States," [49] the simple dichotomy of black/white is inadequate and misleading. Instead, given the modern scientific understanding that surviving a case of yellow fever (even a mild case in childhood) provides immunity against fatal consequences during later epidemics, meaningful conclusions about ethnic differentials can only be expected if the record source specifically list the length of time the dead white (or African-American) had been living in the town, village, or isolated hom estead in which she/he died. Strangers from non-endemic regions where (in pre-vaccination days) the acquisition of immunity in childhood was impossible (i. e. northern Europe or Italy) who had only recently arrived in a place where yellow fever commonly occurred could be expected to be susceptible to sudden death. Thus, for the purposes of objective study, sets of death statistics generated during yellow fever epidemics which do not clearly differentiate between Strangers and life-time residents likely to have undergone a case of yellow fever as children must be considered as irrelevant to the task at hand. [50]

In Kiple's work, there is also the problem of statistical bias. According to Margaret Humphries, in none of the States in the New South, and in only three of the States in the Old South were registers of vital statistics regularly kept. Until 1905 (when yellow fever last was present in force in the USA) in none of the States of the Old Confederacy was any person of color found on a state board of health. Thus when it came to yellow fever (and much else) blacks were all but "invisible." [51] Yet Kiple states; "For studies of the United States scholars are most blessed with source materials: here most of the work on slave demography and black- related disease immunities and susceptibilities has been done." A few lines down the page he adds: "Nor can anyone ... fail to be impressed with the enormous degree of sophistication that studies of the biological past of the black have achieved." [52]

I beg to differ. Statements such as "... disease inexorably selected the black for labor in the tropics and the 'myth'[sic] that the black was singularly suited for such a role had a sound immuniological foundation" [53] and "history makes a very compelling case for ... innate Black yellow fever resistance ..." [54] and "It can be said then, with little fear of exaggeration, that black related disease immunities played a crucial role in the wholesale enslavement of the West African ..." are examples of disease determinism. [55]

Looking beyond the impact Kiple's conclusions might have on conscientious historians, let us consider the impact on tax payers and donors in the Atlantic World as a whole. As several specialists in tropical medicine have recently pointed out, claims that non-white people have inherited genetic immunity to yellow fever (so need not worry about the disease), do not fall on deaf ears. On the contrary, such claims severely hamper efforts to raise the funds needed by the WHO and other international organizations working in the Non-West to control yellow fever, through vaccination campaigns and other appropriate techniques. [56]

Abstract: Sheldon Watts, "Yellow Fever Immunities in West Africa and the Americas in the Age of Slavery and Beyond: A Reappraisal"

This article is a case study in applied objectivity as understood by mainstream historians. It addresses the problem of disease determinism exemplified by late nineteenth and twentieth century interpretations of the role played by yellow fever in "determining" the ethnic composition of the Caribbean Islands, the American South and the Atlantic coastal zones of Central and South America. In its extreme form yellow fever determinism held that the Christian God created Africans immune to yellow fever, with the intention that they should serve white plantation owners in the New World as slaves. The author--a cultural and medical historian long resident in the Non West--hones in on the disease determinism detected in several works written by Kenneth Kiple and systematically deconstructs Kiple's arguments.

ENDNOTES

An earlier draft of this paper was presented at the annual Anglo-American Historical Conference, Institute of Historical Research, University of London, 1 July 1999. A University of Melbourne (Australia) grant as Visiting Research Scholar, early in 2000, funded the block of time needed for writing up this paper in its current form.

(1.) Lawrence Stone, "History and Post-Modernism III," Past & Present No. 135 (May 1992): 189-94.

(2.) William McNeill, Plagues and Peoples (Garden City NY, 1976).

(3.) William Coleman, Yellow Fever in the North: Methods of Early Epidemiology (Madison, 1987), 14.

(4.) K. F. Kiple and V. H. Kiple, "Black Yellow Fever Immunities, Innate and Acquired, as Revealed in the American South," Social Science History I (1977): 419-36.

(5.) K. Kiple, "Survey of Recent Literature," in Kenneth F. Kiple, ed., The African Exchange: Toward a Biological History (Durham, NC, 1988), 24-34.

(6.) Kenneth F. Kiple "Review of Sheldon Watts, Epidemics and History: Disease, Power and Imperialism (New Haven, CT, 1998)," in Journal of Interdisciplinary History 30 no. 1 (summer, 1999): 104-5.

(7.) Claims for present-day: Kenneth F. Kiple, The Caribbean Slave: A Biological History (Cambridge, 1984), 177-8.

(8.) Kiple and Kiple, "Black Yellow Fever Immunities" (1977); Kenneth F. Kiple and Virginia Himmelsteib King, Another Dimension to the Black Diaspora: Diet, Disease, and Racism (Cambridge, 1981); Kenneth Kiple, African Exchange (1987); Kenneth K. Kiple and Brian T. Higgins, "Yellow Fever and the Africanization of the Caribbean," in John W. Verano and Douglas H. Ubelaker, eds., Disease and Demography in the Americas (Washington DC, 1992), 237-48; Kenneth Kiple and Donald Cooper, "Yellow Fever," in Kenneth Kiple, ed., Cambridge World History of Human Disease (Cambridge, 1993); Kiple "Review," (1999).

(9.) Most historians of medicine today recognize the great diversity of African peoples and that power relationships, disease environments of place of birth and residence in childhood etc. can more usefully be regarded as disease determinants than the color of one's skin: Steven Feierman and John M. Janzen eds., The Social Basis of Health and Healing in Africa (Berkeley, CA, 1992), 8-9.

(10.) Kiple, "Yellow Fever and Africanization," 244.

(11.) Kiple, Another Dimension, 29.

(12.) Kiple, Another Dimension, 31;term "biological elite" in Kiple, African Exchange, 269; phrase "powerful testimony to the racial prejudices of falciparium malaria and yellow fever" in Kiple, Another Dimension, 38.

(13.) Kiple, "Review," 105.

(14.) Cert H. Brieger, "Review:, New England Journal of Medicine, 2 July 1998, 55. A. H. Spear praised Kiple and Kiple's Another Dimension (1981), but admitted that he "could not judge their competence in medical and nutritional matters ...:" American Historical Review v. 90, No.2 April 1985): 490.

(15.) Todd L. Savitt, Review of Khaled Bloom, The Mississippi Valley's Great Fever Epidemic of 1878 (1993), American Historical Review 100 no. 5 (Dec. 1995): 1698; Todd L. Savitt, Medicine and Slavery: The Diseases and Health Care of Blacks in Antebellum Virginia (Urbana, IL, 1978), 241. Other supporters include: Donald Cooper, in Cambridge World History of Human Diseases, 1102; Jo Ann Carringan, "Yellow Fever: Scourge of the South," in Todd L. Savitt and James H. Young, eds., Disease and Distinctiveness in the American South (Knoxville, TN, 1988), 59, 73; K. David Patterson, "Yellow Fever Epidemics and Mortality in the United States, 1693-1905," Social Science and Medicine 24 no. 8 (1992): 862; John H. Ellis, Yellow Fever & Public Health in the New South (Lexington, KY, 1992), 31, 57, 108, 180; Margaret Humphries, "Yellow Fever: The Yellow Jack," in Kenneth Kiple, ed., Plague, Pox & Pestilence (London, 1997), 86.

(16.) Thomas P. Monath (U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD), "Yellow Fever: Victor, Victoria? Conqueror, Conquest? Epidemics and Research in the Last Forty Years and Prospects for the Future," American Journal of Tropical Medicine and Hygiene v.45, no. 1(1991): 1-43.

(17.) Sir Rubert Boyce, "The Distribution and Prevalence of Yellow Fever in West Africa," Journal of Tropical Medicine and Hygiene XIII (1 Dec. 1910): 357. For Kiple's comments on Boyce: "in addition to these wrong-headed ... speculations, there were also some badly reasoned arguments that credited acquired immunity": Kiple, Caribbean Slave, 174, See also: Kiple, "Yellow Fever and Africanization," 243.

(18.) W. H. Hoffmann, "Yellow Fever in Africa from the Epidemiological Standpoint," in Mohamed Bay Khalil, ed., Proceedings: Congres international de Medecine Tropicale et d'Hygiene: Le Cairo, Egypte, Decembre, 1928 V (Cairo, 1932), 920.

(19.) G. M. Finlay et al, "Yellow Fever and the Anglo-Egyptian Sudan: Distribution of Immune Bodies to Yellow Fever," Annals of Tropical Medicine & Parasitology v. 35, no. 2 (December 31,1941): 121; Heather Bell, Frontier of Medicine in the Anglo-Egyptian Sudan 1899-1940 (Oxford, 1999), 163-97.

(20.) Monath, "Yellow Fever," 30, 32-5; K. M. De Cock et al, "Epidemic Yellow Fever in Eastern Nigeria, 1986," The Lancet 19 (March 1988): 630-32; WHO, Prevention and Control of Yellow Fever (Geneva, 1986), 3-5, 25-7; J. Thonnon etal, "Re-emergence of Yellow Fever in Senegal in 1995," American Journal of Tropical Medicine and Hygiene v. 59 no. 1(1998): 108. For Kiple's attempt to salvage his thesis by claiming that Senegal was not in the endemic zone: Kiple, "Yellow Fever and Africanization," 243.

(21.) Kiple, Another Dimension, 30.

(22.) Kiple, Caribbean Slave, 5.

(23.) W. C. Gorgas, "Recent Experiences of the United States Army with Regard to Sanitation of Yellow Fever in the Tropics" (paper read before the Egyptian Medical Congress), The Journal of Tropical Medicine v. 6 (February 2, 1903): 49.

(24.) "Discussion of Yellow Fever," Journal of Tropical Medicine and Hygiene v. 14 (February 1, 1911): 42.

(25.) McGrew asserts the first reports from West Africa are from Sierra Leone in 1764 and Senegal in 1778; R. McCrew, Encyclopedia of Medical History (London, 1985), 357.

(26.) Kiple, Another Dimension, 35.

(27.) (Emp mine) Kiple, "Yellow Fever and Africanization," 239. See also: Kiple, Caribbean Slave, 5.

(28.) London, British Library, India Office, V/26/853/2 p. 198.

(29.) Carter's full statement: "That the negro does possess a resistance to yellow fever not shown by any other race is, we think, among the best established facts in the epidemiology of the disease. It is a point on which opinion is all but unanimous and evidence conclusive ... [the negro] has a true racial resistance which is not dependent upon prior infection or exposure": Henry Rose Carter, Yellow Fever, An Epidemiological and Historical Study of its Place of Origin (Baltimore, MD, 1931), 263-4.

(30.) Kiple, Another Dimension, 49, qu. Carter, Yellow Fever, 270.

(31.) Kiple, Another Dimension, 217. See also: Kenneth Kiple, "The Ecology of Disease," in W. F. Bynum and Roy Porter, eds., Companion Encyclopedia of the History of Medicine (London, 1993), 370.

(32.) Kiple, Caribbean Slave, 5.

(33.) Kiple, Another Dimension, 48.

(34.) Kiple, Another Dimension, 32.

(35.) Bell, Frontiers, 190-7.

(36.) WHO, Yellow Fever, 4.

(37.) Kiple, Another Dimension, 45.

(38.) Kiple, Another Dimension, 40.

(39.) Watts, Epidemics and History, 241.

(40.) Kiple, Another Dimension, 57, 244. See also: Eugene D. Genovese, "... And the Children Brought Up," in his Roll Jordon Roll: The World the Slaves Made (New York, 1976); Bertram Wyatt-Brown "The Mask of Obedience: Male Slave Psychology in the Old South," in J. William Harris, ed., Society and Culture in the Slave South (London, 1992), 128-51.

(41.) Kiple, Another Dimension, 58-61, 226; Kiple, African Exchange 8; Kiple, Caribbean Slave, 178.

(42.) Kiple, Another Dimension, 43. See also: Samuel A. Cartwrighr, MD, "Report on the Diseases and Physical Peculiarities of the Negro Race," in Arthur L. Caplin, H. Engelhardt, J. McCartney, eds., Concepts of Health and Disease: Interdisciplinary Perspectives (Reading, MA, 1981).

(43.) (emp. mine) Kiple, African Exchange, 8.

(44.) Kiple, African Exchange, 22. He also holds that [blacks' ability to survive yellow fever] "became crucial to the colonization of tropical America ...": Kiple, Another Dimension, 67; "all of which serves to illustrate the profound role that disease has played in the history of the West Indies": Kiple, Caribbean Slave, 4.

(45.) Robin Blackburn, The Making of New World Slavery from the Baroque to the Modern, 1492-1800 (London, 1997), 156.

(46.) Watts, Epidemics and History, 230-3.

(47.) Quoted in Jack Greene, Imperatives, Behaviors, and Identities: Essays in Early American Cultural History (Charlottesville, VA, 1992), 38; Watts, Epidemics and History, 229. Compare Kiple's comment on "1648" and 1691: "their black chattles seemed impervious to yellow fever's fatal march across the Caribbean:" Another Dimension, 39.

(48.) Kiple, Another Dimension, 48.

(49.) Opportunity ignored: Kiple, Another Dimension, 40-41.

(50.) For an example of contrasting death rates between recently arrived migrant strangers and the locally-born using contemporary statistics: G. Couto and C. de Rezende, "Control of Infectious Diseases in Brazil and especially in Rio de Janeiro," Yellow Fever Bureau Bulletin no. II (1913): 297-8; Watts, Epidemics and History, 250.

(51.) Margaret Humphreys, Yellow Fever and the South (New Brunswick, NJ., 1992), 7-8, 51-2, 59, 179; Watts, Epidemics and History, 245, 247.

(52.) Kiple, African Exchange, 23.

(53.) emp. mine: Kiple, Caribbean Slave, 4.

(54.) Kiple, "Yellow Fever and Africanization," 244.

(55.) Kiple, African Exchange, 8. A further example: "Yet ... these crucial roles played by disease in shaping the black past went unrecognized or ignored by most social scientists ..." whom Kiple accused of" obscurantism:" Kiple, African Exchange, 9, or of having "a shaky grip on epidemiological history", Kiple, "Review," 105. For a listing of disease determinisms used to construct disease, nor generally in the best interests of sufferers: Watts, Epidemics and History, 389.

(56.) Cuts in yellow fever surveillance and delays in including yellow fever into vaccination programs (the Expanded Program on Immunization, EPI) both in Africa and in South America under pressure from Western governments and the I.M.F. has left both Continents dangerously at risk from resurgent yellow fever: K. M. De Cock et al, "Epidemic Yellow Fever in Eastern Nigeria, 1986," The Lancet, March 19,1986: 632; Jocelyn Thonnon et al, "Re-emergence of Yellow Fever in Senegal in 1995," American Journal of Tropical Medicine and Hygiene v. 59, no. 1 (1998): 113; Edward J. Sanders er al, "First Recorded Outbreak of Yellow Fever in Kenya, 1992-1993, I," American Journal of Tropical Medicine and Hygiene v. 59, no.4 (1998): 648; N. Guerin et al, "[Expanded program of vaccination. Results and prospects]" Annales Medecine International (Paris) v. 149, no.6 (1998): 377-8; "Need for Vaccination Against Yellow Fever," Communicable Disease Report Wkly v.9, no.33 (August 13, 1999): 289, 292; Monath, "Yellow Fever", 29; Rich ard L. Guerrant, "Why America Must Care about Tropical Medicine: Threats to Global Health and Security from Tropical Infectious Diseases," American Journal of Tropical Medicine and Hygiene v.59, no. 1(1998): 11-14; Watts, Epidemics and History, 269-79.