History and Geography

American Versus African Hypothesis of Origin

Much historical interest in yellow fever has focused on its place of origin: Africa or the Americas? Those who believe it to have been the latter have emphasized that the disease was described and epidemics were recorded in the Western Hemisphere well over a century before it was recognized in Africa, with the first recognizable epidemic striking Barbados in 1647 and then spreading during the next 2 years to Guadeloupe, St. Kitts, Cuba, and the Yucatan Peninsula. Moreover, Amerindian accounts and records of the early Spanish conquistadores make mention of diseases that could have been yellow fever, such as an epidemic of 1454 on the Mexican plateau, a 1477-

97 epidemic that raged in the Yucatan, and an outbreak of disease in Santo Domingo that assaulted the men of Columbus in 1493.

By contrast, the protagonists of the African hypothesis dismiss these outbreaks as typhus, malaria, or some other disease but not yellow fever, in large part because of immunologic evidence. Whatever the illnesses might have been they argue, the Indians were very susceptible to them; however, any endemic presence of yellow fever should have created a high degree of immunity to it. In addition, American monkeys are demonstratively susceptible to the illness, whereas West African populations of both humans and monkeys have shown themselves to be quite resistant to it, suggesting a history of long exposure.

Indeed, the West Africans' ability to resist yellow fever would explain why recognition of the disease was so slow in coming to that region. In the case of Europeans in Africa, it was difficult to distinguish among the "fevers" that fell upon them (and, in the case of portions of the British army during the early nineteenth century, were eliminating more than half of the troops annually). But judging from the extraordinarily low (by comparison) death rates of black troops serving alongside the Europeans, yellow fever must have been prominent among them, and in this connection it is worth noting that even in this century, physicians in Africa have almost routinely misdiagnosed yellow fever as malaria. Interestingly, too, J. P. Schotte, who is credited with first describing yellow fever in West Africa in 1778, did not claim that it was the first epidemic of the disease in the region. Rather, he discussed previous epidemics, in which he reported (significantly) that only the Europeans had suffered greatly.

A final piece of evidence that may point to an African cradle of yellow fever has to do with the prevalence of its A. aegypti vector. In Africa, many species of mosquitoes are more or less closely allied to the Aedes, whereas very few are thusly related in the Americas, suggesting that the vector, at least, is an import. On the other hand, it is possible (although unlikely) that the yellow fever virus was present in the monkey populations of the New World prior to the arrival of the Europeans but had to await the arrival of the vector in order to be transmitted to humans.

Certainly the timing of yellow fever's recorded appearance in the New World does nothing to detract from the case for an African origin of the vector, and probably of the virus as well, for the decade of the 1640s was one of accelerated slave trade activity to

Barbados as that island was converting its economy to one of a sugar plantation system based on slave labor. The same slave ships that could have delivered the virus in black bodies doubtless did carry the mosquito in their water casks. However, whether the disease achieved endemicity by establishing itself in the monkey populations of those few Caribbean islands that contained monkeys can only be speculated upon, for so many of the serious outbreaks to follow also seem to be traceable directly back to Africa via the slave trade. It does seem, however, that the Yucatan Peninsula and the region around Vera Cruz became endemic foci.

Disease Outbreaks: Seventeenth Through Nineteenth Century

Having reached the Caribbean, the disease began making summer visits northward, striking New York in 1668, Philadelphia and Charleston in 1690, and Boston in 1691, while to the south, yellow fever became a regular visitor to the port cities of Colombia, Ecuador, and Peru. Interestingly, it disappeared from Cuba in 1655 after raging there since 1649 and, save for a visit to Santiago de Cuba in 1695, did not return until 1761, apparently because of the islands' sparse population during this century-long period.

A similar phenomenon appears in the medical literature on Brazil. There seems no doubt that the bicha or molestia da terra that struck Pernambuco in November of 1685 was yellow fever. It killed thousands in Recife and Olinda and spread into Ceard before burning out about 5 years later. As was the case in the Caribbean, the outbreak in Brazil has been attributed to a ship that arrived from the African coast. However, despite a thriving slave trade that presumably could have brought the vector and virus to Brazil in countless ships, and a monkey population that some believe already harbored the virus, the region reputedly was free of the disease for the next century and a half. It is true that many slaves reaching Brazil came from Angolan and, to a lesser extent, East African regions that were outside the endemic zone of yellow fever. But many also came from regions within that zone, which makes it so perplexing that when yellow fever was allegedly reintroduced, some say that it arrived not from Africa but from North America, in 1849, on the brig Brazil, whose crew had been infected either in New Orleans or Havana when the ship had put in to those ports.

Equally perplexing is the selectivity yellow fever demonstrated in seeking out victims as the disease spread from Bahia to other coastal cities, for, al though it fell upon European newcomers with considerable fury, it treated local blacks and whites far more gently, suggesting, of course, that the disease may have been present in the region all along — in its jungle or sylvan form - quietly immunizing the population by periodically producing mild cases in the young. Significantly, in the years immediately prior to the outbreak of the 1849 epidemic, Brazil had been the recipient of a sizable influx of European immigrants, in addition, the population of Rio de Janeiro still included a number of individuals on their way to California. Thus in this epidemic, as in the countless ones to follow, it would be the newcomers who were the chief sufferers of the illness.

Yet yellow fever did not limit its assaults on Europeans to Africa and the Americas, but rather on notable occasions sought them out in their homelands as well, apparently reaching the continent from the Caribbean. The Iberian Peninsula was the most common target, with periodic epidemics reported there throughout the eighteenth and nineteenth centuries. The coastal cities of Oporto, Lisbon, and Barcelona bore the brunt of these attacks, although the disease did penetrate to the heart of the peninsula from time to time, even reaching Madrid in 1878. Small outbreaks also occurred on occasion in France, England, and Italy.

Without doubt, however, yellow fever gained its most fearsome reputation in the Caribbean because of Europeans on hand to host it, often in the form of military personnel who provided the disease with a seemingly endless stream of nonimmunes. In 1655, of the 1,500 French soldiers sent to occupy Saint Lucia, only 89 were reported to have survived an onslaught of disease led by yellow fever. The decade of the 1690s saw yellow fever sweep much of the Caribbean, and whole populations of many islands thinned considerably. In 1693 the English attack on the French at Martinique collapsed in face of yellow fever, whereas in 1741, Admiral Edward Vernon's abortive attack on Cartagena saw the loss of close to half of an original landing force of 19,000 (including many North Americans) to yellow fever.

Prisoners sent as workmen from Vera Cruz to Havana in 1761 are credited with reintroducing yellow fever to Cuba where it proved a formidable ally of the Spaniards the following year in a nearly successful effort to deny Havana to the English. However, it was during European attempts to invade St. Dom-ingue around the turn of the century that yellow fever deaths really peaked in the Caribbean. Over the years 1793-6 the British army in the West Indies lost some 80,000 men, with over half of the deaths attributed to yellow fever. The disease also decimated the French soon after they began their invasion of Hispaniola in 1802 and accounted for a sizable portion of the 40,000 men lost in the first 10 months of the war. After the French retreat to the islands of Martinique and Guadeloupe, yellow fever destroyed any French notions of attempting a second assault by raging among the survivors for another 3 years. It was this tremendous loss of European life to yellow fever (and to malaria) that prompted the English to begin to fill West Indies regiments with black troops who were thought to be immune to the disease and demonstrated over and over again that, indeed, many were.

Because of Philadelphia's brisk trade with the West Indies, yellow fever found its way frequently to that port city during the eighteenth century, with epidemics recorded for the years 1741, 1747, 1762, 1793, 1794, and 1797. The epidemic of 1793 was carried to the city by French refugees from revolution-torn San Domingue. With the turn of the nineteenth century, however, as the West Indian trade was shared to a greater extent by southern ports, it was the South that began to receive most of yellow fever's attention, with New Orleans, Savannah, Mobile, and Charleston the most frequent ports of call for the disease.

During the first 6 decades of the nineteenth century, Savannah suffered from 15 epidemics, Charleston had 22, and New Orleans at least 33. The most notable of the New Orleans epidemics occurred in 1853 during which the city lost almost 8,000 individuals to the disease. Chief among the victims of this and all other epidemics were Northerners and foreigners (especially the Irish), along with white Southerners from the interior. Permanent white residents, however, seldom suffered from fatal yellow fever. Among blacks, it was reported by physicians that mulattoes were the most susceptible (to about the same degree as local whites), and until late in the antebellum period, "pure" blacks were believed to be totally immune. Yet in the decade or so before the Civil War, physicians began to notice that blacks did take the disease in a very mild form during epidemics - so mild that it had heretofore escaped notice.

In Brazil, too, blacks were reputed to be extraordinarily resistant to yellow fever, whereas the European immigrants flocking to South America in large numbers became the primary target. With the end of the slave trade in 1850, the chances of the disease entering the country from Africa were reduced. There was always the possibility that the disease would be imported from the Caribbean or North America as supposedly occurred in 1849, but in view of the almost continual epidemic onslaught of yellow fever on Brazilian coastal cities for the remainder of the century, it seems a reasonable supposition that the disease was endemically established in the country.

Cuba, too, was the nineteenth-century destination of European laborers (from Catholic Europe and the Canary Islands), and these, as well as numerous refugees from Spanish America and numerous Spanish soldiers, assured yellow fever a plenitude of hosts on that island. Moreover, a contraband slave trade continued contact with the reservoir of yellow fever in Africa, and regular trade with Vera Cruz kept Cuba in touch with another endemic focus of the disease. Thus it is not surprising that Cuba became the yellow fever capital of the Caribbean. By contrast, the disease began to wane in most of the rest of the islands as the end of the British and French slave trades and the decline of the sugar industry turned them into economic backwaters seldom visited by outsiders.

The northern blockade of southern ports during the American Civil War, rather ironically, kept the South free of yellow fever for the duration by curtailing West Indian shipping traffic. However, the disease returned to New Orleans in 1867, assaulted inland Montgomery in 1873 and Savannah in 1876, before beginning an ascent of the Mississippi River in 1878 that left countless yellow fever dead in a wake that stretched from New Orleans to Memphis, Tennessee, where 5,000 alone went to a yellow fever grave.

This 1878 epidemic almost certainly reached the United States from Cuba, where the influx of Spanish soldiers sent since 1876 to end the Ten Years' War had provided the tinder for an epidemic that raged on that island from 1876 until 1879. Whether the Cuban epidemic also reached out to slaughter French workers arriving in Panama from 1878 onward to work on Ferdinand de Lesseps' abortive attempt to build a canal across the isthmus, or whether that outbreak came from an endemic jungle source is a matter of speculation. But like their predecessors, who between 1851 and 1855 lost thousands of their numbers to yellow fever in building the Panamanian railroad for American financiers, the French canal workers died in droves, many even bringing their own caskets with them to the isthmus.

Transmission and Control: Twentieth Century

The beginning of the end of yellow fever's seemingly endless onslaughts on the Atlantic coastal regions of the hemisphere came just 3 years after the disastrous yellow fever year of 1878, when Carlos Finlay y Barres of Cuba put forth his theory that the A. oegypti mosquito transmitted the disease. The theory was confirmed in 1900 through the use of human volunteers (three of whom died) by the U.S. Army Commission on Yellow Fever in Havana headed by Walter Reed. Armed with this knowledge, William Gorgas was able, by eradicating the A. aegypti, to rid Havana and consequently much of Cuba (which just 3 years previously had registered 6,000 yellow fever deaths) of the disease. Following this, Gorgas applied the same mosquito eradication methods in Panama, making it possible for workers on the American canal to avoid the fate of so many of their French predecessors. The measures were also quickly applied elsewhere so that the 1905 outbreak of yellow fever in New Orleans and the 1908-9 appearance of the disease in Barbados represented, respectively, the last of the disease on North American soil, and the last reported appearance in the Caribbean for decades.

Plans for eradicating the disease from the entire globe were put forth by Gorgas, and in 1915 the Rockefeller Foundation launched this effort with the creation of its Yellow Fever Commission. The commission began by concentrating on sites in Latin America, but in 1920 shifted much of its attention to Africa. In 1925 the Second Commission to West Africa established itself at Lagos, Nigeria, where, among other things, it was discovered that the rhesus monkey from India, unlike African monkeys, was susceptible to yellow fever. With that discovery, it became possible to use monkeys rather than human volunteers for yellow fever experiments. Nonetheless, yellow fever research remained a dangerous affair, and Adrian Stokes, Hideyo Noguchi, William A. Young, and Theodore B. Hayne all perished from the disease in Africa during these "heroic days" of yellow fever research, which by 1929 had demonstrated beyond doubt that yellow fever was the result of infection by a virus.

In Brazil, the knowledge gained by the Reed Commission in Havana was quickly applied by Oswaldo Cruz to a mosquito eradication campaign that freed major coastal cities from the terror of almost unremitting yellow fever assaults for the first time in over a half-century. Despite the campaign, however, the disease stubbornly refused to disappear from Brazil. Sporadic outbreaks continued with puzzling frequency in that country, and in Peru, Ecuador, and Venezuela and Colombia as well, all of which shared portions of South America's great rain forest.

In 1923 the International Health Division of the Rockefeller Foundation accepted Brazil's invitation to administer the Brazilian Yellow Fever Service and, under the direction of Fred Soper, conducted immunologic surveys which showed that many Brazilians residing close to the forest regions had hosted yellow fever in the past. In 1928 a yellow fever epidemic in Rio, which had been free from the disease for over two decades, triggered investigations revealing that yellow fever could spread in the absence of the A. aegypti mosquito, and that the disease was very much alive in the monkey inhabitants of the great South American rain forest. Jungle yellow fever had been discovered, and with that discovery most of the final riddles connected with yellow fever transmission were resolved.

Meanwhile, as mentioned previously, by the late 1920s workers in Africa had demonstrated that the rhesus monkey was susceptible to yellow fever; thus with an animal that could be used in laboratory experiments, efforts to isolate the yellow fever virus were begun. Shortly afterward Max Theiler discovered that the disease could also be transmitted to white mice, which were less expensive and certainly easier to handle experimental animals. Next Theiler showed that if the virus was transmitted from mouse to mouse, it became sufficiently weakened that it could be used to inoculate and immunize monkeys against yellow fever. More effort on the part of Theiler and co-workers led, by the late 1930s, to a further attenuation of the virus, called the 17D Valline strain, which is a mutation of the virus achieved by successive passage of virus in cultures and chick embryo tissues. It is harmless to humans, but immunizes them against the disease.

The development of a vaccine against yellow fever was crucial, for with the discovery of jungle yellow fever came the realization that yellow fever could not be wiped out after all. This vaccination became the only method of yellow fever prevention in regions where mosquito eradication was not practical. The virus is always present in monkeys and perhaps other wild creatures of the forests, and consequently cannot be pinpointed.

For this reason epidemiologists are particularly alarmed at the relaxation of mosquito control measures in the Western Hemisphere, where very few have been vaccinated. In the southern portions of the United States and much of the Caribbean and Central America, A. aegypti has reestablished itself, and Brazil, once apparently free from the mosquito, has reimported it from North America. With modern air travel, an infected individual - or even mosquito - could easily be whisked from the South American or African forests to any number of large cities where A. aegypti again resides in large numbers, and stands ready to spread the disease throughout nonimmune populations. In addition, Aedes albopictus, a close relative of A. aegypti, has recently (within the last decade) been introduced to the United States from its native habitat in the Orient. Laboratory studies have revealed A. albopictus to be fully susceptible to the yellow fever virus and capable of transmitting it to vertebrates, and it is known to be a prominent vector of dengue as well. Its habits, feeding preferences, and general biology closely resemble those of its more famous congener, and both can inhabit the same areas. Moreover, the newcomer is more tolerant of cold weather, and it has spread widely in the United States. Its spread to the West Indies, and Central and South America is feared. As Wilbur Downs stated in a personal communication, "It could prove to be a most unwelcome contributor to yellow fever epidemiology in coming decades."

Donald B. Cooper and Kenneth F. Kiple

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