by Sean Martin
Yellow fever is first definitively recorded in 1648, when it broke out in Campeche, a Spanish outpost on Mexico’s Yucatan peninsula. The first omen was a thick fog, which appeared in March, according to Diego López de Cogolludo in his Historia de Yucathan. The fog was so dense there was an eclipse-like darkness for several days. The indigenous Mayans took the fog as ‘a sign of great mortality of people in this land, and for our sins’.258 Great mortality did indeed follow. The first cases were reported in June. Cogolludo lamented that Campeche was ‘totally laid waste’.259 He referred to the disease as the peste, noting that victims were ‘taken with a very severe and intense pain in the head and of all the bones in the body, so violent that it appeared to dislocate them or to squeeze them as a press.’ The pains were frequently followed by a ‘vehement fever’, in which they could become delirious. If the disease worsened after that, the victim would vomit ‘putrefied blood and of these very few remained alive.’260
What was this mysterious new disease that was bringing Spanish possessions in Latin America to their knees, and how did it get there? Yellow fever is an acute viral haemorrhagic disease, thought to be native to Africa. It’s what is called an arboviral disease – that is, transmitted by an arthropod vector. In the case of yellow fever, the vector is the female Aedes aegypti mosquito, affecting humans and monkeys with her bite. Aside from the ‘severe and intense pains’ and ‘vehement fever’ recorded by Cogolludo, the symptoms of yellow fever include a slowing of the heart rate – unusual for fevers, which usually cause the opposite. Worsening kidney function causes jaundice, and bleeding can occur from eyes, mouth, nose and rectum. The ‘putrefied blood’ Cogolludo mentions earned the disease the nickname el vomito negro (black vomit).
From its probable home in Africa, yellow fever was almost certainly exported to the New World on slave ships, the mosquitoes laying their eggs in the vessels’ freshwater barrels. In addition, the slave trade was undergoing changes in the seventeenth century. Originally the province of the Spanish and the Portuguese, by the time yellow fever broke out on Yucatan in 1648, the Iberian powers were facing competition from the Dutch, British and French. With more slaves being taken to the Americas, plantations were getting larger, and needed more slaves. To cite the example of Barbados, by mid-century, the number of property holders had fallen from 11,000 to less than 800. This also resulted in plantations amalgamating and with the larger plantations, there came the demand for more labour. When English colonists arrived in 1627, the island had virtually no slaves at all. In 1645 – just three years before the first confirmed case of yellow fever – there were 5,600. By 1667, there were 82,000.261 In addition to the massive increase in slaves, sugar came increasingly to replace – or at least complement – tobacco and cotton.
Not all the ships on the seas in the summer of 1648 were European colonists. Some were probably pirates. But it mattered little: mosquitoes were not fussy travellers, and could hitch a ride on any ship with a fresh water supply. From Yucatan, yellow fever spread to the French colonies of St Kitts and Guadeloupe in the summer of 1648. One-third of St Kitts’s population perished within eighteen months. It then struck Cuba; a third of Havana’s residents died between May and October 1649.262 The disease also seems to have been active on Barbados, where yellow fever (or something very much like it – it was described as a ‘nova pestis’ or a ‘new distemper’), may have broken out in September 1647.263 It remained such a potent threat that it even appears to have slowed down – hindered, certainly – European exploitation of the Caribbean. In 1665, 1,500 British troops seized the French-held island of St Lucia. Within two years, the number of British soldiers on the island had fallen to a rump force of 89. The French were not responsible: yellow fever did most of the work.264
With the increased sea traffic – slavers, imperialists, colonists, traders and pirates – it was only a matter of time before yellow fever reached mainland North America. A British fleet is thought to have introduced the disease into Boston, Massachusetts, in 1693, the first continental North American city to be infected. Charleston, North Carolina, Philadelphia, and New York City were all affected within a decade, losing between seven and ten per cent of their populations. But it proved to be a difficult disease to predict. From 1737 to 1743, yellow fever was an annual visitor to the eastern seaboard of America. It then disappeared until 1762, when it flared up again until 1765. Another long silence ensued, until the 1793 epidemic in Philadelphia.
Yellow fever then began to dog the newly-independent United States, becoming perhaps the most significant disease in the country’s early history, just as it had done in the Caribbean in the seventeenth and early eighteenth centuries. There was so much yellow fever in Louisiana that Napoleon decided to abandon his plan to pursue a North American empire. The disease had already claimed the lives of thousands of French soldiers on Haiti (then fighting for independence), and further losses could not be sustained. Napoleon ordered his foreign minister, Talleyrand, to sell Louisiana to the American government in 1803. (That was certainly not the end of yellow fever in the state: in the 1840s, Irish immigrants, fleeing the great famine at home, are thought to have been responsible for the huge rise in the number of yellow fever cases in New Orleans.) Florida lost so much of its population to yellow fever in the 1820s and 1830s that statehood was delayed, while Memphis, Tennessee, was nearly abandoned as uninhabitable after epidemics in 1878 and 1879. Such continuing disasters would have shocked the Gothic imagination of Brockden Brown and his hero, Arthur Mervyn.
There was very little health officials could do to stop the successive epidemics, which usually struck in the summer. Ships arriving from affected areas were forced to fly a yellow flag – the Yellow Jack – and then had to undergo a period of quarantine. Established to combat the plague (the first quarantine was introduced in fifteenth century Dubrovnik), quarantine was used in the US from the 1793 Philadelphia outbreak onwards. Although one of the few relatively effective tools the urban health boards had at their disposal, it was not always popular. Commercial interests frequently opposed quarantine, as cargoes – such as bananas – wouldn’t keep for 40 days. Opponents pointed out that, of the eight American epidemics following 1793, quarantine had stopped none of them. The problem was simple: although the disease could burn itself out on a ship held for thirty or forty days, nothing prevented the disease-carrying mosquitoes from alighting.
There were those who thought yellow fever was contagious. These ‘contagionists’ were usually to be found supporting quarantine. An opposing camp – unwittingly echoing the miasma theorists of the Black Death – declared the main cause to be dirt and squalor causing ‘bad air’. This ‘explained’ why victims who did not know each other could be affected. However, sometimes all these factors were present, but there was no yellow fever. One doctor in New Orleans noted however, that sometimes all the ingredients for a supposed miasma might be present, but without yellow fever occurring: ‘What a quandary the yellow fever wizards must be in!... We have heat and moisture, dead dogs, cats, chickens, etc, all over the streets, and plenty of hungry doctors; yet Yellow Jack will not come.’265
The American army doctor Walter Reed tried to make Yellow Jack appear in a potentially fatal experiment that took place in Havana in 1900/01. While the US had been the victor in the Spanish-American War of 1898, she had lost more men to yellow fever than to enemy action, and Reed had been appointed by the Surgeon General to look into the matter. Reed and his colleagues, Jesse Lazear, James Carroll and Aristides Agramonte, wanted to test the theory that yellow fever was caused by mosquitoes. The theory had been first put forward by the Cuban doctor, Carlos Finlay (1833–1915), but Finlay never made the decisive discovery that the vector is the female Aedes aegypti mosquito. Another possible source of inspiration was the British army doctor, Ronald Ross, who, in 1897, discovered that malaria was transmitted by mosquitoes (see below). Carroll allowed himself to be bitten by mosquitoes that had fed on yellow fever patients. Despite becoming very ill, he su
rvived. Lazear was not so lucky. He died from yellow fever on 26 September 1900, two weeks after being bitten and so delirious in the final stages that it took five men to hold him down.266
Undeterred, Reed set up another experiment, which took place in wooden huts dubbed ‘Camp Lazear’ in honour of his fallen comrade. Reed had one group of volunteer soldiers placed in a hut full of filthy blankets and clothing covered with blood and vomit from yellow fever victims. But, crucially, there were no mosquitoes. In another hut, conditions were pristine, but Reed introduced mosquitoes. The volunteers in this hut contracted yellow fever; those in the blood-andvomit-infested hovel emerged merely in need of a bath and some fresh air.
Subsequently, a sanitation campaign took place, spearheaded by another army doctor, William Crawford Gorgas, whose previous attempt to clean up Havana in 1898 had failed due to the campaign’s focussing on classic ‘miasma-producing’ areas such as dirty streets and piles of refuse. When Reed told Gorgas about the results at Camp Lazear, Gorgas went on the offensive, draining mosquito breeding grounds – especially any standing fresh water near houses – spraying with insecticide, and introducing screens and insecticides into sick rooms. As a result of Gorgas’s improved methods, Havana was free of yellow fever by 1901, and Gorgas went on to tackle the situation in the Panama Canal (see below), which was decades behind schedule due to yellow fever and malaria. A yellow fever vaccine was finally developed in 1937 by the South African virologist Max Theiler (1899–1972).
Despite these major advances, questions about yellow fever remain. Why has it never invaded Asia, despite the continent’s abundant population of mosquitoes and tropical environments? Do Asians have innate immunity? Or is it because encephalitis occupies the same ecological niche? A further puzzle is that the mosquito aedes albopictus spreads yellow fever and dengue fever in America, but not in Asia. No one knows why it should be a vector on one continent, but not another.
The disease has clear links with emergent capitalism, militarism, and imperialism. Indeed, each of these three inter-related things could be said to have caused yellow fever to become an epidemic disease. As Margaret Humphreys writes,
Yellow fever serves as an early example of an ‘emerging disease’ and as a warning against the disruption of tropical habitats. In its jungle form the disease is not particularly threatening, and where it exists in equilibrium with a stable society, it causes only a minor childhood disease. Developed countries that disrupt such a balance do so at their peril. In many ways it is fair to say that yellow fever is the price that Europeans and their progeny paid for the sin of slavery.267
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While yellow fever was doing its work in the newly-independent United States, and people were lamenting the lack of a health company to deal with the problem – ‘We have fire companies, we have insurance companies, and we have banking companies; but no company could equal the extensive or essential benefits desirable from a health company’268 – a doctor in Berkeley, Gloucestershire, made a momentous discovery. Edward Jenner (1749–1823) noticed that milk maids who had contracted cowpox did not catch smallpox. ‘What renders the Cow-Pox virus so extremely singular… is that the person who has been affected is for ever after secure from infection of the Small-pox,’ he wrote.269
In May 1796, Jenner decided an experiment was in order. He chose James Phipps, the eight-year-old son of his gardener, and a young dairymaid, Sarah Nelmes, who had contracted cowpox. Jenner took a scraping of material from a cowpox pustule on Sarah’s hand and scratched it into the boy’s skin. Six weeks later, Jenner inoculated James Phipps with the smallpox virus taken from the pustule of a smallpox patient. The disease didn’t ‘take’. Jenner then vaccinated his own son with cowpox with equal success. Jenner’s process became known as ‘vaccination’ from vacca, Latin for ‘cow’.
Jenner did not invent the process of vaccination. A semi-legendary account places its origins in eleventh century China.270 However, we’re on firmer ground with evidence from sixteenth century China. Inoculation for smallpox is mentioned in a book of 1549, but not described until the reign of the Longqing emperor, (1567–72).271
The process spread slowly along the Silk Road from China. In 1717, Lady Mary Wortley Montagu (1689–1762), wife of the British ambassador in Istanbul, caused a minor stir in London society circles by having her four-year-old son inoculated against smallpox. This method of ‘engrafting’, as Lady Mary called it, involved rubbing smallpox scabs – ‘as much venom as can lie upon the head of her needle’272 – into open wounds. (It was also known as ‘variolation’.) The method had long been practised by the Turks, who possibly learned it from the people of Circassia in the northwestern Caucasus.
Lady Mary had herself been a victim of smallpox, losing her famous looks (including her eyelashes)273 at the age of 26 (in December 1715). Fascinated by Ottoman culture, Lady Mary resolved to save her son from the possibility of contracting the disease when she heard about the ‘engrafting’ procedure, writing in her Turkish Embassy Letters of how a woman appeared with ‘a nutshell full of matter of the best sort of smallpox’274 when she arranged for her son to be inoculated. (She also had her three-year-old daughter inoculated in 1721.)
Lady Mary’s pioneering efforts started an interest in inoculation in England, although it was not entirely trusted, by dint of its origins in darkest Asia, by way of the Turk. As a safety precaution, engrafting was first tried out on six Newgate convicts who had been condemned to hang – three men and three women – who were offered the choice of being ‘engrafted’ in return for freedom. Although condemned to hang, the six could quite likely have been taken by typhus, or one of the other diseases that were so frequently to be found in the prison that they were virtually members of staff. Conditions in Newgate were so bad – it was little better than an open sewer – that many inmates died before reaching the gallows. King George I allowed the experiment to go ahead on the grounds that ‘carrying on this practice to perfection may tend to the general benefit of mankind’. The engrafting was a success: none of the six became seriously ill, and in September 1721, all six were released from Newgate Prison, free from smallpox.
The need for inoculation was rather more pressing in the Colonies. A smallpox epidemic gripped Boston that same year. The Puritan minister Cotton Mather encouraged inoculation after being told about the process by his African slave. Mather then told Zabdiel Boylston, a physician practising in Brookline (then a village outside the city). Boylston began inoculating patients, but made himself and Mather very unpopular in the process. Despite the epidemic raging around them, many Bostonians – including other doctors – were suspicious of the process of inoculation, and underlined their hostility by firebombing Mather’s house and forcing Boylston into hiding ‘with curses, assault, and threats of hanging.’275 However, it became clear that inoculation worked, when it was found that, out of the 248 people Boylston had treated, only six had died. Both he and Mather were made members of the Royal Society.
Both the Newgate experiment and the experiences of Mather and Boylston made the notion of public health, if not immediately possible, then at least notional. There had been early incarnations of what we would now call public health policy during plague epidemics, but these usually amounted to little more than monarchs or city fathers ordering more plague pits to be dug for the dead, or suggesting measures that we now know to be largely useless, such as hanging heavy curtains in windows to ensure plague-producing miasmas didn’t seep into people’s homes. 1721 marked a turning point, as inoculation showed that procedures could be carried out that actually worked, ‘for the general benefit of mankind’. In Russia the great reforming tsar, Peter the Great, was an advocate and ordered his doctors to begin using inoculation. Spain, on the other hand, was bound by a church every bit as suspicious as New England Puritans, and inoculation didn’t catch on there for nearly a century. Despite these attempts to introduce inoculation, smallpox remained a major killer in eighteenth century Europe.
In Britain, Ed
ward Jenner played a key role in early public health, and the eradication of smallpox in particular. Although initially ridiculed by some, who feared that being inoculated with bovine material would make them develop cow’s heads from various parts of their anatomies, Jenner’s work soon found acceptance from the medical establishment, and he was amply rewarded financially by the government. Safer and more reliable than variolation, vaccination spread to other countries, including Spain. The 1804 expedition to the Americas and China led by Dr Francisco Javier de Balmis (1753–1819) was possibly the first international healthcare undertaking. Balmis set out not to conquer new lands, but to conquer smallpox in Spanish America. Jenner’s work marked a turning point in the struggle against disease, a struggle that, as the new century progressed, gave many indications of being successful.
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While the likes of Jenner and Balmis were trying to rid the world of smallpox, another disease became quite fashionable in polite society. It was known as the White Death because it gave the sufferer a wan appearance that was immortalised in paintings and literature. Such paleness conveyed good breeding, intelligence and sensitivity. It was also called consumption, because it caused weight loss, as if the person were being visibly consumed by the sickness. For some artists and writers, getting it was almost a career move. Lord Byron is said to have remarked ‘I should like to die of a consumption, because the ladies would all say “Look at poor Byron! How interesting he looks dying.”’276
