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How smallpox devastated the Aztecs – and helped Spain conquer an American civilization 500 years ago
Richard Gunderman does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
Indiana University provides funding as a member of The Conversation US.
The Conversation UK receives funding from these organisations
Recent outbreaks in the U.S. have drawn attention to the dangers of measles. The Democratic Republic of Congo is fighting a deadly outbreak of Ebola that has killed hundreds.
Epidemics are nothing new, of course. And some widespread infectious dieseases have profoundly changed the course of human history.
Five hundred years ago, in February of 1519, the Spaniard Hernán Cortés set sail from Cuba to explore and colonize Aztec civilization in the Mexican interior. Within just two years, Aztec ruler Montezuma was dead, the capital city of Tenochtitlan was captured and Cortés had claimed the Aztec empire for Spain. Spanish weaponry and tactics played a role, but most of the destruction was wrought by epidemics of European diseases.
Early Control Efforts
Smallpox was a terrible disease. On average, 3 out of every 10 people who got it died. People who survived usually had scars, which were sometimes severe.
One of the first methods for controlling smallpox was variolation, a process named after the virus that causes smallpox (variola virus). During variolation, people who had never had smallpox were exposed to material from smallpox sores (pustules) by scratching the material into their arm or inhaling it through the nose. After variolation, people usually developed the symptoms associated with smallpox, such as fever and a rash. However, fewer people died from variolation than if they had acquired smallpox naturally.
The basis for vaccination began in 1796 when the English doctor Edward Jenner noticed that milkmaids who had gotten cowpox were protected from smallpox. Jenner also knew about variolation and guessed that exposure to cowpox could be used to protect against smallpox. To test his theory, Dr. Jenner took material from a cowpox sore on milkmaid Sarah Nelmes&rsquo hand and inoculated it into the arm of James Phipps, the 9-year-old son of Jenner&rsquos gardener. Months later, Jenner exposed Phipps several times to variola virus, but Phipps never developed smallpox. More experiments followed, and, in 1801, Jenner published his treatise &ldquoOn the Origin of the Vaccine Inoculation.&rdquo In this work, he summarized his discoveries and expressed hope that &ldquothe annihilation of the smallpox, the most dreadful scourge of the human species, must be the final result of this practice.&rdquo
Vaccination became widely accepted and gradually replaced the practice of variolation. At some point in the 1800s, the virus used to make the smallpox vaccine changed from cowpox to vaccinia virus.
Traces of smallpox pustules found on the head of the 3000-year-old mummy of the Pharaoh Ramses V. Photo courtesy of World Health Organization (WHO)
Edward Jenner (1749&ndash1823). Photo courtesy of the National Library of Medicine.
The human fight against smallpox dates back some 2,000 years. In Asia, a technique known as variolation involved deliberately infecting a person by blowing dried smallpox scabs up their nose. Those who received this treatment contracted a mild form of the disease, developing a lifelong immunity.
A key breakthrough came in 1796 when an experiment by English doctor Edward Jenner showed that inoculation using closely related cowpox could protect against smallpox. Jenner's discovery paved the way for later vaccination programs—especially crucial since there is no effective treatment for smallpox.
In 1967, a year when some 10 million to 15 million people contracted smallpox, the World Health Organization launched a worldwide eradication campaign based on vaccination. Gradually, the disease was pushed back to the Horn of Africa, and the last known natural case occurred in Somalia in 1977.
Did Early European Explorers Really Give Native Americans Smallpox-Infected Blankets?
If asked the question, Did Early European Explorers Really Give Native Americans Smallpox-Infected Blankets?, most people would find the question to be ridiculous. However, it may not be so far fetched. Whether is actually happened or not is opened to debate, but there is sufficient evidence to show that the exact act was contemplated as a war tool against Native American Indians.
History of Smallpox
The first known case of the smallpox occurred in 1507 on the island of Hispaniola. This island is known today as Haiti and The Dominican Republic. Many believe it was Spanish Explorer Herman Cortes and 600 soldiers who used the disease to defeat millions of Aztecs in 1520. Smallpox most likely made its way to America via the pilgrims who landed in Massachusetts. By the middle of the 18th century, smallpox had spread clear across the country. Since the disease can live on cloth or in dust for long periods of time, it spread so rapidly that it is credited with wiping out 30% of all the Indians who became infected. Smallpox may have also played a part in the extinction of the Taino of the Bahamas and Greater Antilles.
The Smallpox Plan
In 1763, the British forces were engaged in battle with the Ottawa tribe during Pontiac’s Rebellion. According to documents discovered by Peter d’Errico, a legal studies professor at the University of Massachusetts at Amherst, Lord Jeffrey Amherst, commander of British forces in North America, allegedly sent a letter to Colonel Henry Bouquet. In this letter, he apparently discussed the possibility of inoculating the Indians with smallpox by the use of blankets. This actual letter has ever been discovered, but other correspondence between Amherst and Bouquet certainly indicated the existence of such a letter.
Was the Plan Executed?
The answer to this question is that no one really knows. What is known is that is was possible as there were blankets available at Fort Pitt where the disease had recently been discovered. The other factor that mades such a crazy plan feasible was Amherst’s view of the Native American Indian as something on the level of a dog. He had indicated he thought is was a waste of good men to go after these animals (the Ottawa) and had been looking for ways to eliminate them without risking the lives of his men. He even referenced copying the same methods the Spanish had used to defeat the Aztecs.
So, what is the answer to the question. Did early European explorers really give Native Americans smallpox-infected blankets? The truth is unknown, but their is circumstantial evidence sufficient enough to make a reasonable assertion. The British officer spoke of the possibility of actually doing it, blankets were available, the devious mindset was in place and many Indians died of the disease. It is such a diabolical notion that most people find it incomprehensible. But the fact remains, these were war times and the British soldiers were at war.
Version One: 1992
Churchill published the earliest known iteration of his smallpox blanket fable in 1992, as one chapter of a book edited by M. Annette Jaimes, who was Churchill's wife at that time. The chapter's authorship, however, was bylined to "Lenore A. Stiffarm with Phil Lane, Jr." They appear to be real people. In 2006, as part of Churchill's defense against charges of plagiarism, he claimed to have ghostwritten this chapter (Wesson et al, 2006, p. 40, fn. 78). The University of Colorado's investigative committee on research misconduct accepted Churchill's ghostwriting claim at face value. Indeed, the chapter does bear Churchill's stylistic tics, and replicates the fabricated details that Churchill would go on to republish under his own name six more times.
However, thus evading a charge of plagiarism made Churchill vulnerable to new charges of fabrication and falsification with regards to his smallpox blanket narrative. The "Stiffarm and Lane" (1992) chapter claims that:
Certainly, the distribution of smallpox-infected blankets by the U.S. Army to Mandans at Fort Clark, on the Missouri River in present-day South Dakota, was the causative factor in the pandemic of 1836-1840. (p. 32)
"Stiffarm and Lane's" endnote reads:
The blankets were taken from a U.S. Army infirmary in St. Louis and sent upriver on the steamer St. Peter's . They were distributed by army personnel on June 19, 1837. See Chardon, Francis A., Journal at Fort Clark, 1834-39 , State Historical Society of South Dakota, Pierre, 1932. (p. 50, fn. 55)
Safely concealed behind a bogus byline, Churchill launches an ad hominem attack on Russell Thornton, the author whose mortality estimates Churchill relies on for his smallpox blanket fable. In the guise of "Stiffarm and Lane," Churchill labels Thornton as "a somewhat confused Cherokee demographer . who appears to have glimpsed an opportunity to acquire 'academic credibility' through adding the weight of his 'native voice' to the chorus of 'respectable scholars'[.]" (p. 27).
Disease Has Never Been Just Disease for Native Americans
Native communities’ vulnerability to epidemics is not a historical accident, but a direct result of oppressive policies and ongoing colonialism.
About the author: Jeffrey Ostler is the Beekman Professor of Northwest and Pacific History at the University of Oregon. He is the author of Surviving Genocide: Native Nations and the United States from the American Revolution to Bleeding Kansas.
As the death toll from COVID-19 mounts, people of color are clearly at greater risk than others. Among the most vulnerable are Native Americans. To understand how dire the COVID-19 situation is becoming for these communities, consider the situation unfolding for the Navajo Nation, a people with homelands in Arizona, New Mexico, and Utah. As of April 23, 1,360 infections and 52 deaths had been reported among the Navajo Reservation’s 170,000 people, a mortality rate of 30 per 100,000. Only six states have a higher per capita toll.
The spread of COVID-19 is reminiscent of previous disease outbreaks that have ravaged Native American communities. Many of those outbreaks resulted in catastrophic loss of life, far greater than even the worst-case scenarios for COVID-19. Even the 1918–19 flu pandemic, in which an estimated 650,000 Americans died (0.6 percent of the 1920 population of 106 million), pales in comparison to the losses Native Americans have suffered from disease.
Until recently, histories of disease and Native Americans have emphasized “virgin-soil epidemics.” According to this theory, popularized in Jared Diamond’s Guns, Germs, and Steel, when Europeans arrived in the Western Hemisphere, they brought diseases (particularly measles and smallpox) that indigenous people had never experienced. Because they had no immunity to these diseases, so the theory goes, the resulting epidemics took the lives of 70 percent or more of the Native population throughout the Americas.
New research, however, provides a much more complicated picture of disease in American Indian history. This research shows that virgin-soil epidemics were not as common as previously believed and shifts the focus to how diseases repeatedly attacked Native communities in the decades and centuries after Europeans first arrived. Post-contact diseases were crippling not so much because indigenous people lacked immunity, but because the conditions created by European and U.S. colonialism made Native communities vulnerable. The virgin-soil-epidemic hypothesis was valuable in countering earlier theories that attributed Native American population decline to racial inferiority, but its singular emphasis on biological difference implied that population collapses were nothing more than historical accidents. By stressing the importance of social conditions created by human decisions and actions, the new scholarship provides a far more disturbing picture. It also helps us understand the problems facing Native communities today as they battle the novel coronavirus.
Virgin-soil epidemics undoubtedly occurred. In 1633, for example, a smallpox epidemic struck Native communities in New England, reducing the Mohegan and Pequot populations from a combined total of 16,000 to just 3,000. The epidemic spread to the Haudenosaunee in New York, but no farther west than that. Smallpox did not hit communities in the Ohio Valley and Great Lakes until 1756–57, a century or more after initial contact with Europeans. When it did, it was because Native fighters, recruited to fight for the French against the British during the Seven Years’ War, had contracted the virus in the east and infected their communities when they returned home. Lack of immunity mattered, but it was the disruption resulting from war that promoted smallpox’s spread.
Smallpox did not arrive in the Southeast until 1696, a century and a half after the Hernando de Soto expedition. It was once thought that de Soto’s men carried smallpox, but this view reflected the flawed assumption that Europeans were always infected with smallpox and always contagious. De Soto’s expedition did cause disease to erupt in Native communities, but the reason was that the expedition’s violent warfare led to outbreaks of pathogens such as dysentery, which was already present in the Americas. When smallpox finally hit the Southeast, it spread rapidly from Virginia to East Texas across networks created by an English trade in Native captives for enslavement in their coastal and West Indies colonies. Raiding, capturing, and transporting human bodies created pathways for the smallpox virus. To make matters worse, those bodies were already weakened by war and its companions—malnutrition, exposure, and lack of palliative care.
By the end of the 18th century, most Native communities in what would eventually become the United States had been exposed to smallpox. Nevertheless, as smallpox recurred in the 19th century, its impact correlated not with a lack of prior exposure, but with the presence of adverse social conditions. These same conditions would also make Native communities susceptible to a host of other diseases, including cholera, typhus, malaria, dysentery, tuberculosis, scrofula, and alcoholism. Native vulnerability had—and has—nothing to do with racial inferiority or, since those initial incidents, lack of immunity rather, it has everything to do with concrete policies pursued by the United States government, its states, and its citizens.
Consider the impact of the Indian Removal Act. Formally adopted in 1830, this policy called for the relocation of Native peoples east of the Mississippi River to “Indian Territory” (what would eventually become Oklahoma and Kansas). Most everyone has heard of the Cherokee Trail of Tears, but it is seldom considered a U.S.-caused health crisis. The expulsion of the Cherokee from their homeland in Georgia, North Carolina, and Tennessee had three phases. In the first, the U.S. Army forcibly evicted Cherokees from their homes and held them for several months in concentration camps with inadequate shelter, insufficient food, and no source of clean water. The camps became death traps. Of the 16,000 people held in them, about 2,000 died from dysentery, whooping cough, measles, and “fevers” (probably malaria). In the second phase, the journey west, an additional 1,500 perished, as people, already sick and further weakened by malnutrition, trauma, and exposure, succumbed to multiple pathogens. In the months after reaching Oklahoma—the third phase—an additional 500 died from similar causes. The death toll was 4,000, or 25 percent of the original 16,000 forced from their homes.
Although the Cherokee Trail of Tears is the most well known, there were dozens of other such forced removals. Creeks, Seminoles, Chickasaws, Choctaws, Senecas, Wyandots, Potawatomis, Sauks and Mesquakies, Ojibwes, Ottawas, Miamis, Kickapoos, Poncas, Modocs, Kalapuyas, and Takelmas represent only a partial list of nations that suffered trails of tears. Not all experienced the same mortality as the Cherokee, but many did, and for some, the toll was even higher. The allied Sauks and Mesquakies were forced to move four times from their villages in western Illinois—once to central Iowa, once to western Iowa, once to Kansas, and finally to Oklahoma. In 1832, the time of the first expulsion, the Sauks and Mesquakies numbered 6,000. By 1869, when they were finally sent to Oklahoma, their population was only 900, a staggering loss of 85 percent. Year after year, unrelenting diseases, including an outbreak of smallpox in 1851, took many lives. Low fertility and infant mortality, the result of malnutrition, sickness, and trauma, hindered population replacement. The Sauk and Mesquakie catastrophe was not an accident. It was a direct and foreseeable consequence of decisions made by the United States and its citizens to dispossess Native people of desirable lands and shove them someplace else.
Navajos (Dinés, as they refer to themselves in their language) were also evicted from their homelands. In the winter of 1863–64, the U.S. Army pursued scorched-earth tactics—destroying their peach trees and cornfields—to drive them to a barren reservation at Bosque Redondo, on the Pecos River in New Mexico. On the 250-mile forced march, known as the Long Walk, several hundred of the 8,000 to 9,000 Dinés died en route. Over the next four years, Dinés lost as many as 2,500 of their people to disease and starvation. In their darkest hour, though, Diné leaders successfully prevailed on government officials to release them from their prison and return home. But even though their population has grown over time, the legacies of the Long Walk remain. The Diné historian Jennifer Denetdale observes that “severe poverty, addiction, suicide and crime on reservations all have their roots in the Long Walk.”
As cases of COVID-19 began to appear on the Navajo Reservation in late March, tribal President Jonathan Nez spoke to his people on Facebook. Summoning memories of the Long Walk, he “called on citizens to help one another,” reminding them “that’s when the best came out of many of our ancestors, helping each other out, carrying the load for the elders, carrying the children for our mothers.” “Now it’s our turn,” he said, “to think of our future, our children, our grandchildren.” Ongoing colonialism makes fighting COVID-19 a challenge. Although the Navajo are a sovereign nation with resources of their own, Dinés have a high incidence of conditions—diabetes, hypertension, and lung disease—that increase their susceptibility to becoming severely ill from the coronavirus. Lack of access to clean water makes hand-washing difficult. Many people cannot afford food, hand sanitizer, and other necessities. And there is an acute shortage of hospital beds and medical personnel.
Many public officials, health experts, and journalists are drawing attention to the disproportionate impact of COVID-19 on communities of color. Even so, large segments of America are indifferent, if not outright hostile, to recognizing these disparities and the inequities underlying them. Native Americans are visible to the general public far more often as sports mascots than as actual communities. The Trump administration initially resisted providing any relief to tribal nations in the $2 trillion stimulus package passed in early April, and although the legislation ultimately appropriated $10 billion to tribal governments, the Treasury Department, tasked with distributing these funds, has failed to disburse them. According to New Mexico Senator Tom Udall, Treasury Department officials “don’t know how to interact in the appropriate way with tribes and they’re just not getting the job done.”
Countering the invisibility of Native peoples, of course, means greater awareness of how COVID-19 is affecting them and enhanced efforts to provide resources to help them combat the current outbreak. It also means creating a deeper understanding of the history of American Indians and disease. Although the virgin-soil-epidemic hypothesis may have been well intentioned, its focus on the brief, if horrific, moment of initial contact consigns disease safely to the distant past and provides colonizers with an alibi. Indigenous communities are fighting more than a virus. They are contending with the ongoing legacy of centuries of violence and dispossession.
The Great Smallpox Epidemic
Elizabeth A. Fenn examines a little known catastrophe that reshaped the history of a continent.
Cruising the northwest coastline of America in 1792, Captain George Vancouver was troubled. Where, he wondered, were all the natives? The land was abundant, with a seemingly unlimited supply of salmon and fresh water, but there were strikingly few people. Instead, the British navigator found deserted villages. The first, encountered south of Vancouver Island on the shores of Discovery Bay, was ‘over-run with weeds amongst which were found several human skulls, and other bones, promiscuously scattered about’.
As Vancouver charted the Strait of Juan de Fuca, the scene repeated itself regularly. ‘During this Expedition’, crew member Thomas Manby noted, ‘we saw a great many deserted Villages some of them . capable of holding many hundred Inhabitants’. For Manby, the conclusion was inescapable: ‘By some event, this country has been considerably depopulated, but from what cause is hard to determine.’ Vancouver agreed. All the evidence, he believed, indicated ‘that at no very remote period this country had been far more populous than at present’.
There had indeed been a disaster, one so vast, in fact, that even its witnesses and victims could not appreciate its extent. In the years from 1775 to 1782, as the Revolutionary War reshaped society and politics along the eastern seaboard, a very different cataclysm shook the entire North American continent. The cataclysm, huge and hideous, was smallpox.
Caused by a moderately contagious virus known as Variola major , the initial signs of smallpox came twelve days after exposure, usually by infection of the respiratory tract. Mild at first, the early symptoms were much like those of the flu. They included headache, backache, fever, vomiting and general malaise. In many cases, victims began feeling better after the first day or two, often thinking that they had indeed suffered a bout of influenza.
Relief, however, was fleeting. By day four, the face flushed and the first painful lesions appeared – not on the surface of the skin, but in the mouth, throat and nasal passages. Within twenty-four hours, the distinctive skin rash surfaced. On some, the rash turned inward, haemorrhaging beneath the skin and through the mucous membranes. These patients died early, bleeding from the eyes, nose, gums or vagina. On most patients, however, the pustules pushed to the surface of the skin. If they did not run together the prognosis was fairly good. But if the pustules ran into each other in what was called ‘confluent’ smallpox, patients stood at least a 60 per cent chance of dying.
As the rash progressed in the mouth and throat, drinking became difficult, and dehydration often set in. Around day ten, when the pustules softened and turned blistery, many dehydrated patients simply reabsorbed the fluid they contained. Soon thereafter, in the words of an eighteenth-century Boston physician, the sores began ‘to crack run and smell’. Even under hygienic conditions, secondary bacterial infections might well set in, with consequences fully as severe as those of the smallpox. Near the end of the second week, scabs started to form. In his description of smallpox among the Narragansett Indians in 1634, William Bradford described this condition:
. they lye on their hard matts, the poxe breaking and mattering, and runing one into another, their skin cleaving (by reason therof) to the matts they lye on when they turne them, a whole side will flea of[f] at once.
By week three, mortality dropped off sharply. Fever subsided, and patients generally improved as unsightly scars replaced scabs and pustules. The usual course of the disease, from initial onset to the loss of all scabs, took roughly one month. Survivors, though often scarred and on rare occasions even blinded by the disease, were also blessed. Having endured smallpox once, they were now immune. They would never catch the disease again.
Fearsome though it was, eighteenth-century Americans did not face smallpox unarmed. Even without an understanding of virology, they employed two weapons against the disease: isolation and inoculation. Isolation or quarantine simply meant avoiding contact between individuals sick with the disease and individuals susceptible to it. Bed linens and clothing might receive special handling. Done properly, quarantine could often halt further contagion. In the colonial period, isolation was used by colonists and Native Americans alike.
The second weapon – employed even after Edward Jenner’s discovery of vaccination in 1796 – was inoculation. Unlike vaccination, which utilised the cowpox virus, inoculation involved the deliberate infection of a susceptible individual with Variola virus, usually through an incision on the hand. For reasons that elude scientists to this day, inoculated smallpox was in most cases much less virulent than the ‘natural’ form of the disease. Survivors won lifelong immunity, just as they would from ‘natural’ smallpox, but mortality was notably lower.
There was, however, a catch: individuals under inoculation did come down with smallpox, and they were therefore fully capable of infecting others with the disease. Unless practised under strict quarantine, the operation was as likely to start an epidemic as to stop one. For this reason, inoculation was highly controversial in the English colonies, where smallpox outbreaks were comparatively rare. In England, however, the disease had long been endemic, and the procedure achieved wider acceptance. These combined factors meant that in the early stages of the American Revolution the British forces were far more likely than the Americans to have acquired immunity to the Variola virus.
There had been devastating outbreaks of smallpox from the time of early Spanish exploration, but none can be so fully documented as the epidemic of which Vancouver had glimpsed the grim remains. The first signs came during the early conflicts of the American Revolution in 1775-76. In three different episodes – the siege of Boston, the siege of Quebec, and the mobilisation of Dunmore’s Ethiopian regiment – smallpox reared its head. In the end, these episodes, particularly the first two, pushed General George Washington and his medical staff to make important policy decisions regarding smallpox control in the Continental Army.
By 1775, the preliminaries were done with. The Sugar Act, the Stamp Act, the Tea Party, the Boston Massacre – each had contributed to the growing rift between the colonies and the mother country. With each new action, meetings convened, crowds gathered, and messengers raced back and forth between the colonies. Historical metaphors that describe the colonists becoming ‘infected’ with a ‘contagion of liberty’ thus seem appropriate: conditions were indeed perfect for actual contagion.
Epidemic smallpox surfaced first in Boston, that hotbed of revolutionary fervor. Isolated incidents had occurred in surrounding towns in 1774, but by January of 1775, the disease had taken hold in Boston itself.
The first battle of the war took place in April, and the disease festered through the summer while the Continental Army was entrenched around the city. To prevent it from taking hold among their troops, the Americans set up a dedicated smallpox hospital at Fresh Pond near Cambridge. On July 4th, 1775, Washington ordered:
No Person is to be allowed to go to Fresh-water pond a fishing or on any other occasion as there may be a danger of introducing the small pox into the army.
Any soldier showing ‘the least symptoms of Small Pox’ faced immediate quarantine.
The efforts at control were successful through the summer. But in November, as Bostonians turned indoors to fend off winter’s chill, the disease surged among them. At the same time, Washington and his men had to contend with a sizeable exodus of refugees from the stricken city. ‘General Howe has ordered 300 inhabitants of Boston to Point Shirley in destitute condition’, wrote Washington to Congress. ‘I . am under dreadful apprehensions of their communicating the Smallpox as it is rife in Boston’. He banned the refugees from the American camp.
Then, in the first week of December, four British deserters arrived with frightening news. Their commander, General William Howe, they claimed, had deliberately infected fugitives ‘with a design to spread the Small-Pox among the Troops’. At first, Washington gave little credit to the rumour. But when smallpox broke out among the displaced Bostonians, the Americans were forced to redouble their efforts at smallpox control.
These efforts paid off. The disease did not spread among the American forces until after the British withdrew on March 17th, 1776. Then, in the aftermath of the siege, people poured into Boston. ‘Boston’, wrote Moses Morse, ‘is become a hospital with the small-pox’. The epidemic peaked in July.
Desperate to control its spread, the town select-men made a dramatic decision: although inoculation was traditionally banned in Boston, they waived the prohibition for a period of twelve days in July. The select-men posted sentinels around the city. No one susceptible could enter no one with visible symptoms could leave. Finally, in mid-September, the epidemic burned itself out.
There was no such good news from other fronts. On May 6th, 1776, after a miserable, five-month siege of the Canadian city of Quebec, more than 1,500 Americans fled up the St Lawrence River as 900 British regulars disembarked to relieve the Quebec garrison. Throughout the siege, the Americans had had to contend with both the British and the smallpox. While quarantine had worked at Boston, it failed from the start at Quebec. On May 1st, 1776, five days before the retreat, 900 of the 1,900 American troops before Quebec were ill, primarily with smallpox.
When the chaotic withdrawal began on May 6th, even the semblance of quarantine disappeared: men in the full throes of smallpox struggled through knee-deep snow alongside men who had never had the disease, while others unaware they were incubating smallpox mingled with healthy troops. ‘My pock had become so sore and troublesome’, soldier Lemuel Roberts recalled, ‘that my clothes stuck fast to my body, especially to my feet and it became a severe trial to my fortitude, to bear my disorder’.
By May 11th, the fleeing soldiers had begun arriving at Sorel, some fifty miles north-east of Montreal, where the Richelieu River enters the St Lawrence. ‘There is Some Regimts all Down in the Small pox not a Single man fit for duty’, wrote one officer on the scene. Among those taken ill was John Thomas, the newly arrived general who had taken charge on May 1st. Thomas relinquished his command on May 21st. By June 1st, he was dead.
Reinforcements now poured into Sorel. The scenes that greeted them were terrifying, and they succumbed to the Variola virus almost as fast as they arrived. On June 11th, General Philip Schuyler wrote to George Washington from Albany, warning him that further reinforcements would ‘rather weaken than strengthen our Army’ unless they had already had smallpox.
By early June, the sight of British sail approaching Sorel had forced the ‘Northern Army’ to continue its retreat along the Richelieu River, eventually pausing at Isle aux Noix near the north entrance of Lake Champlain. Isle aux Noix was hell on earth. ‘My eyes never before beheld such a seen’, wrote John Lacey of Pennsylvania, ‘nor do I ever desire to see such another – the Lice and Maggots seme to vie with each other, were creeping in Millions over the Victims’. Two mass graves consumed thirty to forty bodies per day.
The raging infection caused General John Sullivan to order yet another withdrawal ‘or the Army will be lost, not by the enemy, but by sickness’. And so the army continued southwards to Ticonderoga. At Crown Point in July, the Connecticut painter John Trumbull visited the camp. ‘I did not look into a tent or a hut in which I did not find either a dead or dying man’, he wrote later.
It took until September for the army to cleanse itself. ‘Thank Heaven’, an elated General Horatio Gates wrote to Washington, ‘the small-pox is totally eradicated from amongst us’. The damage is hard to assess, but it is likely that smallpox carried away roughly a thousand men during the Canadian campaign. Returning soldiers, furthermore, launched outbreaks in Connecticut and possibly Pennsylvania.
Native Americans also contracted smallpox during the Quebec invasion, when a British force of Frenchmen and Seneca Indians routed reinforcements sent to the aid of a pox-ridden American garrison at the Cedars. The American patriot John Adams, who bemoaned the general havoc smallpox had created, later noted the results of this episode with satisfaction:
It is some small Consolation that the Scoundrell Savages have taken a large Dose of it. They plundered the Baggage, and stripped off the Cloaths of our Men, who had the Small Pox, out full upon them at the Cedars.
In the months that followed, the disease also appeared further west, striking the Onondaga Iroquois and Indians at Michilimackinac who had assisted in expelling the Americans from Canada.
If the smallpox wreaked havoc on American soldiers retreating from Quebec, their plight remained less poignant than that of a small band of British sympathisers to the south at exactly the same time. The colony was Virginia, where the royal governor, John Murray, Lord Dunmore, had promised freedom to all slaves ‘appertaining to Rebels’ who would fight for the crown. At least 800 African-Americans joined Dunmore, donning uniforms adorned with the words ‘Liberty to Slaves’, and fighting in several skirmishes. But Variola, not patriot Virginians, would be their most formidable enemy.
In February 1776, smallpox appeared among Dunmore’s troops, who had established a precarious camp on a spit of land near Portsmouth, Virginia. By May, nearly 300 had died, and the Governor’s surgeons recommended inoculation. Dunmore decided to leave his vulnerable mainland position and set up an inoculation camp at Gwynn’s Island, where the Piankatank River flows into Chesapeake Bay.
Gwynn’s Island was to Dunmore’s loyalist troops what Isle aux Noix was to the Americans in Canada. An American captive who escaped by swimming to shore in June 1776 claimed that Dunmore lost ‘nine or ten of his black regiment every day by the small pox, &c’.
In July, under a concerted attack by the Virginia rebels, Dunmore and his vastly reduced force gave up the island. Landing within hours of the loyalist departure, the Virginians were appalled at the scene. One described how:
On our arrival, we . were struck with horrour at the number of dead bodies, in a state of putrefaction, strewed all the way from their battery to Cherry-Point, about two miles in length, without a shovelful of earth upon them.
They found ‘others gasping for life and some had crawled to the water’s edge, who could only make known their distress by beckoning to us’. In all, some 500 men had died on the island. The remainder sailed first to the Potomac, and then, in early August, to New York, St Augustine and England. As in the Canadian campaign, returning soldiers and deserters carried smallpox home with them, sparking outbreaks that lasted well into 1777 in tidewater Virginia and Maryland.
In 1777 and 1778, the disease seemed to fade away. In part, the momentary pause in smallpox was due to General Washington’s decision to inoculate the Continental Army. The decision stemmed largely from ‘the deplorable and melancholy situation, to which one of our Armies was reduced last Campaign by the Small pox’ and the certainty that the disease would again take hold if the army was vulnerable. At its core was the recognition that the Revolution had brought about new circumstances in which people and contagious disease circulated rapidly.
So beginning in the spring of 1777 and continuing through the following winter, the American forces went through inoculation at West Point, Morristown, Valley Forge, Alexandria, Dumfries, and Fairfax. The procedure did not always go well for the troops, but quarantine seems to have been secure. There were no complaints of the contagion spreading beyond the designated inoculation sites, and in the difficult Valley Forge winter of 1778, the army managed to keep its temporary debilitation a secret from the British.
The year 1779 was a milestone for smallpox in North America. As the theatre of war moved south, so did the smallpox, primarily affecting civilians, camp followers, and irregular troops in both armies. In early 1779, for example, a combined British force of Waldeckers (German troops) and loyalists from Pennsylvania and Maryland picked up smallpox in Jamaica and carried it to Pensacola Bay.
By mid-October, the disease had reached the Indian town of Little Tallassee, where it ‘reduced them much, and those Towns who have not had it as yet, have fled with their Families into the Woods’. Smallpox also erupted in the cities of Charleston and Savannah, and in the two years that followed, it plagued the southern landscape right along with the war.
Particularly hard hit were the slaves who fled to freedom behind British lines as Cornwallis’s army marched through the south. The retreat to Yorktown, in fact, hearkened back to the Gwynn’s Island epidemic of 1776. But in this instance the British turned their guns on desperately ill African Americans to whom they had promised freedom and instead forced them to return to their masters. Some eyewitnesses believed that this was an attempt to spread smallpox behind the American lines.
But these events paled by comparison to smallpox’s ravages elsewhere. For in 1779, the Variola virus moved westwards, finding its way into the vast susceptible populations it needed to thrive. Now trade, colonial expansion, and the Spanish mission system joined with warfare in transporting and transmitting the disease.
In August 1779, after an eighteen-year hiatus, smallpox struck Mexico City. It moved quickly, and by December 27th the disease had afflicted 44,286 people in the city. ‘A great part of the Mexican youth was cut down that year’, noted the explorer Alexander von Humboldt. By the time it was over, early in 1780, an estimated 18,000 had died.
The virus nevertheless continued to travel. Moving south from Mexico City, the epidemic eventually extended into the South American continent. Traveling north, it arrived in the frontier provinces of Texas and New Mexico in the fall and winter of 1780-81. The historian Hubert Howe Bancroft calculated that in New Mexico alone, the epidemic killed 5,025 mission Indians. If non-mission Indians were included, this number would be much larger.
Even as smallpox ravaged the American southwest and followed Cornwallis’s troops through the southeast, it launched a simultaneous attack on the northern plains and Canadian shield. How did it get there? Very likely by way of the Comanche Indians, the mounted and warlike titans of the southern prairies, who engaged in a spirited horse and slave trade with their Shoshone kinfolk in western Wyoming and Montana.
The great explorer David Thompson recorded the account of an Indian named Saukamappee, who described how, in the summer of 1781, the Piegan Blackfeet had raided a Shoshone village. Knives drawn, the warriors had slashed through their enemies’ tents, and then, Saukamappee said, ‘our war whoop instantly stopt, our eyes were appalled with terror there was no one to fight with but the dead and the dying, each a mass of corruption’. They took no scalps but plundered the village and returned home. Two days later, smallpox broke out.
Before long the disease appeared among the Western Cree and the Assiniboine with whom these Blackfeet traded. On October 22nd, 1781, at a Hudson’s Bay Company post on the North Saskatchewan River, the first Indian turned up with the infection. The man, according to the trader William Walker, had left a tent on the southern prairies
. with Seven Indians laying dead in the Inside that died of the Small pox, and he himself is taken so bad that I believe he never will recover.
Reports of death and disease now poured into the post. Five of Walker’s own men returned from foraging and told of meeting Indians covered with smallpox, trying to cool themselves in the waters of the Eagle River. The dead filled nearby tents, and those who survived ‘were in such a state of despair and despondence that they could hardly converse with us’. From what Walker’s men could discover, ‘three fifths had died under this disease’.
Traders at Fort Vermilion, Portage la Loche, Hudson House, Cumberland House, York Factory, Severn, and Churchill all reported the impact of smallpox in 1781-82. The trading houses of the Canadian Shield, like the missions of the south-west, became deadly centres of contagion, despite the fact that traders often tried to mitigate contact between sick and healthy Indians.
The Shoshones, who were one source of the pestilence that devastated the Canadian interior, appear also to have transmitted the plague to the tribes of the upper Missouri River. Here, in 1805, the explorers Meriwether Lewis and William Clark noted numerous village sites forsaken by the Mandans and Hidatsas ‘about 25 years’ earlier. These towns, Clark said, were ‘destroyed by the Sous [Sioux] & Small Pox’.
The Sioux marauders did not escape unscathed. The surviving evidence does not indicate precisely how the epidemic reached them, but it was very likely in their assaults on the corn-growing Missouri River tribes. The Sioux recorded their fatal encounter with the pestilence in annual chronologies called winter counts. One such count, kept by an Oglala Lakota man named American Horse, designated the year 1780–81 with the simple phrase ‘Many died of smallpox’. In all, the epidemic appears in at least thirteen different winter counts kept by plains Indians in the years 1779–83.
Recorded eyewitness accounts of the pandemic of 1775–82 end at Hudson Bay and the northern plains. The epidemic, however, did not. It struck the northwest coast, where George Vancouver and others observed its depopulating effects.
In 1787, on the coast of what is now south-east Alaska, explorer Nathaniel Portlock spotted what he expected to be a large Tlingit village. But upon landing, he found that only nine people lived there and that the adults bore the marks of smallpox. An animated old man described to Portlock ‘the excessive torments he endured whilst afflicted with the disorder that had marked his face’.
References to abandoned villages and to smallpox-scarred Indians can be found in at least a dozen journals kept on seven different voyages to the Pacific north-west from 1787 to 1795. Even Lewis and Clark, returning through the Cascades in 1806, stopped at a nearly deserted Chinook village where they met an old woman ‘badly marked with the Small Pox’, who remained there still. The woman indicated that the disease had struck ‘about twenty-eight or thirty years past’.
If it is clear that the epidemic did indeed strike the north-west coast, it is not clear exactly how or when it did so. It is most likely that the pox proceeded westward from the Shoshones, following native trade networks down the Columbia River to the sea. Yet no evidence proving this has been found.
It is also possible that the pox arrived by sea. From 1775 to 1779, four Spanish voyages cruised north from San Blas, Mexico, in an effort to stake out and protect territorial claims. Could one of these have carried the infection? Perhaps. But if so, it has not yet turned up in the historical record. Nor, for that matter, does mention of smallpox or depopulation appear in the journals of Captain James Cook’s 1778 voyage, perhaps indicating that the epidemic arrived after that date.
Russians also frequented the north-western coastline, and they had already established trading posts in southern Alaska. Smallpox had ravaged Asia’s Kamchatka peninsula in 1768, and there is some evidence that it was present in 1774. But there is no clear indication that Russians carried the contagion eastwards in these years.
We are left, then, with George Vancouver’s mystery. From 1775 to 1782, as conflict and political upheaval rocked the east coast, smallpox had wreaked its own havoc wherever it found access to susceptible populations. From Quebec to Mexico to Hudson Bay, the continent was alive with human activity. Variola found not just susceptible populations, but connections between them. Transported by human carriers between ports and along rivers, roads, lakes, and trails, the virus showed how closely linked seemingly disparate regions already were. In so doing, it forged a horrific common experience that spanned the continent and reshaped life for years to come.
- Blake, John B. Public Health in the Town of Boston, 1630-1822 ( Harvard UP, 1959)
- Boyd, Robert The Coming of the Spirit of Pestilence: Introduced Infectious Diseases and Population Decline among the Northwest Coast Indians, 1774-1874 (University of Washington Press, 1999)
- Fenn, Elizabeth A. Pox Americana: The Great Smallpox Epidemic of 1775-82 (Hill and Wang, 2001)
- Fenner, F., D. A. Henderson, I. Arita, Z. Ježek, and I. D. Ladnyi Smallpox and Its Eradication (World Health Organization, 1988)
- Roberts, Kenneth, ed. March to Quebec: Journals of the Members of Arnold's Expedition (3rd ed. Doubleday, Doran & Co., 1940)
Elizabeth A. Fenn is an assistant professor of history at Duke University in Durham, North Carolina. Her Pox Americana (Sutton Publishing, 2003) was joint winner of the Longman-History Today book of the year award 2002.
Smallpox kill Native Americans - History
In the years before English settlers established the Plymouth colony (1616–1619), most Native Americans living on the southeastern coast of present-day Massachusetts died from a mysterious disease. Classic explanations have included yellow fever, smallpox, and plague. Chickenpox and trichinosis are among more recent proposals. We suggest an additional candidate: leptospirosis complicated by Weil syndrome. Rodent reservoirs from European ships infected indigenous reservoirs and contaminated land and fresh water. Local ecology and high-risk quotidian practices of the native population favored exposure and were not shared by Europeans. Reduction of the population may have been incremental, episodic, and continuous local customs continuously exposed this population to hyperendemic leptospiral infection over months or years, and only a fraction survived. Previous proposals do not adequately account for signature signs (epistaxis, jaundice) and do not consider customs that may have been instrumental to the near annihilation of Native Americans, which facilitated successful colonization of the Massachusetts Bay area.
Retrospective studies have inherent, sometimes insurmountable, biases, but speculation on past events by historians and anthropologists is commonplace and offers grist for future studies. We offer an alternative hypothesis for the cause of an epidemic among Native Americans in the years immediately before the arrival of the Pilgrims in Massachusetts. During 1616–1619, many persons died of a disease that presumably spared nearby European fishermen and traders (1). The more severe manifestations were fever, headache, epistaxis, jaundice, and skin lesions. Speculations as to the cause have included plague, yellow fever, and smallpox (2–7), as well as influenza, chickenpox, typhus, typhoid fever, trichinosis, cerebrospinal meningitis, and syndemic infection of hepatitis B virus (HBV) and hepatitis D virus (HDV) (Table 1) (6–11). We propose another disease: leptospirosis, accompanied by Weil syndrome. With its more severe manifestations, this syndrome is consistent with available clinical information, the nidality of Leptospira organisms, the introduction of rodent reservoirs, and the presence of favorable ecologic niches. Practices of the local population placed it repeatedly in high-risk exposures to epidemic and hyperendemic environments.
The limited information available notes the following clinical manifestations of the illness: headache and fever with visible signs of epistaxis and jaundice. Mode of transmission was not known. Weather and seasonality are unknown, although tree ring data suggest greater than average rainfall in eastern Massachusetts during 1615–1625 (12). The duration of the epidemic (or epidemics) reportedly ranged from 3 to 6 years. Estimated death rates (which lack reliable numerator and denominator data) range from one third of the local population to as high as 90% (1,13). The Patuxet (Plimouth) Native American village was severely depopulated (14). Referring to conditions along the Newfoundland and Maine coasts, where some believe the epidemic may have originated, Pierre Biard, a Jesuit missionary, noted: “They [the Indians] are astonished and often complain that since the French mingle and carry on trade with them, they are dying fast, and the population is thinning out” (15). In New England, Smith noted “three plagues in three years successively neere two hundred miles along the coast” of southern Massachusetts to Cape Cod and inland for 15 miles (16). Bennett suggested a 50–60-mile interior extension, which corresponds to the area of native corn horticulture (17).
Figure 1. Native American tribes of southeastern Massachusetts in ≈1620.
Figure 2. Plymouth, Massachusetts, harbor showing extensive Native American settlement (a sketch by Samuel de Champlain from his voyage of 1606).
By 1616, several subtribes of the Wampanoag (Pokanoket) Nation were living between the present-day borders of eastern Rhode Island and southeastern Maine (Figure 1). The Patuxet village was localized to an area in and around Plymouth harbor (Figure 2). Demographers and historians disagree about the total size of the Wampanoag Nation, but Salisbury considers an estimate of 21,000–24,000 as “not unrealistic for this region” (13). Gookin also estimated 3,000 men living in Massachusetts before the epidemic (18), which when extrapolated for family size is consistent with Salisbury’s overall estimate. Salisbury estimated that the size of the Patuxet tribe before the epidemic was 2,000.
No estimates are available of the number of Portuguese, Breton, and Bristol fishermen Basque whalers French fur traders or English codders who had established a presence on the North Atlantic coast since the early sixteenth century (10). In 1578, an observer noted 100 Spanish sails, 20–30 Basque whalers, ≈150 French and Breton fishing ships, and 50 English sails along the coast of Newfoundland (19). English traders and fishermen had daily contact with indigenous persons but lived on ships or in segregated enclaves on land where salt-dried codfish stations (favored by the English) were built along Massachusetts Bay.
Indigenous ecology was cataloged in 1604 when hundreds of coastal plants, trees, and animals (but not “vermine”) were described (20). Before 1620, there were no peridomiciliary animals except for small dogs and mice (10), although other rodents (e.g., squirrels) were common. Precolonization and postcolonization English written accounts do not mention rats, the numbers of which may have been influenced by the presence of cats, but aboard ships rats must have been common. An earlier explorer noted “Tant qu’on eut des cuirs on ne s’avisa point de faire la guerre aux rats…” (“As long as there is a cargo of skins, it makes no sense to kill the rats.”) (11). The black rat (Rattus rattus) was common in coastal England at the time (yet to be displaced by the brown rat [R. norvegicus] nearly 100 years later) (21) the black rat and mice were universal companions on ships and must have established themselves early on the coastal mainland, seeking harborage in and around Native American households. Once established, rats and mice would become chronic carriers of disease agents, contaminating water and soil and infecting other commensal rodents (e.g., the local mouse Peromyscus leucopus) and other mammals. Fresh and stored food items such as maize, beans, squash, pumpkin, roots, nuts, berries, meat, fish, and shellfish, were also susceptible to leptospiral contamination.
One hundred years ago, Williams collected all known information about the epidemic in an article that included 23 primary references, 22 of which contained eyewitness accounts or reports (3). He concluded that the disease may have been bubonic plague and supported his proposal by noting that there were abundant fleas in Indian dwellings, survivors had sores suggestive of buboes, and plague was endemic in London during 1606–1611. Eleven of his 23 primary sources disagreed, as did Carter, who without further elaboration stated that he thought the epidemic was influenza (4). Despite allusions to icterus, Williams discounted yellow fever (as did Carter) he also dismissed other febrile illnesses with jaundice, yet he cited Gookin from 1674: “I have discoursed with old Indians, who were then youths, who say that the bodies all over were exceedingly yellow, describing it by a yellow garment they showed me, both before they died and afterwards.” Trumbull, another eyewitness, noted that the Indian word for the disease meant “a bad yellowing” (3). A recent analysis interpreted it as caused by a confluent form of smallpox (6). Clinical and epidemiologic information about classical explanations and some of the more recent suggestions are summarized in Table 2.
The causes of most historical epidemics may never be proven. The new science of paleomicrobiology may provide some answers, but the question will remain about whether a person died of a specific disease or with the disease. However, even when proper evidence is limited, this limitation should not dissuade speculation about the causes of ancient afflictions. Our hypothesis is not meant to be a definite answer but a heuristic for others to criticize and explore. Alfred Crosby, one of America’s foremost medical historians, coined the term “virgin soil epidemics” to describe immunologically unexposed populations exposed to Old World diseases and cited the 1616–1619 epidemic as an example (9). He also proposed that environmental and behavioral factors were equally important (22). The Massachusetts epidemic supports this observation, and evidence may indicate that “genetic weakness” was not as important as the intimate and repeated exposure to an infectious agent among the Indians not shared by Europeans.
All previously proposed explanations for the epidemic are consistent with an Old World importation into a susceptible population (except for Webster’s, who thought yellow fever was of autochthonous origin). Despite its manifestation and subsequent visitations along coastal America in later years, yellow fever is not a plausible explanation given the routes of the trans-Atlantic slave trade at the time. Transportation of the disease, its vector, and human cargo from Africa to the New World was limited to the Caribbean and Central and South America little evidence exists that any ships visited the New England coast after disembarking slaves (23). Alternative arthropod-borne and other non-arthropod–borne viral hemorrhagic fevers are even less plausible candidates.
Clinical descriptions of other proposed diseases (plague, chickenpox, typhus, typhoid fever, and meningitis) are largely inconsistent with the syndrome described and were dismissed by Bratton. Citing Oliver Wendell Holmes, Sr. (7), Bratton concluded that the disease was smallpox, explaining that the confluent form of pustular smallpox might mimic jaundice (6). In 1799, Webster had discounted smallpox because “the Indians, who were perfectly acquainted with the disease [smallpox] after the English arrived, always gave a very different account of it. ” (2). Two diseases not mentioned by Bratton (trichinosis and HBV/HDV infections) are also unlikely. Pigs were absent in the New World, and the finding of a single pig bone in an undated midden makes a most unlikely explanation for the epidemic. Syndemic HBV/HDV infection presupposes aboriginal HBV carriage, HDV importation, and (in the opinion of Speiss and Speiss) an enteric mode of transmission (8).
In 1886, Adolf Weil originally described a constellation of signs and symptoms that is now eponymic for Weil syndrome (his first patient experienced nasenbluten [nosebleed] on the second day of illness) (24). Inada and Ido identified the causative organism 30 years later (25). Subsequent studies have demonstrated that rodents have high rates of leptospiral carriage and shedding (26). Severe (icteric) leptospirosis was also known as infectious jaundice, epidemic jaundice, and icto-hemorrhagic fever (27). Early outbreaks in the United States were recorded by Neill, including a Union Civil War Surgeon General’s report of a large number of “hepatic and haematic disorders” estimated to have affected >71,000 troops during the War (28).
In 1965, Heath et al. summarized the history of leptospirosis in the United States, analyzing 483 cases reported during 1949–1961 (29,30). Twenty-five percent were caused by L. serovar Icterohemorhagiae. Today, L. Icteroheamorrhagiae and other serovars (Canicola, Autumnalis, Hebdomidis, Australis, and Pomona) are endemic in the United States, and isolated instances within the United States continue to be reported (31). More recent reports from the Centers for Disease Control and Prevention (32,33) and ProMED mail (34) demonstrate that leptospirosis is a worldwide, reemerging infection with identifiable risk factors, including immersion in fresh water, exposure to contaminated soil, and antecedent heavy rains (35,36). Unlike hookworm disease, another Old World soil-borne disease that established itself in the more hospitable American South, leptospirosis is a more cosmopolitan fellow traveler and is still recognized as a zoonosis in New England.
Contemporary medical texts conflate signs, symptoms, and death rates of mild leptospiral infection with Weil syndrome, relying on more recent citations in which the nature of exposure, duration, and responsible Leptospira spp. are often not known. Interventional measures (removal from known sources, prompt diagnosis and treatment, and early prevention and control measures) may have decreased overall case-fatality rates and limited the extent of the outbreaks. Nosebleed is rarely mentioned in the recent literature, but “hemorrhages, starting with epistaxis” are noted in a 1944 text on tropical diseases, which also cites high death rates (32% in Europe and 48% in Japan) (27). These surprisingly high death rates in early Japanese reports were attributed to repeated intimate exposure to contaminated water by barefooted mine workers and rice farmers.
Unlike the European experience, epidemics in Japan were rare, and endemic exposures were more common (27). A recent population-based seroepidemiologic study found leptospiral seropositivity rates of 28% in an annually flooded area of the Amazon basin (37). Leptospira spp. were found to cause seasonal outbreaks of a mysterious disease (tentatively named Andaman hemorrhagic fever) during periods of rice paddy sowing and harvesting in the late 1980s on the Andaman Islands in the Indian Ocean (38). Subsequent studies found that leptospiral seroposivity was as high as 62.5% (among agricultural workers) in the Andaman Islands and that the case-fatality rate was 42.9% among hospitalized patients with severe leptospirosis and pulmonary symptoms.
Endemicity and subsequent high case-fatality rates, similar to those reported from Japan, are consistent with a leptospiral etiology for the 1616–1619 epidemic. The Patuxets may not have associated sickness with their environment or traditional ways of living and may have attributed their affliction to many causes, but not to countless exposures and reexposures to the agent. Sporadic, focal mini-epidemics may have played out and coalesced into what was construed as a single “plague” by outside observers. Except for more severe cases of liver failure, the most common cause of death for leptospirosis (renal or respiratory insufficiency) would have not been recognized. The Indian lifestyle, which included constant exposure to rodents and their excreta on land and in water, exposed them to the leptospiral life cycle (Figure 3) (39,40). Bare feet were common in and around houses. Although a rare portal of entry, mucosal exposure may have occurred from ingestion of corn buried in the ground in rodent-accessible baskets and from rodent-contaminated foods in wigwams (weetas). Dermal abrasions offered cutaneous portals of entry. Attendance of the ill and burial of the dead (including those who died from Weil syndrome) would have attracted others who shared local food, water, and camp grounds. It was common practice for entire families to enter sweat lodges followed by immediate immersion in cooling streams and ponds sweat lodges were considered vivifiers and cure-alls for illnesses, a practice that may have reexposed the already ill to contaminated water. Once the spirochete established its presence in numerous foci, it survived for months in water, mud, and moist soil and caused infection in additional mammalian reservoirs. A reduction in the populace may have been incremental, episodic, and continuous daily needs and customs may have exposed the Indians to leptospirosis over many months or years, with only a small fraction of the population eventually surviving. Suggestions that the disease persisted among the Indians after 1619 (perhaps through 1630) support the premise of endemic nidality and selective Indian vulnerability. The fate of nearby European cod fishermen is unknown, but they did not share most of the Indians’ risk factors. Boots would have limited transmission from fresh water exposures, bathing was not a common practice, and work in a saline environment may have curtailed transmission. An occasional case of febrile illness on board ship would have been attributed to many other causes. Disease and death may have occurred among the fishermen but are not recorded.
The exact duration and extent of the epidemic(s) will never be known, but our suggestion offers an alternative explanation. Persistent leptospiral exposures resulted in more severe cases of Weil syndrome and jaundice, a sign that would have been reported by observers the cause of death from other (anicteric) leptospiral infection would not have been recognized. Our proposal is consistent with the historical clinical descriptions, estimated death rates, importation and distribution of its reservoir host, inoculation of the agent in multiple suitable nidalities, spread to other mammalian reservoirs, hyperendemicity, ecologic factors favoring repeated exposure and transmission, and known high-risk activities of the indigenous population.
The name Squanto has entered American history and folklore as the one of the last of the Patuxets who assisted the Pilgrims in 1620. He was one of the few survivors of an epidemic that was crucial to the success of the Plymouth and Massachusetts Bay colonies because remaining Indians had little capacity to resist the new settlers. Two years later, after having fever and a nosebleed, Squanto died of what was then referred to as “the Indean disease.”
Dr Marr is a professor at Virginia Commonwealth University School of Medicine, Richmond, Virginia, and at East Carolina University School of Medicine, Greenville, North Carolina. His research interests include public health history and historical epidemics and diseases.
Mr Cathey is senior editor of the Annals of Saudi Medicine at King Faisal Specialist Hospital, Riyadh, Saudi Arabia, and a professional medical writer. His research interest is historical epidemics.
We thank Alfred W. Crosby, Asim A. Jani, Grayson B. Miller, Myron G. Schultz, and Jack Woodall for critical comments Philip McEldowney for literature search/retrieval Stefanie Nauhardt Parker for translation Mariana Ruiz-Villarreal and David Connell for providing the leptospiral life cycle and Reina Tejano and Samuel de Champlain for providing the maps.
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Disease can drive human history
Of course, the Aztecs were not the only indigenous people to suffer from the introduction of European diseases. In addition to North America’s Native American populations, the Mayan and Incan civilizations were also nearly wiped out by smallpox. And other European diseases, such as measles and mumps, also took substantial tolls – altogether reducing some indigenous populations in the new world by 90 percent or more. Recent investigations have suggested that other infectious agents, such as Salmonella – known for causing contemporary outbreaks among pet owners – may have caused additional epidemics.
The ability of smallpox to incapacitate and decimate populations made it an attractive agent for biological warfare. In the 18th century, the British tried to infect Native American populations. One commander wrote, “We gave them two blankets and a handkerchief out of the smallpox hospital. I hope it will have the desired effect.” During World War II, British, American, Japanese and Soviet teams all investigated the possibility of producing a smallpox biological weapon.
Mass vaccination against smallpox got going in the second half of the 1800s. Photo courtesy of Everett Historical via Shutterstock.cm
Happily, worldwide vaccination efforts have been successful, and the last naturally occurring case of the disease was diagnosed in 1977. The final case occurred in 1978, when a photographer died of the disease, prompting the scientist whose research she was covering to take his own life.
Many great encounters in world history, including Cortés’s clash with the Aztec empire, had less to do with weaponry, tactics and strategy than with the ravages of disease. Nations that suppose they can secure themselves strictly through investments in military spending should study history – time and time again the course of events has been definitively altered by disease outbreaks. Microbes too small to be seen by the naked eye can render ineffectual even the mightiest machinery of war.
This article was originally published on The Conversation. Read the original article here.
Left: A skeleton discovered at a ruined pyramid in Tlateloco in Mexico City February 10, 2009. Archaeologists have discovered a mass grave with four dozen neatly lined up human skeletons in the heart of Mexico City, revealing clues about the Spanish conquest that killed millions in battle and disease. The 49 bodies, all lying face up with their arms crossed over their chests, were discovered as investigators searched for a palace complex in the Tlatelolco area, once a major religious and political center for the Aztec elite. Photo By Daniel Aguilar/Reuters