Category Archives: mortality

Challenging Virgin Soil Epidemic Assumptions 

The depopulation of Native Americans during the 16th to 18th centuries, one result of the ‘Columbian Exchange’, has been held up as the ultimate example of virgin soil epidemics. The emphasis put on the ‘virginity’ of the native population, bordering on biological determinism, has absolved the colonial powers of a multitude of sins. Some archaeologists and historians of early North America have begun to challenge the emphasis placed on the virulence of the new pathogens in the native population without minimizing the depopulation itself. They have uncovered multiple additional factors that led to such a drastic loss of native Americans.

Chiaves la florida, 1584
Chiaves la florida, 1584

I recently finished Paul Kelton’s Epidemics and Enslavement: Biological Catastrophes in the Native Southeast, 1492-1715 (2007) and it was illuminating. He is covering the area of the modern Carolinas, Georgia, northern Florida, and Alabama and contiguous frontiers. This area was colonized by the Spanish, English and the French toward the Mississippi. These infant colonies set off an extensive reorganization of native tribes as trade goods shifted the balance of power throughout the region.

The colonial powers were initially interested in resource extraction over building large colonies. This region had only two easily exploitable resources — deer skins and slaves. This sparked a period of nearly constant intra-tribal warfare and the creation of confederations for protection.

Kelton shows that native depopulation did not occur solely due to epidemics, but due to a set of actions taken by the colonial powers primarily in Carolina. In the first century of the English colonies, native tribes became dependent upon trade good especially guns, powder and shot that were paid for with deer skins and captives. Moreover, the English wanted primarily women and children as captives. Eventually this led to a gender imbalance in most tribes preyed upon for captives. This made it nearly impossible for the tribes to recover from severe epidemics. Having enough women of reproductive age is absolutely necessary for population recovery after an epidemic or any other sudden population loss.

Kelton does not look at human genetic analyses but this makes me think of population analyses in Central and South America where native mtDNA lineages (via matrilineal only) are common but native Y chromosomes are very rare. Many female captives would become wives to immigrant men and their offspring are advantaged over all North American native children. Kelton never really explores the destination of native captives/slaves but implies that many went to markets outside of the English colonies. He implies that it was primarily when native captives were exhausted that Carolina turns to more African slaves.

As the tribes disintegrated from the stresses of warfare and slave raiding, they reorganized into the confederations we are more familiar with, like the Cherokee, Creeks, and Choctaw. None of the groups existed before the colonial period.  In the process of reformation many villages were abandoned. They resettled in a tighter configurations and some built palisades for the first time. In the past many of these settlements were claimed to have been depopulated by epidemics.

Natives in the south-east were primarily farmers who supplemented their diet with venison, fish and other salvaged sources of protein. Without domestic animals for protein, their nutrition was maintained by a precarious balance of crops liable to be disrupted by climate and social disruption. Evasion of slave raiding parties made it difficult to grow crops (most maize) and gather supplementary wild food (deer, fish, oysters, fruit/berries etc). Famine coupled with enteric disease has to be a significant factor in any explanation of native depopulation.  Even before 1492, native populations showed signs of nutritional stress and short lifespans, sometimes with average lifespans in the low twenties.

I’ve focused on non-epidemics causes of depopulation so far because this was the newest material to me. Kelton postulates that malaria was the first epidemic disease to spread among the native population. Malaria is likely to have become entrenched in wetlands early, but how quickly it spread is more questionable and he seems to minimize its demographic impact.  From my own research on the mid-Mississippi valley, malaria makes its first appearance in the records with the arrival of the English even though the French and Spanish had been in the valley long before.

Smallpox is generally considered the most dangerous pathogen of the Columbian Exchange. Kelton acknowledges that smallpox first came to the Spanish missions in Florida and Georgia, but asserts that these epidemics were limited to the mission system. Native North Americans did not have the population density or extensive trade networks found in Mexico and further south. He shows that smallpox (and perhaps measles) did not begin to spread between tribal groups at distance from the colonial settlements until the English facilitated native enslavement system, always done through native partners, developed. By the mid-18th century, native tribes stopped cooperating with the British to sell captives creating a more direct confrontation between the European colonies and all native groups, and increasing the importation of African slaves.

Supposed virgin soil epidemics have been an attractive explanation for demographic collapses in part because it comparatively simple, absolving humans of more responsibility. Humans are portrayed as being victims of biology. Finding other causes does not clear new pathogens of a significant role in native depopulation. Epidemics remain an integral piece of the puzzle, but only a piece.

Reference: Paul Kelton, Epidemics and Enslavement: Biological Catastrophe in the Native Southeast, 1492-1715. Lincoln & London: University of Nebraska Press, 2007.

An Anniversary year for Natural Disasters: 1815, 1665, and 1315

There are major natural disasters every year. In the last year alone we have had the major earthquake in Nepal just in the last couple days and a historic epidemic of Ebola. It’s too soon to tell how these latest disasters will seen by history and effect historical interpretations. This year there are three natural disaster anniversaries that stand out from the rest not just due to their mortality but also because of their impact on how we interpret the past.

Tambora, 1815

Mount Tambora Volcano, Sumbawa Island, Indonesia
Mount Tambora Volcano, NASA image (public domain)
Just a few weeks ago there was a minor splash in the news to mark the 200th anniversary of the eruption of Tambora on April 5, 1815. The photo to the right is the caldera of Tambora taken from space. As tragic as the thousands of deaths directly related to the eruption are, 1815 is best known as the ‘year without a summer’, a volcanic winter. It is impossible to know how many deaths resulted from crop failures and unseasonable weather. As the most recent volcanic winter, 1815 is an important because we have the most reliable scientific data, economic data, and descriptions of the effects on health and culture from people in all walks of life all over the globe. I don’t know as much about Tambora and its after effects as I would like, so I’m planning on reading The Year Without a Summer by historian William Klingman and meteorologist Nicholas Klingman (2013). If I like it, maybe you will hear more about it later this year.

Great Plague of London, 1665

This year is also the 350th anniversary of the Great London Plague that was followed closely by the Great London fire. Despite its reputation, the great plague of London was not the last major plague of Europe by a long shot.

17th century London
17th century London

The 1665 plague of London claimed up to 100,000 lives, about as many as died in the Marseille plague of 1720-3. Fifty years later, a similar size plague struck Moscow under Empress Catherine the Great. Yet, the London Plague is the one that gets the most attention.

A great deal of the notoriety of the Great Plague of London comes from the amount and quality of resources available in English.  Daniel Dafoe immortalized the plague in his novel, Journal of a Plague Year written in 1722. A savvy author, Dafoe timed it to take advantage of plague fears in southern Europe, concurrent with the plague in Marseille. It is testament to the Dafoe’s skill as a writer than his novel is often taken as historical evidence. I think I’ll mark the anniversary by reading Defoe’s classic.

The London plague has also been magnified by it linkage with the great fire of London in 1666. The relationship between the fire and the plague has been controversial. It has been sometimes assumed that the fire ended the plague, but the plague was winding down before the fire began. However, it is likely that the fire removed the environment that had supported the plague preventing its return; over 80% of the citizens of London were left homeless. Restoration of the capital city after the great fire also immortalized 1665-6 in the history of London.

Great European Famine, 1315

A less combustible but perhaps equally deadly anniversary this year is that of the Great Famine of 1315 that effected most of continental Europe. Seven hundred years ago the famine began and, while its hard to estimate famine mortality over three to seven years, perhaps up to 15% of Northern Europeans died. It began with soaking and then flooding rains that destroyed winter crops for two years with yields of wheat and rye in England and Wales 60% below normal in 1316, and again in 1321 with similar drops in yield. Also beginning in 1315 the great bovine pestilence, possibly rinderpest,  begins in Central Europe and spread across the continent: France and Germany, the Low Countries,  Denmark and England by 1319. In just one year, England and Wales lost approximately 62% of all bovines (Slavin 2012). The loss of dairy and beef was compounded by the fact that oxen provided the vast majority of traction and fertilizer. With similar losses across Europe, it took nearly 25 years to return cattle numbers to the pre-epizootic levels.

There was no respite for the 14th century. The childhood survivors of the famine and food shortage were the adults who were cut down by the Black Death in the 1340s. What effect malnutrition had on their developing immune system is a line of inquiry being explored by anthropologists Sharon DeWitte and historian Philip Slavin (2013). Let us not forget, it still got worse, between the crop failures and panzootic of 1315 and the Black Death in 1346 , the Hundred Years’ War begins in 1337.


Devaux, C. A. (2013). Small Oversights That Led to the Great Plague of Marseille (1720-1723) Lessons From the Past. Infection, Genetics and Evolution, 14(C), 169–185. doi:10.1016/j.meegid.2012.11.016 (for comparisons to other epidemics)

Slavin, P. (2010). The Crisis of the Fourteenth Century Reassessed: Between Ecology and Institutions — Evidence from England (1310-1350). EHA Paper, 1–14.

Slavin, P. (2012). The Great Bovine Pestilence and its economic and environmental consequences in England and Wales, 1318–501. The Economic History Review, 1–28.

Dewitte, S., & Slavin, P. (2013). Between Famine and Death: England on the Eve of the Black Death—Evidence from Paleoepidemiology and Manorial Accounts. Journal of Interdisciplinary History, 1–25.

Ebola’s Chain of Infection

Chain of Infection A chain of infection is a method for organizing the basic information needed to respond to an epidemic.  I’ve gathered the best information I’ve been able to find. As the current epidemic is analyzed, there is no doubt some of the recommendations and basic knowledge will change.

The Ebola Virus (EBOV)

img8The Ebola virus is a Filovirus, an enveloped RNA virus containing only eight genes. Three of the five ebola virus species are highly pathogenic to humans: Zaire ebolavirus (Case fatality rate (CFR) 70-90%), Sudan ebolavirus (CFR ~50%) and Bundibugyo ebolavirus (CFR 25%). The 2014 epidemic is caused by the  Zaire ebolavirus.

Ebola attaches to the host cell via glycoproteins that trigger absorption of the virus. Once inside the cell it uncoats and begins replicating the eight negative sense RNA genes (seven structural genes and one non-structural gene). It initially targets immune cells that respond to the site of infection; monocytes/macrophages carry it to lymph nodes and then the liver and spleen. It then spreads throughout the body producing a cytotoxic effect in all infected cells. Death occurs an average of 6-16 days after the onset of symptoms from multi-organ failure and hypotensive shock.

Symptoms present 2-21 days after infection and the patient is contagious from the onset of symptoms.  Symptoms include a fever, fatigue, headache, nausea and vomiting, abdominal pain, diarrhea, coughing, focal hemorrhaging of the skin and mucus membranes, skin rashes and disseminated intravascular coagulation (DIC). In the 2014 epidemic, abnormal bleeding has only occurred in 18% of cases and late in the disease process.

The Reservoir

Fruit bats in Africa are believed to be the primary reservoir. Transmission between bats and other animals is poorly understood.


Portal of Exit

Ebola leaves its reservoir by contact with body fluids of an infected animal, often by bushmeat hunters. The spill-over is usually very small with the vast majority of human cases being caused by human to human transmission.


Transmission between humans occurs by contact of skin or mucus membranes with the body fluids of an infected person. Viral particles are found in all body fluids: blood, tears, saliva, sputum, breast milk,  diarrhea, vomit, urine, sweat and oil glands of the skin, and semen. Ebola can be found in semen three months after recovery from an infection but transmission by this route is poorly understood. Viral particles are found in other body fluids for 15 days or less after the onset of symptoms. It lasts the longest in convalescent semen and breast milk. All fluids from dead bodies are highly infectious.

All materials touched by the infected person, body fluids, medical waste, and used PPE must be discarded and destroyed as infectious medical waste. Non-disposable items like rubber boots, furniture, and building structures must be professionally decontaminated.

Ebola virus is a Biosafety Level 4 pathogen and a category A bioterrorism agent along with other viral hemorrhagic fevers.

Portal of Entry

Ebola enters the human body through breaks in the skin, including micro-abrasions and splashes on mucus membranes. Personal protective equipment (PPE) includes full body coverage including hood, mask or face shield, a tight fitting respirator, boots or shoe coverings, and double gloving. A buddy system should be used for dressing and disrobing. Removing PPE is a point of frequent contamination and should be done with help from another robed person.

Vulnerable populations

The most vulnerable populations for ebola are defined by their occupation. Care givers in medical facilities are at the highest risk because the viral titers reach the highest levels in fatal cases shortly before death. Mortuary and burial workers are also at high risk. The infectiousness of the bodies means that the usual burial practices can not be done in any setting or country. Home caregivers and decontamination workers would also be at a higher risk.

Information is lacking on survival vulnerabilities such as age, gender, pregnancy, or pre-existing conditions. More information on these aspects should be available in the post-epidemic analysis of the current epidemic.


References and further reading:

Martines, R. B., Ng, D. L., Greer, P. W., Rollin, P. E., & Zaki, S. R. (2014). Tissue and cellular tropism, pathology and pathogenesis of Ebola and Marburg Viruses. The Journal of Pathology, n/a–n/a. doi:10.1002/path.4456 [in press]

Chowell, G., & Nishiura, H. (2014). Transmission dynamics and control of Ebola virus disease (EVD): a review. BMC Medicine, 12(1), 196. doi:10.1186/s12916-014-0196-0

Toner, E., Adalja, A., & Inglesby, T. (2014). A Primer on Ebola for Clinicians. Disaster Medicine and Public Health Preparedness, 1–5. doi:10.1017/dmp.2014.115

Bausch, D. G., Towner, J. S., Dowell, S. F., Kaducu, F., Lukwiya, M., Sanchez, A., et al. (2007). Assessment of the Risk of Ebola Virus Transmission from Bodily Fluids and Fomites. Journal of Infectious Diseases, 196(s2), S142–S147. doi:10.1086/520545

CDC: Ebola Virus Disease portal