Category Archives: North America

Disease and Discrimination in Colonial Atlantic America

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Reviewed by Michelle Ziegler

Dale Hutchinson. Disease and Discrimination: Poverty and Pestilence in Colonial Atlantic America. University of Florida Press, 2016. $85

Dale Hutchinson’s latest book fits into a recent trend of a more critical analysis of the role disease played in the demographic collapse of Native Americans in the Colonial period. After spending most of his career working on the Spanish Colonial system in Florida,  in Disease and Discrimination, he discusses the English and French colonies along the Atlantic seaboard.

By his own description, “this book is a series of narratives about changing landscapes of America — not only the natural landscapes, but the social, political and economic landscapes — and how they all contributed to the nutrition and health of natives and newcomers in the Atlantic coastal colonies” (p. 10) He goes on to warn the reader that landscapes he intends to paint are “neither exhaustive nor completely factual representations”; he has “chosen what to accentuate” (p.11).   In painting his landscapes he chose to use an informal, conversational tone that should make it the science easier to understand but also leads to a somewhat rambling style that sometimes lacks structure and yields uneven coverage. Disease and Discrimination is divided into four sections: ‘Of Apples and Edens’,  ‘Natives and Newcomers’, and Planters and Pestilence, and ‘Measuring the Lands’.

In the first section, he discusses landscapes and disease processes.  He opens the second chapter with a nice introduction to disease ecology and terminology but then moves on build off of McNeill’s “civilized disease pools”, which is now quite outdated. This would have been an ideal place to discuss syndemics, but he does not apply syndemic theory anywhere in the book. From here he moves into a rather free flowing discussion of plague pandemics. To be honest, I felt this discussion was out of place in a book that does not otherwise discuss bubonic plague. If he wanted to discuss the Old World origins of New World epidemics, then wouldn’t it have been better to discuss the disease ecology of an organism that made the ‘Columbian exchange’?

Opening with a discussion of syphilis, the next chapter discusses historical epidemiology and then the virgin soil epidemic hypothesis. As he notes, attenuation (weakening over time) is a core principle of the virgin soil hypothesis that lacks pervasive scientific evidence. It is not always in the best interest of a pathogen to become less virulent. Indeed, some times it’s quite the opposite.  Hutchison correctly points out that many of the examples of virgin soil epidemics were more likely to be caused by environmental contingencies like over crowding and poor sanitation on Indian reservations. Consulting David Jones (2003) work on refuting the virgin soil hypothesis would have been helpful here.

In the second section, Hutchinson reviews the European settlement, resource extraction and interactions with the Native tribes. He pays particular attention to the interactions between the French, Dutch and English colonists with the tribes, providing a handy table of seventeenth-century epidemics (table 4.1). It is interesting that all but one of these epidemics are credited to viruses (smallpox, measles, and influenza). Just over half of these epidemics were recorded by the Jesuits working in the French colonies. The 1630s were a particularly bad time for the colonies with measles, smallpox and other poorly recognized diseases impacted both the colonists and the Native American tribes in the Northeast. Hutchinson spends some valuable time discussing the differential impacts of the French and English interests in resource extraction, how that affected the landscape, and how the tribes moved, mixed and formed new entities due to attrition. Despite the reputation of epidemics among native tribes, the Europeans and Africans were ravaged by smallpox and measles as well.  Children born to both Europeans and Africans would have been as immunologically naive as the Native Americans (although variolation would have protected the few who received it from smallpox). Malnutrition affected all three groups but in different circumstances and to different degrees, as did the effects of war. A key difference between natives and newcomers is that more Europeans and Africans could immigrate to bolster their numbers, while Native Americans were still being enslaved or facing hostile encounters.

As the English began to attempt to transform the landscape, to ‘improve’ it, they began to build plantations, essentially recreating English manors in the New World. The New World landscapes did not yield easily and it dragged out long enough to spawn its own pestilence, known by contemporaries as ‘the seasoning’.  Hutchinson discusses the ecological causes including rice farming, deforestation, and diseases clusters (primarily typhoid and malaria).  The ‘seasoning’ is discussed in terms of immunology but it would have been helpful to consider the seasoning as a type of syndemic. In addition to gaining some immunological protection, the mortality rate was often very high in the first few years after arriving on the frontier.  In the Carolinas, rice farming learned from West African slaves quickly went from sustenance to export along with indigo and timber, taken for lumber and pine tar. The radical changes to the Carolina landscape primed it for its own blend of ‘seasoning’ microbes led by malaria.  The production environment of the Carolinas stimulated the import of African slaves who brought more malaria and were vulnerable to infections primed by enslavement conditions.

As the plantation landscape developed beyond the coast the stratification of society became extreme enough to be detected in osteological assessments of their health. Indentured servants and slaves both show evidence of a very hard life with overdeveloped muscle attachments on their bone indicating hard labor and evidence of malnutrition including signs of rickets, scurvy, and protein malnutrition. Corn (maize) replaced European grains, especially for servants and slaves. The caloric intake may be similar but the nutritional value is not. The typical diet of cornmeal, fatback, molasses, and an assortment of vegetables given to slaves is not a balanced diet. Fatback is a slice of pork under the back skin with hard fat with little or no muscle. It was often left to slaves and indentured servants to hunt or fish for most of their protein. Protein malnutrition is particularly evident in the remains of children who got the proportionally worst diet.  Through at least the early seventeenth century Native Americans continued to be a significant percentage of slaves, 20% in one Carolina census, and when census are compared, proportionally more Native American slaves were added than African. It was not until the end of the seventeenth century that the birth rate exceeded the death rate in Chesapeake, and even then, parents “were about as likely to die before their children reached their teens as their children were to reach maturity” (p. 137). Many children would be forced into early hard labor to survive. Although Hutchison does not discuss infection and nutrition as a syndemic, he does recognize the “synergistic relationship between nutrition and infectious disease” (p. 139). He notes that slave owners treated infectious disease but tended to ignore chronic or nutritional disorders that made the slaves more prone to serious infectious disease. I do wonder if this was not the attitude of most people except the richest families. It is unclear if they understood the nature of their malnutrition.

In the last section, Hutchinson turns more toward the first cities and urban life. In the last full chapter, he discusses the rapid development of New York City from the original Dutch colony to New York City on the verge of the Civil War. Early New York did not have a sanitary infrastructure so that it quickly became an extremely contaminated environment that was unhealthy for all of its inhabitants. Poverty was an issue for the inhabitants of New York from its earliest days. A constant stream of new poor immigrants meant that the labor market always had access to laborers for less than a living wage. Crowd diseases like smallpox and measles and filth diseases like dysentery always had a constant supply of vulnerable people to prey upon. The city streets were a zoo of animals that contributed to its disease ecology: hogs roamed the street eating refuse, mice and rats multiplied along with stray dogs and constant horse traffic. The city buzzed with urban mosquitoes and New York fell victim to Yellow fever 19 times between 1702 and 1822, but it still did not suffer as much or as often as Philadelphia or Charlestown (p. 166). By 1760 Beloe Island in New York Bay hosted a pesthouse for smallpox and yellow fever; fifty years later the island was ceded to the federal government for the construction of Fort Wood, now the foundation for the base of the Statue of Liberty. A sewage and water system was not installed in New York City until 1850.  As with other large cities in the more distant past, New York’s high mortality rate was offset by an even higher immigration rate into the city.

Hutchinson accomplished his goal of painting a very complex landscape of disease in Colonial America. To gain a more complete picture of the causes and effects of malnutrition and disease, social, cultural and economic factors have to be brought into play along with biological and ecological conditions.

It seems that this book overlapped in the publication process with the collected study Beyond Germs: Native Depopulation in North America, published in 2015. These two books complement each other even though there does not seem to be any contact between the authors. It seems we are on the verge of a new era of Native American studies that will be very welcome.


References

Jones, D. S. (2003). Virgin soils revisited. The William and Mary Quarterly, 60(4), 703–742. http://doi.org/10.2307/3491697

Catherine Cameron, Paul Kelton, Alan Swedlund, Eds. Beyond Germs: Native Depopulation in North America. University of Arizona Press, 2015.

 

Dogs as Plague Sentinels and Vectors

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Marmot fighting a wild dog in northern Tibet (Source: China Tibet Online/ Xinhua)

I’ve been a little obsessed with thinking about dogs and the plague lately. Dogs are often overlooked in historic plague discussions because they usually survive plague and dog-specific fleas are not associated with transmitting plague. Yet, dogs can host many of the fleas common among rodents and others that do transmit the plague including the cat flea (Ctenocephalidis felis) and the human flea (Pulex irritans) (Gage, Montenieri, & Thomas 1994). In a case controlled study of nine US cases of bubonic and septicemic plague in 2006, having dogs in the home and particularly sleeping with a dog was a significant risk factor, probably by flea transfer (Gould et al, 2008).  There is also a growing awareness that dogs can also transmit pneumonic plague directly to humans. Like other aspects of plague biology, there is a lot going on under a veneer of normalcy.

Dogs do readily contract the plague; it’s just not apparent to casual observation. In the American state of New Mexico, 62 domestic dogs were diagnosed with plague just between the years 2003 and 2011 — 97% survived (Nichols et al, 2014).  The dogs were diagnosed by an increase of Yersinia pestis F1 antibody greater than four times greater than the recovered level, by isolation of Yersinia pestis from a body fluid or by direct flourescent antibody assay of a tissue specimen. All of them had some physical sign of infection with fever and lethargy being found in 100% of cases, but buboes or lymphadenopathy (enlarged lymph nodes) were found in only 23% and these were all in the jaw and neck region. The mean time for recovery was two days, although all but one did receive at least one dose of antibiotics. Potential sources of plague exposure are from prairie dogs, ground squirrels, chipmunks, and rabbits. Only three of the dogs had any fleas at all, but as these dogs were pets, most had received anti-flea treatment.

Monitoring plague in working dogs and other carnivores is the most efficient method of doing plague surveillance in the vast semi-arid grasslands that harbor some of the most enduring plague reservoirs. Dogs are especially useful because their immunity only lasts about six months, so a detectable level (titre) of plague antibody indicates recent contact with an infected animal. Gage, Montenieri, and Thomas (1994:6) estimated that  “sampling even a few rodent consuming carnivores, such as coyotes, can be roughly equivalent to sampling hundreds of rodents for evidence of plague infection”. The earliest serologic survey that I have found was done in Navajo lands in 1966-1968. In this same survey  in 1968, “the plague organism was isolated from a pool of fleas (Pulex irritans) taken from the household dogs of a person with plague” (Archibald & Kunitz 1971). Carnivores are now routinely monitored in the US.  Surveying herding dogs in Iran was able to show that the long unmonitored plague foci is still active (Esamaeili et al., 2013). Recent Chinese F1 antibody surveys in the Gansu province are more ominous: in 2012 4.55% of dogs were positive, but it had jumped to 10% of dogs by 2014 (Ge et al, 2014). Another  2014 survey of multiple Yersinia species in dogs found 25% of dogs in Gansu province and 18% of dogs in Qinghai province to be positive for Yersinia pestis F1 antibody, while no plague-free provinces had a single dog that had a positive antibody titre (Wang et al, 2014).

Consumption is the likely primary route of infection for dogs.  The 62 dogs from New Mexico are believed to have been primarily infected by consumption of a plague infected rodent or rabbit (Nichols et al, 2014). In a 2014 case study from China, an infected marmot was taken from a dog, butchered and divided among five dogs. All five dogs developed positive antibody titers for  plague and the shepherd who took the marmot from the dog developed pneumonic plague (but not his brother who butchered the marmot). Aerosol transmission was supported by  the isolation of Y. pestis from sputum and throat samples (Ge et al, 2014). One dog not fed the marmot was negative for the F1 antigen. Three of the 151 human contacts given prophylactic antibiotics developed an antibody titre but did not manifest disease. According to Chinese policy, the five positive dogs were euthanized and the local marmots were depopulated (Ge et al., 2014).

Dogs can transmit plague to humans through fleas that feed on the dog, fleas carried by the dog from the rodent source of the infection,  through bites or scratches, or by aerosols from dogs that develop a systemic infection. While dogs are usually thought of transmitting infected fleas to people, the  number of pneumonic cases linked to dogs is increasing. The first confirmed transmission of pneumonic plague from a dog to a person occurred in China in 2009 (Wang et al, 2015). The index case in turn transmitted pneumonic plague to eleven people. Three of these twelve cases died with the other nine cases confirmed by Y. pestis F1 antibody titres. All of the Y. pestis isolates were later typed to “biovar antiqua” — a reminder that older strains are still very virulent (Wang et al, 2009). In June 2104, in Colorado, a dog transmitted pneumonic plague to three caregivers, one of whom transmitted it to another person. All of four of these cases survived and 88 additional people were given prophylactic antibiotics (Runfola et al, 2015). Three of China’s 2014 plague cases in Gansu province within the Qinghai-Tibet plague focus area  were pneumonic plague in herders.  All three arrived at the medical center too late for effective antibiotic treatment and died (Li et al, 2016). Chinese authorities believe that two of these men may have contracted plague from infected dogs and the third directly from a marmot (Lie et al, 2016).

Dog transmitted plague seems to usually result in family or small settlement size outbreaks. I do wonder about the potential role of dogs in the Bronze Age cases of plague (Rasmussen et al, 2015). Dogs contracting plague by consumption of infected rodents and passing it on to human contacts seems possible with the tools of the Bronze Age strains. It might also be worth investigating the potential role of dogs in the beginning of the Great Manchurian Plague of 1910-1911, which focused on hunters who likely used dogs extensively. Indeed hunters in this region would feed sick marmots to their dogs believing that they could not contract the disease. Outbreaks of 100% lethal plague were not unknown among hunting families in Manchuria (Summers 2012: 122-124). Such a high mortality rate would suggest pneumonic plague.

References:

Archibald, W. S., & Kunitz, S. J. (1971). Detection of plague by testing serums of dogs on the Navajo Reservation. HSMHA Health Reports.

Esamaeili, S., Azadmanesh, K., Naddaf, S. R., Rajerison, M., Carniel, E., & Mostafavi, E. (2013). Serologic Survey of Plague in Animals, Western Iran. Emerging Infectious Diseases, 19(9). http://doi.org/10.3201/eid1909.121829

Gage, K. L., Montenieri, J. A., & Thomas, R. E. (1994). The role of predators in the ecology, epidemiology, and surveillance of plague in the United States, 20.Proceedings of the 16th Vertebrate. Pest Conference (W.S. Halverson& A.C. Crabb, Eds.) Published at Univ. of Calif., Davis. 1994.

Ge P, Xi J, Ding J, Jin F, Zhang H, Guo L, Zhang J, Li J, Gan Z, Wu B, Liang J, Wang X, Wang X, Primary Case of Pneumonic Plague in Marmata himalayana natural focus area Gansu Province, China, International Journal of Infectious Diseases (2014), http://dx.doi.org/10.1016/j.ijid.2014.12.044

Gould, L. H., Pape, J., Ettestad, P., Griffith, K. S., & Mead, P. S. (2008). Dog-Associated Risk Factors for Human Plague. Zoonoses and Public Health, 55(0), 448–454. http://doi.org/10.1111/j.1863-2378.2008.01132.x

Li, Y., Li, D, Shao, H., Li, H and Han, Y. (2016) Plague in China 2014 — All sporadic case report of pneumonic plague. BMC Infectious Disease. 16: 85.

Lin, Karen. (2014-07-02) Photo: Himalaya marmot eaten by wild dogs in N. Tibet. China Tibet Online. http://www.vtibet.com/en/news_1746/focus/201407/t20140703_209395.html

Nichols, M. C., Ettestad, P. J., Vinhatton, E. S., Melman, S. D., Onischuk, L., Pierce, E. A., & Aragon, A. S. (2014). Yersinia pestis infection in dogs: 62 cases (2003-2011). Journal of the American Veterinary Medical Association, 244(10), 1176–1180. doi:10.2460/javma.244.10.1176

Rasmussen, S., Allentoft, M. E., Nielsen, K., Orlando, L., Sikora, M., Sjögren, K.-G., et al. (2015). Early Divergent Strains of Yersinia pestis in Eurasia 5,000 Years Ago. Cell, 163(3), 571–582. http://doi.org/10.1016/j.cell.2015.10.009 [Bronze Age cases]

Runfola, J. K., House, J., Miller, L., Coltron, L., Hite, D., Hawley, A., et al. (2015). Outbreak of Human Pneumonic Plague with Dog-to-Human and Possible Human-to-Human Transmission — Colorado, June–July 2014. MMWR. Morbidity and Mortality Weekly Report, 64(16), 429–434.

Salkeld, D. J., & Stapp, P. (2006). Seroprevalence Rates and Transmission of Plague (Yersinia pestis) in Mammalian Carnivores. Vector-Borne and Zoonotic Diseases, 6(3), 231–239. http://doi.org/10.1089/vbz.2006.6.231

Summers, William C. (2012) The Great Manchurian Plague of 1910-1911: The Geopolitics of an Epidemic Disease. Yale University Press.

Wang, H., Cui, Y., Wang, Z., Wang, X., Guo, Z., Yan, Y., et al. (2015). A Dog-Associated Primary Pneumonic Plague in Qinghai Province, China. Clinical Infectious Diseases, 52(2), 185–190. doi:10.1093/cid/ciq107

Wang, X., Liang, J., Xi, J., Yang, J., Wang, M., Tian, K., et al. (2014). Canis lupus familiaris involved in the transmission of pathogenic Yersinia spp. in China. Veterinary Microbiology, 172(1-2), 339–344. doi:10.1016/j.vetmic.2014.04.015

Beyond Germs: Native Depopulation in North America

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Beyond Germs: Native Depopulation in North America. Edited by Catherine Cameron, Paul Kelton and Alan Swedlund. University of Arizona Press, 2015.


With the number of emerging infectious diseases climbing and new revelations about plague’s past, this book is a timely caution to the rhetoric surrounding so-called virgin soil epidemics. This book is the publication of an interdisciplinary conference held to discuss the causes of Native American depopulation hosted by the Amerind Foundation. Essays by David Jones, George Milner, Clark Spenser Larsen, Debra Martin, Gerardo Gutiérrez, Alan Swedlund, Catherine Cameron, Paul Kelton, Katheleen Hull, and James Brooks are included. Most of these essays are case studies in depopulation of specific areas.

David Jones opens the book with a discussion of the rhetoric surrounding so-called virgin soil epidemics that are credited with being the primary cause of native depopulation. Admitting the influence of his mentor evolutionary biologist Stephan J Gould, Jones favors social and contingent causes for depopulation over biological determinism. Perhaps the influential role that Gould played in my own formation as a biologist makes me sympathetic to Jones’ argument, but I can certainly live with that. Genetic determinism, in my opinion, is the easy way out to explain what can not be yet understood. His argument against the sweeping rhetoric of ‘virgin soil epidemics’ is, I think, very effective.

Milner’s chapter tackles the tricky problem of the pre-contact population collapse of the Mississippian culture centered at the mid-continent site of Cahokia, near St. Louis. This had been the largest and most (archaeologically) complex native culture in North America but it collapsed so entirely that the mid-continent was still sparsely populated when Europeans arrived a couple of centuries later. Medieval Cahokia had been more populous than contemporary London. The example of Cahokia must give us pause for assuming that unrecorded demographic collapses that lack signs of massive destruction must be due to epidemics.

Larsen, Martin, Gutiérrez, and Hull cover the effect of the Spanish mission system in Florida, the Pueblo of the Southwest,  Mexico, and California respectively. Structural violence was seen throughout the Spanish mission system from hard, forced labor. Larsen discusses how changing landscapes and lifestyles make natives more susceptible to infection. He sees a dramatic rise in cribra orbitalis/porotic hyperostosis as a sign of iron deficiency when it may actually be malaria. Wet Florida would have been susceptible to endemic malaria and a reservoir for it to spread through the southeast. Martin looks at the bioarchaeological evidence for a ‘creeping genocide’ in the peublos of the south west. Sporatic massacres of pueblo communities were used to enforce compliance by the wider culture. Cultural resilience was also stressed to the breaking point by a prolonged period of drought and environmental deterioration in the southwest that left them with marginal nutritional sufficiency. In this stressed environment, smallpox spread widely among the pueblo communities. Epidemics were part of a set of practices used to destroy or reorient native culture to make it acceptable, and more importantly controllable for the Spanish. Gutiérrez focuses on the methods and effects of identity erasure on demographics. The caste system that developed was very systematic “virtuous cycle”  with the goal of eliminating native identity and indeed native (and African) ‘blood’ while maximizing Spanish identity and ‘blood’.

Chapters by Swedlund,  Cameron, and Kelton examine tribes that dealt more closely with the English colonies and early American states. Swedlund looks at the great smallpox epidemic of 1633-34 beyond coastal New England up into the Connecticut River valley. Cameron reviews the demographic effects of warfare and captive taking had on the Southeast, the northern Pays d’en Haunt (Great Lakes region), and the Southwest tribes. Colonial politics and trade caused more intertribal warfare than warfare directly with European colonists. Kelton writes about the disastrous experiences of the Cherokee with warfare, famine, and disease during the American Revolutionary War.

One of the overarching problems is the difficulty in determining population size before contact and then for the first couple centuries of the colonial period. Problematically, in the past, abandoned villages have been assumed to be extinct due to disease rather than simply relocation or the movement of refugees to other tribes. The reality is that many areas that are fertile with Old World methods and domestic livestock were very difficult to make products with native resources.

Over arching themes that I noticed which point toward other factors than just “germs” causing depopulation:

  1.  Use of starvation as an intentional weapon accomplished by burning fields and disrupting the agricultural cycle.
  2. The selective taking of women of reproductive age as captives/slaves causing a gender imbalance that prevented populations from rebounding.
  3. Selling captives to slavers rather than incorporating them into the tribe as pre-contact tribes often did to bolster their numbers and replace their dead. Sales were often to repay debts for European trade goods, especially weapons and ammunition.
  4.  Use of tribes as proxy militias by European powers to create intertribal warfare and recruitment of tribes by the British during the American revolution and war of 1812. Set up an adversarial relationship with the young American nation.
 In effect, I think the process they are all searching for is a syndemic that combined epidemics, nutritional deficiencies, systemic violence, slavery, and forced assimilation. Unfortunately, they didn’t really consult the syndemic literature.

One of the things I took away from this collection is an appreciation for how long it takes to develop a fully agricultural culture. Many Native American groups were still in transition. Lacking domestic animals other than the dog, they were very vulnerable to climate and social disorder disrupting their agricultural cycle and yield. Some tribes adopted domestic animals from Europeans quickly. Colonists were greatly alarmed at how quickly the Cherokee adopted raising hogs and European crops, bringing them nutritional stability. Of course, horses are were adopted so well by natives that its hard for many of us today to even think of Native Americans without them.  The idea that domestic animals were worth the effort may have been what was missing most, rather than a lack of animals capable of being domesticated.

I highly recommend this book for anyone interested the dynamics of depopulation, “dark ages”, and most importantly for comparison to other “virgin soil” epidemic situations. I don’t think it’s a coincidence that other renowned virgin soil epidemics like the first and second plague pandemics occurred in times of ecological and social stress in addition to the epidemic in question. By opening the explanations for Native American depopulation up to other causes than the disease,  it also opens up views into colonial life that even contemporaries tried to ignore. Whether their demise to disease was believed by contemporaries to be the divine will or by modern historians as biological determinism, it has diverted attention away from the very human causes of depopulation and in some cases genocide.