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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disease ecology and terminology but then moves on build off of McNeill’s “civilized disease pools”, which is now quite outdated.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 arrive 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 built 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 from under the back skin containing 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.
The Genoese have always been central in the legend of the start of the Black Death, by their own claim, linking a siege of the Genoese at Kaffa to the spread of the epidemic in the Mediterranean. Last month the first confirmed plague graves in the region of Genoa were reported by Cesana, Benedictow, and Bianucci in the cemetery of the ospitali (hospital) of San Nicolo. The hospital of San Nicolo was located at a node along the route connecting the hilly backcountry of Genoa to the main travel routes of medieval Italy.
The quadruple grave consisted of a woman in her 30s with full-term fetus in the birth canal (a ‘coffin birth’), and two children aged approximately 3 and 12 years, based on their growth and tooth eruption. Dated stratigraphically to the second half of the 14th century, they are a very rare multiple grave for Northern Italy. No plague pits have been discovered in this region.
They were screened for plague with the RDT dipstick (here and here) that detects the F1 antigen of Yersinia pestis (see also Bianucci et al, 2008 and Pusch et al, 2004). This test has proven quite reliable for archaeological material and is a useful tool for modern diagnosis in resource-poor areas. The RDT dipstick is a more sensitive test than aDNA so we should not expect every positive skeleton by the RDT to produce aDNA but it is a good screening tool prior to aDNA surveys and useful for epidemiological purposes. The adult female, the fetus and the oldest child all gave positive results by the RDT dipstick. I would consider these to be positive plague cases with or without aDNA confirmation. Now I do have one caveat at this point, I’m not ready to assume that the fetus is a true positive, although it is certainly possible. Since it was present in a decaying maternal body with lots of F1 antigen around, the protein could have been absorbed into the fetal bones during the decomposition process. If there is enough aDNA to be detected and readable in the fetal bones, then I would consider it a stronger case. Regardless, the plague was at least the secondary cause of death for the fetus since it claimed the life of its mother. Without more genetic testing, we will not know the relationship between the two older children and the woman. They could be one family, although at a hospital they could be of no relation to each other.
Without a more precise date or ancient DNA, we can not predict which plague epidemic produced this grave. Raffaella Bianucci has informed me that these graves will be part of a large aDNA project currently underway, so more information will be available eventually. Then the historical analysis of Ole Benedictow in this article will be very helpful in placing them in a more precise context.
My main interest lies with the pregnant plague victim and her fetus. A coffin birth is caused by the build up of gasses in the corpse that pushes the fetus out of the birth canal. Given that plague victims die of septicemia, possibly infecting the placenta, it’s not all that surprising (at least to me).
Given a high medieval birth rate, I am surprised that more pregnant women have not been found in plague graves. Stephen Ell (1989) found that 8.5% of all women between ages 15 and 50 were reported as pregnant in the death records he analyzed for three days in an October 1630 epidemic in Venice. So why haven’t fetuses or newborns been found in more plague graves?
There are a few possible reasons for fewer fetuses than expected: early pregnancies are unlikely to leave fetal bones, and in a stacked mass grave, tiny fetal bones would easily get jumbled with all the other bone bits. When fetal bones are found in these mass burials it may be difficult to determine how many fetuses they represent. Reports from the third pandemic and later may provide a few more clues.
So let’s look at a parallel late-term pregnancy infection from 1975 (Welty et al, 1985, 641-2): a 31-year-old Navajo Arizona woman in her 9th month of pregnancy presented at a clinic with a high fever, headache and a tender right axillary node whose aspirate produced the bipolar safety pin looking bacillus suggestive of Yersinia pestis. This was later confirmed by culture and she was started on Streptomycin. On the first day of admission, the baby’s heart rate was already at 200 beats per minute suggesting fetal distress so she was induced, and she delivered a healthy baby boy. His cord blood was negative for plague and he never developed a plague antibody titer. Two days later the mother’s two and a half-year-old child was admitted with a fever (104 F), cough, headache, and vomiting. Her axial lymph nodes were also positive for Yersinia pestis and she was started on antibiotics as well. All three were recovering well when released from the hospital nine days after the mother’s original admission.
Clearly, antibiotics and the ability to induce the birth made all the difference in this case. The placental blood barrier seems to have held just long enough for a healthy delivery. In the few other cases in the literature, antibiotic treatment appears to rescue the pregnancy, although induction of delivery is recommended if there are signs of fetal distress at 36 weeks of gestation or later. The pre-antibiotic scenario is much grimmer:
“In the preantimicrobial era, plague reguarly resulted in abortion, and the aborted tissues were occasionally infected with plague bacillus. In 1903 Jennings reported 10,000 cases of plague, 14 of which occurred during pregnancy. Four of the mothers survived, but spontaneous abortions or still births occurred in 13 of the patients, including the four survivors. One of the 14 patients was near her expected date of delivery. The child was born apparently well, but the mother died of postpartum hemorrhage. Ten hours after birth, lymphadenopathy was noted in the infant’s groins and axillae and it died one day later.” (Welty et al, 1985, 645)
In another case report from 1975, Mann and Maskowitz (1977) opined that “fetal wastage resulting from a maternal infection with plague probably results from the systemic effects of illness rather than direct placental or fetal infection, although true intrauterine infection with plague as been described.” Fetal distress detected in the case described above and in the other case reported by Mann and Moskowitz both support a risk to the pregnancy prior to fetal infection. Infection of the fetus and/or placenta would have been a very grave development without access to antibiotics. I can not imagine how a maternal immune system could clear such an infection. At any rate, it seems likely that most infected pregnant women lost their fetus to miscarriage or stillbirth prior to their own death. This would account for a lower than expected number of pregnant women found in plague burials. Given that fetuses and infants are underrepresented in normal cemeteries, it is possible that many of these unbaptized infants in plague times were not buried with the rest of the community.
All of the modern cases would have been managed slightly differently today. The Navaho woman’s entire family would have been examined and given antibiotics immediately. It is hard to believe today they waited until the two-year-old had a 104-degree fever before being examined. Modern plague management guidelines have detailed instructions for treating pregnant women for bubonic and pneumonic plague to maximize safety and limit side effects of the drugs on the fetus (Inglesby et al, 2000). However, saving the mother’s life trumps all considerations if ideal antibiotics are not available or working sufficiently. Prior to 36 weeks of gestation when it can be induced, this is also the best chance the fetus has for survival.
Bianucci, R., Rahalison, L., Massa, E. R., Peluso, A., Ferroglio, E., & Signoli, M. (2008). Technical note: a rapid diagnostic test detects plague in ancient human remains: an example of the interaction between archeological and biological approaches (southeastern France, 16th-18th centuries). American Journal of Physical Anthropology, 136(3), 361–367. http://doi.org/10.1002/ajpa.20818
CESANA, D., BENEDICTOW, O. J., & Bianucci, R. (2017). The origin and early spread of the Black Death in Italy: first evidence of plague victims from 14th-century Liguria (northern Italy). Anthropological Science, 1–10. http://doi.org/10.1537/ase.161011
Ell, S. R. (1989). Three days in October of 1630: detailed examination of mortality during an early modern plague epidemic in Venice. Reviews of Infectious Diseases, 11(1), 128–141.
Inglesby, T. V., Dennis, D. T., Henderson, D. A., Bartlett, J. G., Ascher, M. S., Eitzen, E., et al. (2000). Plague as a biological weapon: medical and public health management. Working Group on Civilian Biodefense (Vol. 283, pp. 2281–2290). Presented at the JAMA : the journal of the American Medical Association.
Mann, J. M., & Moskowitz, R. (1977). Plague and pregnancy. A case report. Jama, 237(17), 1854–1855.
Pusch, C. M., Rahalison, L., Blin, N., Nicholson, G. J., & Czarnetzki, A. (2004). Yersinial F1 antigen and the cause of Black Death. The Lancet Infectious Diseases, 4(8), 484–485. http://doi.org/10.1016/S1473-3099(04)01099-0
Welty, T. K., Grabman, J., Kompare, E., Wood, G., Welty, E., Van Duzen, J., et al. (1985). Nineteen cases of plague in Arizona. A spectrum including ecthyma gangrenosum due to plague and plague in pregnancy. The Western Journal of Medicine, 142(5), 641–646.