Category Archives: anthropology

A Migration Age Anglo-Saxon Leper

Paleomicrobiology and isotopic analysis has the ability to completely change what we know of past infectious diseases. A study published this month on a fifth century Anglo-Saxon skeleton is one of the most complete I have read.

Lesions on skeletons found at Great Chesterfield in Essex, England, suggested possible leprosy. To confirm this diagnosis, they chose one skeleton that is nearly complete and in good shape for further analysis.

Grave GC86 from Great Chesterford, excavated in a rescue archaeology operation in 1953-4.
Grave GC86 from Great Chesterford, excavated in a rescue archaeology operation in 1953-4. (Inskip et al, 2015)

The skeleton (GC96) shown to the right is of a 25 to 35-year-old male buried in modestly furnished grave in an area of the cemetery with other visibly disabled people. Radiocarbon dating places these remains at AD 415-545, and thus Migration Age for the Anglo-Saxons. The Great Chesterford cemetery is located roughly in an approximate border area between the kingdom of the East Saxons and East Angles at the site of a ford of the River Cam (or Granta) downriver from Cambridge. He was buried with a slender knife secured by a belt with an oval buckle. Over his left shoulder, a spear and a conical ferrule were found.  Lesions consistent with lepromatous leprosy were found on the lower legs with extensive remodeling of the right foot. A bronze shoelace tag found near the right foot suggests the diseased foot covered with a shoe.  Given the lesions found on the foot and lower legs, the ferrule may have capped a walking staff. His facial bones were missing losing a common, distinctive site of leprosy lesions. The disorganized and rough appearance of new bone growth suggest that the lesion was active at the time of death.

Profile of the mycolic acids extracted from the indicated bones.
Profile of the mycolic acids extracted from the indicated bones. (Inskip et al, 2015)

Selections of bone were taken and powdered to extract aDNA and for lipid analysis. Mycobacterium species that cause leprosy and tuberculosis have distinctive lipid profiles that have been successfully extracted and identified by archaeological remains in the past. Their analysis of lipids from the bones confirmed the presence of Mycobacterium leprae and excluded the presence of Mycobacterium tuberculosis.  The aDNA analysis confirmed identified the presence of Mycobacterium leprae strain 3I-1, that has been previously found in later medieval England, Denmark and Sweden. Inskip et al (2015) suggest a possible Scandinavian origin for the strain.  The VNTR analysis used to produce ‘genetic fingerprints’ shows that this strain of M. leprae is unique among other ancient isolates and should be useful in the comparative analysis of other early remains. Other remains in the same cemetery have similar lesions and will be investigated in the future.

Isotopic analysis of his tooth enamel provide an indication of childhood location and adult nutrition. Carbon analysis showed a diet of primarily C3 plants, consistent with southern Britain. Analysis of oxygen and strontium isotopes suggest he did not spend his childhood in the area of Great Chesterford.

The combination of the two isotopes gives his best probable origin to be between north-central France and the north-central Germany, in other words, the region of the Anglo-Saxon homeland. A continental origin coupled with the dating range between 415 and 545 suggests that he was part of the migration of the peoples who later called themselves Anglo-Saxons. He was likely no more Scandinavian than any of the other migration era ‘English’. This is further supported by a relatively high level of leprosy (by osteological analysis) in medieval city of Schleswig, the very area where the Angles are most specifically located. Further analysis of migration era remains should refine the origins of this strain of leprosy and determine its frequency.

Reference:

Inskip, S. A., Taylor, G. M., Zakrzewski, S. R., Mays, S. A., Pike, A. W. G., Llewellyn, G., et al. (2015). Osteological, Biomolecular and Geochemical Examination of an Early Anglo-Saxon Case of Lepromatous Leprosy. PLoS ONE, 10(5), e0124282. doi:10.1371/journal.pone.0124282.s001

Kristina Killgrove, 14 May 2015 “Earliest Case of Leprosy in Britain reveals Scandinavian Origins of the Disease”, Forbes.com

SIMON MAYS, SONIA R. ZAKRZEWSKI, SARAH A. INSKIP, STEPHANIE WRIGHT and JOANNA R. SOFAER. (2015) Anglo-Saxon concepts of dis/ability: placing disease at Great Chesterford in its wider context. Poster at The 84th Annual Meeting of the American Association of Physical Anthropologists.

Contours of the Black Death Cemetery at Charterhouse Square, London

Excavations for the Crossrail Extension project discovered the second major Black Death cemetery in London in 2013. This week the first peer-reviewed publication of findings from the site appeared (in press).  As a rescue excavation in the midst of a construction project, the site had to be quickly surveyed for the extent of the cemetery and this is what is contained in this publication.

This site is part of 13 acres leased by Sir Walter de Mauny from St Bartholomew’s Priory for an emergency cemetery for plague victims in 1349 AD.  The site has been used for a variety of purposes over the centuries and currently is a four acre green space called Charterhouse square. The site is graphically displayed below with the locations of later structures.

Crossrails site, London
Crossrails site in Charterhouse Square, London (Dick et al., 2015)

The initial discovery came in a shaft just to the southwest of the Charterhouse Square. There they found three layers of graves with a total of 25 bodies lacking signs of trauma and with pottery shards from 1270-1350 AD. Subsequent radiocarbon dating and aDNA analysis confirmed that they were victims of the Black Death.

The surveys conducted over just two days were able to outline the broad contours of features at the site. These included a 15th century building, a priory kitchen, a probable World War II submerged emergency water tank, and a possible ditch and bank along the cemetery that is mentioned in descriptions. They believe that a disturbed area in the southwest corner represents about 200 individual graves, although only excavation can confirm these graves. They concluded that their ability to detect medieval objects in such an intensely used urban area suggests these methods are a good option for similar future situations.

The scans also revealed some surprises. There are not as many graves as descriptions suggest should have been there, though bodies may be more dense that suggested by the scans. They also did not find any large pits of  stacked bodies. This indicates that even during the height of the Black Death, many people were still buried in individual graves. Graves were found in three phases with layers of clay-rich earth in between perhaps in an attempt to seal the graves. These scans should allow them to target future excavations to areas with a high probability of dense graves.

Reference:

Dick, H. C., Pringle, J. K., Sloane, B., Carver, J., Haffenden, A., Stephen Porter, H. A., et al. (2015). Detection and characterisation of Black Death burials by multi-proxy geophysical methods. Journal of Archaeological Science, 1–50. doi:10.1016/j.jas.2015.04.010 [In press, accepted manuscript]

Syndemics and Historic Diseases

I’ve been looking for a model or framework to bring together interdisciplinary evidence on diseases of the past. There are a variety of disciplinary approaches but few that can readily incorporate very different types of evidence well.

Apart from past discussions of discrete co-morbidities, the most common framework for understanding historic disease ecology has been pathocoenosis or ‘disease pools’ originated by M. D. Grmek in 1969 and popularized as ‘disease pools’ through McNeill’s Plagues and Peoples (1976). While this concept has proven popular among historians of medicine in high level overviews of human history, the concept begins to break down when practically applied to specific problems, as outlined by Robert Sallares (2004). It is hard enough to identify all of disease-causing microbes in a modern environment, much less a historic environment or population. It is often the minor or chronic disease-causing agents that make the most difference during a co-infection; malaria being a prime contender for the most important.  Pathocoenosis doesn’t adequately take into account the dynamic complexity of microbes in any population (however defined) and the idea that epidemics are disruptions in the equilibrium of pathogens in the population caused by new entrants to the population often doesn’t hold up.

Syndemics is a related concept emerging among biologists and medical anthropologists as a way to understand the diverse complex outcomes of diseases in populations. Syndemic comes from the terms synergistic and epidemic; it is a synergistic epidemic. A synergism exists when two conditions together produce a much greater effect than either individually added together ( ex. 1 +1 = 5 not 2).

A syndemic, in short, involves a set of enmeshed and mutually enhancing health problems that, working together in a context of deleterious social and physical conditions that increase vulnerability, significantly affect the overall disease status of a population (Singer, 2014).

The theory of syndemics is still evolving. The CDC’s definition refers specifically to two epidemics in the same population that produce a synergistic adverse outcome in human health. Consequently biology and medicine focus primarily on coinfections with an occasional look at nutrition. So far they are beginning to find some fascinating insights into how the immune system copes with two or more disease-causing microbes at once. We have to really take in that we are all coinfected all of the time. It comes down to if there is a significant interaction between multiple microbial species and the immune system. (It should be also said that coinfection can occasionally be protective as well.) Not surprisingly medical anthropologists insist on there always being a social component like malnutrition causing events, human behaviors like drug abuse and sexual practices,  or social disorder and inequality. So far from what I’ve read, these different focuses are complementing each other pretty well.

Some of the well-recognized syndemics include:

  • malaria + malnutrition
  • influenza + bacterial pneumonia
  • HIV + TB
  • HIV + HCV
  • HIV + HCV + IV drug use
  • Lyme disease + other Tick Borne Diseases
  • malnutrition + war (social disruption) + infectious disease (mostly diarrhea)

HIV has had a critical role in recognizing syndemics. Not unexpectedly, HIV coinfection with multiple organisms causes recognized synergetically worse outcomes. In many parts of the world, liver disease is a leading cause of HIV+ patient deaths due to Hepatitis C (HCV). It has also highlighted social conditions and behaviors that increase risk and vulnerability. The massive size, duration and amount of research done on AIDS is what has really allowed syndemic theory to become established.

Syndemics is just beginning to look at zoonotic disease but the future is already promising. As has already been suggested by work on pathocoenosis, malaria is a leading candidate to understand the syndemics of zoonoses. Syndemic effects have been suggested for malaria plus malnutrition, HIV and influenza.  Patients with long-term and serious health outcomes from Lyme disease are often coinfected with other less common tick born infectious diseases that are often undiagnosed (Singer & Bulled, 2014).

From what I have read so far, syndemics appears to take the best parts of the pathocoenosis paradigm, while jettisoning the unsupportable, over-reaching baggage. As we can already see for HIV and malaria, the syndemics approach has the potential to build up a foundation to understand the multifaceted outcomes of disease causing agents in different environments and provide insights into how the human microbiome and immune system interact. While its not perfect and doesn’t incorporate all of the disciplines needed to understand historic disease, it may provide a basis to build upon.

References and further reading:

Sallares, R. (2005). Pathocoenoses ancient and modern. History and Philosophy of the Life Sciences, 27 (2): 201–220. [Malaria]

Singer, M. (2014). Pathogen-pathogen interaction.Virulence, 1(1), 10–18. doi:10.4161/viru.1.1.9933

Singer, M., & Clair, S. (2003). Syndemics and public health: reconceptualizing disease in bio-social context. Medical Anthropology Quarterly, 17(4), 423–441.

Rock, M., Buntain, B. J.,Hatfield, J. M., & HallgrImsson, B. (2009). Animal–human connections, “‘one health,’” and the syndemic approach to prevention. Social Science & Medicine (1982), 68(6), 991–995. doi:10.1016/j.socscimed.2008.12.047

Singer, M. C. (2009). Doorways in nature: Syndemics, zoonotics, and public health. A commentary on Rock, Buntain, Hatfield & Hallgrı ́msson. Social Science & Medicine (1982), 68(6), 996–999. doi:10.1016/j.socscimed.2008.12.041

Ostrach, B., & Singer, M. (2013). Syndemics of War: Malnutrition-Infectious Disease Interactions and the Unintended Health Consequences of International War Policies.  Annals of Anthropological Practice, 36(2), 257–273. doi:10.1111/napa.12003

Morano, J. P., Gibson, B. A., & Altice, F. L. (2013). The Burgeoning HIV/HCV Syndemic in the Urban Northeast: HCV, HIV, and HIV/HCV Coinfection in an Urban Setting. PLoS ONE, 8(5), e64321. doi:10.1371/journal.pone.0064321.t003

Kwan, C. K., & Ernst, J. D. (2011). HIV and Tuberculosis: a Deadly Human Syndemic. Clinical Microbiology Reviews, 24(2), 351–376. doi:10.1128/CMR.00042-10

Conant, K. L., Marinelli, A., & Kaleeba, J. A. R. (2013). Dangerous liaisons: molecular basis for a syndemic relationship between Kaposi’s sarcoma and P. falciparum malaria. Frontiers in Microbiology, 4(article 35), 1–14. doi:10.3389/fmicb.2013.00035/abstract

Faure, E. (2014). Malarial pathocoenosis: beneficial and deleterious interactions between malaria and other human diseases. Frontiers in Physiology, 5. doi:10.3389/fphys.2014.00441/abstract

Herring, D. Ann, & Sattenspiel, L. (2007). Social contexts, syndemics, and infectious disease in northern Aboriginal populations. American Journal of Human Biology, 19(2), 190–202. doi:10.1002/ajhb.20618   [1918 influenza]

Singer, M., & Bulled, N. (2014). Ectoparasitic Syndemics: Polymicrobial Tick-borne Disease Interactions in a Changing Anthropogenic Landscape.Medical Anthropology Quarterly, n/a–n/a. doi:10.1111/maq.12163