All posts by Michelle Ziegler

CFP: Medieval Landscapes of Disease

Call for Papers
Medieval Landscapes of Disease
International Congress of Medieval Studies
Kalamazoo, MI  May 12-15, 2016

Following on a successful session last year, I’m offering another session on Medieval Landscapes of Disease this year at Kalamazoo.

In recognition that diseases are manifestations of their environment, this session seeks papers that place medieval diseases within their environmental context. Just as a seed must be placed in good soil to grow, infectious disease requires a permissive environment to develop into an epidemic (or epizootic) and an ideal environment to bloom into a pandemic or panzootic.  I am open to all manner of studies and disciplines that address these issues.

Examples of acceptable topics:
  • Historic impacts of  epidemics and/or epizootics
  • Endemic disease in medieval environments
  • Environmental causes of disease such as malnutrition or industrial pollution related disease
  • Health effects of human-animal interactions
  • Applications of the One Health Approach to medieval disease
  • Archaeological assessments of human health and disease
  • Landscape alterations intended to improve human or animal health
  • Ecology of the built environment

Abstracts of no more than 300 words and the Participant Information Form should be sent to Michelle Ziegler at ZieglerM@slu.edu by September 15. Pre-submission queries are welcome.

The Participant Information Form and additional information be found at  http://www.wmich.edu/medieval/congress/submissions/index.html .

Multi-strain Plague Blooms Over Landscapes

Two articles have come to my attention over the couple months that argue strongly for an environmental role in plague epidemics/epizootics over clonal expansion. Taken together these studies suggest that multiple strains of Yersinia pestis percolate out of multiple reservoirs at the same time.

Sites of Madagascar cases, 2007 (Riehm et al, 2015)
Sites of Madagascar cases, 2007 (Riehm et al, 2015)
Strains isolated in Madagascar, 2007 (Riehm et al, 2015)
Strains isolated in Madagascar, 2007 (Riehm et al, 2015)

The strongest support comes from Madagascar where ten MLVA defined strains from 93 human clinical specimens representing the two major groups of Yersinia pestis (based on, if I recall correctly, their introduction source) all emerged within one single year, 2007, scattered over a large range of the central island. These ten strains represent eight previously known strains and two discovered in this investigation. As the map shows, several locations had cases from more than one lineage.  This pattern does not suggest to me that one strain was more successful than another; there is no new mutation that allowed one strain to erupt on the scene or transmission advantage caused by chance or mutation. (Yes, chance does play a role sometimes.) That one strain is more widespread than another probably represents years of enzootic spread and so multiple emergences of a more common strain. With multiple strains emerging at the same time, there is relatively little clonal or territorial expansion, and no reason to expect a major selective advantage by any particular strain. They are emerging where ever the right environmental conditions exist. This study is not directly informative on the underlying epizootic. There may have been even more strain diversity in the epizootic.

There are at least two relevant findings for future surveillance. First, these strains were genotyped directed from DNA in clinical specimens without culturing the specimen. This means that specimens that previously were difficult to culture can still be genotyped and it also should be safer for lab staff to handle. It suggests again that they need a new case classification system since only culturable isolates are considered confirmed. As encouraging as this is, the bad news for reservoir surveillance is that they will have to monitor very large zones based on climate and other environmental factors instead of just trying to project the direction of an ongoing outbreak.

This is supported by another study published in May by Jennifer Lowell’s team on plague in the western US. They analyzed 34 isolates of Yersinia pestis collected from fleas, humans, cats, and a variety of other animals between 1980 and 2006 primarily in Colorado (21) and some scattered sites across the southwest. In Colorado isolates geographically close but temporally spaced showed an evolutionary relationship demonstrating that they had evolved in place over seven years. Mountain isolates were also distinctive between valleys and on the plains suggesting that they evolved in isolation.

During the initial introduction of Yersinia pestis to a region, there is a rapid spread of a single clone but following this, there the creation of local reservoirs with evolution occurring in place. Subsequent epizootics emerge from these new reservoirs and remain small. It follows that large epizootics are usually the emergence of several reservoirs stimulated by the right environmental conditions.

What I take from this is the idea that large scale spread of epizootics or epidemics over different ecological regions require human assistance. There is a anthropogenic factor to the largest epizootics/epidemics. Left to their own means, epizootics remain local spreading only as far as the contiguous environment allows. Some agent, usually humans, must carry them between permissive environments. It is possible that the permissive environment will be urban as it was in Madagascar in the 1990s (Vogler et al, 2013).

Now thinking historically, what we need is serial aDNA results from the same city over many centuries. London and Marseille would be good options, so would Constantinople and Alexandria. With enough aDNA samples it should be possible to estimate how many introductions of Yersinia pestis from the Asia occurred for each pandemic and to discern a role for European or Mediterranean local reservoirs. These modern studies are absolutely necessary to make sense out of the patterns that will eventually emerge when we have enough aDNA specimens.

References:

Riehm, J. M., Projahn, M., Vogler, A. J., Rajerison, M., Andersen, G., Hall, C. M., et al. (2015). Diverse Genotypes of Yersinia pestis Caused Plague in Madagascar in 2007. PLoS Neglected Tropical Diseases, 9(6), e0003844. doi:10.1371/journal.pntd.0003844.s002 (h/t to Matt Wilson for this one!)

Lowell, J. L., Antolin, M. F., Andersen, G. L., Hu, P., Stokowski, R. P., & Gage, K. L. (2015). Single-Nucleotide Polymorphisms Reveal Spatial Diversity Among Clones of Yersinia pestis During Plague Outbreaks in Colorado and the Western United States. Vector Borne and Zoonotic Diseases (Larchmont, N.Y.), 15(5), 291–302. doi:10.1089/vbz.2014.1714

Vogler, A., Chan, F., Nottingham, R., Andersen, G., Drees, K., Beckstrom-Sternberg, S., Wagner, D., Chanteau, S., & Keim, P. (2013). A Decade of Plague in Mahajanga, Madagascar: Insights into the Global Maritime Spread of Pandemic Plague mBio, 4 (1) DOI: 10.1128/mBio.00623-12

Spring Reading

spring1
It has been a busy spring. I haven’t had a chance to blog as much as I would have liked to, but I have done quite a bit of reading. Some of my reading has been on the complex world of the first plague pandemic. To say that it was transformative would be an understatement.  One of the social questions for the first plague pandemic is how does plague and other natural disasters effect a population that is the midst of conversion?  When the Black Death came it encountered a fully Christian and Muslim world, but not so during the first pandemic. Most of Europe was not yet Christian in 541. There were some Jews, Christians of several varieties, Roman pagans, Germanic pagans, Celtic pagans, Zoroastrians, North African and Middle Eastern pagans, etc. Yet at the end of the pandemic period, Islam is born (and fast growing) and Christianity is dominant in Europe (and united by Rome). The plague began in a polytheistic world and ended in a monotheistic one. What role did the plague play, if any? Yet to be determined. This really isn’t a peripheral issue. Every writer of the first pandemic was involved in this transformation (winners and losers) in some way and it effected how they wrote about the plague and other calamities. So I have a lot of reading to do; below is a start and a few other things that caught my attention.

Books:

Marilyn Dunn. (2010) The Christianization of the Anglo-Saxons, c. 497- c.700: Discourses of Life, Death and Afterlife.

Marilyn Dunn (2013) Belief and Religion in Barbarian Europe, c. 350-700. Bloomsbury.

Peter Brown (2015) The Ransom of the Soul: Afterlife and Wealth in Early Christianity. Harvard University Press.

Peter Heather (2013) The Restoration of Rome: Barbarian Popes and Imperial Pretenders. Oxford University Press.

Articles:

Balbir Singh and Cyrus Saneshvar (2013) Human Infections and Detection of Plasmodium knowlesi. Clinical Microbiology Reviews. 26 (2): 165-184.

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.

Smith-Guzmán, N. E. (2015). Cribra orbitalia in the ancient Nile Valley and its connection to malaria. International Journal of Paleopathology, 10, 1–12. doi:10.1016/j.ijpp.2015.03.001

Benovitz, N. (2014). The Justinianic plague: evidence from the dated Greek epitaphs of Byzantine Palestine and Arabia. Journal of Roman Archaeology. doi:10.1016/S1473-3099(13)70323-2)

Bernard Bachrach, (2007) Plague, Population, and Economy in Merovingian Gaul. Journal of the Australian Early Medieval Association. 3: 29-57.

Sarris, P. (2002). The Justinianic plague: origins and effects. Continuity and Change, 17(02), 169–182. doi:10.1017/S0268416002004137

Newfield, T. P. (2015). Human–Bovine Plagues in the Early Middle Ages. Journal of Interdisciplinary History, 46(1), 1–38. doi:10.1179/146141010X12640787648612

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

Shanks, G. D., & White, N. J. (2013). The activation of vivax malaria hypnozoites by infectious diseases. The Lancet Infectious Diseases, 13(10), 900–906. doi:10.1016/S1473-3099(13)70095-1

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

Lowell, J. L., Antolin, M. F., Andersen, G. L., Hu, P., Stokowski, R. P., & Gage, K. L. (2015). Single-Nucleotide Polymorphisms Reveal Spatial Diversity Among Clones of Yersinia pestis During Plague Outbreaks in Colorado and the Western United States. Vector Borne and Zoonotic Diseases (Larchmont, N.Y.), 15(5), 291–302. doi:10.1089/vbz.2014.1714

Neil, B. (2013). The Papacy in the Age of Gregory the Great. A Companion to Gregory the Great, 3–28.

Brogiolo, G. P. (2015). Flooding in Northern Italy during the Early Middle Ages: resilience and adaption. Post-Classical Archaeologies, 5, 47–68.

Kostick, C., & Ludlow, F. (2015). The dating of volcanic events and their impact upon European society, 400-800 CE. Post-Classical Archaeologies.  5, 7–30.

Riehm, J. M., Projahn, M., Vogler, A. J., Rajerison, M., Andersen, G., Hall, C. M., et al. (2015). Diverse Genotypes of Yersinia pestis Caused Plague in Madagascar in 2007. PLoS Neglected Tropical Diseases, 9(6), e0003844. doi:10.1371/journal.pntd.0003844.s002

Makundi, R. H., Massawe, A. W., Borremans, B., Laudisoit, A., & Katakweba, A. (2015). We are connected: flea–host association networks in the plague outbreak focus in the Rift Valley, northern Tanzania. Wildlife Research, 42(2), 196. doi:10.1071/WR14254