Since I last wrote about Bavaria, the aDNA centers have been busy. With the accepted manuscript of the second new paper available this past week, its time for an update. The fourth paper on Aschheim not only confirmed the first three, but it also produced the first full genome of Yersinia pestis for the Plague of Justinian (Wagner et al, 2014). This paper also confirmed the Bavarian strain’s placement in the phylogeny of Y. pestis. The availability of the first full genome will primarily be important for comparison to newly discovered samples from elsewhere. Using newer technology, the newest paper refined some of the Aschheim sequence and produced a full genome of Y. pestis from a woman buried at Altenerding, about 20 km from Aschheim (Feldman et al, 2016). Radiocarbon dating from both sites places the epidemic in the mid-sixth century; it can not differentiate which specific epidemic ‘wave’. The Altenerding epidemic was from the same Y. pestis lineage as Aschheim proving that this was a regional epidemic, possibly the same epidemic event. The phylogeny for the first pandemic is still based on a single epidemic from one geographic region, so the time is not yet ripe to use the phylogeny to tell inform us on the transmission or route of the pandemic.
Map of Roman Bavaria showing the Roman roads with Aschheim and Altenerding marked. The half circle/mound mark designates Roman villas. (modified from the Pelagios project)
It is, however, time to start thinking a little more about the environment of these sites. They are both located on the Munich gravel plain, foreland (foothills) north of the Alps. Aschheim is located closer to the Alps at an elevation of 500 meters with Altenerding 20 km further north at a lower elevation in small valley formed by a tributary of the River Isar. The Roman road running horizontally across the map runs west to Augsburg, the capital of the Roman province of Raetia Secunda and east to the city of Batavia, a colony in the province of Noricum. The road running by Altenerding would take traffic eventually north toward Regensburg (Casta Regina).
Large water feature is Speichersee lake with a man-made 20th century reservoir used to power hydroelectric plants and serve some of the water needs of the Munich region. As far as I can tell, none of this would have been present in the Late Antique period. The River Isar is the green line to the west of both sites. Munich will later be founded where the road crosses the river from monastic land in about 1158. There was nothing special at the river crossing in the sixth century. Although the road crosses the river, there is no indication of a Roman bridge on the map.
Both Aschheim and Altenerding are located in what would have been the province of Raetia II. While they are along Roman roads, this would have been a rural area. Both Aschheim and Altenerding were sites of Roman villas and Dornach near Aschheim was a small settlement. How much of this would have been occupied and further developed (or not) after the Roman army left is unclear. The cemetery at Altenerding is triple the size of Aschheim. Yet, there is reason to think that Aschheim was hit harder by the plague and based on the carbon dates of graves with some molecular plague signal, probably more than once. Michael McCormick (2015:83) suggests that the Aschheim cemetery gathered graves from a dispersed settlement that probably had fewer than 70 people at any one time.
A living history museum in Munich area at Kirchheim has reconstructed typical buildings from the early medieval Merovingian period. Although this area was nominally under Merovingian Frankish hegemony there is little specifically Frankish about the archaeology. They were all wooden construction. Below is a picture of a sunken pit building, an ‘out building’ and a long house.
Continue to think of the Plague of Justinian in Constantinople and Pelusium, it was surely there. Just remember that most of its geographic spread may have looked more like this picture.
References:
Feldman, M., Harbeck, M., Keller, M., Spyrou, M. A., Rott, A., Trautmann, B., et al. (2016). A high-coverage Yersinia pestis Genome from a 6th-century Justinianic Plague Victim. Molecular Biology and Evolution, 1–31. [Accepted manuscript]
McCormick, M. (2015). Tracking mass death during the fall of Rome’s empire (I). Journal of Roman Archaeology, 28, 325–357.
Wagner, D. M., Klunk, J., Harbeck, M., Devault, A., Waglechner, N., Sahl, J. W., et al. (2014). Yersinia pestis and the Plague of Justinian 541–543 AD: a genomic analysis. The Lancet Infectious Diseases, 14(4), 1–8. http://doi.org/10.1016/S1473-3099(13)70323-2
Over the coming year, I would like to organize a new society specifically on the study of infectious diseases in the past. It is called Contagions: Society for Historic Infectious Disease Studies. It is open to everyone working on contemporary or historical aspects infectious diseases that can be studied in the past. Examples of these diseases include plague, cholera, smallpox, leprosy, influenza, tuberculosis, malaria, brucellosis, rinderpest, potato blight, typhoid fever, parasites (worms, mites), etc. As this list illustrates, I think diseases of humans, animals, and plants should all be included because they all affect human health and nutrition. The organisms themselves are a point of continuity throughout time. As ancient DNA technology expands the list of ancient infectious diseases that can be identified in time and place is likely to grow by leaps and bounds. I believe that it is helpful to have people who study them today in communication with those who study them in the past via biology, history, epidemiology, public health, archaeology, ecology, climate and more. This is a true interdisciplinary topic.
To begin, there are only two goals:
Organize sessions for academic conferences. Initially, the International Congress on Medieval Studies at Kalamazoo, but perhaps others as well.
Create an email discussion list on google groups open to all members. Membership in the google group will constitute membership in the group. I can act as a gatekeeper but otherwise unmoderated. The message archive will be available to members only.
I do not see any reason for a fee. I think we can get things started for a couple years at least with volunteers.
To get things started I have arranged for the society to sponsor two sessions at the upcoming ICMS at Kalamazoo in May 2017. There will be a round table on Bruce Campbell’s new book The Great Transition: Climate, Disease and Society in the Late Medieval World. This is the first book that I know of that examines the Black Death with the new genetic paradigm in the context of the entire 14th century throughout the Old World. The second will be a session of papers on “Historic Landscapes of Disease” which will continue the series I have been personally sponsoring for the last couple of years. I am looking for papers that focus on epidemiology, ecology of disease, environmental history and disease, history or archaeology of human health and disease, and related topics.
If you are interested in joining the society or participating in the Congress next May, please contact me with the form below. Abstracts are due by September 15. I am really looking forward to gathering a truly interdisciplinary group of people who are all interested in historic diseases.
In our previous blog post, Monica and I discussed how different lineages of plague – Yersinia pestis – collected their own genetic signature (SNP profile) as they diversified from a common ancestor. Monica also summarized in broad terms what ancient DNA samples of Y. pestis (extracted from plague victims) are now available from the initial Black Death outbreak and how they are related, using the latest plague studies of Haensch, Bos and Spyrou.
In this blog post Monica will delve into the nitty gritty details of these aDNA plague studies, and give an example of how to transform those details into a new understanding of the past rodent reservoirs and global mobility of plague, one of the deadliest diseases of our collective past. And I close the post by reflecting on the potential of aDNA to connect the fields of history and biology.
Monica:
Thanks, Boris. It might be important to remind readers that we don’t have any aDNA evidence from past rodent populations yet. All the samples to date have been retrieved from human victims. But the SNP study that Seifert et al. published earlier this year from samples in Brandenburg, an inhumation from the time of the 30 Years War (1618-1648); the whole genome study that Bos and Herbig et al. also published this year, reporting on the samples from 18th-century Marseille; and the sample from Ellwangen included in the new study by Spyrou et al., all document that Branch 1A (see tree in our previous post) “focalized,” that is, it set up shop in some rodent population(s) and happily continued to proliferate for another 400 years. But all that happened, it is clear, separately from what was going on with Branch 1B, what I have taken to call the pestis secunda.
In their most recent study, the Tübingen/Jena team headed by Krause give us further insight into the early stages of Branch 1B. The beginning of Branch 1B was first documented in the 2011 London study, though it was only earlier this year that I realized that London sample 6330 likely dates from the 1360s and does not come from the initial Black Death outbreak. (It comes from a different burial ground, St Mary Graces.) In Bos and Herbig et al. 2016, it was reported that sample 6330 differed from the 1348-50 London Y. pestis genome by two SNPs. In the present study, interestingly, Spyrou et al. report something slightly different. Sample 6330 does indeed differ from the London Black Death genome by two SNPs (p3 and p4), but a third SNP in sample 6330 they are reporting here for the first time (p5) seems to be unique, a ‘G’ to ‘T’ switch at position 4,301,295 not found in any other historic genome or in the reference strain, CO92. (Spyrou et al. did not include London 6330 on their Table 1, so we offer a modified version of it here in fig. 3.)
Fig. 3: (a) Detail of Spyrou et al. 2016, fig 2B: Yersinia pestis phylogeny – SNPs distinguishing Branches 1A and 1B; (b) Spyrou et al. 2016, Table 1, modified with data on London sample 6330 drawn from Spyrou et al. 2016, Table S4, SNP table. The SNPs unique to London 6330 and Bolgar City are highlighted in yellow.
First of all, we might say that those three SNPs are significant for the time gap they suggest between the Black Death and the 2nd wave of plague to hit London in 1361-63; for the sake of argument, we’ll say “21 years,” to use your formula (3 x 7 years), Boris. But think about the implications of that: plague arrives in London at the end of 1348 as a new disease, and a new strain (with 3 new SNPs) is causing a major new outbreak in 1361-63, which is when this burial seems to date from. 21 years have not passed since the previous outbreak. So what gives? Obviously, the “time-to-SNP” calculus we’re using is an average, not an absolute. But it does make us stop and wonder: did all this really happen so fast? And did it really happen in western Europe?
Which brings us to the Bolgar City sample. It, clearly, is a “descendant” of the same strain as London 6330: it has the two new SNPs, p3 and p4. (It doesn’t have that unique p5 SNP of London 6330, but that may have arisen as little as three days before this person died. We cannot attach any evolutionary significance to it until we see it documented somewhere else.) But note this: the Bolgar City strain has evolved further. It now has the p6 SNP that will define all the rest of Branch 1B and it has its own unique SNP, p7. And again, we have a problem of time compression: the Bolgar City sample (if we can trust the dating of the coins which were said to have been found with the body) may date as early as the late 1360s.
Remember what we need to have an outbreak in humans from a new lineage of Y. pestis: not simply does that new lineage have to arise from a single change in a single cell of Y. pestis, but that new SNP needs to proliferate enough in a reservoir rodent population to cause a new epidemic in humans. So looking over all these SNPs, p1-p7, we can see that they cluster into two “founder effect” phenomena: one that creates the initial Black Death lineage (Branch 1A) and one that creates the pestis secunda lineage (Branch 1B).
Where did those two lineage foundations happen? Let’s go back to Caffa, the “hurling bodies over the walls” scenario. Clearly, if we can believe that story (and remember, we have only one account of it, and that from a non-eye-witness), it tells of an already proliferating plague outbreak. By October 1346, Y. pestis was multiplying by the millions in rats and mice and rodents of whatever kind that lived in and around Caffa.
One, and only one, of those gazillions of Caffese offspring gave rise to Branch 1B. It, too, needed to find a place to set up shop and proliferate to make gazillions of (nearly) identical copies. And where was that place? Was it (as Krause seemed to imply in his April lecture) in London? Maybe it was in or near Bergen op Zoom (NL), where we find a sample with the same SNP profile as the London 6330 sample (Haensch et al. 2010)? Or was it near the same place where Branch 1A had already established its original home, before it reached the Black Sea? Haensch et al. had already proposed in 2010 a “northern” route for the introduction of the pestis secunda strain that reached the Netherlands. I’ll admit, I was skeptical for the longest time. But now I see that this possibility might bear more analysis. At the very least, the question shifts our focus away from western Europe and back to the areas around the Black and Caspian Seas. And that’s exactly where our Bolgar City sample is from, the one that is already showing two SNPs of further evolution beyond London 6330 but might not be a whole lot younger than it. As we said, jetting out of Heathrow wasn’t yet an option in the 14th century. But there was plenty of activity in these central Eurasian areas dominated by the Mongol Golden Horde to connect lots of rodent reservoirs to a bacterium looking for a new place to call home.
Boris:
Thanks Monica! The amount of information that follows from a few different nucleotides between aDNA samples is quite amazing, and learning how to interpret this data historically is rightly one of the transformative processes now happening in Biology (and if I say so, in Medical History as well).
Monica’s interpretation of plague’s past mobility is based on the same genetic data as the one sketched out in Spyrou 2016, and highlights the challenge of interpreting ancient DNA, given that the ancient DNA sequences of plague are still so sparsely sampled across time and space. One thing that strikes me as especially important is how much the argument of “favor the most simple, parsimonious explanation” changes based on whether you think of plague largely in terms of a human epidemic (which Wagner 2014, and by extension Spyrou 2016 appear to do), or as a disease that spread through human and wildlife both, as Monica and I do. If you include the possibility of new wildlife reservoirs of plague (and plague has created numerous new wildlife reservoirs in time), say near Bolgar City, the logic of how plague moved across Eurasia changes.
As more aDNA data becomes available, it will be very interesting to see the geographic range that a lineage of plague bacteria can spread without collecting changes in its SNP profile. Once we have a good idea of that, and a more complete view of the SNP profiles that existed during the past pandemics, SNP profiles might be used to shed light on the actual source of a historic plague outbreak, and thus offer an independent way of checking the reliability of historic sources that blame particular smugglers, ships, refugees or clothing as the source of a plague outbreak.
Wow, thanks, Monica, for this great discussion. This is an example on how history and biology can intertwine, and while we are all waiting for more revelations from aDNA and historic sources, it seems prudent to start more interactions between historians and biologists. There is an inherent bias to doubt your own data too much, and trust another fields’ data too blindly, leading to mistakes at both sides: we blindly pick some historic report as authoritative, or put too much faith in a report on the (in-) efficiency of plague transmission by different flea species, whilst a single mutation that causes the loss of a gene can have drastic effects on how well the disease transmits (Hinnebusch, 2016). The only practical way to avoid falling into such pitfalls is by investing in cross-talk between scholars of the humanities and natural sciences!
Monica:
Thank you, Boris. This was great. And very special thanks to Michelle Ziegler, for hosting our discussion on her super blog, Contagions.
References
Bos, K. I., Herbig, A., Sahl, J., Waglechner, N., Fourment, M., Forrest, S. A., et al. (2016). Eighteenth century Yersinia pestis genomes reveal the long-term persistence of an historical plague focus. eLife, 5, 17837. http://doi.org/10.7554/eLife.12994
Cui, Y., Yu, C., Yan, Y., Li, D., Li, Y., Jombart, T., et al. (2012). Historical variations in mutation rate in an epidemic pathogen, Yersinia pestis. Proceedings of the National Academy of Sciences, 110(2), 577-582. http://doi.org/10.1073/pnas.1205750110/-/DCSupplemental/sd01.xls
Haensch, S., Bianucci, R., Signoli, M., Rajerison, M., Schultz, M., Kacki, S., et al. (2010). Distinct Clones of Yersinia pestis Caused the Black Death. PLoS Pathogens, 6(10), e1001134. http://doi.org/10.1371/journal.ppat.1001134.t001
Hinnebusch, B. J., Chouikha, I., & Sun, Y.-C. (2016). Ecological Opportunity, Evolution, and the Emergence of Flea-borne Plague. Infection and Immunity, IAI.00188–16–31. http://doi.org/10.1128/IAI.00188-16
Seifert, L., Wiechmann, I., Harbeck, M., Thomas, A., Grupe, G., Projahn, M., et al. (2016). Genotyping Yersinia pestis in Historical Plague: Evidence for Long-Term Persistence of Y. pestis in Europe from the 14th to the 17th Century. PLoS ONE, 11(1), e0145194-8. http://doi.org/10.1371/journal.pone.0145194
Spyrou, M. A., Tukhbatova, R. I., Feldman, M., Drath, J., Kacki, S., de Heredia, J. B., et al. (2016). Historical Y. pestisGenomes Reveal the European Black Death as the Source of Ancient and Modern Plague Pandemics. Cell Host and Microbe, 19(6), 874–881. http://doi.org/10.1016/j.chom.2016.05.012
Wagner, D. M., Klunk, J., Harbeck, M., Devault, A., Waglechner, N., Sahl, J. W., et al. (2014). Yersinia pestis and the Plague of Justinian 541–543 AD: a genomic analysis. The Lancet Infectious Diseases, 14(4), 1–8. http://doi.org/10.1016/S1473-3099(13)70323-2
