Category Archives: bioarchaeology

Plague in 6th century Aschheim and Altenerding, Bavaria

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.

6th cent Bavaria
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.

1280px-Bajuwarenhof_Kirchheim_Übersicht_2012-08-05
Reconstruction of 6th-7th century Bavarian buildings at Kirchheim in the Munich district close to Aschheim. (Photo by Leporollo, Wikipedia CC3.0)

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

cropped-venice-plague.jpg

Plague Dialogues: Monica Green and Boris Schmid on Plague Phylogeny (II)

Monica H. Green (monica.green@asu.edu,@MonicaMedHist) is a historian of medieval medicine. An elected Fellow of the Medieval Academy of America, she teaches both global history and the global history of health. She was the editor in 2014 of Pandemic Disease in the Medieval World: Rethinking the Black Death, the inaugural issue of a new journal, The Medieval Globe.

Boris Schmid (@BorisVSchmid) is a theoretical biologist at the University of Oslo, Norway, and specializes in disease ecology and epidemiology. He recently described a link between climate fluctuations in medieval Central Asia and what looks like repeated introductions of plague into Europe’s harbors, a hypothesis that can be tested by the analysis of ancient DNA samples of Y. pestis. He works in a multidisciplinary team of theoreticians, archeologists, microbiologists and historians, led by Nils Chr. Stenseth.


Boris:

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.)

CORRECTED fig03 for Contagions blog, (a) Spyrou et al 2016 fig02B Y pestis phylogenetic tree (detail of origins of Branches 1A and 1B), (b) Table 1 with 6330 SNPs added (06272016)
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

Krause, Johannes (4-12-2016)  Oral Presentation #S577:  Ancient pathogen genomics: what we learn from historic pandemics. European Congress  of Clinical Microbiology and Infectious Diseaseshttp://eccmidlive.org/#resources/ancient-pathogen-genomics-what-we-learn-from-historic-pandemics

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

cropped-venice-plague.jpg

Plague Dialogues: Monica Green and Boris Schmid on Plague Phylogeny (I)

In keeping with this blog’s goal to be a meeting ground for interdisciplinary discussions, I’ll be hosting a series of dialogues between scholars in the humanities and sciences. If you would like to be involved in one of these dialogues, please use the contact form on the about page.

On behalf of today’s participants, I invite you to post comments on this dialogue or on twitter.


Monica H. Green (monica.green@asu.edu, @MonicaMedHist ) is a historian of medieval medicine. An elected Fellow of the Medieval Academy of America, she teaches both global history and the global history of health. She was the editor in 2014 of Pandemic Disease in the Medieval World: Rethinking the Black Death, the inaugural issue of a new journal, The Medieval Globe.

Boris Schmid (@BorisVSchmid) is a theoretical biologist at the University of Oslo, Norway, and specializes in disease ecology and epidemiology. He recently described a link between climate fluctuations in medieval Central Asia and what looks like repeated introductions of plague into Europe’s harbors, a hypothesis that can be tested by the analysis of ancient DNA samples of Y. pestis. He works in a multidisciplinary team of theoreticians, archeologists, microbiologists and historians, led by Nils Chr. Stenseth.


“Tiny Changes with Huge Implications: Counting SNPs in Plague’s History”

Monica:

I’d like to raise the question of SNPs and why understanding them is so important for those keeping an eye on the “plague aDNA debates.” SNPs – single nucleotide polymorphisms, one of the smallest levels of genetic change you can document on a genome — are critical to the evolutionary, and historical, story of Yersinia pestis (the causative agent of plague), because Y. pestis in fact has been proven to change so little over time. Nucleotide changes are a normal part of evolution. They just happen. But they don’t necessarily happen at the same rate in all organisms, or even necessarily at the same rate in the same species in all circumstances. On top of that, sudden proliferation of an organism — say, in the context of an epidemic in the case of pathogenic organisms — may increase the rapidity with which a random evolutionary change gets fixed in a population. (See Cui et al. 2013)

In the case of Y. pestis, it’s actually been shown to be “genetically monomorphic.” That’s another way of saying, it doesn’t change very much or very often. Within its core genome (the common set of genes shared by all Y. pestis bacteria), most any Y. pestis cell you find is going to look pretty much like every other one across much of its ±3.5 million nucleotides, differentiated only by a few dozen or a few hundred different SNPs (Achtman 2012). So when a ‘C’ (cytosine) in one position on the genome changes to a ‘G’ (guanine) or ’T’ (thymine) or ‘A’ (adenine), that can actually be a historically significant change. And when that new SNP suddenly shows up in a whole population, that’s a sign that something major has happened. That’s what Cui et al. 2013 talked about in the “Big Bang” they posited for the later medieval period: the old Branch 0 of Y. pestis (see fig. 1) suddenly split into four new branches, each characterized by a different SNP signature. And the sequencing in 2011 of the first three Y. pestis genomes from the London Black Death cemetery (Bos et al. 2011; I’ll want to talk about the 4th genome, London 6330, later), made clear that that split did indeed happen quite suddenly. The split happens (presumably somewhere in western China or central Eurasia) and then, “two SNPs later,” Y. pestis shows up in London. Given the distances involved in transmitting this single-celled organism — several thousands of kilometers —  and the fact that there are no airplanes in the 14th century to account for rapid dissemination, that’s quite significant.

Cui et al 2013 fig S3B Minimum spanning tree, with SNP counts (post-polytomy branches only)
Fig. 1: Cui et al 2013 fig S3B Minimum spanning tree of relationships between 133 core genomes of Y. pestis based on 2298 SNPs. Detail to show post-polytomy branches (the “Big Bang”), at the middle of the tree. Branch 0 is the vertical stem below that. New aDNA work in 2016 has added additional sub branches just after the polytomy on Branch 1 (upper left).

 

Boris:

The mutation rates of bacteria is indeed a topic with quite some nuance, and one that is worth delving into in order to understand the slew of aDNA plague papers that are currently coming online.

The rate at which plague accumulates new point mutations has been calculated from the plague outbreaks in Madagascar (Morelli 2010) to be on average of 1 mutation for every 100 million nucleotides copied (Cui 2013). While that sounds like a very uncommon event, it really is not, given the length of its genome – a single bacterium that is replicating itself would after 4 generations (so roughly 7 hours within a human (Chauvaux 2007)) be a small colony of 16 bacteria, with a total of 105 million nucleotides of core genome copied, and therefore most likely already with 1 SNP among them. But here we are comparing two different things – the mutation rate used by Morelli and Cui is valid for the amount of variation you’d expect to accumulate in each surviving lineage of plague during an epidemic; many of the mutations that were generated are lost again simply because those bacteria were not the ones that continued the epidemic.

Bos (2011) notices with surprise that the plague at the time of the Black Death differed just 97 SNPs from CO92 (a sample collected from a human patient in 1992 in Colorado, and the plague strain that by convention is used as a baseline against which to compare other plague strains). So that is 1 accumulated mutation every 6.6 years, counting from 1348 to 1992. That compares pretty well to the mutation rate in a plague focus we in Oslo are currently studying, where we see an accumulation of mutations along each lineage of about 1 mutation every 8 years. Continuing with our back-of-the-envelope calculation, this “two SNPs later” since the sudden divergence of plague into 4 lineages puts the date of the “Big Bang” at just 10-20 years prior to the arrival of the Black Death in Europe in 1347. There are some caveats that come with this analysis, notably that the rate at which mutations are accumulated can be quite slower in some branches of plague (up to 6-fold, Cui 2013), but for now let us continue with a simplistic 1 new SNP being fixed into a plague lineage approximately every 7 years.

With that 1 SNP per 7 years rate in mind, let’s look at the stylized version of the evolution of Yersinia pestis, recently presented by Johannes Krause (fig. 2 below), with the recently published medieval plague sequences (and now the new publication from Spyrou et al. 2016), and see what it tells us in terms of the history of plague.

last-tree-plague-krause
Fig. 2: A simplified diagram of the “Big Bang” (polytomy) proposed by Cui et al. 2013, where plague split up into its 4 branches in the 13th or 14th century. Branch 1 is the lineage responsible for both the Second (medieval) Pandemic in western Eurasia and Africa and the Third (modern, global) Pandemic. Moving along Branch 1 from the initial split, two SNPs after the “Big Bang,” we see the introduction of the Black Death into Europe (the red-darkred circle). In our discussion, we call the branch leading to Marseille (the grey circle) “Branch 1A”; the branch leading to the rest of Branch 1 we call “Branch 1B.” (Source: Krause 2016.)

 

Monica:

Thanks, Boris, for laying out these calculations. So, we’ve established that, even though Y. pestis is genetically monomorphic—that it doesn’t have sex and doesn’t even often switch genetic material laterally—that it does have a tendency to develop random mutations over time. Par for the course for basic biology. I’d like to return now to a point I already made, which is more historical: “And when that new SNP suddenly shows up in a whole population, that’s a sign that something major has happened.” The big question we’re looking at with the Black Death strain and the “founding” of Branch 1 of the Y. pestis phylogenetic tree is: how did one—just one—Y. pestis cell get its SNP profile to be the founder of the whole lineage that caused millions of deaths in the first wave of the Black Death? This seems to be a classic “founder effect” scenario, the Mitochondrial Eve of this new phase of plague history. (And yes, I know that Y. pestis doesn’t have mitochondria.) Granted, we only have fully sequenced aDNA from two Black Death sites: London and Barcelona. But Spyrou et al. report that the Barcelona sample is identical in every respect with the three London Black Death genomes that were sequenced in 2011.

Let us assume then, for the moment, that our historical sources are correct that the famous outbreak of plague in Caffa in 1346 (the bodies being hurled over the walls) caused a single chain of events that carried our one strain of Y. pestis all the way to Barcelona and London within a two-year period. Presumably, if we had samples from all the other places plague struck in those brutal first years as it spread from the Black Sea to the Mediterranean—Alexandria, Aleppo, Almeria, etc., etc.—they would all have the same SNP signature that Haensch et al. 2010 reported from sample SNP typing for Hereford (UK) and Saint-Laurent-de-la-Cabrerisse (France), and that Seifert et al. 2016 reported, also from sample SNP typing, for Manching-Pichl (Bavaria). None of those sites are as precisely dated as the first three genomes sequenced from the East Smithfield cemetery in London (which is dated from documentary records to late 1348 to 1350). But for the sake of argument let’s assume that they are, in fact, all first outbreak burials. So all those human deaths are caused by an identical organism, moving into new vulnerable hosts at the same time.

But now we have to ask: what happened after the Black Death? What was Y. pestis’s next stage of evolution? The samples we have thus far, whether whole genome sequences or just SNP profiles, are all taken from human bodies. But humans are not natural carriers of plague. Every aDNA sample found thus far is probably a dead end, literally: the end of the line for the unique SNP profile (if it had one) of the Y. pestis that infected that individual. It died with them. If we’re going to look for what sustained plague, what allowed it to focalize and continue replicating for centuries thereafter, then we need to look at what plague strains survived in rodent populations.

Boris:

The question of where plague’s reservoir was in medieval Eurasia is indeed the question that, as a biologist, I was eager to work on, Monica. Validation of any theory of how plague has moved across Eurasia in the past would have to come from the analysis of the SNPs that plague gathered along the way. However, the interpretation of those medieval SNPs turns out to less clear-cut than most of us had anticipated, as we will discuss in the next blog post.

References:

Achtman, M. (2012). Insights from genomic comparisons of genetically monomorphic bacterial pathogens. Philosophical Transactions of the Royal Society B: Biological Sciences, 367(1590), 860–867. http://doi.org/10.1098/rstb.2011.0303

Bos, K. I., Schuenemann, V. J., Golding, G. B., Burbano, H. A., Waglechner, N., Coombes, B. K., et al. (2011). A draft genome of Yersinia pestis from victims of the Black Death. Nature, 478(7370), 506–510. http://doi.org/10.1038/nature10549

Chauvaux, Sylvie, Marie-Laure Rosso, Lionel Frangeul, Céline Lacroix, Laurent Labarre, Angèle Schiavo, Michaël Marceau, et al. 2007. “Transcriptome Analysis of Yersinia Pestis in Human Plasma: An Approach for Discovering Bacterial Genes Involved in Septicaemic Plague.” Microbiology 153 (Pt 9): 3112–3124

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

Krause, Johannes (4-12-2016)  Oral Presentation #S577:  Ancient pathogen genomics: what we learn from historic pandemics. European Congress  of Clinical Microbiology and Infectious Diseases http://eccmidlive.org/#resources/ancient-pathogen-genomics-what-we-learn-from-historic-pandemics

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. pestis Genomes 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