Molecular Confirmation of Yersinia pestis in 6th century Bavaria

Erasing any lingering doubts about the agent of the Plague of Justinian, a group of German biological anthropologists have shown conclusively that Yersinia pestis caused an epidemic in a 6th century Bavarian cemetery at Aschheim. Harbeck et al (2013) provide a convincing refutation of previous theories about the etiologic agent of the Plague of Justinian.   Returning to the same cemetery where plague was previously reported, two independent labs using the most modern standards to prevent contamination confirmed Yersinia pestis from multiple burials within the cemetery making this the best characterized Early Medieval plague cemetery.

The cemetery, called Aschheim, is in Bavaria outside of Munich. It contains the remains of 438 people with an unusually high number of multiple graves but no disordered mass graves. The 19 multiple burials contained two to five individuals arranged in lines. The cemetery was dated archaeologically to 500-700 AD with remains being carbon dated ranging from 530 to 680, all consistent with the 541 pandemic and its aftermath. Harbeck et al (2013) tested 19 individuals from 12 multiple graves. From these, there were eight positive samples, but only one produced enough aDNA to do some SNP genotyping. Added to the previous paper, this makes 11 positive individuals from this cemetery. Given the tenuous survival of aDNA, 11 positive individuals out of 21 tested in the two combined papers is a very good success rate. This is a cemetery that the F1 antigen test would be interesting since it could be used on the entire cemetery without great cost or labor. More sensitive than aDNA, the antigen test could tell us the percentage of plague deaths in the cemetery.

Individual A120 was screened with several SNPs that mapped it to an early region of the phylogenetic tree in the 0.ANT section. This makes the Plague of Justinian isolate ancestral to the Black Death isolates (yellow boxes below) from East Smithfield. This section whose only point of diversity is 0.ANT1 at node 4. Date predictions for the nodes of diversity in the tree fits with the Plague of Justinian falling in this region.  Modern isolates that  form this region of the phylogenetic tree all come from central Asia (around Tibet), suggesting that like the Black Death, the Plague of Justinian also originated in Asia. Overall, everything fits in well with expectations for the first pandemic.

(Harbeck et al, 2013. Fig. 1)

Reference:

Harbeck M, Seifert L, Hänsch S, Wagner DM, Birdsell D, et al. (2013) Yersinia pestis DNA from Skeletal Remains from the 6th Century AD Reveals Insights into Justinianic Plague. PLoS Pathog 9(5): e1003349. doi:10.1371/journal.ppat.1003349

Wiechmann I, & Grupe G (2005). Detection of Yersinia pestis DNA in two early medieval skeletal finds from Aschheim (Upper Bavaria, 6th century A.D.). American journal of physical anthropology, 126 (1), 48-55 PMID: 15386257

Visualizing the Plague of Justinian in the Mediterranean

Browsing through Academia.edu this morning I came across some graphics from the Topographies of Entanglements project from the Austrian Academy of Sciences, Division of Byzantine Research. Unfortunately there is very little explanation with these graphics.

Comparing these two graphs they are not conveying exactly the same information.  How do we define a wave of plague? Does it have to show directional movement? How far does it have to go?  Given the sparse information from this period, accurately defining waves must be tentative.   The second graph, may be a more realistic representation. The second graph charts individual epidemic outbreak records giving a better representation of scale and that the gaps between the waves are not plague-free. Given the sparse records in the early medieval period, we can not take the lack of reports in 580 and 610 to mean that the plague disappeared completely. Plague was also occurring outside of the Mediterranean in these low years. For example the major wave of plague to devastate Britain and Ireland was from 664-668.

From: Visualising waves of Plague epidemics in the Mediterranean and the Near East, 541-750 AD by Topographies of Entanglements. Graphics by Johannes Preiser-Kapeller, 2013. (Here converted from tiff files to jpg.)

They took their data from Dionysios Stathakopoulos, Famine and Pestilence in the Late Roman and Early Byzantine Empire: A Systematic Survey of Subsistence Crises and Epidemics (Ashgate, 2004).

Toward a Molecular History of Yersinia pestis (AHA)

This post a resource for the presentation I gave at the AHA meeting in New Orleans on January 5, 2013. A color handout of the slides can be downloaded here.

This map will be continually updated as new finds are published. Some of the balloons mark sites with multiple studies. Click on the balloons for citations.

View Larger Map

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. doi: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, 1–5. doi:10.1038/nature10549

Bos, K. I., Stevens, P., Nieselt, K., Hendrik N Poinar, DeWitte, S. N., & Krause, J. (2012). Yersinia pestis: New Evidence for an Old Infection. PLoS ONE, 7(11), e49803.

Drancourt, M., & Raoult, D. (2005). Palaeomicrobiology: current issues and perspectives. Nature Reviews Microbiology, 3(1), 23–35. doi:10.1038/nrmicro1063

Drancourt, M., Houhamdi, L., & Raoult, D. (2006). Yersinia pestis as a telluric, human ectoparasite-borne organism. The Lancet Infectious Diseases, 6(4), 234–241. doi:10.1016/S1473-3099(06)70438-8

Haensch, S., Bianucci, R., Signoli, M., Rajerison, M., Schultz, M., Kacki, S., et al. (2010). Distinct Clones of Yersinia pestis Caused the Black Death. (N. J. Besansky, Ed.)PLoS Pathogens, 6(10), e1001134. doi:10.1371/journal.ppat.1001134.t001

Houhamdi, L., Lepidi, H., Drancourt, M., & Raoult, D. (2006). Experimental model to evaluate the human body louse as a vector of plague. The Journal of Infectious Diseases, 194(11), 1589–1596. doi:10.1086/508995

Little, L. K. (2011). Plague Historians in Lab Coats*. Past & Present, 213(1), 267–290. doi:10.1093/pastj/gtr014

Malou, N., Tran, T.-N.-N., Nappez, C., Signoli, M., Le Forestier, C., Castex, D., et al. (2012). Immuno-PCR – A New Tool for Paleomicrobiology: The Plague Paradigm. (S. Bereswill, Ed.)PLoS ONE, 7(2), e31744. doi:10.1371/journal.pone.0031744.g006

Morelli, G., Song, Y., Mazzoni, C. J., Eppinger, M., Roumagnac, P., Wagner, D. M., et al. (2010). Yersinia pestis genome sequencing identifies patterns of global phylogenetic diversity. Nature Genetics. doi:10.1038/ng.705

Nguyen-Hieu, T., Aboudharam, G., Signoli, M., Rigeade, C., Drancourt, M., & Raoult, D. (2010). Evidence of a Louse-Borne Outbreak Involving Typhus in Douai, 1710-1712 during the War of Spanish Succession. PLoS ONE, 5(10), e15405. doi:10.1371/journal.pone.0015405

Parkhill, J., Wren, B. W., Thomson, N. R., Titball, R. W., Holden, M. T., Prentice, M. B., et al. (2001). Genome sequence of Yersinia pestis, the causative agent of plague. Nature, 413(6855), 523–527. doi:10.1038/35097083

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. doi:10.1016/S1473-3099(04)01099-0

Raoult, D., Dutour, O., Houhamdi, L., Jankauskas, R., Fournier, P.-E., Ardagna, Y., et al. (2006). Evidence for louse-transmitted diseases in soldiers of Napoleon’s Grand Army in Vilnius. The Journal of Infectious Diseases, 193(1), 112–120. doi:10.1086/498534

Schuenemann, V. J., Bos, K., Dewitte, S., Schmedes, S., Jamieson, J., Mittnik, A., et al. (2011). PNAS Plus: Targeted enrichment of ancient pathogens yielding the pPCP1 plasmid of Yersinia pestis from victims of the Black Death. Proceedings of the National Academy of Sciences, 1–22. doi:10.1073/pnas.1105107108

Tran, T., Forestier, C., & Drancourt, M. (n.d.). Brief communication: Co‐detection of Bartonella quintana and Yersinia pestis in an 11th–15th burial site in Bondy, France. American Journal of ….

Tran, T.-N.-N., Signoli, M., Fozzati, L., Aboudharam, G., Raoult, D., & Drancourt, M. (2011). High throughput, multiplexed pathogen detection authenticates plague waves in medieval venice, Italy. PLoS ONE, 6(3), e16735. doi:10.1371/journal.pone.0016735

Wiechmann, I., & Grupe, G. (2004). Detection ofYersinia pestis DNA in two early medieval skeletal finds from Aschheim (Upper Bavaria, 6th century A.D.). American Journal of Physical Anthropology, 126(1), 48–55. doi:10.1002/ajpa.10276

Wiechmann, I., Harbeck, M., & Grupe, G. (2010). Yersinia pestis DNA Sequences in Late Medieval Skeletal Finds, Bavaria. Emerging Infectious Diseases, 16(11), 1806–1807.

Remodeling the Plague Phylogenetic Tree

Understanding the molecular history of any organism requires fitting together ancient DNA with the phylogenetic tree constructed with living exemplars. Constructing a bacterial phylogenetic tree is a snapshot of a moving target because its impossible to sample all of the strains.  A recent study by the East Smithfield group ( Bos et al, 2012 [2]) seeks to fit the recent near complete genomic sequence of Yersinia pestis from the Black Death cemetery at East Smithfield into the current phylogenetic tree.

They pooled their SNP database with those used by Morelli et al [3] for a total of 311 strains, plus the parental species Yersinia pseudotuberculosis as its foundation.  The East Smithfield group expect that the SNP comparison “could provide a qualitative indication of phylogenetic signals that were lost via our original, more conservative analytical approach based strictly on complete genomes.” [2]

New phylogeny of Yersinia pestis (Bos et al, 2012)

Their analysis confirmed that the Black Death strain settles into the base of split between branch 1 & 2. This matches what Haensch et al [4] found in 14th century sites at Hereford and Saint-Laurent-de-Cabrerisse. This indicates that the split occurred after the Black Death, probably due to microevolution in geographically distinct regions. Branch 2 is localized primarily along the Silk Road route in Central Asia, while branch 1 is far more widely distributed  and produced the third pandemic strain [3].  Bos et al further identified two living strains, designated 3.ANT, with SNP profiles that match their East Smithfield Black Death SNP profile [2]. These strains have not been completely sequenced and the plasmid profiles of these strains and the Black Death strain have not been characterized, so we can not yet say that these strains are genetically identical in sequence or genomic architecture to the Black Death strain [2]. Note that genomic architecture (placement of genes in chromosome) will mostly likely effect gene expression and therefore function of the microbe.

The East Smithfield group  observed that a small group of three strains diverged from the main descent line immediately before the Black Death, designated here as 0.ANT3, were all isolated from China [2]. They suggest that these strains may have been produced during a diversifying event that produced the main Black Death strain, possibly in Asia before it reached Europe.

They also observed 11 strains of Yersinia pestis clumped at the 0.ANT1 branch point [2]. By their calculations this split would have occurred between the 8th and 10th century (732-980 AD) overlapping with the documented period of the Plague of Justinian. They suggest that these strains represent genetic radiation that occurred during the Justinian expansion. This is a change from their observations based solely on comparisons of complete genomes [1].

The East Smithfield genomic group still have not incorporated ancient DNA data from any other group in their analysis.

References:

[1] Bos KI, Schuenemann VS, Golding GB, Burbano HA, Waglechner N, et al. (2011) A draft genome of Yersinia pestis from victims of the Black Death. Nature 478: 506.510.

[2] Bos KI, Stevens P, Nieselt K, Poinar HN, DeWitte SN, et al. (2012) Yersinia pestis: New Evidence for an Old Infection. PLoS ONE 7(11): e49803. doi:10.1371/journal.pone.0049803

[3] Morelli G, Song Y, Mazzoni CJ, Eppinger M, Roumagnac P, et al. (2010) Yersinia pestis genome sequencing identifies patterns of global phylogenetic diversity. Nat Genet 42: 1140.1143.

[4] Haensch S, Bianucci R, Signoli M, Rajerison M, Schultz M, et al. (2010) Distinct Clones of Yersinia pestis Caused the Black Death. PLoS Pathog 6(10): e1001134. doi:10.1371/journal.ppat.1001134

Gothic Epidemiology? or Gothic Historiography?

I was reading David Mengel’s recent article on plague in Bohemia and he kept referring to this apparently well-known concept, gothic epidemiology. Being the early medieval geek that I am, my first thought was Ostrogoth or Visigoth, and what do they have to do with epidemiology, especially in Bohemia? Feeling that I was clearing missing out on an important concept in plague studies, I looked up the original paper by Faye Marie Getz in 1991.

It turns out that Getz was referring to the genre of Gothic literature that began in the 18th century when Gothic came to mean anything that “offended Enlightenment sensibilities”, anything anti-modern to the new men of the age of reason. ‘Gothic’ architecture gave way to neo-classical architecture, and Roman and Greek revival artistic motifs were everywhere. Yet, Gothic literature typified by Mary Shelly’s Frankenstein, and the works of Lord Byron and Edgar Allen Poe also developed during this time.  Getz characterized the essential elements of Gothic literary sensibility as

“an interest in distant and exotic places and times, especially in the Middle Ages and the Orient; the celebration of the power of nature and the ineffability of nature’s essence; the unity of disparate elements – of good and evil, the hideous and the beautiful, the dead and the living; the seduction of the primitive and wild in nature, of the bizarre; the insignificance of human beings against nature; the existence of geniuses; the importance of individual experience; and finally the emphasis on suffering, death, and redemption.” (p. 279)

Getz and others have found that from the mid-eighteenth century historians wrote of the plague as typifying and glorifying this Gothic sensibility. It was these early historians who made the plague a symbol of all that is dark, deadly and medieval.

The most influential gothic epidemiologist was Justin Hecker whose influential book Der schwarze Tod im vierzehten Jahrhunder  (The Black Death in the Fourteenth Century) in 1832 began modern plague studies. Getz characterizes Hecker’s book as seeing the plague as an inescapable force of nature that swept away the old, bringing historical change and most importantly progress.

“The miasma of plague was in Hecker both literally and figuratively atmospheric. It rolled like a fog out of the mysterious East, a crawling miasma exhaled by earthquakes and volcanoes, by the rotting dead in graveyards and battlefields, by decaying matter in marshes and swamps. Plague leveled all those who stood before it and spared no person. It seeped into churches, castles, and cottages. There was no escape. Nature herself spoke of the coming disaster. Comets, earthquakes, and volcanoes shattered man’s complacency. A pillar of fire appeared over the papal palace at Avignon. Plants and animals behaved in a bizarre manner. The very heavens rained disaster.” (Getz 1991: 276-277)

The plague itself was as heroic as disastrous.   Nature becomes God’s avenging army that sweeps away a whole civilization that has gone astray. Getz believes that Hecker set the foundation for most 19th and 20th century plague scholarship on four basic pillars: 1) the Black Death marked the end of an era and the start of a reinvigorated, more industrious society; 2) the plague was a natural phenomenon that was beyond human understanding,  awesome in its power, and unlike anything before or since;  3) the Black Death was a double-edged sword that was both terrible  in its destruction but also culturally transformative, begetting the Renaissance, and 4) a focus on the bizarre and morbid facts and behaviors. Getz notes that Hecker was the first person to focus on Flagellants or the massacre of Jews during the Black Death, two aspects of the pandemic that still draw an extraordinary amount of attention.  These four elements compromise what Getz calls Gothic epidemiology.

Many plague historians followed in Hecker’s footsteps (and occasionally still do). The morbid and bizarre feature more in plague history than in any other area of the history of medicine. The plague doctor has become an icon of  the Middle Ages.  Claims that the plague is the root cause behind vampires, werewolves and revenants/zombies are still made. The awesomeness of the plague as a natural phenomenon is still with us and can almost border on nature worship. Nearly 150 years after Hecker’s paradigm emerged, Robert Gottfried’s The Black Death: Natural and Human Disaster in Medieval Europe (1983) opens with a Chaucer  quotation, “Nature, the vicaire of the almyghty lorde” (The Parliament of Fowls, c. 1380). So two of Hecker’s four pillars are still with us in varying degrees. Given how popular Gothic culture still is, these elements are likely to remain.

The dilemma for plague historians and scientists comes in attracting interdisciplinary and public attention for their work without distorting the history and/or science. The easiest way to attract attention is by focusing on either the bizarre and morbid, or on nature’s power and plague’s uniqueness. This is the same compromise documentary films must make.  To avoid this fate some will be happy writing only for other academics of their ilk, but for all except the most specialized topics this is short-sighted. First, as one of the most interdisciplinary topics available today it is necessary to write so that other disciplines can understand and follow the argument, and to highlight aspects that are interesting to other disciplines. It not fair to complain about the misuse of our work if we don’t write at an interdisciplinary level. Given the wide range of disciplines involved in plague studies this is essentially a college-level general public audience. Second, the plague’s attraction for those who like elements of  Gothic culture means that there are educational opportunities for history and science. The CDC received a fair amount of attention for its Zombie apocalypse  preparedness educational program and the Zombie Research Society has a real epidemiologist on their advisory board. Of course, zombies being entirely fictional gives them a lot of latitude. However, if done carefully the plague can still be used to teach history and science without over focusing on only the most bizarre aspects or distorting its history.

The other two of Hecker’s pillars are the creation of academics rather than appealing to the public. Did the plague end an era and create a positive cultural transformation? Most plague historians can dispatch the idea that the Black Death was a great boundary in time after which everything changed. This is not to say that the plague didn’t have a cultural impact but it did not beget the Renaissance or the Reformation. It is just as likely that in periods of cultural transformation and upheaval, humans are more vulnerable to the plague and its transmission patterns. Meaning the plague gathered momentum because of cultural changes rather than being the cause of cultural change.

This also makes me think of the questions that surround the Plague of Justinian that began in 541. Did it end antiquity? Did it prevent the Western Roman Empire from recovering and reasserting itself? No. How odd that we place a plague pandemic at the beginning and end of the Medieval period.  Who determined when ‘classical antiquity‘ was as a period? Those same 17-18th century elites who developed Gothic literature. As modern historians show more continuity across time periods, there is a tendency to chip away at the length of the medieval period. The new designation of Late Antiquity is chipping the period of c. 500-750 away from early medieval, taking the Plague of Justianian with it. Fitting for a plague named for a Roman emperor?

In the Gothic epidemiology paradigm, the plague of Justianian must have been minimized to the point that it was forgotten for a long time. Afterall, it didn’t create a reinvigorated society; it marked the beginning of the medieval period, the ‘dark ages‘. The term ‘dark ages’ being contrasted with the supposed light of Rome. Perhaps we should refer to Gothic historiography rather than epidemiology since the paradigm clearly goes beyond just the Black Death.

References

Getz FM (1991). Black death and the silver lining: meaning, continuity, and revolutionary change in histories of medieval plague. Journal of the history of biology, 24 (2), 265-89 PMID: 11612554

Mengel DC (2011). A plague on Bohemia? Mapping the Black Death. Past & present, 211 (1), 3-34 PMID: 21961188

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Plague Detection by Immuno-PCR

Once again the Marseille research group is pushing the bounds of plague detection. This time their target is looking for a more sensitive method of detecting non-nucleic acid biomolecules from Yersinia pestis, ‘the plague’. We have now moved into an era where PCR is being used in the mechanics of testing, rather than amplifying the ultimate target of the test.

Immuno-PCR

The immuno-PCR (iPCR) method is outlined in the figure. The selective component of the assay is the mouse polyclonal anti-Yersinia pestis antibody. Polyclonal antibodies are the products of several different B lymphocytes reacting to the same antigen, protein in this case. This means the antibodies in preparation will bind to different parts (epitopes) of the same protein. This should be an advantage in working with badly degraded material.

In iPCR the selective reagent is the non-human antibody generated against the microbial target. The second antibody is against the non-human antibody (mouse, rabbit, etc) and carries biotin as a marker. These biotinylated antibodies are a very common and widely available immunology reagent. The third antibody is against the biotin and carries a reporter sequence of DNA. Quantitative real-time PCR is then done on the reporter DNA sequence attached to the antibody. This amplified reporter DNA can easily measure very tiny amounts of DNA. The iPCR system utilizes advances in PCR technology to measure specific protein levels.

Malou et al (2012) took  known positive and negative teeth, and subjected them to iPCR, PCR and the standard ELISA antibody assay.   They first determined the detection limit for ELISA and iPCR, and set a threshold for a positive iPCR result with 10 known negative teeth (5 ancient and 5 modern). They then coded and randomized  34 historically known positive teeth, the 10 negative teeth (5 ancient and 5 modern) and two blanks for testing with ELISA, PCR, and iPCR. The results and how they compare are shown in the diagram below. The ELISA only picked up four teeth with one being a known negative resulting in a sensitivity of 9% and specificity of 90%. Of the three ELISA true positives, two were from a 17th century site at Lariey and one from a 6th century site at Sens, both in France. For the iPCR, 14 of 34 exceeded the threshold and were considered positive for a 41% sensitivity with a 100% specificity (all positives were historically positive, no false positives). These teeth came from Lariey, Bourges, Sens, Bondy, and Venice with a date range from the 6th to 17th century. Traditional PCR identified 10 out of 34 historically positive teeth fora  sensitivity of 29% with 8 of 10 also being identified by iPCR.

Venn diagram of positive teeth detected by ELISA, PCR, and iPCR.

Immuno-PCR compares well with the efficiency and specificity of standard PCR for Yersinia pestis DNA and is more sensitive than the standard ELISA antibody assay. A standard ELISA produced the worst results. Although not quantitative, it would have been interesting if they had also done the Rapid Diagnostic Dipstick Test (RDT), another antibody based protein detection method, that has been used in several studies.  They are suggesting that iPCR be added to traditional PCR as a method of further confirmation of Yersinia pestis at a site. Immuno-PCR can be done on the same teeth as traditional PCR and should be easily doable with the expertise and equipment in labs that conduct traditional aDNA PCR.  By identifying both aDNA and protein, the confirmation of Yersinia pestis in the ancient remains should become quite strong.

Reference:

Malou, N., Tran, T., Nappez, C., Signoli, M., Le Forestier, C., Castex, D., Drancourt, M., & Raoult, D. (2012). Immuno-PCR – A New Tool for Paleomicrobiology: The Plague Paradigm PLoS ONE, 7 (2) DOI: 10.1371/journal.pone.0031744

 

Black Death Genome Fished Out of East Smithfield

Fishing just isn’t what it used to be, and neither is DNA sequencing. Reconstructing the ancient plague genome required the development of new technology that was able to enrich the sequencing sample by concentrating the Y. pestis sequence fragments from the brew of human DNA and contaminants in all aDNA extracts.

Using an Agilent Capture Array (above), a large international group led by Johannas Krause and Hendrik Poinar [1] fished ancient, degraded fragments of Yersinia pestis out of bone and teeth extracts from the East Smithfield Black Death cemetery using lures (probes) composed of short fragments of a modern Y. pestis strain. These lures (probes) are attached to the slide and the extracts are washed over the slide. Complementary ancient fragments in the extract will hybridize with the single stranded probes while the remainder of the extract is washed away. (The match does not have to be exact for these probes to hang on to the extract fragment allowing them to pull out fragments with minor sequence variants.) The fragments can then be released from the slide and sequenced. Using two of these slides (one in Canada and one in Germany?) they captured over two million unique fragments. Overlapping regions of sequence were lined up to reconstruct “93.48% of the targeted regions” (complementary to the modern CO92 strain of Yersinia pestis). All genes of the modern Y. pestis strains appear to be accounted for, although the existence of any part of the ancient genome that is completely foreign to modern strains can not be ruled out.

When they analyzed the ancient sequence they found that it is surprisingly similar to modern Y. pestis strains. It differed from modern strains at only 97 positions all of which matched the ancestral genes from Yersinia psuedotuberculosis. The most important information in this paper is that the genes of the Black Death clones do not have significant genetic differences that would make the ancient clone(s) more virulent than modern strains.

They also went on to place their reconstructed genome on the phylogenetic tree of Y. pestis relative to public sequences of modern Y. pestis strains. They placed the East Smithfield Black Death clone at the node where modern Y. pestis strains branch from the ancestral stem leading to Yersinia pseudotuberculosis, its parent species. Actually it is the primary East Smithfield clone because they also found another derivative clone in the extracts from only four people at East Smithfield. Placing the Black Death strain at the branch point is basically the same finding as Haenesh et al, 2010 [2] that I’ve discussed in a previous post. Apart from having much more sequence to compare, the finding really isn’t new. It also doesn’t really tell us anything new about the earlier, first pandemic known as the Plague of Justinian. Despite their assertion that the Plague of Justianian was “distinct from all currently circulating strains commonly associated with human infections, or it was another disease all together” [1], they can not rule out that the Black Death strain itself is not identical to or a descendant of the Justinian strain. I see no reason to think that it was another disease. Two previous groups, Drancourt’s group in Marseille [3] and Wiechmann and Grupe in Bavaria [4], have found Yersinia pestis in 6th century remains.  Further, the speed, virulence, and signs and symptoms of the Plague of Justinian match descriptions of the Black Death.

The similarity of the Black Death strain with modern Yersinia pestis strains validates modern public health and biosecurity concerns over the plague. Although this ancient strain would be susceptible to modern antibiotics — if they are administered in time, we will need all the information we can get for a potential arms race with the plague.

[1] Bos, K., Schuenemann, V., Golding, G., Burbano, H., Waglechner, N., Coombes, B., McPhee, J., DeWitte, S., Meyer, M., Schmedes, S., Wood, J., Earn, D., Herring, D., Bauer, P., Poinar, H., & Krause, J. (2011). A draft genome of Yersinia pestis from victims of the Black Death Nature DOI: 10.1038/nature10549

[2] Haensch, S., Bianucci, R., Signoli, M., Rajerison, M., Schultz, M., Kacki, S., Vermunt, M., Weston, D., Hurst, D., Achtman, M., Carniel, E., and Bramanti, B. (2010). Distinct clones of Yersinia pestis caused the Black Death. PLoS Pathogens, 6 (10)

[3] Drancourt M, Signoli M, Vu Dang L, Bizot B, Roux V, Tzortzis S, et al. Yersinia pestis Orientalis in remains of ancient plague patients. Emerg Infect Dis [serial on the Internet]. 2007 Feb [date cited]. Available from http://wwwnc.cdc.gov/eid/article/13/2/06-0197.htm

[4] Wiechmann I, & Grupe G (2005). Detection of Yersinia pestis DNA in two early medieval skeletal finds from Aschheim (Upper Bavaria, 6th century A.D.). American journal of physical anthropology, 126 (1), 48-55 PMID: 15386257