Category Archives: Black Death

Contours of the Black Death Cemetery at Charterhouse Square, London

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

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

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

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

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

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


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

Expanding the Historical Plague Paradigm

When the first complete genomic sequence of Yersinia pestis was published on October 4, 2001 the world was naturally focused elsewhere, on anthrax bioterrorism — the Amerithrax incident was then in its second week– and the September 11 attacks were just over three weeks old. As the world redeveloped bioterrorism assessments and plans, plague was placed on lists along with anthrax, smallpox and yes, ebola as agents of national security concern and response.  Although plague produced more annual cases than most agents on the category A bioterrorism list, it was placed on the list primarily based on its historical reputation and past attempts to weaponize it (also based on its reputation). Yet, in 2001 there was a fierce debate ranging among historians and others on whether Yersinia pestis was the agent of the Black Death at all.

It would take another ten years before genomics would revolutionize our understanding of the historical plague. On October 12, 2011 the first draft sequence of an ancient plague genome was published. Finally, adding to the detection of Yersinia pestis DNA tests previously done on remains, the draft sequence isolated from the East Smithfield Black Death cemetery in London solidified consensus that Yersinia pestis is the agent of the Black Death pandemic.  Meanwhile, the phylogenetic tree of Yersinia pestis had been constructed based on the genetic sequence of isolates from all over the globe. Ancient and modern Yersinia pestis genomes were opening a new window into the history of the species.

As fundamental as genomic analysis is to the new understanding of historical plague, it is a skeleton of data that is open to many different historical interpretations. Science can’t adequately explain the historic plague epidemics alone; it takes historical context. In the inaugural double issue of The Medieval Globe,  Pandemic Disease in the Medieval World: Rethinking the Black Death (open access) begins this process. The eleven articles in this issue take the genetic identification of Yersinia pestis  as the agent of the Black Death as foundational and integrate modern biological and epidemiological information into a new global Old World assessment of the history of the Black Death and subsequent epidemics. Each of these articles lays the groundwork for future interdisciplinary work between historians, anthropologists, biologists, epidemiologists and others.

In my own contribution to this issue, “The Black Death and the Future of the Plague” I discuss why plague is still important in the modern world and for our future. Plague has played an integral role in the development of the re-emerging infectious diseases paradigm and is an agent of biosecurity concern. I review the current state of plague around the world, what we have learned about plague epidemiology and transmission, and how it can be applied to historic epidemics. I also make my case for why the study of the entire history of plague is uniquely important and why the sciences and humanities must move forward together.  I hope we can engage in a discussion on these issues here in the comments section, on twitter or by email.

My own interest and awareness of the issues surrounding the study of the plague was transformed when I had the great fortune to be invited by Monica Green to participate in a session at the American Historical Association annual meeting in New Orleans, January 2013. The group of plague scholars gathered there has largely remained in contact and expanded our network into an informal working group that has enriched all of our scholarship.  No one can become fully conversant with all of the disciplines involved in the study of even one epidemic, much less the entire history of the plague.  Working in disciplinary seclusion will not produce a satisfying paradigm or widespread consensus. It takes work, patience and some tolerance of how other disciplines work, but I have found it to always be worth it. I hope you will agree.

Some references for the milestones mentioned:

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

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, 1–20. doi:10.1038/ng.705

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

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

Pandemic Disease in the Medieval World: Rethinking the Black Death. Edited by Monica Green. The Medieval Globe, 1 (1), 2014.

Academic Plague Identity Wars Continue

Just when you think the academic wars over the identity of the medieval plague are over, another volley is cast by Samuel Cohn. In the past I haven’t mustered the energy to respond to his papers and books because there are just so many scientific misunderstandings, but its time to respond. Obviously, scientific studies that cover all the bases aren’t enough, so for now I’ll to correct some of his misinformation (leaving most of his historical analysis to the historians to critique).

Samuel K. Cohn, Jr. (2013) “The Historian and the Laboratory: The Black Death Disease” pp. 195- 212 in Society in the Age of Plague. The Fifteenth Century XII. Clark, L and Rawcliffe, C. Eds. Boydell Press.

Cohn portrays the discovery of Yersinia pestis at the turn of the 20th century as yet another French vs British competition in a partisan British manner. While trying to undercut the importance of French findings, he does not include the political context of Victorian India and particularly English trade interests in his discussion of the Indian outbreak. He does blame harsh British tactics in India on their recognition that Yersinia pestis was the pathogen (which he questions). This whole section needs a good going over by an modern historian.

In his criticism of the aDNA work, he claims that most researchers had “negative findings” but Gilbert et al is the only paper he cites that really failed to find plague. If he is referring to the number of negative specimens, then he doesn’t understand how rare the survival of aDNA is in general and the importance of the more sensitive protein methods. Like most of the press, he makes way too much out of the observation that the East Smithfield isolates represent an ‘extinct’ clade. It would be far more surprising if a Black Death isolate were identical to a modern strain. Evolution does not stop, especially not in the accumulation of polymorphisms (neutral mutations). He ignores the fact that the Third Pandemic strains are descendants of the Black Death isolates. He doesn’t seem to understand that genetic diversity is produced in every epidemic and that most of it is lost at the end of the epidemic. This is especially true of Yersinia pestis diversity generated in humans because it must be transmitted to a reservoir species to be preserved.

Not for the first time, I wonder if he understands what natural immunity is and he uses references from the 1950s or before on human immunity to the plague. All medieval immunity is natural. They did not have the means to generate artificial immunity. Natural immunity can be passive (mother to child) or active (generated after exposure).   He misrepresents Li et al (2012) as an indication that immunity is short-lived when in fact the study shows the antibody response is strong (69.5% at 10+ years) and correlated with the strength of their response at the time of the initial infection. Just because we are having problems generating a vaccine that can repel pneumonic plague doesn’t mean that a response generated against an active infection couldn’t repel bubonic plague.  It takes a much stronger response to cope with an aerosol exposure.  When plague epidemics are coming about every 10-15 years, an immunity that lasts 10-20 years would be enough to produce an age differential in the mortality rate. I will leave his analysis of the mortality from historic sources to historians to comment upon. While childhood mortality rates in plague epidemics are clues toward immunity, they are only one variable in comparing the epidemics. We also have to look at what else is occurring among the children such as normal childhood mortality, co-infection and other co-morbidity.

He makes the leap of logic that decreases in total mortality rates equals changes in human immunity. There are many variables that effect the intensity of an epidemic. Decreases in human mortality may suggest changes in the rodent population and/or rodent immunity. If epidemics occur too closely spaced the rodent population will not have recovered enough to generate a large outbreak. Of course, other environmental changes can alter the rodent population and exposure of humans to rodents.

He makes assertions on vector transmission that are not referenced and uses a reference from 1913 (!) to assert that the septicemia in humans is not high enough to allow human-to-human flea transmission. He seems to be assuming that transmission would need to be accomplished by a single flea or louse, which is unlikely. He gives no reference for his assertion that the bacterial load in plague is lower than insect vector transmitted typhus or Lyme disease. He seems to think that only one vector could be at work in the second pandemic rather than rat fleas, human fleas, and lice all transmitting Y. pestis in the same epidemic. Pathogens will take any opportunity available to transmit.

He starts reaching for straws in the conclusions:

There are statements like this: “The ancestor of this family, Yersinia psuedotuberculosis, which geneticists argue gave birth to this new strain of Yersinia, perhaps as late as the eve of the Black Death” (p. 210) Yersinia pestis is not a new strain of Yersinia pseudotuberculosis! It is a species in its own right. A strain is a distinctive subpopulation of a species.  Emerged as late as the eve of the Black Death? Nonsense. There is the little thing of the Plague of Justinian about 800 years earlier, with aDNA and protein evidence. This emergence involving genome rearrangement, loss of genes, gain of chromosomal genes and plasmids would likely have taken at a minimum centuries before 541.

“Could an earlier variety of the ancestor Yersinia suddenly have developed pathogenic factors such as plasmids or, on the level of protein biosynthesis, abilities form a capsule or to release endotoxin, thus suddenly transforming the benign pseudotuberculosis into a new and vicious pathogen, but without diminishing its ability to spread effectively from person to person?” (p. 211)

This one is easy…. NO! Bacteria do not suddenly develop plasmids; they acquire them from other species. In Y. pestis’s case, all of these plasmids are significantly modified from the ancestral plasmids they received. It also takes more than one gene or even plasmid to produce Y. pestis virulence from Y. pseudotuberculosis. He seems to also be implying that a change to increased virulence in humans is the species differentiating event for a primarily rodent pathogen.  Then he strangely follows this (a few sentences down) with the speculation that the “modern bacillus may actually be more toxic than that of the pathogen of the historic plague.”(p. 211) Huh? What happened to his speculation above that “a new and vicious pathogen” was at work?

“As regards Black Death and the ‘Third Pandemic, when and by what criteria does ‘a strain’ of a pathogen come to be reckoned as the causal agent of another ‘disease’, which has to be classified differently from that caused by a related pathogen of the same genetic family, as is currently recognized in the case of Yersinia pestis and its older relative, Yersinia pseudotuberculosis? Even if scientists thought that a pathogen is the equivalent of the disease it in part causes, that is the only pertinent defining feature? Even if scientists thought that the pathogens of the ‘Second’ and ‘Third’ Pandemics were identical (and now they do not), should we then return to the strict reductionism of Koch circa 1890, that a pathogen is the equivalent of the disease it in part causes, that it is the only pertinent feature?” (p. 212)

What? Now we have to reargue germ theory? Pathogens can have different presentations and different epidemic dynamics; some transmit by a variety of means. Co-infections and other co-morbidities certainly matter, but you don’t have the disease without the pathogen.  This is not a type of disease like pneumonia where multiple pathogens cause similar effects. Cohn is grasping at straws and bending scientific concepts to suit his purposes.