Category Archives: aDNA

Historians Chronicling Plague Genetic Discoveries

After my last post critiquing Cohn’s scientific interpretations, I think its only fair to write about all the historians who are actively engaging and incorporating scientific findings in their work. I’ve communicated with a lot of historians who are following the scientific work on the plague and I know there will be some articles and books coming out over the next year or so that incorporate some of new genetics in historical analysis.

So for science folks, these two articles give us some insight into how historians see plague genetics unfolding. Little concentrates on the early drama over plague genetics. Bolton covers that material also, but also looks at newer information on transmission dynamics too.

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

Bolton, J.L. ‘Looking for Yersinia pestis: scientists, historians and the Black Death’ in L. Clark and C. Rawcliffe (eds.), Society in an Age of Plague, The Fifteenth Century XII (Woodbridge: Boydell, 2013), publication date 15 August 2013, ISBN 9781843838753. (In the same book/issue as Cohn’s paper discussed in the last post.)

Overall, I am really optimistic about the interdisciplinary work that can be done on the plague.

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.

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)
(Harbeck et al, 2013. Fig. 1)


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