Category Archives: Black Death

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.

Wendy Orent on the Plague

13548013 Plague: The Mysterious Past and Terrifying Future of the World’s Most Dangerous Disease

Wendy Orent, New York: Free Press, 2004, reprinted 2013

I’ve been way for far too long. One of the reasons for the quiet is because I’ve been reading quite a few books this summer. This book was one of them. I wouldn’t normally review a nine-year old book, but it was just reprinted unrevised this year so I think it’s fair for review. Published in 2004 it can’t be expected to have hardly any of the recent genetic work.

Wendy Orent has a PhD in anthropology but has always worked as a freelance writer. Her journalistic history shows. The sensationalist title put me off reading this book for a long time. Unfortunately, it continued in the book. The material is attention-getting enough without adjectives like “chilling”. She also overused interviews as sources. Some of the interviews are interesting and provide opinions not found in print. In my opinion, interviews should not be used for material that has been published.

One of her primary sources is a Russian biologist named Igor Domaradskij whose Cold War career ran the gamut of roles in the Russian plague system from anti-plague epidemiologist to biological weapons designer. Orent previously was co-author of his autobiography and considers him a friend. Her theories and even terminology are heavily influenced by Domaradskij to the degree that it seems to compromise her objectivity. Sources like Domaradskij are difficult, divulging their version of events that their government will never acknowledge even occurred. We have to keep in mind that one reason men like Domaradskij write books is to get recognition for their secret work and get vengeance on a system they feel wronged by. Cold war Russian research was also warped by the influence of Lysenkoism and by its self-imposed isolation from the rest of the world of science making reconciliation of scientific theories and philosophies difficult. Even those like Domaradskij who say they always renounced Lysenkoism were still trained and worked in an environment that warped the scientific method.  We are forced to use their information because we can’t afford not to but we have to approach it with caution and skepticism.

Her reconstruction of the first two plague pandemics is a mixed bag. She supported Yersinia pestis as the agent of both pandemics and asserts that the human flea was the primary vector.  It’s interesting to see how she argues for the human flea as vector but she never really presents evidence to support this method. She also posits that there were fundamental differences between the first and second pandemics that I do not believe the sources support. We don’t have enough sources from the first pandemic to judge. She does not seem to recognize that although early plague records are primarily coastal, plague is mentioned in all areas of Europe that we have written records. It is likely that the perceived area restrictions are due more to our records than the actual spread of the plague. She makes some predictions about the evolution of Yersinia pestis, especially the Black Death clone(s), that have not panned out in modern genetic studies. Depending on Russian evolutionary theories rooted in Cold War philosophies is just not sound.  She argues for a major role for pneumonic plague early during the Black Death that transitions into a vector borne disease. These are just a few areas where she argues for explanations without enough scientific or historic evidence to back them up.

There is some thought-provoking material in this book primary on plague in the 20th century but there is a lot of chaff to sift to find the wheat. It may be useful to people who are well read on the plague literature, historic and scientific, but I can’t recommend it to those who have not done a lot of previous study on the plague.

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.

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.