While autumn is not officially over yet, December always seems like winter to me so here is my reading review from autumn.
This season I’m introducing a book review rating system. On my scale, an average book would get three scopes; a good book, four; and only the extraordinary book gets five scopes. I probably will not rate translations because I don’t feel qualified to evaluate them.
Books
Paul Kelton. Epidemics and Enslavement: Biological Catastrophes in the Native Southeast, 1492-1715. University of Arizona Press, 2007.
Catherine Cameron, Paul Kelton, and Alan Swedlund, eds. Beyond Germs: Native Depopulation in North America. U of Arizona Press, 2015.
Pseudo-Dionysius of Tel-Mahre: Chronicle, Part III edited by Withold Witakowski, Liverpool University Press, 1997. (includes the largest section of John of Ephesus’ Church History/History of the Plague)
Zlata Blažina Tomic and Vesna Blažina Expelling the Plague: The Health Office and the Implementation of Quarantine in Dubrovnik, 1377-1533. McGill-Queens University Press, 2015.
Dorothy Crawford. Deadly Companions: How Microbes Shaped Our History. Oxford University Press, 2007.
Susan Mattern. The Prince of Medicine: Galen in the Roman Empire. Oxford University Press, 2013.
Papers
Meier, D. (2004). Man and environment in the marsh area of Schleswig–Holstein from Roman until late Medieval times. Quaternary International, 112(1), 55–69. http://doi.org/10.1016/S1040-6182(03)00065-X
Stanley, J.-D., Bernasconi, M. P., & Jorstad, T. F. (2008). Pelusium, an Ancient Port Fortress on Egypt’s Nile Delta Coast: Its Evolving Environmental Setting from Foundation to Demise. Journal of Coastal Research, 242, 451–462. http://doi.org/10.2112/07A-0021.1
Schats, R. (2015). Malaise and mosquitos: osteoarchaeological evidence for malaria in the medieval Netherlands. Analecta Praehistoricaleidensia, 45, 133–140.
MacMaster, T. J. (2015). “Not With a Bang?” The Economics of Trade and the End of Byzantine North Africa. In M. Di Rodi, P. Frankopan, M. Lau, & C. Franchi (Eds.), Landscapes of Power: Selected Papers From the XV Oxford University Byzantine Society International Graduate Conference (pp. 73–91).
SHWARTZ, L. (2013). Gargano Comes to Rome: Castel Sant“Angelo”s Historical Origins. The Journal of Ecclesiastical History, 64(03), 453–475. http://doi.org/10.1017/S0022046912001704 (Blogged about here: St Michael, the Plague and Castel Sant’ Angelo, in 2012 after his Kalamazoo talk. I just found in in print much as I remembered in the blog post.)
Rasmussen, S., Allentoft, M. E., Nielsen, K., Orlando, L., Sikora, M., Sjögren, K.-G., et al. (2015). Early Divergent Strains of Yersinia pestis in Eurasia 5,000 Years Ago. Cell, 163(3), 571–582. http://doi.org/10.1016/j.cell.2015.10.009 (See the previous post on this blog!)
Sun, Y.-C., Jarrett, C. O., Bosio, C. F., & Hinnebusch, B. J. (2014). Retracing the Evolutionary Path that Led to Flea-Borne Transmission of Yersinia pestis. Cell Host and Microbe, 15(5), 578–586. http://doi.org/10.1016/j.chom.2014.04.003
McCormick, M. (2015). Tracking mass death during the fall of Rome’s empire (I). Journal of Roman Archaeology, 28, 325–357.
Daniel Melleno. (2014) North Sea Networks: Trade and Communication from the Seventh to the Tenth Century. Comitatus. 45:65-90.
The latest plague news to splash across headlines is the discovery of Yersinia pestis aDNA in seven Bronze Age remains from Eurasia. The most important findings in this new study are not anthropological; they are evolutionary. This paper allows us to drop a couple more evolutionary mile markers. Finding 7% of the tested remains (7 out of 101) positive for plague is surprising, but I’m not yet ready to believe that it was endemic over such a huge area scattered over 2000 years. Not yet anyway.
The new phylogenetic tree places Y. pestis in humans since the Bronze Age and the origin of the species as far back 50,000 years ago. It also opens up questions on the original reservoir species and the location of the birth of the species, although central Asia is still the most likely location.
Stretching out the Yersinia pestis tree. Blue arrows are gains and red arrows are losses. (Rasmussen et al, 2015)
So let’s look at the genetic results in three areas highlighted by Rasmussen et al: flea transmission, Pla activity, and suppression of the immune response stimulating flagellin production. These traits are critical to producing bubonic plague as we know today.
Late phase flea transmission of modern Yersinia pestis is dependent on the ability to survive in and colonize the flea. The Bronze Age strains have all of the plasmids and virulence genes of modern strains except one, the ymt gene that encodes the murine toxin. The basic tool set of modern strains also have deactivated or knocked-out the protein products of three ancestral genes that hinder Yersinia pestis biofilm formation. Remnants of these genes persist as pseudogenes in modern strains. (A pseudogene is the corpse of a former gene.) This genetic combination allows Y. pestis to survive in the mid-gut of the flea, persist longer and form a biofilm; a necessity for late phase flea transmission. However, as Monica Green reminded me, ymt is not required for early phase flea transmission, dirty-needle style (Johnson et al, 2014). In fact, since Y. pestis does not need to persist long or multiply at all, there are no known genes needed to be present or absent for early phase transmission. As I recently reviewed, early phase transmission is very common and effective (see Eisen, Dennis & Gage, 2015). Based on the dates of their samples, they estimate that ymt was gained in about 1000 BC. In the RISE509 strain from Afanasievo Gora in southern Siberia, the pde3 is inactive but the other two, pde2 and rcsA, are still functional. Taken together this genetic combination should allow early phase flea transmission but not late phase flea transmission that requires biofilm formation. They are still mid-way in developing late phase flea transmission. This makes sense for a microbe being transmitted dirty-needle style, providing the opportunity for natural selection to develop late phase transmission bit by bit. While early phase transmission can support regional epizootics and epidemics, late phase flea transmission is probably important for long distance transmission by fleas in grain or textiles, or by sea.
The recent discovery of the Pla gene in Citrobacter koseri and Escherichia coli, other enteric opportunistic flora, but not found in Yersinia pseudotuberculosis, suggests that lateral gene transfer brought the plasmid to the young Y. pestis while still in the enteric environment (Hänsch et al, 2015) . This is consistent with Y. pestis Pla and Salmonella enterica PgeE both evolving from the same ancestral omptin ancestor in an enteric environment (Haiko et al, 2009). This suggests that Y. pestis may have remained an enteric organism for some time after it split from Y. pseudotuberculosis.
Six of seven Bronze Age Y. pestis strains contain the Pla gene required for deep tissue invasion and bubo formation. Rasmussen et al (2015) suggest that the strain lacking the Pla gene has lost it and that this gene has been lost more than once in the phylogenetic tree. In other words, Pla was present in the common ancestral strain. However, to support development of bubonic plague Pla needed to gain a mutation at position 259 that these strains lack (Haiko et al, 2009). So the Pla gene without the mutation at position 259 can support pneumonic plague but not bubonic in the Pestoides F strain (0.PE2) of Y. pestis (Zimbler et al, 2015). On the other hand, Sebbane et al (2006) showed that strains completely lacking Pla can still develop primary septicemic plague following flea transmission. They can envision an “evolutionary scenario in which plague emerged as a flea-borne septicemic disease of limited transmissibility”(Sebbane et al, 2006). Without the polymorphism at position 259, bubo formation should be retarded, if not suppressed.
A third genetic difference of possible significance is the apparent ability to produce flagellin, a major activator of the human innate immune system. Modern Y. pestis strains have deactivated the production of flagellin by a frameshift mutation in the regulatory gene flhD. The Bronze Age strains lack this frameshift and so presumably had normal flagellin production. However, Y. pseudotuberculosis and Y. enterocolitica down regulate production at mammalian body temperatures. If the ancestral Y. pestis did also then its possible that it wasn’t a factor in human infections. Experimentally recreating the regulatory environment from Y. pseudotuberculosis would be much more difficult than simply inserting an intact copy of the gene in a modern strain of Y. pestis.
Predicting the impact of these ancestral genes is highly conjectural. This combination of genes has never been studied together. Since these strains were isolated from human remains we can assume that there is a path for transmission and pathogenesis. The reliance on early phase flea transmission, the less virulent pla allele and the possible production of flagellin suggest that Bronze Age local (dermal) infections from flea bites would be less virulent (more survivable). Interestingly, these milder local infections may have been immunogenic.
As Y. pestis moved away from an enteric lifestyle, producing a septicemia was necessary for either flea transmission or development of a secondary pneumonia with aerosol transmission. I find it hard to believe that Bronze Age Siberia or Estonia had a large enough population for sustained pneumonic transmission. Since Pulex irritans can transmit Y pestis without development of a biofilm, there is no reason to see humans as a dead-end to flea transmission even as early as the Bronze Age.
Humans could have also contracted septicemic plague by ingesting infected meat. Although natural ingestion infections are very rare today, this mode remains effective. A village size outbreak could easily occur from sharing a large infected animal as happened in Afghanistan in 2007. In that outbreak a single infected camel shared among two villages produced 83 probable cases of plague with 17 deaths, a case fatality rate of 20.5%. (Leslie et al, 2011). Last but certainly not least, the further back we go in Yersinia pestis‘ evolution the more likely ingestion is to be a mode of transmission like its ancestor Yersinia pseudotuberculosis.
Its takes more than good transmission to cause a demographic changing epidemic over large areas like the Eurasian continent. It also requires a fairly high human density and good trade or communication routes. Humans play the the most important role in transmitting plague of pandemic size. I can’t say if the cultural factors that make such large epidemics possible were in place in Bronze Age Eurasia.
Let’s keep things in perspective before we conjure up the specter of virgin soil epidemics of plague in the Bronze Age. Yersinia pestis is the kind of over achiever that may have been a player in Bronze Age demographics but it would be nice to have a lot more evidence before jumping to that conclusion.
References:
Rasmussen, S., Allentoft, M. E., Nielsen, K., Orlando, L., Sikora, M., Sjögren, K.-G., et al. (2015). Early Divergent Strains of Yersinia pestis in Eurasia 5,000 Years Ago. Cell, 163(3), 571–582. http://doi.org/10.1016/j.cell.2015.10.009
Eisen, R. J., Dennis, D. T., & Gage, K. L. (2015). The Role of Early-Phase Transmission in the Spread of Yersinia pestis. Journal of Medical Entomology, tjv128–10. http://doi.org/10.1093/jme/tjv128
Johnson, T. L., Hinnebusch, B. J., Boegler, K. A., Graham, C. B., MacMillan, K., Montenieri, J. A., et al. (2014). Yersinia murine toxin is not required for early-phase transmission of Yersinia pestis by Oropsylla montana (Siphonaptera: Ceratophyllidae) or Xenopsylla cheopis (Siphonaptera: Pulicidae). Microbiology, 160(Pt_11), 2517–2525. http://doi.org/10.1099/mic.0.082123-0
LESLIE, T., WHITEHOUSE, C. A., YINGST, S., BALDWIN, C., KAKAR, F., MOFLEH, J., et al. (2011). Outbreak of gastroenteritis caused by Yersinia pestis in Afghanistan. Epidemiology and Infection, 139(5), 728–735. http://doi.org/10.1017/S0950268810001792
Sebbane, F., Jarrett, C. O., Gardner, D., Long, D., & Hinnebusch, B. J. (2006). Role of the Yersinia pestis plasminogen activator in the incidence of distinct septicemic and bubonic forms of flea-borne plague. Proceedings of the National Academy of Sciences of the United States of America, 103(14), 5526–5530. http://doi.org/10.1073/pnas.0509544103
Zimbler, D. L., Schroeder, J. A., Eddy, J. L., & Lathem, W. W. (2015). Early emergence of Yersinia pestis as a severe respiratory pathogen. Nature Communications, 6, 1–10. http://doi.org/10.1038/ncomms8487
Hänsch, S., Cilli, E., Catalano, G., Gruppioni, G., Bianucci, R., Stenseth, N. C., et al. (2015). The pla gene, encoding plasminogen activator, is not specific to Yersinia pestis. BMC Research Notes, 1–3. http://doi.org/10.1186/s13104-015-1525-x
Haiko, J., Kukkonen, M., Ravantti, J. J., Westerlund-Wikstrom, B., & Korhonen, T. K. (2009). The Single Substitution I259T, Conserved in the Plasminogen Activator Pla of Pandemic Yersinia pestis Branches, Enhances Fibrinolytic Activity. Journal of Bacteriology, 191(15), 4758–4766. http://doi.org/10.1128/JB.00489-09
Nükhet Varlık. Plague and Empire in the Early Modern Mediterranean World: The Ottoman Experience 1347-1600. Cambridge University Press, 2015.
Zlata Blažina Tomic and Vesna Blažina Expelling the Plague: The Health Office and the Implementation of Quarantine in Dubrovnik, 1377-1533. McGill-Queens University Press, 2015. [Dubrovnik = Ragusa]. [An English edition of Blažina-Tomić, Zlata. Kacamorti i kuga. Utemeljenje i razvoj zdravstvene službe u Dubrovniku. [The Cazamorti and the Plague: Founding and Development of the Health Office in Dubrovnik] Zagreb: HAZU, 2007.]
Comparing the Ragusan Republic to the Ottoman Empire is a little like comparing an ant to an anteater, but nevertheless they managed to coexist as neighbors throughout the plague years. They were both carved out of the relic of the Byzantine empire. If you have never heard of the Ragusan Republic, that is probably because the city of Ragusa is now called Dubrovnik and the republic was limited to that small coastal area of modern Croatia. It was one of the smallest city states of the Mediterranean world. On the other hand, by 1600 the Ottoman Empire included almost all of what had been the Eastern Roman Empire or Byzantine Empire.
It seems natural to assume that the larger, more powerful nation should be able to do everything better, but when it comes to public health the opposite is often true. Quarantines are much easier to develop and maintain in a smaller state with limited points of access like Ragusa. The fact that smaller wealthy states often have better health care does not prevent contemporaries from still expecting the larger state to do better. Expectations are rarely realistic. The Ottoman empire was not well understood by contemporary Europeans and the growth of the empire over the 14th and 15th centuries terrified them. The second plague pandemic hit the Ottoman empire at least as hard as elsewhere and yet, it continued to grow. This alone gives the Ottoman experience a unique position in plague history.
Each book naturally is focused on their unique contributions to plague studies. Varlık reconstructs the movements of the plague on a grand scale as it ebbed, flowed, and pulsed through the Ottoman empire by 1600 encompassing about a third of the Mediterranean rim. It has become clear that we can not understand the Black Death without the Ottoman experience. Tomic and Blažina provide a microhistory of the public health and medical practices in the single city of Ragusa (Dubrovnik). They remind us that even in a city that was extremely diligent with their quarantine measures, security and economics often trump public health and that medical care was a contracted service to meet the needs of city administrators.
Turning to the Ottoman empire first, Varlık has to begin with some damage control on assumptions about the Ottomans. She made me grateful that I don’t have any assumptions about the Ottomans to be be undone; sometimes its good to be a blank slate. This is an important chapter for historians who deal with opinions of 14th centuries sources and their impact on subsequent historiography. For most of us, the Ottoman experience during the Black Death as been a black hole in history– until now.
Her chapter on the natural history of the plague in Ottoman lands is a gold mine of information on fleas and hosts. It is clear that there were plenty of black rats in Constantinople at the onset of the Black Death and Istanbul in subsequent epidemics. Fleas and lice were such a common way of life that people who did not have fleas or lice were considered suspect of either being lepers or having foul body odor! (p. 34) This is the kind of historical evidence we need for most regions of the world with plague histories.
In most of the book, Varlık traces the trajectory of the plague to Constantinople / Istanbul and the rest of the Ottoman empire ultimately through four phases. When the Black Death first arrived, Constantinople was still part of the Byzantine empire and the Ottomans were a small Anatolian group. This was followed by three phases of plague activity from the time the Ottoman’s conquered Constantinople, renaming it Istanbul. In the first phase (1453-1517), the Ottomans were besieged by plague imported from the West in multiple ‘waves’. Remarkably, it did not check population or urban growth. Plague pulsed in and out of the empire’s regional networks during the second phase (1517-1570). By the third phase (1570-1600), Istanbul has transformed to a plague hub reflecting its centralizing role in the empire. She finished the last section of the book with a discussion of new understandings of the plague and social experience of the Ottomans during the plague.
Varlık looks forward to others examining other contemporary major states like the Hapsburg empire for comparative analysis. Personally, I look forward to a comparison between the first pandemic in the Roman/Byzantine Empire and the second pandemic among the Ottoman Empire. It is essentially the same territory, both seated from Constantinople / Istanbul. Did Roman Constantinople have the same ‘capital effect’ that Varlık outlines in this book? An obvious difference being that the Ottomans waxed during the second pandemic, while Byzantium waned from the first pandemic onward. What role, if any, did the plague have in their polical trajectories? The rise of the Ottomans straight through the second pandemic should make people pause in their eagerness to claim the first pandemic doomed the Roman empire. Or did their political trajectories explain how plague was transmitted within or through the respective empires? I suspect the later is the right question. I rather suspect, as Varlık shows here, that the plague is reflecting social and political changes rather than causing those changes. And, this does not diminish the importance of the plague in any way.
Pivoting to the Ragusan Republic, the scale has shrunk so much that it seems like a different world (even though the Ottoman’s had hegemony over Ragusa for part of the period covered). The entire Ragusan Republic was perhaps on par with a medium size Ottoman city. Comparing the differences in attitude toward each other between Ragusa and Istanbul in these two books is interesting. The Ragusan Republic had a peculiar organization owing to its foundation by a group of Byzantine businessmen, who created a state to allow their business and lifestyle to continue but with little if any political or religious ambitions. Due to its small size it had to contract most professionals like physicians, surgeons, and clergy from outside the republic, primarily from Italy. Their position on the frontier between Christendom and Islamic lands gave them unusual religious independence especially considering they had to import their clergy.
Ragusa’s primary claim to plague fame is having established the first quarantine zone to protect the city of Ragusa. Fair enough, though as small as the republic was, the protected zone was limited to the city of Ragusa itself with its peripheral islands used for isolation of the sick and quarantine of the suspected. Their plague program had to be set up and maintained while business continued in the city. Ragusa was too small to stop imports. It couldn’t feed itself, much less keep its economy moving enough to pay for the security it needed, with its port closed. They were in constant fear that the plague would make them vulnerable to conquest by their neighbors.
Tomic and Blažina utilize a unique archive of government actions and contracts for health services to reconstruct the health care program of Ragusa. Their interaction with the physicians they contracted for services was fascinating. First, physicians never were in control or even had a significant influence on the function of the health office. They were contracted like any other professional. During plague outbreaks, they granted leaves of absence to the regular physicians that they valued. They were apparently too important to risk during the plague (p. 173). They then contracted specific plague physicians (medi pestis) who were only allowed to evaluate suspected plague cases and treat those who had plague. I previously wrote about one of their plague doctors here. They were not allowed to do other services and had to live in essentially quarantined due to their contact with possible plague victims. These plague doctors were paid by the state and were required to treat people of all classes the same, so the poor could expect to have the same attention as the wealthy. Ragusa’s health office was an experiment in socialized medicine. Those interested in the evolution of public health should be interested in this book.
Between these two books the eastern Mediterranean can begin to take the pivotal place that its geography suggests it must have in understanding the second plague pandemic. In the 15th and 17th century the Ottoman Empire linked together the three continents all ravaged by the pandemic. In the decades leading up to 1600 when Istanbul became a plague hub, it reflected Istanbul’s essential role in controlling all movement within the empire and thus within this connecting zone between the three continents. Tracking the plague may well inform political and economic history as well as the history of health in this critical region.
