Sorry, this blogpost is in German. However, corrections are welcome.
New plague research has just been published with particular importance for the discussion of the early-phase transmission and transmission by proventricular blockage. B.J. Hinnebusch, Senior Investigator at the Laboratory of Zoonotic Pathogens, NIH, NIAID, Rocky Mountain Laboratories, has long been one of the sharpest critics of the early-phase theory of transmission, see, for instance, his article “Biofilm-Dependent and Bio-Film-Independent Mechanisms of using Transmission of Yersinia pestis by Fleas”, Advances in Experimental Medicine and Biology, 954; 2012: 237‒243. In these days, he publishes with co-authors an evidently crucial article on this topic: Hinnebusch, B.J. Bland, D.M., Bosio, C.F., Jarrett, C.O., “Comparative Ability of Oropsylla montana and Xenopylla cheopis Fleas to transmitt Yersinia pestis by two Different Mechanisms” PLOS Neglected Tropical Diseases | DOI: 10…1371/journal.pntd.0005276 January 12, 2017: 1-15.
They used fleas of Oropsylla montana provided by two of the central advocates of the early-phase theory, which excludes that different strains of this flea could affect the outcome. The conventional vector of plague ‘par excellence’, Xenopsylla cheopis, was used for comparison. Contrary to earlier assertions by the advocates of the early-phase theory that Oropsylla montana rarely develop proventricular blockage, it was shown to block earlier and surviving longer after becoming blocked than X. Cheopis, and that transmission by blockage was as good as or better than observed for X. cheopis. This (re)confirmed earlier research on the vector capacity of this species of flea (see, e.g., the fully referenced comments in my monograph The Black Death and Later Plague Epidemic in the Scandinavian Countries, 2016: 377, 403, 630, 658).
In this article, the early-phase theory is dismantled as an important or significant means or mechanism of transmission of plague. In a personal communication by email of 01.03.17, Hinnebusch states that “In fact, I think early-phase transmission only has a role in very special circumstances, such as during an epizootic of plague in a dense [rodent] population that is both highly susceptible (LD50< 10) and that routinely develops very high bacteremia levels (>108 to 109 Y. pestis/ml) before death. High flea density is also a likely precondition, as intermittent challenges from just a few fleas at a time would frequently lead to resistance rather than productive, transmissible disease (bacteremia).”
This also means that early-phase transmission is of no significance in plague epidemics, except perhaps, at the individual level, the occasional transmission of immunity-inducing tiny doses of plague bacteria (that will be easily dealt with by the human immune apparatus). It will also become clear that Hinnebusch et al. corroborate and deepen earlier plague research: it is pointed out that this type of early-phase transmission was identified by the Indian Plague Research Commission (IPRC) in 1907 and that the pioneering studies of Bacot of the IPRC on blockage in fleas IPRC 1914 and 1915, are still tenable and relevant. The bibliography contains studies from the entire 1900s, not least 1940s, which have kept their value as fine research.
Finally, I will point out that my recently published monograph contains a long study of early-phase transmission in Chapter 12: 625-655 (with bibliographic references included in the General Bibliography). Its conclusions and basic analysis agree with this recent study by Hinnebusch et al.
Ole J. Benedictow,
The following session report by Doris Gutsmiedl-Schümann (Freie Universität Berlin, Germany), Sacha Kacki (Université de Bordeaux, France), Marcel Keller (MPI-SHH Jena, Germany) and Christina Lee (University of Nottingham, UK) will be published in The European Archaeologist. With kind permission of the EAA.
Edit 17-02-07: filmed talks are now linked under the respective name.
Plague, an infectious disease caused by the bacterium Yersinia pestis, occurred in at least three major historical pandemics: the Justinianic Plague (6th to 8th century), the Black Death (1348-1352, with further epidemic outbreaks until the 18th century), and the Modern or Hong Kong Plague (19th to 20th century). However, it appears that the disease may be much older: DNA from Bronze Age human skeleton has recently shown that plague first emerged at least as early as 3000 BC. As any disease, plague has both a biological as well as a social dimension. Different disciplines can therefore explicate different aspects of plague which can lead to a better understanding of the disease and its medical and social implications.
The session was held on 2nd September 2016 as part of the 22nd Annual Meeting of the EAA with the aim of bringing together researchers from different disciplines who work on plague. It addressed a series of research questions, such as:
- Which disciplines can contribute to the research on plague?
- What are their methodological possibilities and the limitations of their methodologies?
- How can different disciplines work together in order to gain a more realistic and detailed picture of plague in different periods and regions?
- How did different societies react to plague? In which way may we prove or disprove evidence for such reactions – and which disciplines may contribute to the debate?
- What where the common aspects, and what the differences of the various plague outbreaks? Are there any epidemiological characteristics that are essential and/or unique to plague?
- What are possible implications of the pandemic spread and endemic occurrence of plague through the ages for the interpretation of historical and cultural phenomena?
I am a PhD student in the department Archaeogenetics of the Max Planck Institute for the Science of Human History in Jena, Germany. My academic background is Biology (B.Sc./M.Sc.) with specialization in Anthropology and Human Biology. The main project of my PhD is the reconstruction of genomes of Yersinia pestis of both the first (Justinianic Plague) and second pandemic (following the Black Death) in Europe. Additional ancient genomes of Y. pestis are crucial for phylogenetic analyses and allow a more detailed picture of the spatiotemporal distribution of plague.
Neither the 14th century, nor a scientific paper, but probably nevertheless of some interest
Over the last decade a substantial amount of molecular evidence confirming the etiology of the plague over virtually the entire medieval period has been produced. In this rapidly evolving field, evidence for the Black Death of the 14th century has been produced by each new method in turn.
Given the conditions of remains sampled to date, the methods fall into two main categories: genomics and immunology. There are pros and cons to each. Genomics has well-recognized specificity and the ability to compare with living and ancient strains, but non-nucleic acid methods are both specific and far more sensitive. Non-nucleic acid methods (using immunology) will give a better indication of the true incidence within a population, especially important when testing moves beyond mass graves. Immunologic methods have been the primary means of diagnosing clinical infectious disease for at least 30 years. The Rapid Diagnostic Test (RDT) now used to diagnose ancient and modern plague uses technology that has existed for over 25 years with a good track record. The downside of immunology is that it doesn’t give strain specific information. On the other hand, detection of degraded DNA much less getting good enough sequence for strain matching is difficult and inefficient.
This map charts all of the medieval plague molecular data that I have seen (view Plague Map in a larger map). The red balloons mark 6th-9th century, Plague of Justinian, sites. All three early medieval sites are beyond the Alps proving that the plague of Justinian penetrated well beyond the Mediterranean basin. The yellow balloons represent 14th century data, with the starred balloon specifically dated to the first wave of the Black Death pandemic. The blue balloons represent post-14 century data (14th-17th century). Click the balloons for references.
Even a cursory look at the map makes it apparent that both pandemics reached beyond the Alps into the European plain. Further, the distribution represents the areas of activity of 3-4 research groups rather than as an indication of plague incidence across Europe. Every region so far examined and published has found some evidence of plague. There is both DNA and immunological evidence for the 14th century. Unfortunately, DNA data has been produced by three different groups who have not yet produced a consensus sequence or analyzed their differences. Despite the differences between their sequences, there is plenty of homology between their data and modern reference sequences to ensure that they all identified Yersinia pestis. Their differences are most likely to be primarily related to interpretations of degradative changes in the ancient DNA, though it is possible that more than one strain was active in 14th century Europe.
The map also makes it apparent that we only have molecular evidence from a very small sliver of the territory covered by the medieval pandemics. There are too few sites so far to make any predictions about the routes the plague traveled based on molecular evidence. It never travels from point A to point B as the crow flies! Plague spreads more like a spiderweb than a wave. So, long distance transmission may well exist before lateral spread fills in the countryside. It is absolutely necessary to take in consideration medieval trade and communication routes.
This is an exciting time to be working on the plague. So far, only the tip of the iceberg has been exposed. To date, the molecular evidence has been the most useful for confirming the etiology of the plague of Justinian, the Black Death pandemic, and plague’s endurance in western Europe. We have the technology now to map the geographic extent of Yersinia pestis for the first and second pandemic. It will take at least a generation of work from archaeologists, geneticists, and paleomicrobiologists to gather enough sites and resolve the fine-detail sequencing issues to begin to do strain mapping.