31 Matching Annotations
  1. Nov 2025
    1. genetic evidence alone is not enough to reconstruct the timing and spread of short-term plague pandemics, which has implications for future research related to past pandemics and the progression of ongoing outbreaks such as COVID-1

      This is the perfect quote to use in my proposal! The top scientists at McMaster are literally saying that to understand the plague, I need the historical and social context alongside the genetic data.

    2. The team studied genomes from strains with a worldwide distribution and of different ages and determined that Y. pestis has an unstable molecular clock. This makes it particularly difficult to measure the rate at which mutations accumulate in its genome over time, which are then used to calculate dates of emergence. Because Y. pestis evolves at a very slow pace, it is almost impossible to determine exactly where it originated.

      This explains the scientific limitation that creates the big debate. Since the plague genome evolves so slowly, they can't even tell where it started!

    1. These changes from the Y. pseudotuberculosis progenitor included loss of insecticidal activity, increased resistance to antibacterial factors in the flea midgut, and extending Yersinia biofilm-forming ability to the flea host environment.

      This is the technical explanation for the famous "blocked flea" which is the key to the rat theory. The biofilm is what clogs the flea's gut and forces it to bite more.

    2. the interactions of Y. pestis with its flea vector that lead to colonization and successful transmission are the result of a recent evolutionary adaptation that required relatively few genetic changes.

      This is a great detail for my argument! The article calls the flea jump a "recent evolutionary adaptation." This suggests the mechanism might have been imperfect or inefficient in the 14th century, which actually strengthens the argument against the rat-flea model being the sole cause of the Black Death's incredibly fast spread. It provides scientific backing for why I need to seriously consider the human ectoparasite model and not just discard it immediately.

    3. The Yersinia–flea interactions that enable plague transmission cycles have had profound historical consequences as manifested by human plague pandemics. The arthropod-borne transmission route was a radical ecologic change

      This is the whole mechanism behind the classic rat-flea theory that my map needs to test. The article is basically saying the history of the plague is tied to this interaction. When I map the spread, I have to remember that this theory relies on a slow, multi-step process involving rats and fleas, which is the main reason I'm testing it against the faster human-to-human transmission idea.

    1. Alternative putative etiologies of the Black Death include a viral hemorrhagic fever [16] or a currently unknown pathogen [19]. In part, these alternative etiologies reflect apparent discrepancies between historical observations of extremely rapid spread of mortality during the Black Death with the dogma based on Indian epidemiology that plague is associated with transmission from infected rats via blocked fleas

      This is a perfect summary of the whole problem I'm trying to solve. Historians originally doubted the Y. pestis theory because the plague spread way too fast to be the slow rat-flea model. This confirms that I'm right to use my map to visually test the difference between the slow rat spread (the "dogma") and the rapid human spread (my hypothesis).

    2. Our finding of identical genotypes (based on 20 markers) in Saint-Laurent-de-la-Cabrerisse and Hereford thus lends support to historical evidence [2,25] which suggest that plague spread from France to England (Fig. 1) in the second half of the 14th century.

      The fact that they share the exact same plague strain means I have a confirmed, solid connection across the English Channel. This established route will be my baseline when I look at the historical records and chronicles. (Saint-Laurent-de-la-Cabrerisse and Hereford)

    3. our aDNA results identified two previously unknown but related clades of Y. pestis associated with distinct medieval mass graves. These findings suggest that plague was imported to Europe on two or more occasions, each following a distinct route.

      This is good for my hypothesis! It proves that the plague was too complex to have followed just one simple path. Since the scientists found two different strains, my map must show two separate main routes into Europe, which means I can directly test the differences between the rat theory and the human flea theory.

    4. Here we identified DNA and protein signatures specific for Y. pestis in human skeletons from mass graves in northern, central and southern Europe that were associated archaeologically with the Black Death and subsequent resurgences. We confirm that Y. pestis caused the Black Death and later epidemics on the entire European continent over the course of four centuries.

      This could be the best starting point for my project. It shuts down the argument about what caused the plague, so I don't have to waste time debating the pathogen itself. I can now focus 100% on mapping the how and when of the spread, which is the whole point of my research.

    1. Rats and fleas and thus the contagion itself could also be spread by transport going in the opposite direction, carrying residues of grain and grain-based provisions that would feed the carriers of the disease on their journey.

      This is a deeper detail for my map. I shouldn't only map where things were exported, but also mention/point out the return trips of ships, as they could have also carried the disease.

    2. it struck Norway on two fronts: in Oslo, by then the largest town in the southern part of the country,40 and Bergen on the west coast.41 From these two points the infection spread inland along main roads and pilgrim routes, both south of the Oslo fjord and all the way up north to the Archdiocese of Nidaros, where the archbishop himself succumbed in 1349.42From Norway the plague must have been transmitted to Denmark, where, in the autumn of 1349, it erupted in the port of Halmstad

      Oslo, Bergen, Norway and Halmstad, Denmark. Date: 1349. This gives me key points for mapping the very northern part of Europe.

    3. The rat flea, Xenopsylla cheopis, admittedly had the most favourable conditions to do so, but research demonstrates that it was extremely sensitive to changes in temperature and humidity

      This is a specific scientific detail that helps me understand why the rat theory might be wrong in places like Scandinavia. My map can visually test if the plague slowed down in colder areas.

    4. However, there is no evidence to suggest that rats were involved in the spread of the plague in the Middle Ages. No contemporary historical accounts exist of dead rats being found ahead of an outbreak of the plague

      This is a great piece of evidence for the human parasite side. It tells me to look for things in the old chronicles that don't mention rats, which strengthens the argument against the rat theory.

    5. the hypothesis that the plague was bubonic in origin and spread along the trade routes of Europe, carried like metastases by the black rat and its parasitic fleas.

      This clearly backs up the old idea (the rat-flea theory) that I need to test with my map. It gives me a clear route to follow.

    6. The purpose of the present research is to examine various theories concerning the origin of the Black Death, to record its routes of dissemination in the Nordic countries and across the British Isles, and to compare the pattern of that dissemination with trade routes carrying grain throughout northern Europe

      This is exactly what my project aims to do. I can use this quote to show that comparing the plague's spread with trade routes is the right way to study this problem.

  2. Dec 2021
    1. Note also that testators left cloth as bequests during the epidemic. Apparently they were not as concerned with clothes retaining miasma as were anti-plague ordinances of the government.

      I did not know what the word miasma meant, after searching it up I learned that it was a "highly unpleasant or unhealthy smell". I wanted to learn more about what personal hygiene was like and how it changed during the time of the plague. I learned that it was a very unsanitary time and this helped to spread the plague. The doctors were unsure where the plague could spread from some, the community continued on with their everyday routine in little sense of where the disease came from which made the plague spread more.

  3. Aug 2021
  4. Apr 2021
  5. Mar 2021
  6. Jul 2020
  7. May 2020