What we have done is compare the rise and fall of daily or weekly mortality levels during plague outbreaks against three models of plague transmission - two that are generally accepted (rat-borne plague and pneumonic plague), and one that has been speculated about for a long time (human ectoparasites like body lice and fleas). We allowed the models to achieve the best fit they could within biological parameter constraints, and see how well each of these models could mimic the observed mortality curve.
There is a bit more detail in this interview: https://news.nationalgeographic.com/2018/01/rats-plague-blac...
The code/models we used are available online for one of the outbreaks (Barcelona 1490) https://zenodo.org/record/1043924
A pre-review version of the paper is available as a poster here: http://www.mn.uio.no/cees/english/people/phd/katharrd/kd_yer... Note that we changed the lice model a bit since then, on recommendation of one of the reviewers.
Xavier Didelot did some work on testing mixed models for two cities, 17th century Eyam and 19th century Cairo. He did have to further simplify the models though - there are some restrictions on how many floating parameters you can have while the models are trying to converge to the parameter set that results in the best match with the observations.
Epidemiological analysis of the Eyam plague outbreak of 1665–1666:
Model-based analysis of an outbreak of bubonic plague in Cairo in 1801:
And we can treat the plague today.
I also put a popular science summary of the paper online here:
That said, there are some long-standing questions in plague research, one of which is why the first and second plague pandemic were that much more lethal than the third plague pandemic. Prior to the aDNA work, people speculated that medieval plague was a different pathogen altogether, but that hypothesis has been put to rest now. An alternative theory has been that plague could spread through human ectoparasites, and we found a novel way to test that theory. That resulted in this paper.
Better yet, those who survived prior plagues were more likely to already be immune to the disease, and evolutionary pressure led to a more resilient population against this type of disease.
One of the groups that is doing most of the research on body lice as vectors of plague is the group of Didier Raoult. Michelle Ziegler made a nice summary of that work here:
We didn't use all of the cities for which we had outbreaks, but selected nine that covered a large part of the time period, and a large geographic region. Here is the list:
Givry, France, 1348.
Florence, Italy, 1400.
Barcelona, Spain, 1490.
London, England, 1563-1564.
Eyam, England, 1666.
Gdansk, Poland, 1709.
Stockholm, Sweden, 1710-1711.
Moscow, Russia, 1771.
Malta, Malta, 1813.
Also it makes a certain novel sound a little bit less realistic.
Not that they must be the same, but at least they might have an explanation as to why modern infections would be different from historical ones, if they are any different.
Piarroux R, et al. (2013) Plague epidemics and lice, Democratic Republic of the Congo. Emerg Infect Dis 19:505–506.
Laudisoit A, et al. (2007) Plague and the human flea, Tanzania. Emerg Infect Dis 13:
Ratovonjato J, Rajerison M, Rahelinirina S, Boyer S (2014) Yersinia pestis in Pulex irritans
fleas during plague outbreak, Madagascar. Emerg Infect Dis 20:1414–1415.
One more: has this raised any doubts that the Black Death was a Bubonic Plague?
If it is about the manifestation of the disease (the clinical symptoms), those we only know from historical descriptions and that is not something a model can change :-). So yeah, many infected people would still have had buboes. Buboes are also the expected result from plague acquired from fleas (whether they were human fleas or rat fleas).
What might be less known is that there is a pretty high chance (10-20%) that a person suffering from bubonic plague progresses to pneumonic plague. That basically is a death warrant for that person, but it also means that he/she might spread the disease further through air-droplets. If the conditions are right, you might get a pneumonic plague epidemic intermingled with a bubonic plague epidemic. Model-wise, that is one scenario we haven't looked into, but we have seen something like that play out in Madagascar last year.
Another factor is rats. They are killed by plague just like humans. At least one person should have noted large volumes of rats dropping dead everywhere, but that isn't mentioned in writings of the time.
rats dont travel as much as you think, even within cities. only when the rats piggy back on human travel, could they have spread the disease.
"But feral cats won’t stray three blocks beyond where they were born, and few mice will venture more than a hundred feet from their burrows in a lifetime."
In what way is that obvious?