**Group 6**
The multiple paths to plague outbreaks
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===== Introduction =====
Black Death was part of a pandemic that killed up to a half of
Eurasian population in the 14th century. This series of epidemics was
attributed to bubonic plague, as well as the Justinian Pandemics and
the recurrent plague epidemics that burst over Europe until the 17th
century.
{{ https://upload.wikimedia.org/wikipedia/commons/thumb/4/4e/1346-1353_spread_of_the_Black_Death_in_Europe_map.svg/1200px-1346-1353_spread_of_the_Black_Death_in_Europe_map.svg.png?450 | https://en.wikipedia.org/wiki/Black_Death#/media/File:1346-1353_spread_of_the_Black_Death_in_Europe_map.svg }}
Many rodents are reservoirs of the
bacteria that causes plague (//Yersinia pestis//).
Urban outbreaks have been explained by the transmission of the
disease from infected rats to humans through flea bites.
Nevertheless, this epidemiological model does not match some
key features of the Black Death and other pandemics attributed to
bubonic plague. For instance, many ancient epidemics spread over large
areas faster but had larger recurrence times than
the plagues of the 19-20th centuries,
from which the classic rat-flea-human cycle was deduced.
A recent review (Setenseth et al. 2008) concluded that there are many other
transmission pathways to humans, which can be more or less important
according to the ecological context. Such variation in the main transmission
routes might explain the marked differences in the
epidemiological dynamics among ancient and modern plague
outbreaks.
{{ :2019:groups:g6:stenseth_fig2.png | Stenseth et al. PLOS Medicine 2008 }}
For instance, there was a higher prevalence of blood-sucking
bugs in humans ((the [[https://en.wikipedia.org/wiki/Human_flea|house flea]],
and [[https://en.wikipedia.org/wiki/Body_louse|body]], [[https://en.wikipedia.org/wiki/Head_louse|head]], and [[https://en.wikipedia.org/wiki/Crab_louse|pubic]] lice))
at the time of the Black Death than in recent times.
The human-to-human transmission by way
of these ectoparasites has been advanced as a route that could speed up
the spread of plague (Drancourt et al. 2006).
On the other hand, Appleby (1980) claimed that
the way that plague spread over London during the 1665 epidemic is
better explained by the rat-flea-human pathway.
According to this author, acquired immunity by rats
explains why plague suddenly disappeared from England since then.
===== Assigment =====
Propose simple but realistic mathematical model(s) to describe the dynamics of plague epidemics. The model(s) should address at least one issue of the classic rat-flea-human model, taking into account alternative transmission pathways. Any other aspect that can help to address the issues is also welcome, such as acquired immunity (by humans or rats). Key parameters of your model should be well-grounded in the available knowledge about plague transmission and ecology of vectors and reservoirs.
===== Suggested questions =====
* Does your model predict single or recurrent epidemics? Why?
* Can the alternative pathway(s) you modeled explain (some of) the distinct patterns between recent and ancient plagues?
===== References =====
* Appleby, A. B. (1980). The disappearance of plague: a continuing puzzle. The Economic History Review, 33(2), 161-173.
* Drancourt, M., Houhamdi, L., & Raoult, D. (2006). Yersinia pestis as a telluric, human ectoparasite-borne organism. The Lancet infectious diseases, 6(4), 234-241.
* Stenseth, N. C., Atshabar, B. B., Begon, M., Belmain, S. R., Bertherat, E., Carniel, E., ... & Rahalison, L. (2008). Plague: past, present, and future. PLoS medicine, 5(1), e3.