The Black Death: a New Approach
April Liske-Clark, Brendan Clancy, Katie O'Brien, and Rob Muollo
Advisor: Dr. Todd Livdahl
The Black Death, an epidemic that forever changed the Western
world, began in 1347 and continued for a full five years, sweeping
Europe, leaving in its wake more than twenty million people dead.
One-third to one-half of the European population was wiped out
(Duncan, 2006). Trade was the most influential factor in the quick
spread of the disease. It spread first through some of the biggest
trading cities of the time in Italy and France, followed by a
somewhat slower diffusion across the rest of Europe, until reaching
the Russian cities of Moscow and Kiev in 1351. Iceland, despite its
geographical isolation, was struck by the disease in 1402 during a
second outbreak of the plague in Norway.
Yersinia pestis, The Plague:
Yersinia pestis occurs in two predominant forms,
bubonic plague and pneumonic plague (Huang et al. 2006).
Bubonic plague is primarily transmitted to humans from
zoonotic reservoirs, usually oriental rat fleas, Xenopsylla
cheopis that have contracted Y. pestis from an infected wild
rodent. Under normal circumstances the X. cheopis would
not bite a human; however when the flea is infected with Y.
pestis its gut becomes blocked, starving the flea. This results
in the flea seeking out any blood meal source that it can
find, including humans (Eisen, 2006).
The spread of the Black Death across Europe
Modeling the System
The Perfect Storm Hypothesis
Bubonic Plague:
Day 1-2: Fever, headache, and fatigue, followed by
aches in the upper leg and groin, a white tongue, rapid pulse,
slurred speech, and confusion.
Day 3: Swelling of the lymph glands in the neck,
armpits, and groin occur, Bleeding under the skin follows,
causing purplish blotches. Dark-ringed red spots on the skin
from infected fleabites eventually turn black, producing
putrid-smelling lesions. Nervous system collapses.
Day 4-6: Symptoms worsen. Skin blackens, inspiring the
name “The Black Death” (Perlin, 2002).
Day 7: Death.
In order to test the validity of Y. pestis as the cause of the Black Death, using the software, STELLA, a model was
created illustrating the effect of the Black Death on a population, using rats as the required transmission factor (fig 1). As
can be seen in figure 2, the bubonic plague was followed by the pneumonic plague and only after the population had been
significantly lowered the plague subsided allowing the population to slowly grow again. These results were very similar to
that which was seen in England. For Iceland, there were no rats, meaning the bubonic factor had to be discounted, leaving
only the effect of pneumonic plague (fig 3). Although there were probably more, it effect on a population if only one carrier
of the pneumonic plague were to be involved was tested. Figure 4 shows that despite the lack of rats, a plague transmissible
solely from person to person is just as likely to similarly devastate a population, thereby proving rats were not a necessary
factor in the pandemic and that Y. pestis most likely caused the Black Death.
Model Parameters*:
Pneumonic plague:
Transmissible directly from person-to-person. Occurs
when bubonic plague travels from the lymph nodes to the
lungs were it can then be transmitted through the air (Gani,
2004). Symptoms are similar to pneumonia, and death is
almost certain (Center for Disease Control, 1996).
Human Population
Susceptible
- 100**
BR= birth rate - 3%
DR= death rate - 2.7%
Rate of infection - 1% sick rats x Susceptible***
~Bubonic infected reservoir~
Bubonic DR
- 90%
Recovery rate
- 5%
Respiratory infection
- 5%
~Pneumonic infected reservoir~
Pneumonic DR - 100%
Pneumonic transmission - 2%
Fig. 1 Ecological model illustrating the effect of Y. pestis on two
populations
Rat Population
Susceptible
- 1,000**
BR
- 100%
DR
- 50%
Rate of infection
- 1%***
~Bubonic infected reservoir~ begins at 50
Bubonic DR
- 100%
Fig. 3 Ecological model illustrating the effect of Y.pestis
on a population like Iceland
Case of Iceland
As there were no rats present the
influence of the Bubonic plague on the
population could not be accounted for
and therefore only pneumonic
transmission would have an effect. All
values remain the same except that the
starting population of Pneumonic
Infected is 1
Fig. 2 The effect of Y. pestis on a human population based
on the model
Figure 1: Y. Pestis Life Cycle
In recent years there has been disagreement over the epidemiology
of the Black Death. In late Medieval Europe they lacked medical
ability to properly diagnose disease, and we are therefore left with
little more than a list of common symptoms as well as the ecology of
the disease. It is widely held that the epidemic was caused by Y.
pestis with an emphasis on rats facilitating the spread. However,
records show that there were no rats present in Iceland until the 18th
century, thereby calling the bubonic plague hypothesis into doubt.
Fig. 4 The effect of Y. pestis on the population of Iceland based
on the model
*
These numbers are all based on data taken from the records of the time as well as information known regarding the ecology of Y. pestis.
**
Because there are so many other factors involved that a simple biological model cannot take into account, matching the human population exactly was
counterproductive and wouldn’t model the ecology as accurately as a relatively smaFig. 3 Ecological model illustrating the effect of Y. pestis on a population like
Iceland ll starting population would. The rat population (as well as death and birth rate) was decided with the idea that it was safe to say that for every person, there
was at least 10 rats that could have had sufficient contact with them. Also the lifespan of rats is significantly shorter hence the larger birth and death rates.
***
For a rat to become infected with the Y. pestis, it must be bitten by an infected flea. This was determined to be relatively unlikely so a 1% transmission rate
seemed appropriate. For a human to become infected, he or she must be bitten by a flea that has bitten an already infected rat in which Y. pestis has incubated. This
was also determined to be unlikely so it was determined that the infection rate of the plague was the amount of susceptible humans multiplied by 1% of the infected
rats.
The killing success of the Black Death was due, in
part, to several key social conditions including crowding,
famine, trade, and weather. During the years before the
plague Europe suffered a cooling period, which decreased
agricultural productivity causing widespread famine. By
the 14th century, trade kept the different kingdoms of
Europe in constant communication. Crowding and famine
would have primed a city for an outbreak of a disease by
leaving most of the population suffering from
malnutrition, making it vulnerable to an outbreak of any
major crowd disease.
While it can be argued that other diseases caused
the Black Death, it is generally accepted that Y. pestis, is
the culprit. Our models support Y. pestis as the cause of
the epidemic even in the absence of rats. However, the
disease itself was not solely responsible for the severe
death toll, as multiple social, political, and environmental
factors also played a role in making the population
vulnerable. Evidence also suggests that under the right
conditions in a crowded population, any disease with
similar modes of transmissibility and effects could have
had the same devastating effect.