Epilogue• 281A possible explanation is that rats have a habit of going back to their nests
when they become ill. The Pasteur Institute’s researchers, from Henri Molla-
ret to Elisabeth Carniel, have emphasized this characteristic. Dead rats in
the alleys and cellars of London in 1665 may not have been present in suffi-
cient number to capture people’s attention. The ratcatcher, after all, was a
regular feature of this society; rodents abounded, and some of them turned
up dead. Charles I’s French physician Theodore Mayerne voiced a rare suspi-
cion of a connection between rat and pestilence. Most people pointed to live
dogs and cats prowling the city streets as the most likely animal carriers of
the disease.
Two British historians and an anthropologist from the United States
argue that the Black Death spread too rapidly across Europe to have been
dependent on rats for dispersal.^36 Perhaps they have not considered fleas on
travelers’ clothing as a likely medium for the plague’s rapid advance. Medical
observers in 1665 knew nothing of the etiology of plague. Yet they suspected
that the disease entered a community frequently on cloth and clothing, espe-
cially light-colored material, which is particularly attractive to fleas. This not
only fits with the role of fleas as a vector of the disease but helps to explain
how plague could travel great distances and strike persons at places, like
Eyam in Derbyshire, that were remote from the source of infection.
Some Yersinia pestisskeptics look to the temperature charts of the mid–
seventeenth century and say that it was too cold for the rat flea,Xenopsilla
chopsis,to be a key link in the chain causing a human plague epidemic.^37 In
response, continental European researchers suggest that human fleas played a
crucial role during this period. They argue that the human flea,Pulex irritans,
could withstand the temperatures of early modern Europe’s Little Ice Age.
These fleas could have spread the disease from person to person and did not
need rats as a source of the plague bacillus once it entered the human arena.
Many researchers, however, point out that P. irritansis not a good vector.
At least at the beginning and through much of the Great Plague of 1665 ,it
seems likely that an epizootic in rats caused by bites from infected rat fleas
was needed for the human epidemic. Rats in the “pestered places” of Lon-
don’s poor attracted infected rat fleas, which may have come by a cargo ship
from an infected port. The fleas could have survived in the warmth of the rat
habitat. It follows logically that, when rat die-off began in the late winter and
early spring of 1665 , isolated cases of human plague followed. An occasional
infected flea, ravenous after its proventriculus (the pouch of the esophagus
leading to the midgut) became blocked with bacteria, searched for a warm-
blooded meal. These fleas, in a feeding frenzy, abandoned dead rats and went