280 • The Great Plague1665 would fit a present-day diagnosis. Their external observations mirror
with considerable precision what was happening internally. Their greatest
contribution is letting us know that the disease’s pathology has not funda-
mentally changed during a long history.
What has fluctuated over time is the plague bacillus’s cohabiting relation-
ship with vector fleas, primary host animals, and incidental human hosts.
The result has been an ebbing and flowing of plague in the human popula-
tion. This is partly explained by the plague genome’s elasticity; it can inte-
grate small snips of foreign or rogue DNA, called plasmids, which have infil-
trated the bacterial DNA. Some added pieces of DNA increase the bacilli’s
virulence, and other plasmids give adaptability to insect vectors. These snips
of DNA are so well integrated that researchers can’t distinguish them from
the rest of the Yersinia pestisgenome.
The role of the black rat poses the most problematic link in the chain of
human plague infection. Rats were virtually unmentioned in 1665 , yet they
were presumably the primary hosts of fleas searching for a warm bloodmeal.Fig. 16 .Plague victim with bubo on the neck, detail of Saint Sebastian Intercedes dur-
ing the Plague,Josse Lieferinxe, 1497 – 99. This fifteenth-century artistic rendition of a
plague scene, featuring Saint Sebastian as a spiritual consoler and aid to the victims,
displays on a victim’s neck the bubo swelling of the lymph nodes that has been the
most common identifying sign of plague since the Black Death. Other diseases can
also cause this swelling but without the other common body signs and symptoms and
high mortality rate characteristic of plague.The Walters Art Museum, Baltimore