282 • The Great Plaguelooking for the closest warm body. Thus an epidemic began. When the rats
started dying in large numbers, the plague mortality in humans shot up as
the secondary human host alternated with the primary one.^38 This chronol-
ogy fits the early stages of Great Plague mortality.
One last point about the causal organism concerns the multiple diseases
reported at the time of the Great Plague.^39 Certainly, there were cases of
smallpox at the beginning and perhaps other diseases as well. Since the mor-
tality curves of all nonplague diseases reported in 1665 mirror the distinctive
plague death curves, as shown by graphs, it seems obvious that the parish
clerks and searchers frequently listed plague as other diseases. This side-
stepped quarantine and masked the enormity of a crisis that left uncounted
victims dead in the streets.
As medical science now understands it, plague in humans usually begins
with infective fleas piercing the skin. Fleabites are known to regurgitate
25 , 000 to 100 , 000 bacilli into the victim’s tissue.^40 With radarlike certainty
these invading microbes attach to approaching white blood cells that have
been alerted by chemicals released from the invaded tissue at the site of the
injection. The people of 1665 could not have seen this first stage of a battle
royal within the body, but they did see the resulting tokens that accounts de-
scribed as resembling fleabites.
What happens next could be neither seen nor imagined by the humorally
centered medicine of 1665 , though Fracastoro’s invading seedlets of disease
and the body’s sentinel-like archeus imagined by Thomson vaguely fit the
two sides of the microscopically detected battle: the microbes and the body’s
defense system. Among the first white cells to arrive at the site of the invasion
are large macrophages from the blood, lymph, or tissue. These baglike cells
are phagocytic—that is, they engulf the bacteria and release killing enzymes.
The plague bacillus, in turn, has two avoidance mechanisms: antiphagocytic
surface molecules and a capsule that prevents destruction by cellular en-
zymes.^41 Protected by these two defenses, the plague bacteria proliferate and
turn the macrophages into centers of multiplying Yersinia pestisorganisms.
Other white cells (T cells) carry the infected macrophages through blood ves-
sels or tissue to the nearest lymph nodes, where more white cells try to de-
stroy the organisms.
At this point in the battle within the human body, the physicians in 1665
picked up the external signs again. They could see the protruding buboes and
observe the victim’s excruciating pain as the parasitic bacteria and host blood
cells proliferated rapidly there,causing the nodes to swell. The buboes are