Biology Reference
In-Depth Information
Access to medicines has become the test above all others by which the rich world
will be judged in its dealings with the poor.
285
Richard Horton
Scientific agreement about the imminent danger of an avian flu pandemic is almost as broad and all-en-
compassing as the consensus that humans are largely responsible for global warming. All the summit or-
ganizations responsible for world health, including the WHO and the CDC, have warned that the coming
viral hurricane might be even more deadly than the 1918 pandemic. The major dissenter to this view is
Amherst biologist Paul Ewald, a controversial advocate of “evolutionary medicine.” In his view, the lead-
ing influenza experts have failed to grasp elementary principles of viral evolution, especially “the selective
processes that favor increased or decreased virulence of virus strains.” The 1918 pandemic, in his view, was
a unique historical event whose catastrophic outcome depended upon the evolution of influenza virulence
in the extraordinary conditions of the Western Front. “Both theory and the evidence,” he claims, “implicate
the Western Front as the source of the epidemic.” Ewald doubts that environmental conditions so favorable
to the emergence of hypervirulence in influenza A will ever reappear. “We will fail to see,” he predicts, “a
recurrence of a pandemic influenza with the kind of lethality that characterized the 1918 pandemic.”
286
Some scholars, of course, would dispute that the virulent second wave of the 1918 virus originated in
France at all: Kansas, in fact, seems a better bet. Ewald also skirts over the geography of the great pandem-
ic, whose deadly epicenter was India, not the Western Front; nor does he engage theories about how malnu-
trition and malaria amplified influenza mortality. Still, Ewald may be correct that crowded Army training
camps, hospitals, and ships, as well as the trenches themselves, were the bellows that turned outbreak into
conflagration. The 1918 pandemic dramatically grew in virulence between its initial spring outbreak and
the deadly second wave in the early fall, so the key variables must have been crowded, often unsanitary
conditions with large concentrations of sick victims able to transmit an evolving virus quickly to distant
locations. Ewald calls such an environment a “disease factory.”
287
He might also have called it a slum.
The Western Front of the world's first industrialized war recapitulated much of the disease ecology
of the classic Victorian slum—the
locus classicus
of most discourse about infectious disease. In the nine-
teenth century, the great slums of Europe, America, and Asia had a total population of perhaps 25 mil-
lion; today, according to UN-Habitat, there are 1 billion slum-dwellers: a number expected to double by
2020. Is there any reason to assume that today's
bustees, colonias,
and shantytowns are any less efficient
“disease factories” than Victorian slums or crowded 1918 army camps? If, according to Ewald, the
sine
qua non
of a deadly airborne pandemic is “host density” in poor sanitary conditions, then—as
Table 12.1
shows—today's megaslums are just as fetid and overcrowded as any of their notorious Victorian prede-
cessors. With population densities as high as 200,000 residents per square kilometer, they offer perfect en-
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