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in the world. The prevailing winds reverse twice annually, churning up the waters of the bay,
while the summer rains create a vast freshwater runoff from the rivers. Mile-wide phytoplank-
ton blooms, on which great colonies of
v. cholerae
depend, surface at the river mouths and
glide along the coast by the East India coastal current according to a distinct but variable sea-
sonal pattern that drives the bay's dynamic interaction with the cholera microbe.
Answers to the question of why a new and deadly cholera strain developed in Bengal in
1817 had been mostly speculative until the complete sequencing of the cholera genome was
an evolutionary narrative for cholera, by which the post-1817 pathogenic strains of the bac-
teria separated themselves from their benign or strictly endemic marine ancestors.
In a series of articles, University of Michigan ecologist Mercedes Pascual has explicitly re-
visited the early nineteenth-century debate between meteorological and contagionist theories
of cholera, proposing to “integrate” them and thereby return medical science full circle to an
logy of cholera has shown “interannual variability” of climate—that is, weather anomalies
such as drought, flood, and unseasonable temperatures—to be a strong driver of outbreaks.
In addition to threatening the security of water infrastructure, excessive rainfall alters the sa-
linity levels of water and promotes the growth of nutrients conducive to bacterial production.
Conversely droughts, by increasing the temperature of reduced standing bodies of water and
concentrating the bacterial population, also promote disease transmission.
Fellow cholera epidemiologist Rita Colwell has likewise singled out extreme meteorolo-
gical events, with their impacts on water temperature, salinity, and conditions of flood or
drought, as capable of both amplifying transmission of cholera and producing the nonlinear
transformation of organic pathogens into new and potentially deadly forms. For the new gen-
eration of cholera epidemiologists, such as Pascual and Colwell, the trigger for cholera is thus
climate, specifically climate
change
. Lateral genetic transfer, by which the cholera bacterium
is modified by foreign elements, is promoted by changes in environment—in the temperature,
salinity, and alkalinity of the aquatic habitat.
If a cyclical meteorological event such as an El Niño is capable of amplifying cholera con-
ditions, as Pascual has shown, then a truly bizarre monsoonal anomaly such as the Tamboran
Asian weather regime of 1815-18 would certainly have been sufficient for the evolution of a
new microbial strain. In 1817, the aquatic environment of the Bay of Bengal had deteriorated
radically owing to the disrupted monsoon, a consequence of Tambora's dimming presence in
the stratosphere. By a process that remains mysterious in its details, the altered estuarine eco-
logy then stimulated an unprecedented event of genetic mutation in the ancient career of the
cholera bacterium.
From this point the cholera's path is chillingly clear. Changes in water temperature and
salinity promote the bloom of zooplankton, the cholera's main aquatic host, while flood-
ing dredges up deep-welling nutrients and transports the pathogen into the water system of
coastal human communities. Barely above sea level, the waterways of the Bengal delta ebb
and flow with the tides of the bay. If changes in rainfall patterns drive sea levels higher, bay
waters ooze and swell inland, infiltrating the ponds and tanks dedicated to human use. The
mix of fresh and salt water keeps the plankton blooms, and their bacterial tenants, at the sur-
face. From there, the
v. cholerae
is but a cup of water, rice pot, or shellfish meal away from
colonizing its first human victim. And if that first host is tended to in unsanitary conditions
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