Tambora: The Eruption That Changed the World (14 page)

CHOLERA AND CLIMATE CHANGE

Endemic cholera in Bengal had traditionally been associated with the “winter” months of November to January, with a smaller peak in the hot, dry months of April and May. The reach of the disease remained limited, in any given year, for the simple reason that it soon ran out of fresh victims. Explanations for the unprecedented epidemic outbreak in Bengal in 1817 depend upon the putative emergence of a new strain of cholera capable of bypassing the built-up immunity of its
indigenous hosts, then spreading rapidly to successive populations in various directions.
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Energized by its passage through the human intestine, the cholera microbe achieves a temporary hyperinfective state. Density of human traffic is thus essential to its continued transmission. Carrying the fatal microbe with them in their bowels, soldiers, pilgrims, and traveling merchants in 1817 dispersed the infection to unsuspecting fresh host communities north and west across India. In the following years and decades, these same human vectors, following the webs of global trade, brought cholera southeast to the Dutch Indies and East Asia, and northwest across the great trading routes of Arabia to Russia, Europe, and finally the Americas. The eventual global death toll of nineteenth-century cholera stands in the tens of millions.

The “father of British medical writers on cholera,” Calcutta physician James Jameson, traced the cause of the 1817 cholera to abnormalities in the Bengal climate in the two-year period leading to the outbreak. His classic 1820 report to the Calcutta Medical Board includes a ninety-page prefatory description of the “distempered” state of the weather beginning in late 1815. By attributing the outbreak of cholera to meteorological causes, Jameson placed himself within an established tradition of environmentalist medical theories dating back to the Hippocratic revival of the late seventeenth century. The pathogens of disease, whether produced by the noxious exhalations of the Earth or the “vitiated” state of the atmosphere, were airborne. The Indian cholera, Jameson concluded, had been spread by the strangely humid atmosphere, drought, and unusual winds of 1816–17. With its detailed synoptic data—based on one hundred survey reports from physicians across British India—Jameson’s report is a landmark in medical and public health literature and was the most quoted text by English writers on cholera for decades.

Already by the Tambora period, however, debates over the etiology of cholera were shifting. In subsequent decades, a new legion of medical theorists of cholera would come to reject Jameson’s meteorological emphasis in favor of an emerging liberal paradigm that captured the imaginations of progressive physicians and public officials through the Victorian age. Infectious disease was not “natural” but rather the product
of human-created filth, of the open sewers and fetid air of slums and industrial tenements. Cholera was a social disease, an index of failures by nation-states to regulate and sanitize their colonial ports of trade and booming industrialized cities. In the pulpits of Europe, the cholera would accordingly change shape from a divine punishment for wickedness to a progressive moral calling for social reform, to provide hygienic living conditions for the newly urbanized masses.

Thus the early climatological theories of cholera rapidly lost ground during the heroic age of nineteenth-century sanitarianism. For almost a century after the apparently definitive discovery of the comma-tailed cholera bacterium in a Calcutta pond by pioneer bacteriologist Robert Koch in 1883, both clinical theory and public health policy surrounding the disease endorsed the emerging contagionist consensus, focusing on its human-to-human transmission. The fecal matter of infected persons in waterways was simply the pathogen’s mode of transit from one human host to another, which might be denied by proper investment in sanitary engineering. This dominant model of twentieth-century cholera science relegated Jameson—and a host of other pre-Victorian writers in the medico-meteorological tradition—to the dustbin of history, as embarrassing examples of the puffed-up guesswork and shamanistic fantasies that passed for medical science before the discovery of bacterial infection. Jameson’s enlightenment medical geography, with its environmentalist perspective on disease transmission, had lost the battle of ideas, which resolved by century’s end into a narrower medical-scientific practice focused on the career of pathogens, to be charted by the new techniques of laboratory biology.

Now, however, at the beginning of the twenty-first century, the medico-meteorological worldview of James Jameson has experienced a second coming. The post-Victorian bacteriological consensus on cholera has been overtaken by a new, more complex etiological paradigm that restores credibility to the early nineteenth-century model of climatic disease dynamics. Beginning in the late 1960s, epidemiologists utilizing the tools of modern molecular biology discovered the
vibrio cholerae
thriving in nonendemic form among the zooplankton and protozoa of a wide range of aquatic environments—from the Chesapeake Bay to
the lochs of Scotland—independent of human hosts. Not the “Asiatic” cholera after all! Nor are humans the end point or object of the cholera. We are merely accidental part-time hosts to a pathogen that enjoys ancient privileges in a range of aquasystems outside the human intestine. From its ancestral origins in the deep sea, the
v. cholerae
resides year-round in brackish reservoirs around the globe, while its pathogenic strains are favored only within dense human communities situated at low elevation along estuarine coasts, in tropical climates characterized by high temperatures, humidity, and heavy seasonal rain.
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To succeed in this global role, the cholera bacterium possesses an unusually flexible and adaptive genetic structure highly sensitive to changes in its aquatic environment. In the monsoonal waters into which the five major rivers of the Ganges delta flow, the
vibrio cholerae
prospers by attachment to benign organic hosts—plankton, algae, crustaceans, and even tiny insects—where they participate in the mineralization of matter vital for the replenishment of the aquatic food web. The circulation patterns and organic life cycles of the northern Indian Ocean are unique on account of the monsoonal climatic regime. Over the Bay of Bengal in June and July, the water vapor content of the atmosphere reaches its highest level anywhere 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 phytoplankton 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 seasonal 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 published in 2000.
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Since then, investigations of cholera genetics have drawn the outline of an evolutionary narrative for cholera, by which the post-1817 pathogenic strains of the bacteria separated themselves from their benign or strictly endemic marine ancestors.

In a series of articles, University of Michigan ecologist Mercedes Pascual has explicitly revisited 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 understanding of “the influence of climate on disease dynamics.”
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Pascual’s theoretical ecology 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 salinity 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 meteorological 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 generation 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 conditions, 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 ecology 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 flooding 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 surface. 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 and his waste finds its way back to the water sources of the community, the stage is set for cholera to rise up from the waters in its ghoulish mortal shape.

In short, cholera outbreaks are climate driven, and cholera is a climate change disease. In our Tambora case study, droughts
and
floods—twin climatic extremes characteristic of the 1815–18 period in Bengal—provided hospitable conditions for the emergence of a new epidemic strain of cholera, with devastating global consequences. The sustained weather anomalies in Tambora’s wake impacted, by the physical laws of teleconnection, molecular processes in faraway Bay of Bengal. The long-forgotten “father of cholera science,” James Jameson, was thus right to contemplate the distempered skies over Bengal when charged with reporting on the 1817 cholera epidemic for the Calcutta Medical Board. Because of his meticulous record keeping, we are able to reconstruct the deteriorated monsoonal conditions in South Asia in the aftermath of Tambora. And with India’s Year without a Monsoon brought into focus, the vision of a nineteenth-century world shaped by climate-driven epidemic cholera emerges for the first time. Tambora’s Frankenstein weather, wild and weird, created a microbial time bomb in the waters of the estuarine Bengal delta. Once exploded, life on Earth, at least for human beings, became a far more dangerous proposition.

CHOLERA GOES GLOBAL

In the years after the 1817 epidemic, of course, none of this was known, which made the mysterious new global scourge all the more terrifying. The disease soon confounded the Jameson school of medico-meterological scientists, since cholera declared itself at home across multiple latitudes and climatic zones. In 1819–20, the epidemic retraced the path of Tambora’s volcanic plume southeast across Burma and Siam (Thailand), where cholera’s victims clogged the rivers and canals of Bangkok, plunging the kingdom into crisis. From there the epidemic spread to Java, where Tambora’s curse performed a kind of tragic second coming, killing an estimated 125,000 people, more than died in the volcanic eruption itself.