Skip To Content Skip To Left Navigation
NSF Logo Search GraphicGuide To Programs GraphicImage Library GraphicSite Map GraphicHelp GraphicPrivacy Policy Graphic
OLPA Header Graphic

Dr. Colwell's Remarks


"The Spiral of Complexity: Connecting Climate and Health"

Dr. Rita R. Colwell
National Science Foundation
Lecture at the Royal Swedish Academy of Sciences
Stockholm, Sweden

October 23, 2002

See also slide presentation.

If you're interested in reproducing any of the slides, please contact
The Office of Legislative and Public Affairs: (703) 292-8070.

Good evening, President and members of the Academy, and ladies and gentlemen. Thank you, Professor Carlsson, for a kind introduction. It is an honor to have the opportunity to speak to you and I would like to thank the Royal Swedish Academy of Sciences for this invitation. My links to Sweden go back many years. It is a pleasure to see old friends here in Stockholm.

Science and engineering have always flourished across national borders, but the global scale of research in the 21st century is unprecedented. As research grows increasingly interdisciplinary, more scientific questions cross national borders. Such is the case with the study of climate and health. Both are global phenomena, and for the first time, we can begin to look at them from a global perspective and explore their linkages through many dimensions.

Science of today's breadth and depth calls for new frameworks. The framework I wish to explore today is called biocomplexity. This is a way of thinking about the relationships between life and its environment that has emerged from a lifetime of research examining the complex interactions between climate and health.

[first slide: title slide: The Spiral of Biocomplexity]
(Use "back" to return to the text.)

Biocomplexity denotes the study of complex interactions in biological systems, including humans, and their physical environments. Ecosystems do not respond linearly to environmental change, nor do the pathogens that live in them. Here, I use the form of a spiral, so symbolic of life at every level, to underscore the point that understanding demands observing at multiple scales, from the nano to the global.

[new biocomplexity slide]
(Use "back" to return to the text.)

The spiral of complexity begins to unfurl at the most minute scale of the atom, and curves up through successive levels of life, through the cell, the organism, the community, the ecosystem. Complexity principles emerge at each level. With the perspective of biocomplexity, disciplinary worlds, formerly discrete, intersect to form fuller, more nuanced viewpoints.

Much of modern science, up to now, has followed a reductionist approach. We have sought understanding by taking things apart, and this has been a dominant trend in medicine and health as in many disciplines. This approach has given us the lion's share of scientific knowledge to date. Now we're ready for a new perspective that integrates across disciplines and scales, a perspective that roots epidemiology firmly in ecology. The spiral of complexity curves both ways--outward, integrating the levels of life, and inward, back to the center.

Patterns, like the spiral, draw scientists and artists alike. "Patterns are often coded messages," notes Horace Freeland Judson in his book, The Search for Solutions. "Once the key is discovered, the pattern can be read like a story."

Biocomplexity reaches beyond the scope of ecology, linking the molecular level to forces operating at the planetary scale, such as climate. It encompasses time as well. Biocomplexity also differs from biodiversity. We recognize that to stem the loss of diversity, we must understand how it functions.

Biocomplexity is a 21st century term, because only now do we have the tools to sharpen our vision at the smallest and largest scales. These tools--optics, sensors, remote sensing, nanotechnology and information technology, among them--let us take the measure of the breadth and depth of life on our planet.

[Emerson quote against spiral backdrop]
(Use "back" to return to the text.)

What is the lineage of biocomplexity as an idea? American essayist Ralph Waldo Emerson wrote, "Certain ideas are in the air. We are all impressionable, for we are made of them; all impressionable, but some more than others, and these first express them. This explains the curious contemporaneousness of inventions and discoveries. The truth is in the air."

Looking back to the 1990s, biocomplexity indeed seemed to be "in the air." It was defined and selected as an initiative for the National Science Foundation in 1998 when I arrived at NSF. For the tracing of biocomplexity's antecedents, I would like to thank Bruce Heyden, formerly of NSF.

[UNEP defn]
(Use "back" to return to the text.)

An international root of the biocomplexity concept traces to 1995, to the United Nations Environment Program, which conceived of the concept as "biodiversity within an ecosystem and social systems context," and critical for sustainable development.

[Dutch definition of biocomplexity]
(Use "back" to return to the text.)

In 1996, the Netherlands Organisation for Scientific Research held a symposium on "Biocomplexity and the Essence of the Living State." The organizers defined biocomplexity as "the difference between any integral biological system and the sum of its components," and called for concepts to describe how the living cell emerges from molecules.

[NIH biocomplexity]
(Use "back" to return to the text.)

Another root traces to the U.S. National Institutes of Health, which convened a workshop in 1997, described in a workshop report in 1998, on complex biological processes. The concept reached only to the level of the organism at NIH. The report noted that individual parts did not account for the behavior of the whole, and called for predicting the behavior of complex phenomena across dimensions.

(Use "back" to return to the text.)

Biocomplexity as we define it, from atoms to the planetary level, is now a priority research area at the National Science Foundation.

Here is an example of a biocomplexity study we support--work by Richard Lenski of Michigan State University and his team, which includes a microbiologist, computer scientist and physicist. They study how biological complexity evolves using two kinds of organisms--bacterial and digital.

Here, the two graphs show the family trees of digital organisms--artificial life--evolving over time.

On the left, the digital organisms all compete for the same resource, so they do not diversify and the family tree does not branch out. On the right, the digital organisms compete for a number of different resources, and diversify.

In the background are round spots--actually laboratory populations of the bacterium E. coli, which also diversified both morphologically and metabolically over time when fed different resources. In vivo derives insight from in silico, in this instance.

[Endosymbiosis/Battacharya 1: dinoflagellate bloom in St. Lawrence River and haptophyte bloom]
(Use "back" to return to the text.)

Here is another complex mystery with global implications that has been unlocked with the small-scale key of genomics. It involves two species of microorganisms that are of economic and ecological importance. On the left is an aerial view of the St. Lawrence River in Canada, with the purplish color of a harmful algal bloom circled, caused by the dinoflagellate Alexandrium, which is shown in the slide. This bloom results in paralytic shellfish poisoning and has cost millions of dollars in lost revenue.

On the right, encircled, is an algal bloom of another organism, a haptophyte. Inset is a close-up of Emilinia, an open-ocean organism that is a major sink for carbon on this planet and, therefore, of interest in global climate research. Genomics has revealed that these two organisms have an unexpected relationship.

[Endosymbiosis/Bhattacharya 2: primary, secondary, tertiary]
(Use "back" to return to the text.)

The story involves endosymbiosis, the process in which one cell engulfs and captures another, free-living cell. The process turns out to have unexpected significance in evolution.

The cartoon at left shows primary endosymbiosis: the yellow cell engulfs a green cyanobacterium which is destined to become a plastid, resulting in the first alga.

Next, in the center, the same cell, the alga, is itself engulfed by a non-photosynthetic protist. Such a process gave rise to the haptophytes and the dinoflagellates.

At right is the third step: tertiary endosymbiosis, in which the dinoflagellate has engulfed a haptophyte. The unexpected discovery is the relationship between these two important organisms--the haptophyte contributed genes to the dinoflagellate. This is the work of a team led by Debashish Bhattacharya of the University of Iowa.

Genomics has unraveled this bewildering pedigree of complexity-within-complexity, the record of each genetic engulfment nested within the next, like a series of Russian dolls. Such processes are now thought to have generated much of the variation in life on our planet.

The lens of biocomplexity helps to focus on the links between climate and health in another case. Biocomplexity's perspective was critical to solving a mystery that began in 1993 in the Four Corners area of the United States, when young and otherwise healthy people began dying from an unknown disease.

The culprit turned out to be a Hantavirus unknown in the New World until the outbreak. The mortality rate of those infected with the virus--more than 50%--is second only to Ebola. Was the new virus a mutant, or had the environment been harboring it all the time?

The carrier turned out to be a rodent, the deer mouse pictured here. Biologists working at an NSF-supported Long-Term Ecological Research site, led by Terry Yates of the University of New Mexico and his team, were able to detect the deadly virus in mouse tissue that had been archived years before. As it happened, Native American legends corroborated a history of outbreaks.

In addition, the investigators showed a link between climate and the outbreak of disease. Mild and wet winters associated with a periodic climate pattern, El Nino-Southern Oscillation, had provided more food for the rodents, whose populations had increased dramatically in 1993.

[global spread of cholera-recent]
(Use "back" to return to the text.)

I turn now to the central focus of my talk: my own research on cholera as a case example for the interrelationship between climate and health.

Cholera is an excellent example of how investigation of environmental factors--climate foremost among them--gives a clearer picture of a disease, from virulence to transmission to epidemiology.

Cholera has plagued humankind since ancient times, but is still very much with us today, as this global perspective shows. Cholera occurs worldwide, and is a major public health problem in more than 75 countries in Asia, Africa and South America. We are still in the seventh pandemic, which has persisted, unlike earlier epidemics, for more than 40 years.

[pictures of Bangladesh people]
(Use "back" to return to the text.)

Cholera remains a major public health problem, causing significant mortality wherever it arises--despite the fact that it is simple and inexpensive to treat, if committed health workers and adequate medical supplies are available.

Many factors combine to create outbreaks: poor sanitation, lack of clean water, wars, and economic displacement. Those who live near water, especially along a seacoast, are most at risk.

[Cholera statistics, WHO, 2000]
(Use "back" to return to the text.)

As you know, cholera is still a deadly scourge in developing countries. The latest numbers of cholera cases from the World Health Organization are for the year 2000: 137,071 cases and almost 5,000 deaths. But note that those figures don't include Bangladesh, Pakistan, both North and South Korea, and several other countries, whose aggregate numbers may equal those reported for the rest of the world, shown in this slide.

To give an idea of possible worldwide totals, especially during epidemics, a representative year is 1991, when more than 200,000 cases were counted in three months in Bangladesh alone. From August through November of that year, a thousand cholera victims entered the hospital daily in Dhaka, Bangladesh.

[old map of cholera from medical textbook]
(Use "back" to return to the text.)

Sanskrit records from the 5th to 6th century B.C. describe a disease like cholera. Other records in Greek and Sanskrit, 2000 years old, also describe cholera-like diseases. Cholera's "traditional home" has been the Ganges Delta and Southeast Asia, and we know that cholera existed on the Indian subcontinent centuries before Europeans arrived. Cholera has determined the course of wars.

It actually may have emerged in its violent epidemic form in the 19th century; the first pandemic of cholera began in 1817.

[Cartoon: "death" with pump]
(Use "back" to return to the text.)

The second pandemic spread from Russia, to the Americas, and then reappeared in London. Here a landmark advance in epidemiology occurred. John Snow, an obstetrician to Queen Victoria, suspected that cholera was spread by contaminated water--specifically from a contaminated public pump on Broad Street.

[Snow's map]
(Use "back" to return to the text.)

In the first use of epidemiological data to identify a specific cause of a disease, and to recommend a specific remedy, Snow plotted the occurrence of epidemiological deaths, showing that they clustered around the pump. Here is a crystal clear example of how pattern can lead to discovery.

[Picture of cholera bacterium]
(Use "back" to return to the text.)

Italian scientist Filippo Pacini first described the cholera bacterium in 1854. However, he was ignored because at that time the germ theory of disease was not yet accepted.

[new Koch quote slide]
(Use "back" to return to the text.)

German physician Robert Koch redefined the bacterium as the causative agent of cholera and isolated what he called "V. comma" --because of its curved shape-- in pure culture in 1883. Koch's speculation, as seen here in his words, was prescient.

"I am not a supporter of the exclusive drinking water theory," he said. "I think that the ways in which cholera can spread in a place are extremely diverse, and...almost every place has its own peculiar conditions..." Nonetheless, for a hundred years, it was not considered possible for cholera to survive longer than a few hours outside the human intestine.

[intestinal chemistry diagram]
(Use "back" to return to the text.)

It wasn't until 1959, more than 140 years after the beginning of the first pandemic, that an Indian scientist, Sambhunath De, discovered and described the Vibrio cholerae toxin.

The production of this toxin by the bacterium changes the permeability of the cell membrane in the intestine of infected individuals, enabling secretion of massive amounts of water and electrolytes into the lumen of the intestine. If these fluids and electrolytes are not replaced rapidly, death follows.

Although not all members of the genus Vibrio produce toxins, many do. Twelve of the 30 known species of this bacterial genus cause human diseases.

Today we can bring ecological insight to such questions as: Why is the history of cholera so elusive? Why have pandemic strains naturally disappeared, and been replaced by others? How might we predict a coming epidemic or pandemic?

I would like to take us briefly to Bangladesh, where cholera is endemic, using a brief video. The video, please.

[Modified and shortened Bangladesh video: TRT 1:27]video not available

[Biocomplexity spiral with molecular level highlighted]
(Use "back" to return to the text.)

Today we are beginning to trace the spiral of complexity that surrounds the mystery of cholera, yielding insights from the smallest to the largest scale. Solutions also rest upon the integration of research from across the disciplines of science and engineering. Let us begin with insights from the smallest scale.

[picture: life at undersea vent]
(Use "back" to return to the text.)

Where did cholera come from? The requirement of Vibrio cholerae for salt to grow led us to suggest that its ancestral home is the sea. Genomics has helped to substantiate this theory.

Here is a community of life around a deep-sea vent. The isolation of the genus Vibrio from deep-sea hydrothermal vents was first reported in 1981. Vibrio species have also been found in a variety of deep-sea habitats.

[East Pacific Rise: map]
(Use "back" to return to the text.)

In 1999, during dives by the submersibles Alvin and Nautile, sulfide chimneys were collected from undersea hydrothermal vents on the East Pacific Rise. Vibrio species isolated from the chimneys were identified that bore significant similarity to Vibrio cholerae, suggesting that it is autochthonous, or native, to the deep sea. V. cholerae may well serve important functions in ocean ecosystems, such as chitin digestion and nitrogen cycling.

[Doolittle family tree]
(Use "back" to return to the text.)

Here is another strand supporting cholera's deep-sea ancestry, from the research of Yan Boucher and Ford Doolittle of the Canadian Institute for Advanced Research and Dalhousie University.

I show here a simplified version of their phylogenetic tree of genes coding for a key enzyme in certain metabolic pathways; it shows that "V. cholerae always groups with the archaea..." Archaea are microorganisms associated with hydrothermal vents. The researchers theorize that an ancestor of V. cholerae acquired material from an archeon through lateral transfer.

[small chromosome]
(Use "back" to return to the text.)

In 2000, the genomes of the two chromosomes possessed by V. cholerae were sequenced. The discovery of two chromosomes was interesting, because bacteria were presumed to have a single chromosome. Both chromosomes are necessary for metabolism and replication.

[Large chromosome]
(Use "back" to return to the text.)

The toxin genes, of which there are fifty, reside on the large chromosome. The sequencing data confirm that V. cholerae is a versatile organism, able to live in several habitat types, as well as to infect the human gastrointestinal tract.

As S. Sozhamannan and others have reported, Vibrio cholerae has a gene acquisition system located on its small chromosome as well as hot spots for DNA rearrangement. Lateral transfer of genetic material is clearly occurring in this organism.

[spiral with organism level highlighted]
(Use "back" to return to the text.)

Moving up the spiral of complexity to the level of organism lends insight into the remarkable capacity of V. cholerae to evolve. V. cholerae's classical serogroup 01 caused the sixth pandemic. However, in the seventh pandemic, the El Tor biotype--the same as the classical 01 genetically, but new in physiology and pathogenicity--emerged and replaced the classical form.

[graph of % of cholera cases in age classes caused by 01 versus 0139, from Sack et al. paper]
(Use "back" to return to the text.)

Now, there has been another development. Since 1992, a new serogroup, 0139 Bengal--different from 01--has caused explosive outbreaks in the Bay of Bengal region.

We can see by this graph of cholera cases in Bangladesh that serogroups 01 and 0139 affect people of different ages differently. 01 afflicted significantly more younger patients, while 0139 afflicted mainly older people.

0139, the new serogroup, acquired novel DNA. Before this, non-01 serotypes were not known to cause diarrhea epidemics.

This is a significant turning point in the history of cholera because the strain arose from genetic recombination and horizontal gene transfer--the acquisition of unique DNA through introduction of a block of foreign genes.

A serotype that does not cause epidemic cholera picks up toxin genes from other cholera bacteria in its environment. This complicates understanding the genetics of cholera, yet makes it a very versatile organism.

[pic of VBNC cholera]
(Use "back" to return to the text.)

A major insight from the organism level of complexity is the discovery that pathogens can exist in a viable state even though they cannot be cultured. Here we see actual Vibrio cholerae that are in that state.

[List of VBNC organisms]
(Use "back" to return to the text.)

This list gives a quick glimpse of pathogens in which the "viable but non-culturable" phenomenon has been studied, from E. coli to Helicobacter pylori (the cause of ulcers), to Legionella and Salmonella.

[Chesapeake Bay sampling sites]
(Use "back" to return to the text.)

In the 1970s, my students and I discovered that the ocean itself is a reservoir for V. cholerae, when we identified the organism in water samples from the Chesapeake Bay off the coast of Maryland and Delaware. You see some of our regular sampling sites here.

Earlier detection methods for V. cholerae were developed strictly for testing clinical, infectious samples. In environmental samples, V. cholerae is more difficult to detect. The organisms may be more dispersed in the water and they may be dormant--not actively metabolizing, viable but non-culturable.

Most recently, we have used molecular genetic methods--PCR and gene probes--to detect Vibrio directly from environmental samples, confirming earlier immunofluorescent-detection results employing monoclonal antibodies.

We also know that cholera in its non-culturable but viable state can revert back to being culturable and infectious, not only in the environment but also after passage through the human gut. Now we seek to better understand the genetic regulation controlling passage into and out of the "somnolent," viable but non-culturable state.

[spiral with habitat highlighted]
(Use "back" to return to the text.)

Moving up the complexity spiral to the levels of population and habitat, we trace the ecological interactions of V. cholerae populations in two distinct habitats: the human intestine and the aquatic environment.

It turns out that the populations of toxigenic V. cholerae, whether in the environment or the gut, are genetically the same.

Rapid transfer of microorganisms between habitats, or the mingling of clinical and environmental strains, produces a dynamic equilibrium, as evidenced by data published in the October Proceedings of the National Academy of Sciences.

However, spatial and temporal fluctuations in the composition of toxigenic V. cholerae populations in the environment can alter disease dynamics. Such genetic fluctuations of cholera bacteria in the environment can be caused by seasonal change, microevolution, or introduction from elsewhere.

We hypothesize that the dynamics of V. cholerae populations in the aquatic environment contribute significantly to the variation in cholera epidemics.

Recent research by Andrew Camilli and colleagues, reported in the journal Nature this June, even suggests that when V. cholerae passes through the human gut, certain genes appear to greatly accelerate their activity--becoming up to 700 times more infectious than control bacteria.

[copepod cartoon]
(Use "back" to return to the text.)

As the film clip explained, cholera's ecology is intimately linked with the copepod, a microscopic relative of shrimp. This animal lives in rivers and salt or brackish waters, and travels with currents and tides. We first reported the association of vibrios with zooplankton in 1973, and with copepods, in particular, in 1983.

Copepods harbor both dormant, or nutrient-deprived, and culturable vibrios. The bacteria can survive as an inactive, spore-like form--the viable but non-culturable state--in the gut and on the surfaces of the copepods between epidemics.

[copepod with egg case]
(Use "back" to return to the text.)

This copepod is a female whose egg case, on the left, is covered with vibrios. V. cholerae colonizes the oral region and egg sacs of copepods. The oral location probably reflects the normal ingestion of bacteria as a food source, but the egg sac substrate is more intriguing.

Our hypothesis, in fact, is that cholera originally evolved commensally with marine animals such as copepods, which provided them a surface to grow, nutrition and perhaps other mutual benefits.

One such advantage is that as the copepod egg sac ruptures in the water, the cholera bacteria are dispersed with the eggs. In turn, the copepod or other hosts may benefit from the ability of vibrios to break down protein--that is, the possession of a powerful protease--in rupturing the egg sac.

Vibrio cholerae is part of the natural flora in the gut of zooplankton whose exoskeletons are chitin, like the copepod. It is also present in shellfish such as crabs, shrimp, and crayfish. As shown in the 1970s by our group and others, V. cholerae secretes a powerful chitinase, an enzyme that breaks down the chitin molecule, which assists its growth on chitin surfaces.

[new/old figs from Colwell and Kaneko]
(Use "back" to return to the text.)

In the early 1970s, we found that the efficiency of adsorption of a Vibrio species depends on pH and on the concentration of other seawater ions. The graph shows how adsorption percentage of Vibrio varies as pH increases.

The data in the table illustrate how different species of microorganisms vary in their ability to adsorb onto chitin by digesting the chitinous exoskeleton. The extent of adsorption also varied with salinity.

The top of the table shows--for various species--the numbers of free bacteria remaining in a 1% NaCl solution after exposure to chitin particles for six hours. The bottom part of the table shows adsorption in water of the Rhode River, Chesapeake Bay, of 4.2% salinity.

In the early 1980s, we hypothesized that the V. cholerae toxin in the crab may play a role in osmoregulation--and, therefore, provide protection to crabs migrating from the open ocean to the uppermost reaches of the Chesapeake Bay. In addition, in the human gut, chitin of the V. cholerae's host--which humans can't digest--may help protect V. cholerae from stomach acidity, as proposed.

[3 copepod species; pics from Rawlings]
(Use "back" to return to the text.)

Currently, my student, Tonya Rawlings at the University of Maryland, is investigating whether the seasonality of cholera in endemic areas is associated purely with temperature and salinity, or whether V. cholerae's interactions with its hosts--such as these copepods--also affect seasonality.

Specifically, she is investigating whether two epidemic variants of cholera, O1 and 0139, may have preference for attaching to specific genera of copepods. Here we see three copepod genera: Oithona, Eurytemora, and Arcatia. Not all bacteria compete well for space on surfaces. The pathogenic species of V. cholerae attach best.

[spiral: ecosystem level]
(Use "back" to return to the text.)

Let's move up the spiral staircase to take in a broader view, looking at cholera from the perspective of the ecosystem.

Recently we have used remote sensing to track sea surface temperature and sea surface height. We discovered that temperature patterns were clearly linked to the pattern of cholera outbreaks in Bangladesh and in South America. Simply stated, we have found a positive correlation between increased sea surface temperature and sea surface height and subsequent outbreaks of cholera.

Heating of surface waters, especially off a tropical or subtropical coast, results in an increase in phytoplankton. Through remote sensing, we can now determine when that bloom is occurring. The phytoplankton, in turn, provides food for zooplankton, including the copepods, which then increase.

[cholera outbreaks, SST and SSH]
(Use "back" to return to the text.)

We know that cholera epidemics are seasonal. Using remote sensing imagery, we discovered that, in areas of Bangladesh, cholera outbreaks occur shortly after sea surface temperature and sea surface height are at their zenith. This usually occurs twice a year, in spring and fall.

The following video of satellite imagery of the Bay of Bengal will show how sea surface temperature changes with the seasons over the year. We'll see the waters warm in spring--denoted by green and yellow, even red colors, and then the monsoon cooling. Then, the ocean warms again in fall, with some red visible at the mouth of the Ganges River. This cycle repeats every year. The video, please.

[SST in Bay of Bengal]
(Use "back" to return to the text.)

[Chesapeake Bay]
(Use "back" to return to the text.)

What factors influence V. cholerae distribution in another ecosystem in another Bay in another hemisphere--the Chesapeake Bay? Here, native V. cholerae populations fluctuate with the seasons just like in Bangladesh.

My student, Valerie Louis, has investigated how salinity affects cholera concentrations in the water. V. cholerae is more common in the northern part of the bay where salinity is low and when the weather is warmer.

In fact, temperature and salinity combined predict the presence of V. cholerae with an accuracy between 75.5 and 88.5 %.

Furthermore, changes in salinity from year to year, due to the influx of freshwater from the Susquehanna River at the head of the Bay, may cause V. cholerae populations to fluctuate greatly.

With climate change--with carbon dioxide increasing in the atmosphere, global warming, and more rainfall--river flow could increase, lowering salinity and driving up V. cholerae populations in the Bay.

[Heidelberg: Choptank map]
(Use "back" to return to the text.)

Populations of bacterial species such as Vibrio cholerae are very patchy in distribution--they vary over both time and space. Vibrio species vary seasonally from spring to winter in the Choptank River, a tributary of the Chesapeake, and even markedly from one week to the next.

Work on this question by my student, John Heidelberg, now at The Institute for Genomic Research, is important for decisions based on environmental sampling, when samples at two nearby locations, or a few days apart, may differ greatly.

[Heidelberg: graphs]
(Use "back" to return to the text.)

The upper graph shows how numbers of vibrios, measured by FISH--fluorescent DNA probes--vary over spring to winter, from one week to the next. The lower graph shows the variation from week to week of the number of V. cholerae cells found on just one zooplankter such as a copepod.

The highest measurement was 7,100 vibrios on a single copepod, which approximates an infectious dose--a dose, based on human volunteer studies, that could cause cholera in a human being. We see how factors at scales large and small, seasonal and microscopic, might interact to shape populations of cholera bacteria.

[Bangladesh picture: woman straining water]
(Use "back" to return to the text.)

In cholera-endemic areas, human beings are part of the cholera bacteria's ecosystem. Yet there is a simple and inexpensive tool available.

A sari cloth such as this, available even in the poorest household, can be folded eight to ten times. This creates a 20-micron mesh filter, as we determined by electron microscopy. As we saw in the film excerpt from Bangladesh, we have found that straining water through several layers of sari cloth may be enough to prevent ingestion of infectious levels of cholera bacteria.

[micrographs of old and new sari cloth]
(Use "back" to return to the text.)

The pictures show why old sari cloth, not new, is essential--because its holes are smaller and better able to trap the plankton. Laboratory studies show that old sari cloth folded at least eight times filtered out more than 99% of the V. cholerae attached to plankton.

[Filtration fig]
(Use "back" to return to the text.)

We have just submitted results for publication on a three-year study carried out in 65 villages in Matlab, Bangladesh, comprising a total study population of about 133,000 people. You can see the result here for filters made of sari cloth and nylon net versus the control group.

The incidence of cholera was reduced more than 50% in villages that used sari filters. The severity of disease also appears to have been reduced in villages that filtered, but this will need confirmation.

[ballast ship]
(Use "back" to return to the text.)

Another way human beings might interact with V. cholerae in the ecosystem is through discharge of ship ballast, and I thank my former student, Dr. Ivor Knight, now at James Madison University, for his insights on this topic.

[scientist with test tubes, inside ballast tank]
(Use "back" to return to the text.)

The scientist we see here is inside a ballast tank of a ship collecting water samples.

Cholera bacteria have been detected in ballast water of ships entering the Chesapeake Bay and the U.S. Great Lakes after an ocean crossing. It has still not been shown that cholera can colonize a new area this way. Nonetheless, if coastal environments warm, an organism adapted to warmer temperatures and frequently transported in ballast water may be established more easily.

[spiral: global level]
(Use "back" to return to the text.)

We move up the spiral of complexity to the planetary perspective, to examine the largest epidemic of cholera to strike toward the close of the last century.

After a century of absence, cholera surfaced in Latin America in 1991, beginning in Peru.

I would like to use a short video segment to set the scene for the planetary link between cholera and climate--specifically between the cholera outbreak and the climate pattern known as the El Nino/Southern Oscillation, or ENSO for short. The video, please.

[Peru-El Nino video: TRT 2:03] video not available

[slide of Peruvian coast]
(Use "back" to return to the text.)

The cholera epidemic of 1991 hit Peru most severely, both in terms of number of cases and in economic impact.

It has been proposed that cholera arrived on an Asian ship which contaminated coastal water with fecal material, but the data we see here suggest multiple cholera outbreaks along the coast.

Noted are the location and date of first appearances of clinical cholera cases. Also given is the distance from Lima for each coastal city.

Seven patients had cholera-like symptoms at least four months before the epidemic was recognized. This pattern along the coast suggests wide dispersion of vibrios in the water.

We hypothesize that toxigenic V. cholerae 01 El Tor was present along the coast at least since October 1990, causing sporadic cases until the epidemic began full force in January 1991. Continuing work during and after the 1997-98 El Nino shows that, indeed, the coastal waters of Peru harbor V. cholerae 01 in seawater and associated with zooplankton.

We hypothesize that the El Nino event triggered the resurgence of cholera in Peru. Warm water along the coast, coupled with plankton blooms fostered by El Nino rains, may have helped amplify the population of cholera bacteria already in the environment.

A short animation will give a better look at the dynamics of El Nino.

[animation of El Nino: TRT about one minute; it has its own soundtrack; then blank slide up] animation not available

Work by Mercedes Pascal, myself and my students suggests that the ENSO pattern also affects atmospheric circulation in the Indian Ocean and South Asia. El Nino may influence regional climate in Bangladesh--potentially affecting the prevalence of cholera.

The spiral of biocomplexity comes full circle, connecting climate patterns to the vicissitudes of cholera in Latin America, Bangladesh and even the Chesapeake Bay.

Now we are poised on the threshold of prediction for complex systems such as cholera ecology.

For example, satellite data suggest that it is to the north of Bangladesh, over the Himalayas, that certain temperature patterns unfold six months before the incidence of cholera rises in Bangladesh.

We want to be able to incorporate such climate patterns into an early warning system for cholera, and this is now becoming feasible. As science moves from reduction to integration, so we move from reaction to prediction.

Hungarian Nobel Laureate Albert Szent-Gyorgyi voiced a wish: "To see what everyone has seen and think what no one has thought." How much grander our vision, and how much greater the thoughts, when viewpoints are combined from many disciplines.

Connecting cholera to climate has required insights from sociologists, physicians, field extension agents, microbiologists, epidemiologists, ecologists, statisticians, remote sensing scientists, and environmental scientists.

How much more we see, and how much more revolutionary our thought, when we blend insights from the smallest to the largest scales.

Patterns can embody messages. Simple and ancient archetypal patterns like the spiral--termed "metapatterns"--occur repeatedly in nature and seem to yield clues to complexity.

We know that cholera itself is an ancient scourge to humankind, and that Hippocrates recognized the pattern, the link between disease and climate.

Today, however, the spiralling perspective of biocomplexity shows how cholera and climate entangle, how epidemiology and ecology intertwine.

Only now, with new tools of vision, with the integration across disciplines, and the explosion of opportunities to share scientific insights around the world, can we begin to pull the separate pieces together into patterns, and to collectively see what no one else has seen.



National Science Foundation
Office of Legislative and Public Affairs
4201 Wilson Boulevard
Arlington, Virginia 22230, USA
Tel: 703-292-8070
FIRS: 800-877-8339 | TDD: 703-292-5090

NSF Logo Graphic