Mercedes Pascual's computational models have generated evidence that complex climate patterns influence the incidence of infectious disease epidemics.

These were heady times in the field, Pascual says. Scientists in theoretical ecology, including Caswell, were pioneering mathematical studies of “nonlinear” dynamics, which describe how ecological systems change and respond to their environments over time. Because of internal feedback between their components, natural systems almost never exhibit linear or proportionate responses to environmental influences. Plankton populations, for instance—the subject of Pascual's doctoral research—don't grow twice as large if their food supplies double. Many factors play into those growth rates, including competition among individuals. Given that, plankton populations exhibit complex, nonlinear responses to food increases that can be challenging to quantify.

Nonlinear dynamics have been central to Pascual's work ever since. But her emphasis has gradually shifted from their role in marine ecology to their expression in patterns of infectious disease. The transformation toward human illness began when Pascual moved to Baltimore in 1997 to work at the Center of Marine Biotechnology at the University of Maryland.

The Center for Marine Biology was headed by Rita Colwell (who later was director of the National Science Foundation from 1998 to 2004). Colwell had spent years studying cholera and was the first to propose that this water-borne illness—the result of Vibrio cholera bacterial infections—could be linked to climatic factors. Her research had shown that the bacteria can survive in aquatic environments in association with plankton. When a massive cholera outbreak struck Peru in 1991, killing 10,000 people and sickening 1 million, Colwell proposed that a recent and remarkably strong El Niño was the underlying cause. In her view, unusually warm Pacific waters and heavy rains induced by the El Niño Southern Oscillation (ENSO) triggered a proliferation of cholera bacteria that fueled the epidemic.

In thinking about the epidemic, Pascual wondered if cholera's response to climate variability was nonlinear and governed not just by ENSO and its effects on the pathogen but also by an important limiting factor—i.e., the fraction of susceptible people in the at-risk population.

Infectious diseases need fuel to spread, Pascual explains, and that fuel comes in the form of susceptible individuals. Those who survive cholera develop temporary immunity to future exposure. When immunity predominates in a population, cholera outbreaks don't spread no matter how strong the environmental pressures. But when the pool of susceptible people rises—perhaps because of new births or human migration patterns—vulnerability to environmental pressures increases, making outbreaks more likely and intense.

Pascual wanted to study the interaction between ENSO and cholera outbreaks, but to do that she had to look beyond the Peruvian epidemic. El Niños occur every three to seven years, but before the 1991 event Peru hadn't experienced a cholera outbreak of any significance for more than a century. To model disease dynamics over multiyear timescales, Pascual needed to look at more than a single outbreak. She needed data from a country that faced cholera threats on a regular basis.

Photo: Brian Ulrich

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