The Ecology of Epidemics
by Kim Carlyle

A recent study of measles and whooping cough epidemics in 19th century European cities shows that microbes compete with each other for human hosts. This finding sheds new light on the underlying mechanisms of cyclical epidemics.

“The idea we have explored is that one pathogen can crowd the field for others,” said Pejman Rohani, a University of Georgia ecologist. “This means that when sick people are home recuperating or when they are killed by an infection, they are not ‘available’ to other pathogens.”

The research has implications for epidemiologists working worldwide, especially for those in developing nations where concurrent epidemics are common and can significantly contribute to mortality rates.

“A lot of work has been done on the diseases in isolation, but not too many people look at whether the diseases affect each other or how,” said Natalia Mantilla-Beniers, a UGA visiting scholar and Rohani’s co-author on the paper “Ecological Interference Between Fatal Diseases” published in Nature in April 2003.

“This work shows that sometimes it might be impossible to understand epidemics by studying diseases in isolation,” she said.

Rohani’s research team analyzed and modeled records of measles and whooping cough infections in 32 European cities from 1883 to 1932, before vaccinations became widely available.

Their research predicts that when one disease removes enough susceptible hosts from a given population — by convalescence or death — the infection rate for the “competing” disease also diminishes. The researchers mapped both outbreaks simultaneously in a certain population and found that infections peaked in alternating, two-year cycles.

“Certain biennial epidemics like measles and whooping cough outbreaks are negatively correlated — much more so than if their dynamics were independent,” said Rohani, one of 10 scientists named in 2003 to the Ellison Medical Foundation’s New Scholars Program in Global and Infectious Disease.

Rohani’s team developed a three-strain extension of the model that also showed pronounced out-of-phase patterns as either the convalescence period or the fatality probability increases. These patterns are consistent with observations of dengue fever or strains of echoviruses.

“Until now, it was thought the dynamics of dengue fever were largely determined by the number of mosquitoes available to transmit the disease or by some complex immunological interactions between the strains’ so-called antibody dependent enhancement,” Rohani said. “What we see now is that there may be something more complex at play. We see that one strain actually competes with the other for susceptible hosts.”

For more information, contact Pejman Rohani at or visit