, Volume 4, Issue 2, pp 121–124

Trophic Cascades and Disease Ecology


DOI: 10.1007/s10393-007-0099-z

Cite this article as:
STAPP, P. EcoHealth (2007) 4: 121. doi:10.1007/s10393-007-0099-z

The ecology of infectious disease is an important, growing sub-discipline of ecology that combines field studies, epidemiology, molecular approaches, and modeling to understand interactions among wildlife hosts, vectors, and pathogens, and to better forecast risk of disease. At its core, disease ecology is population and community ecology, and many of the concepts and paradigms of these well-established sub-disciplines can be effectively applied to studies of the ecology of infectious disease. Several recent articles have attempted to place ecological studies of disease systems in the context of food-web ecology. Yates et al. (2002), building upon results and arguments in Parmenter et al. (1999), proposed a “trophic-cascade hypothesis” to explain how climatic variation affects the probability of outbreaks of hantavirus pulmonary syndrome (HPS), a disease spread by small rodents, in the southwestern United States (also see Enscore et al., 2002; Davis et al., 2005). In this scenario, mild weather conditions increase primary production and the availability of food for small rodents, resulting in higher rodent population density and, eventually, increased risk of HPS transmission to humans in rural areas (see Brown and Ernest, 2000, for an alternative view). Collinge et al. (2005), in a recent article in EcoHealth, tested the generality of this “trophic-cascade hypothesis” as an explanation for outbreaks of plague in prairie-dog colonies in Colorado and Montana.

The evidence of a link between climate, rodent population density, and risk of disease outbreaks is compelling, and suggests several interesting hypotheses about the possible effects of climate change on risk of disease. However, it is important to point out that the “trophic-cascade hypothesis” described by Yates et al. (2002), and addressed by Davis et al. (2005) and Collinge et al. (2005), is not a trophic cascade in the way that the term was first defined (Paine, 1980; Carpenter et al., 1985), and has come to be used widely in the ecological literature (e.g., Persson, 1999; Schmitz et al., 2000). Trophic cascades describe indirect top-down regulation of productivity, abundance or biomass at one trophic level (usually, primary producers) by higher-level consumers at least one trophic level removed, e.g., predators. The sequence of events described by Yates et al. (2002) and others, in fact, suggests quite the opposite: bottom-up control of primary and secondary production driven by abiotic factors that percolates upward through all trophic levels. Interestingly, Ostfeld and Holt (2004) recently proposed that predators might exert top-down control of rodent reservoirs of human disease, an argument that is more consistent with the accepted concept of a trophic cascade, though without the explicit consideration of indirect effects of pathogens on primary production, which is considered by some to be a necessary condition for a trophic cascade (Persson, 1999).

Nonetheless, it is not unreasonable to expect that pathogens may cause trophic cascades, especially when host species involved have large, ecosystem-level effects. For example, plague, which is caused by the bacterium, Yersinia pestis, causes nearly complete mortality of colonies of black-tailed prairie dogs (Cynomys ludovicianus) in the western Great Plains of the United States (Cully and Williams, 2001). Plague was introduced to North America in the past century, and represents a significant threat to persistence of prairie dogs, whose numbers were greatly reduced by habitat conversion and poisoning programs. By clipping vegetation and constructing burrows, prairie dogs alter plant communities and ecosystem function across thousands of hectares of grasslands. Elimination of colonies, either by plague or by human activities (e.g., Klatt and Hein, 1978; Uresk, 1985; Stapp, 2007), can result in substantial re-growth of vegetation, depending on local plant species composition, productivity, climate, and the length of time that a colony is unoccupied. Notwithstanding biological control programs involving exotic pests, there are likely many instances where pathogens or parasites of dominant native herbivores or even key predators might be expected to exert top-down control of production, though relatively few studies have been cast in the context of trophic cascades and food-web ecology. The increasing efforts to bridge the fields of epidemiology and ecology will undoubtedly be fruitful, but researchers must take care that they are using each other’s terminology consistently.


Support for my research was provided by the U.S. National Science Foundation (EID-0327052, DEB-0217631).

Copyright information

© Ecohealth Journal Consortium 2007

Authors and Affiliations

  1. 1.Department of Biological ScienceCalifornia State UniversityFullertonCA