Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers


Johnson, PTJ and JM Chase. 2004. Parasites in the food web: linking amphibian malformations and aquatic eutrophication. Ecological Letters 7: 521–526.



Johnson and Chase propose that the cause of outbreaks of frog deformities can be traced to the increased frequency of eutrophication of waters where tadpoles hatch and then metamorphose into frogs.

Eutrophication favors expansion of the populations of a family of snails, Planorbidae, which are hosts to a parasitic trematode. The trematode has been shown to cause deformities in frogs by forming cysts around developing limbs of the tadpole.

In essence: eutrophied waters means more snails. More snails lead to more trematodes. More trematodes lead to more deformed frogs.

Other factors, such as pesticides and UV, may also contribute. But Johnson and Chase suggest that the increase in frog deformities is part of a broader phenomenon, in which ecological changes caused by human activity--in this case eutrophication--are increasing human and wildlife diseases.

Background biology

Ribeiroa ondatrae is a parasitic flatworm (trematode) that forms cysts around developing limb buds of tadpoles. The cysts cause the buds to develop abnormally, so that after metamorphosis the adult frog has deformities.

This flatworm has a complex life cycle that requires it to live in several different hosts.

The first stage is spent in Planorbid snails, in which the flatworms reproduce asexually and the progeny become free-swimming "cercariae."

In the second stage, the "cercariae" burrow into tadpoles and form cysts around developing limb buds.

The third stage requires that the infected tadpole or frog be eaten by a suitable predator, such as a water bird. In this host, the flatworm reproduces sexually. Its eggs are dispersed by the host, and the cycle begins again.



What did they do? Johnson and Chase present data on three relationships:

  • Between phosphorus levels and the biomass of Planorbella snails. This genus of snails is an obligate host of the trematode parasite that causes deformities in frogs.

    Ponds with higher phosphorus levels have more snails (graph to left).


These data are from 27 Michigan ponds.

  • Between the abundance of snails and the number of amphibian infections by trematode cysts.

    Where there are more snails, there are more infections (graph to right)


These data are from surveys of ponds in
16 "deformity" hotspots in western and central USA.

  • Between the number of infections and the frequency of deformities.

    More infections lead to higher rates of deformities (graph to right).


These data are from surveys of 56 amphibian
populations in CA, OR, WA, MN and WI.

What does it mean? Johnson and Chase offer a highly plausible model to explain epidemics of frog deformities in agricultural areas, caused ultimately by heavy fertilizer run-off into frog habitat. It would be even stronger if all the data were from the same system, instead of from different areas.

They acknowledge that they have not considered the role of other factors that could also affect the frequency of amphibians deformities. The most prominent of these are UV and chemical pollution. For example, exposure to pesticides can reduce a frog's ability to resist parasitic infection by trematodes, because of impacts on the frog's immune system.

Taken together, these studies point toward two broader conclusions:

  • The epidemics of frog deformities are indeed not 'natural' even though one of the principal causal mechanisms involves a highly evolved parastic relationship between flatworm and host.
  • Multiple factors can contribute simultaneously to causing outbreaks --clusters--of adverse effects like frog deformities, and research that pits one cause against another, instead of looking for their interactions, may impede efforts to understand what is happening. This is as likely to be true for clusters of human disease as it is for wildlife.

Johnson and Chase conclude with a discussion of the "unprecedented number of diseases [that] have emerged or re-emerged in recent years, frequently owing to changes in the ecological interactions among a pathogen, its hosts and the environment in which they co-occur.

"Considering that human and wildlife populations depend upon freshwater for survival and that many diseases are transmitted via waterborne stages, interactions between pathogens and aquatic eutrophication are an important frontier for understanding current--and forecasting future-- disease epidemics."






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