Article: AR Blaustein and PTJ Johnson. 2003. The complexity of deformed amphibians. Frontiers in Ecology and the Environment 2(1): 87-94


Two global environmental concerns, biodiversity loss and increasing numbers of emerging diseases, are the context for a worldwide decline of amphibian populations and large numbers of deformed amphibians. In this article, Blaustein and Johnson give examples of these deformities and describe three possible causes. They propose that trematode infection is the most likely cause of amphibian limb deformation but also acknowledge contradictory evidence and the possibility of interacting causes.

Frogs, toads, and other amphibians with extra limbs have long been a rare curiosity. Over the last few decades however, frequency and severity of deformities in frog populations has greatly increased. According to Blaustein and Johnson, frequency of severe deformities (e.g., missing or partly missing limbs, misshapen eyes and tails) is as high as 15-90% in some populations. They state that, since the 1990s, over 60 frog species in the United States, Japan, Canada, and Europe have been identified as “deformed.”

The three most likely causes of amphibian deformities are ultraviolet (UV) radiation, chemical contamination, and trematode infection. Blaustein and Johnson discuss each briefly, including physiological mechanisms, types of evidence, and, in their opinion, degree of support for the three proposed agents. Their description of the “pros” and “cons” of each agent is quite useful for students. For example, while frogs exposed to UV-B radiation can develop misshapen limbs, the patterns of deformation recorded in the lab are different from those seen in the field (e.g., no lab experiments resulted in extra limbs which is commonly seen in the field).

Blaustein and Johnson favor parasitic trematodes as the likely agent because a combination of laboratory and field experiments plus field observations supports this idea. Trematodes are parasitic flatworms with several hosts for its different life stages. Figure 3 of their article illustrates the following cycle: eggs inside snails develop into aquatic larvae; these then burrow into hind limbs of amphibians where adult trematode worms develop; amphibians are in turn are eaten by wading birds; the trematode then reproduces asexually inside the bird producing eggs that are released into water to be eaten by snails.

Perhaps the most convincing evidence for the trematode argument, according to Blaustein and Johnson, is data showing a positive correlation between amphibian infection by the trematode Ribeiroia ondatrae and limb deformity. However, parasites are not the sole agent of amphibian deformities because misshapen frogs have been found where trematodes appear to be absent and some of the deformities (e.g., misshapen eyes) are not caused by parasitic worms.

The authors conclude by discussing possible interactions between parasitic infections in amphibians and other stressors. For instance they cite a study linking amphibian deformities, presence of Ribeiroia, and number of highly productive, artificial ponds such as farm ponds for cattle. Perhaps more hosts are becoming parasitized by trematodes because other environmental factors (in this case use of fertilizers which stimulate algal growth and subsequently more snails in farm ponds) favor success of trematodes.