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Prairie Wanderings: Deformed frogs

By PAUL G. JANTZEN

Contributing writer

In late April of 2001, about three dozen of us explored the prairie streams and ponds of the sandhills in western Harvey County listening for frog calls. It was night and Dwight Platt was identifying various amphibian species. We heard the northern cricket frog's sound of jostling marbles, the plains leopard frog imitating a clucking mother hen, the western chorus frog stroking the teeth of a plastic comb, and the Woodhouse's toad with its distant call of a screaming child.

The Harvey County expedition was probably organized in part to call attention to the alarming decline in amphibian populations around the world. Herpetologists were searching for explanations and their possible implications for our own human species.

One suspected cause of the decline was the increased exposure to ultraviolet radiation as chlorofluorocarbons and other human-produced contaminants reduce the screening effect of stratispheric ozone. Laboratory investigations showed that this radiation disrupts development of amphibians by killing their embryos and causes serious deformities in adult frogs and salamanders. Without protective shells, their eggs are easily penetrated by ultraviolet radiations.

Other researchers noted that many reports of amphibian ailments came from areas subjected to liberal applications of insecticides and fertilizers. Laboratory work showed that many pollutants can kill amphibians. With a moist skin and no protective scales, they are vulnerable to the action of insecticides. The popular herbicide, atrozine, causes male leopard frogs to develop eggs in their testes. But after testing more than 60 agricultural chemicals, workers concluded that, while the damage done by both water pollutants and ultraviolet radiation cause serious problems for amphibians, the rate of population decline was too rapid to be caused by these factors alone.

In 1995, on a hot summer day near Henderson, Minnesota, eight middle school students studying wetland ecology discovered that half the leopard frogs they caught were severely deformed. Some had extra hind legs; others had stubs where legs should be, or one or two legs growing from the abdomen; some had no legs at all.

The story attracted media attention and, since 1995, investigators in other states found that in some local areas 80 percent of the amphibians were deformed. By now, deformed amphibians have also been found in Europe, Asia, and Australia. The most common deformities worldwide were extra legs and missing legs.

But what caused the extra legs?

Experiments showed that, while both ultraviolet radiation and some pesticides can cause some deformities, neither lead to the development of extra legs.

In the mid-1980s, even before the deformed frogs in Minnesota attracted attention, a biologist collecting data in ponds of California discovered hundreds of tree frogs and salamanders with missing legs and extra legs. All of the deformed amphibians were also infested with a parasitic fluke related to tapeworms. Later studies found that the affected amphibians came from ponds that contained a certain aquatic snail. The deformed frogs were dissected and found to harbor the cysts of a parasitic fluke just under the skin near the base of the hind legs. When normal tadpoles were exposed to the suspected snails, the tadpoles developed extra limbs or missing limbs while unexposed tadpoles developed normally.

The first larva of the fluke develops inside the snail into a second, free-swimming form. This larva escapes the snail and swims to a tadpole and embeds itself near the tadpole's future rear leg where it forms a cyst. This cyst disrupts normal leg development. The crippled frog that develops is easy prey for large wading birds such as herons and egrets. As the parasite matures inside the bird, the fluke releases its eggs into the bird's intestine from which they pass into the water with the bird's droppings. As the eggs hatch, the first larva repeats the cycle by infecting the snail, etc.

Recently, zoologist Andrew Blaustein and limnologist Pieter Johnson suggested that "human alteration of habitat" accounts for the epidemic of the fluke. Their survey of 59 wetlands in western U.S. revealed that the 44 pools infected by the fluke were "reservoirs, farm ponds or other artificial bodies of water." Fertilizer runoff and livestock manure near these habitats can encourage population explosions of algae providing food for the snail that hosts the parasitic fluke capable of producing deformed frogs. Herons and egrets that eat frogs are often abundant at these altered habitats and serve as temporary hatcheries of the fluke's eggs.

Joseph T. Collins, veteran Kansas herpetologist, does not know whether the guilty fluke is present in the artificial ponds and reservoirs of Kansas. But he speaks of the takeover of

wild areas by humankind (including the draining of wetlands) which certainly contributes to the decline of amphibian populations in Kansas.

So we know that environmental hazards contributing to the dramatic decline of amphibians include over-exposure to ultraviolet radiation, the release of agricultural chemicals into water, and especially, infestation by a flatworm. And all of these factors result from human activities.

Will the human species be affected by the same or similar self-induced environmental hazards?

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