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in North American Amphibians
In 1995, a group of Minnesota school children on a biology field trip were shocked by finding dozens of misshapen Northern Leopard frogs, Rana pipiens. This highly publicized incident led to an international media frenzy! Never has a herpetological phenomenon received such wide-spread publicity with such little scientific writing (or perhaps knowledge) to back it up. Within weeks the Minnesota Pollution Control Agency and the federal Environmental Protection Agency began a statewide survey. Early results exhibited a malformation rate as high as 80% in some ponds and lakes.
The United States Geological Survey in conjunction with several researchers formed the North American Reporting Center for Amphibian Malformations (NARCAM). Reports of deformities have come from almost every state. Minnesota, Vermont and Quebec to date have reported the highest abnormality rates in the continent. No one knows for certain what is causing increased levels of deformed amphibians or if there really are more abnormal frogs than in the past. Currently there are a number of hypotheses being investigated: Parasitic trematodes (Riberoria ondatrae); increased ultra-violet radiation from ozone thinning; chemical pollution from pesticides, insecticides, herbicides, or fertilizers; and attempted predation or cannibalistic activity.
Hearsay and hypothesis have been misrepresented as fact in many media accounts of amphibian malformation. A few historical accounts of deformed anurans can be found in scientific literature over the past two centuries. In 1986, biology teacher Steven Ruth discovered large numbers of multi-limbed Pacific Treefrogs Hyla regilla in two ponds in Aptos, California. Ruth contacted Dr. Stanley Sessions of Monterey Peninsula College. The team extensively surveyed and collected hundreds of deformed treefrogs and Long-toed salamanders, Ambystoma macrodactyum.
Sessions and Ruth discovered that the specimens were heavily infested with parasitic cysts. The parasites where Riberoria ondatrae a type of flatworm or trematode. Trematodes typically have a complex life-cycle that involves more than one host. Riberoria has a five-part life cycle that involves aquatic snails, amphibians and aquatic birds. At the third phase of its life-cycle (cercariae) the parasite forms a hardened cyst inside the body of it's host. If the trematodes host is a tadpole, the cyst can damage and disrupt normal limb development.
In 1999, the peer-reviewed journal SCIENCE published two papers on amphibian limb abnormalities caused by trematode infestation. Sessions has proven a dose responsive relationship between increased cercariae and severe limb mis-development. Dr. Pieter Johnson of Stanford University, has captured free swimming Riberoria and has allowed them to infect developing Pacific treefrogs. The resulting abnormalities were consistent with malformations found throughout the North American continent. At present it is still not known why or if there are increased incidences of Riberoria infections occurring in native amphibians.
Ozone-thinning is believed to be causing heightened levels of ultra-violet radiation (UVBs) to penetrate the earth. Dr. Andrew Blaustein at Oregon State University has been focusing on increased amphibian mortality and mis-development caused by UVBs. Experimenting with salamander spawn, Blaustein exposed some eggs to normal sunlight while others were shielded. Some of the of the exposed spawn did not hatch and a number of those that did had congenital malformations. The shielded eggs hatched with a decreased level of mortality and no abnormalities.
Research teams in Canada and Austria are attempting to prove a relationship between UVBs and increased amphibian mortality. The premise is that damage occurs in the DNA of certain species at an embryonic level. Furthermore, high levels of photolyase, an enzyme which repairs DNA after damage from UVBs, has been found in species that are not suffering from decline compared to minute levels in some species that are near extinction.
A paper published in 1998 in Environmental Science and Technology demonstrated that an IGH, or common insect growth hormone (used to control mosquito populations) could induce abnormalities. The experiment involved exposing embryonic Xenepus laevis to a photo sensitive IGH. The IGH affected development and increased mortality levels in the juvenile African Clawed Frogs. The deformities observed were at an early stage of development so they could not accurately be compared to those found in the wild.
A research team led by Tyrone Hays at the University of California Berkeley has found that the popular weedkiller, Atrazine, can cause abnormalities in the reproductive systems of frogs. The studies showed that the herbicide acted as an endocrine disrupter creating frogs that had both male and female reproductive organs. Even at small levels, the herbicide caused the conversion of testosterone to estrogen in developing Xenepus laevis. Apparently the male frogs not only had decreased levels of testosterone, but also had much smaller larynxes than normal, which could affect their ability to call and attract mates. If wild frogs are unable to attract a mate or are physically unable to reproduce this may be a major factor in global amphibian declines.
Amphibians are particularly sensitive to certain chemicals. Retinoic acid (RA) has been proven to induce abnormal development in laboratory specimens. RA is a basic building block in nature. In tadpoles, vitamin A (a retinoid) is transformed into all-trans RA and 9-cis RA. These bind with precise RA receptors to form a 'heterodimer'. The complex then binds with DNA, which turns the animal's genes on or off. So in theory if too much RA or an RA mimicker is present in the animal's body, misdevelopment may occur.
Canadian researcher Dr. Martin Ouellet has collected thousands of malformed amphibians over the past ten years. He has been able to show an increased incident level of ectromelia (missing limbs) and ectrodactyly (extra limbs) in amphibians from agricultural habitats. Other studies show affected development in species believed to be exposed to high levels of nitrogenous fertilizer. Increased levels of agricultural run-off and excess minerals from eroded soil have been shown to cause eutrophication in wetlands. Eutrophication is the process by which a wetland becomes overloaded with nutrients. This fluctuation in nutrient load can rapidly change the structure of a wetland. The resulting chemical shifts can cause algae blooms and increased populations of aquatic snails. More snails may cause more trematode parasites which may equal more deformed amphibians.
The debate on amphibian malformations is far from closed. If the occurrences are being caused primarily by parasites, are there more trematodes than in the past? or are there more of us looking for them? If the cause is UVBs then why are some high altitude species (where UVBs would be the most intense) not effected? If the cause is chemical pollution then certainly more research is needed to locate the culprit or culprits. Are all these agents synergetically effecting amphibian physiology? Does this phenomena contribute to the amphibian population decline occurring globally?
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