While working on her PhD in 1992, Karen Lips went to Las Tablas, Panama, to study the biology of a tree frog, Hyla calypso, an inch-long, spiny, bright-green creature. As she walked through transects in the forest, measuring and sexing frog individuals, here and there she noticed a handful of dead frogs on the forest floor. Collecting them, but not thinking much of it, she took the dead frogs to a veterinarian. The vet examined the frogs and noticed something strange on their skin, but could not explain their deaths.
When Lips returned to Las Tablas two years later, she couldn't find any frogs. Soon after, Lips found 50 dead frogs at another collection site, Fortuna, further east in Panama. "As soon as I got there I could see things weren't quite right," Lips says. "And just by complete dumb luck, [I] was in the right place at the right time."
Without knowing it, Lips had managed to arrive in Panama just as the amphibian populations were starting to crash from infections of a fungus, Batrachochytrium dendrobatidis (Bd). The fungus coats the frog skin, fatally interfering with how the creatures can absorb water. Global decline of amphibian populations was well underway when Lips consulted with a group of Australian researchers who had already pinpointed the fungus as responsible for frog deaths. In 2004, the Australians discovered the fungus on museum frog samples of Xenopus laevis obtained in southern Africa in the 1930s. This observation sparked a theory that perhaps the fungus was spread around the globe by frogs from Africa that were used as pregnancy tests in the 1930s and 1950s. (The Xenopus frog is injected with a woman's urine; if the frog drops its eggs, the woman is pregnant.) However, the first known amphibian declines began in the 1970s - far too long after the fungus had supposedly spread around the globe via pregnancy tests.
Currently, there are two predominant theories about the origin of the fungus: Either it is endemic to many regions and emerged in response to favorable changes in environmental conditions, or it has recently spread to new environments with naïve hosts.
In Panama, Lips continued to work in sites further east, where frog populations remained intact. But by 2002, frog populations crashed at Santa Fe, about 90 km from Fortuna, and then in El Cope, about 50 km farther east of that.
In a PNAS paper published in August (104:13845-50, 2007), Jessica Morgan of the Animal Research Institute, Australia, and colleagues found that the fungus had diversified genetically among nearby populations in the Sierra Nevada mountains in California, suggesting that genetic recombination allows the fungus to specialize to a particular site. The fungus appears to be sexually reproducing as well, producing sporangia that can resist drought or high temperatures, which may have enabled the fungus to spread widely. "This finding offers an alternative means of global dispersal," Morgan writes in an e-mail. "Without a resistant spore, the only way the fungus could move between continents was by human-assisted movements of infected frogs involved in the food and pet trades."
Since last year, the fungus seems to have stopped its 28 km-per-year spread east across the isthmus, likely because it encountered temperatures too high to sustain it. Other researchers around the globe continue to work on discovering the origin of the fungus, requiring extensive genetic examination of all its varieties. "Bd is not just one thing," says Lips. "There are a couple different genetic forms, and likely have been multiple introductions." Some strains cause mortality, while others have less virulent effects. "It means we can't lump everything in one category and call it Bd."