In the mid-1990s, people in the United States and Canada began to notice something grotesque. The frogs in their local ponds were sprouting extra legs.
As news of the deformed frogs spread, the Minnesota state government set up a hot line for sightings, and soon they got hundreds of calls from 54 out of 87 counties. “I’ve seen a lot of frogs over the years, and I’ve never seen anything like that,” a University of Minnesota herpetologist told the New York Times in 1996.
Citizens and scientists alike feared that whatever was altering the frogs–pesticides perhaps–was also having an effect on humans. But researchers didn’t find any compelling link between frog deformities and humans diseases such as cancer. In fact, within a few years it looked as if the frogs were getting their legs naturally–through the manipulations of a parasite.
The parasite in question is a flatworm called Ribeiroia. It starts out life in snails. It grows and reproduces inside the snails, which it castrates so that they don’t waste time on making eggs or looking for a mate. In its castrated host, the parasite produces a new generation of flatworms that can escape the snail and swim in search of a vertebrate host. They typically infect fish or tadpoles. When they invade tadpoles, the parasites bury themselves in the tiny buds that will eventually grow into legs.
As the frogs develop their legs, the parasites wreak havoc. In some frogs they will stunt the growth of a leg, leaving it a stump. In other frogs, a developing leg forks in two. A single frog may even sprout a dozen legs. It’s not clear yet how the parasites manage this feat, but one recent experiment offers a clue.
In order for a limb bud to develop properly, its cells have to produce certain molecules. The molecules spread out across the limb bud, causing other cells to make other molecules, to grow faster, to die off, and to do all the other things required to make a limb. (See my article in the New York Times for more on this process.)
One of the crucial molecules for building legs is a version of Vitamin A, known as retinoic acid. Dorina Szuroczki and Nicholas Vesprini of Brock University and their colleagues found that before the swimming parasites find a tadpole, they are producing retinoic acid. Once they’re buried in the frog’s limb bud, their level of retinoic acid drops. Meanwhile, the level of retinoic acid in the limb bud shoots up 70 percent. All of these findings are consistent with the idea that the parasite is injecting limb-deforming drugs into their host.
The deformities of the frogs are not merely a side effect of their getting sick, in other words. They’re part of a strategy that the parasite uses to advance its life cycle. To understand why this would be so, you have to bear in mind that the frog is just a way station for the parasites. They cannot mate or reproduce in frogs. Instead, they have to wait to get into a bird, where they take up residence in the gut and produce eggs that are shed by their host. And they can only make that trip if the frog they inhabit is caught by a bird. Some frogs get eaten, and some don’t. A parasite in a frog that escapes death by bird will die without reproducing.
Brett Goodman and Pieter Johnson of the University of Colorado ran an experiment in 2011 to see what effect the limb deformities have on the frogs. They infected frogs in their lab and then compared their performance to healthy animals. The scientists found that the jumps of malformed frogs were 41 percent shorter than those of healthy frogs. They swam 37% slower and had 66% less endurance. They tried just as often to catch crickets, but they caught 55% fewer insects.
Goodman and Johnson then studied the frogs in the wild, observing how well they survived in a pond in California. Surprisingly, extra legs had no significant effect on the survival of the frogs–as long as Goodman and Johnson kept their ponds free of predators. The deformed frogs could still get around well enough to find enough food to stay alive. But in ordinary ponds, the parasitized frogs were at grave risk. Over a fifth of them died every two weeks, and when a given generation of frogs became adults, there were almost no deformed frogs left among them. Instead, they had delivered their parasites to their next home.
The discovery of this parasite manipulation was not the end of the story, though. Even though Ribeiroia has probably been infecting frogs long before people showed up in the United States, the level of infection might be influenced by a number of factors. Johnson and his colleagues have found, for example, that frogs that live in water contaminated with high levels of fertilizers were more likely to be infected with Ribeiroia. Pesticides can kill off the parasites, some studies show, but they also lower the defenses of the frogs, which may lead to higher infections.
In this week’s issue of Nature, Johnson and his colleagues now offer evidence for another factor in the success of leg-deforming parasites: biodiversity.
For some years now, a number of ecologists and parasitologists have developed the idea that biodiversity protects against disease. The notion is this: parasites in search of a new host sometimes end up in the wrong species. A bird flu virus that gets into a bird, for example, can make billions of new viruses that are shed in the bird’s droppings, which can then infect other birds. But bird flu sometimes gets into a human and cannot spread any further. The more species in an ecosystem, the argument goes, the more likely parasites are going to hit a dead end and get diluted. In low-diversity ecosystems, parasites will be more likely to hit the right host, make more copies of themselves, and cause more disease.
It’s a very influential idea, but, like many ideas in ecology, very hard to test. Johnson and his colleagues realized that Ribeiroia offers a very good opportunity to do so. The parasite only manages to trigger limb deformities in some of its hosts, and it has more success in some amphibian species than others. What’s more, each pond occupied by the parasite and its hosts is like a test tube in which the experiment is replicated. Johnson and his colleagues have visited 345 sites in California wetlands to examine Ribeiroia and its hosts. All told, they studied 24,215 amphibians and dissected 17,516 snails.
In these wetlands, the parasite is most successful when it infects Pacific tree frogs. But it can infect other frog species and even the salamanders that live alongside the frogs. Johnson and his colleagues found that in ponds with high biodiversity–up to six species of amphibians–the parasites did much worse at getting transmitted than in low diversity ponds. This was no minor difference: there was a 78.5% decline in deformed frogs in high-diversity sites. To test this pattern, Johnson and his colleagues put groups of amphibians into tanks along with infected snails. The frogs in high-diversity tanks had half the parasites as the ones in low-diversity tanks.
It seems, then, that we can add low biodiversity to the list of factors that can produce a flurry of frog legs, along with pesticides and fertilizer. Johnson also suspects that the snails are important too. As the parasite population grows, it castrates more and more snails, until their population crashes. Once the snails become scarce, the parasites become scarce, too, giving the frogs a break. Unfortunately, no one has yet conclusively shown that any of these factors has driven a long-term change in frog deformities of the sort that made headlines in the 199os.
Nevertheless, this study is important for a few reasons. For one thing, frogs are in big trouble these days. Species are winking out around the world, and diseases appear to play a big part in their demise. Biodiversity itself may defend the frogs against dangerous outbreaks.
It also tells us something about our own well-being. We don’t have to worry about frog flatworms getting into our bodies and causing us to sprout extra legs, thank goodness. But many other pathogens that do make us sick also lurk in other species, such as West Nile virus and hantavirus. And the more species that can dilute those pathogens, the healthier we’ll be.