Since the 1990s, the world has witnessed the rise of one of the most terrifying diseases to afflict any animal group: a doomsday fungus that is ripping through the world’s frogs and amphibians. Known as Batrachochtyrium dendrobatidis, or Bd for short, it causes a disease that has wiped out dozens of species and endangered hundreds more. It’s a global problem and earlier this year, it was finally found in Madagascar—the last Bd-free amphibian stronghold. “That’s it. The worst news imaginable,” wrote one herpetologist.
Bd news is almost always bad news. But this week, Taegan McMahon from the University of South Florida has a more positive to tell—or, at least, what passes for positive when you’re dealing with Bd. Her team showed that frogs become more and more resistant to the fungus if they are repeatedly infected and cured. They even became more resistant after the team exposed them to dead fungus.
These results offer a small sliver of hope. Perhaps conservationists might be able to vaccinate frogs against Bd using dead versions of the fungus, just as humans protect ourselves from polio or rabies. They could inoculate captive individuals before releasing them, prepared and protected, into the big, bad, Bd-filled world.
“This is the beginning to a long line of work—the first information that we need to figure out whether it’s really practical in the field,” says McMahon. “We need to test this on a larger scale, but we’re super-optimistic with it.”
Other frog specialists are more skeptical. Lee Skerratt from James Cook University in Australia praised the team’s experiments but said, “The fungus still appears to be highly virulent after four previous exposures, which fits with our current understanding. It still kills the majority of frogs after a short period of time. In comparison, inoculations with many other pathogens provide almost complete protection against future exposure.”
Karen Lips from the University of Maryland also doubts that the results will make much practical difference. “It’s already a Bd world. Essentially all amphibian species have already been exposed at some point. Many have been shown to self-clear infections, some get reinfected, some die, some don’t.” The point is that they’ve already had a chance to become resistant, only some have taken it, and we still don’t understand why.
However, she adds, “Any evidence that some amphibians are surviving with disease is good news. [And] anything that zoos and NGOs can do to promote or allow evolution of captive assurance populations would be good.”
McMahon’s team repeatedly exposed Cuban tree frogs to Bd and then raised their temperatures to clear their infections. With each passing exposure, the team found that the frogs became more and more resistant to the fungus. By the third exposure, they carried 75 percent less of it on their skins. They also mounted stronger immune responses and made more white blood cells in response to the threat. That was a surprise—Bd can suppress amphibian immune systems but it seems that, over time, the frogs can compensate.
Spraying live fungus onto frogs, especially endangered species or those only exist in captivity, would be a non-starter. So the team exposed the frogs to dead fungus to see if they could trigger the same resistance. It did, and to almost the same extent as the live fungus. “I was hopeful but not as confident that the dead fungus would work,” says McMahon. “It did, and that’s extremely exciting.”
But Lips warns that strong immune responses aren’t necessarily cause for celebration. In her own research, she found that harlequin frogs that naturally recover from a bout with Bd will die just as fast as naive frogs if re-infected, even though they mount vigorous immune responses.
In McMahon’s experiment, only 20 percent of the animals that had acquired “resistance” to the fungus were still alive after five months. They fared better than the completely naive animals, all of whom were killed, but a survival rate of 20 percent is probably not good enough to sustain a wild population. And what happens after five months? Does their shred of immunity disappear, or do the frogs lose it over time?
There are other unknowns. Bd has wildly varying effects on different frogs—harlequin frogs almost always die, but cane toads (predictably, sadly) are almost impossible to kill. It’s not clear if other frogs would react to the fungus in the same way that the Cuban tree frogs did.
Most importantly, what would happen in the wild? Lips adds that when she pits amphibians against Bd in her lab, context is everything. The same fungal strains will kill infected salamanders at 13 degrees Celsius but spare their lives at 17 degrees. “In terms of relevance for wild populations, what will happen when winter comes and temperatures drop?” she asks. Field tests are everything.
McMahon agrees. She now wants to expose frogs in mesocosms—enclosures that sit in natural settings, but that can still be carefully manipulated. That will tell her not only whether the frogs can resist the fungus outside of a lab, but also whether spraying dead fungus has any unintended consequences. After all, she previously showed that Bd can release an unknown toxin that can kill crayfish at a distance. “We want to make sure that if we’re spraying the fungus, there aren’t effects we don’t expect,” she says.
Reference: McMahon, Sears, Venesky, Bessler, Brown, Deutsch, Halstead, Lentz, Tenouri, Young, Vicitello, Ortega, Fites, Reiner, Rollins-Smith, Raffel & Rohr. 2014. Amphibians acquire resistance to live and dead
fungus overcoming fungal immunosuppression. Nature http://dx.doi.org/10.1038/nature13491