The New York Times, July 9, 2014

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In the 1990s, a disturbing silence began to settle across the world. From mountain lakes to tropical streams, the music of singing frogs began to disappear.

It took a few years for scientists to figure out what was happening. A species of fungus — Batrachochytrium dendrobatidis, or Bd for short — was infecting and killing amphibians.

Two decades later, Bd has proved itself an exceptional biological catastrophe. It afflicts amphibians on every continent, and scientists suspect it has driven hundreds of species to extinction since its discovery.

“Even Ebola doesn’t cause extinctions,” said Jason R. Rohr, an expert on the fungus at the University of South Florida. “This makes it arguably the second most deadly organism on the planet, behind humans.”

In a new study published on Wednesday in Nature, Dr. Rohr and his colleagues offer what they consider cause for hope. They’ve discovered that frogs can acquire defenses against the fungus. The results might lead to a vaccination-like campaign to slow the epidemic, Dr. Rohr said.

Other researchers were cheered by the conclusions of the new study, although some were skeptical about its usefulness. In the study, the amphibians did not develop overwhelming defenses against the fungus. So even if scientists did start a sweeping campaign to save them, their defenses might not become strong enough to stop the destruction.

The stakes of this debate are high. If Bd continues to spread unchecked, it could drive many more species extinct, with huge ecological consequences. In the forests of the northeastern United States, the biomass of amphibians outweighs birds, mammals and all other vertebrates. Many predators depend on amphibians for food; algae in streams depend on amphibian larvae to release nitrogen that fertilizes them.

We humans benefit from amphibians, too, and not just thanks to their appetite for mosquitoes and other pests. Amphibians produce many unusual chemicals that have been turned into useful compounds, from cancer drugs to powerful adhesives. When an amphibian species becomes extinct, millions of years of evolutionary experimentation disappear with it.

Only in recent years have scientists gotten a basic understanding of how Bd kills. Its spores land on the skin of amphibians, and the fungus burrows down to deeper layers, where it releases a toxin that paralyzes immune cells.

But there have long been tantalizing hints that some amphibians can fight back. Some species, such as bullfrogs, haven’t declined despite being exposed to Bd. In other species, certain populations have vanished, while others have endured. In Australia, scientists have even discovered that a frog species that was decimated by Bd has been bouncing back.

Dr. Rohr and his colleagues wondered if these amphibians were developing immunity to the fungus. They might have a response similar to the way we develop immunity to influenza and other pathogens after exposure.

To find out, the scientists swabbed Bd onto the bellies of Cuban tree frogs. After the frogs became infected, the scientists cured them by taking advantage of a weakness of the fungus: it can’t survive for very long at high temperatures.

Dr. Rohr and his colleagues kept their frog chambers heated to 86 degrees for 10 days, after which the fungi disappeared. The scientists then repeated this procedure three more times.

Frogs that had already been exposed to Bd produced a much stronger immune response to a new infection, the scientists found. They produced more immune cells, and the fungus produced fewer spores.

The exposed frogs were also much more likely to survive an infection than a frog exposed for the first time. What’s more, these effects became stronger after each exposure.

Dr. Rohr and his colleagues also found that amphibians can learn to avoid the fungus. In another experiment, they put oak toads in a chamber. One side of the chamber was contaminated with fungal spores, while the other was fungus-free. They found that toads that had never been exposed to the fungus would explore both sides of the chamber, becoming infected along the way.

But toads that had previous been exposed (and cured with heat) tended to avoid the side of the chamber with the fungus. If they were exposed more than once, they were even less likely to go to there. Dr. Rohr and his colleagues are investigating how the toads learn to avoid exposure to Bd. It’s possible that the toads can detect a chemical made by the fungus.

Dr. Rohr thinks the new study helps explain why Bd has eradicated some populations of amphibians and not others. When the fungus invades, it can sweep through the animals quickly — possibly killing them all.

But in some cases, a few amphibians survive that first attack. They may find refuge in a sunny spot, for example, where Bd can’t grow quickly. Their immune system may vanquish the fungus. Perhaps they learn to avoid the fungus and develop a stronger immune response.

Doug Woodhams, a postdoctoral researcher at the University of Colorado who was not involved in the study, said that it might be possible to strengthen the defenses of captive amphibians before releasing them into the wild. “This may provide the head start that is needed to avoid immediately contracting lethal infections,” he said.

Instead of infecting amphibians with live fungi and then heating them, Dr. Rohr suggests that scientists might be able to use a simpler method. His research suggests that dead spores might spur stronger defenses, or even just a Bd protein. It might even be possible to release Bd-protecting proteins into the waters where wild amphibians live.

“We have to stay optimistic that we can find some sort of solution,” said Dr. Rohr.

Such a strategy will work, though, only if the defenses it produces are powerful enough to overcome the fungus. And Lee F. Skerratt of James Cook University in Australia, who wasn’t involved in the new study, doesn’t see much hope of that in Dr. Rohr’s research.

“The size of the effect is relatively small,” he said, calling its potential value for saving amphibians “highly uncertain.”

Karen R. Lips of the University of Maryland also questioned how effective such a campaign would be. After all, wild amphibians are already exposed to both live and dead spores. “We live in a Bd world,” she said.

Despite her reservations, Dr. Lips said that understanding how amphibians fight Bd was crucial in the struggle to save them. “Any evidence that some amphibians are surviving with disease is good news,” she said.

Copyright 2014 The New York Times Company. Reprinted with permission.