Болезнь называется хитридиомикоз, и вызвается грибом Batrachochytrium dendrobatidis (прям как

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But amphibian specialist Reid Harris has hope. Harris has discovered a possible way of protecting these animals from their fungal foes. In the early 2000s, he found that the red-backed and four-toed salamanders – two small, sinuous species from the eastern USA – are covered in a rich cocktail of antifungal chemicals. These substances aren’t made by the animals themselves but by the bacteria on their skin. They might help to protect the salamanders’ eggs from fungi that would otherwise thrive in the humid underground nests. And as Harris later found, they can also stop Bd from growing. Perhaps, he thought, this explained why some lucky amphibian species seem to resist the killer fungus: their skin microbiomes act as symbiotic shields. And perhaps, he hoped, those microbes could help to save vulnerable species from the looming Amphibiageddon.
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In lab tests, Vredenburg and Harris confirmed that J-liv can indeed protect naïve frogs from Bd – but how? Does it kill the fungus directly by making antibiotics? Does it stimulate the frogs’ own immune system? Does it reshape the frogs’ native microbiome? Does it simply take up space in the skin, physically preventing the fungus from taking hold? And if it is so useful, why is it only found on some frogs and not others? And why is it relatively rare even when it is present? “It would be great to figure out every little detail but we don’t have time,” says Vredenburg. “If we take time, the frogs won’t be around any more. We’re really working in a crisis.” Forget the details. What mattered was that the bacterium worked, at least in the cosy confines of a lab. Would it also work in the wild?

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“The results were phenomenal,” says Vredenburg. As predicted, Bd arrived that summer. The fungus took its usual toll on the frogs that had just been soaked in pond water – dozens of spores became thousands of spores, and each frog became an ex-frog. But in the animals that were dunked in J-liv, the fatal accumulation of spores not only plateaued early, it often reversed. A year later, around 39 per cent of them were still alive, while their peers were all dead. The trial had worked. The team had successfully protected a wild population of vulnerable frogs with a microbe. And they had established J-liv as a probiotic: a term that is most commonly linked to yoghurts and supplements, but really applies to any microbe that can be applied to a host to improve its health.
But conservationists can’t very well catch and inoculate every amphibian that’s threatened with Bd – that would be all of them. Instead, Harris is thinking about seeding soils with probiotics so that any passing frog or salamander would automatically dose itself. Alternatively, threatened frogs that are already bred in captivity could be dosed in the lab before being released as a group. “There is a lot of potential,” says Vredenburg, “but this is not a silver bullet. Like any complex problem, we can’t expect it to be a winner all the time.” Indeed, Matthew Becker, one of Harris’s former students, found that the same approach failed completely with captive Panamanian golden frogs. This species is a ghost in a bumblebee’s colours: a gorgeous black-and-yellow creature that has already been exterminated from the wild by Bd. Today, it exists only in zoos and aquariums and cannot be reintroduced to Panama as long as Bd persists. J-liv, despite its initial promise, won’t help with that.”