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Amphibians across the globe are facing calamitous declines. Around a third of species are critically threatened, while extinction rates for amphibians are 200 times higher than for other vertebrates. Several factors underlie these changes: widespread habitat loss, climate change and toxic chemicals in environmental run-off, among others. However, the most prominent cause of epidemic mortality is the fungal pathogen Batrachochytrium dendrobatidis, known more simply as Bd. Where it is common, Bd decimates populations. Puzzlingly, however, while Bd infection rates in some ponds are extremely high, other ponds are hardly affected. New research published in Current Biology offers a compelling explanation for this variation. Simultaneously, the results offer a novel route to mitigate Bd-induced amphibian loss.

Bd in nature can be divided into two stages: a host-associated stage and a free-living motile stage called a zoospore. Zoospores are the agents of new infections, and where there are lots of zoospores there tends to be lots of disease. But why are some ponds zoospore hotbeds while others are not? The simple answer, it turns out, is in the water.

Dirk Schmeller from Leipzig in Germany and an international team of collaborators compared zoospore survival in water taken from ponds with a high incidence of infection with survival in water from ponds with little infection. They observed striking differences: zoospores incubated in water from sites with little infection died much more rapidly. But this difference was not caused by pH, temperature or, indeed, anything chemical in the water. Instead, the team found that the zoospores were being eaten by tiny rotifer, paramecium and ciliate predators that were abundant in ponds with low rates of infection but largely absent from ponds with lots of infection. Moreover, if they removed the predatory microfauna using filters, the survival of the Bd zoospores dramatically increased. In short, the parasites had become prey.

But how does zoospore predation influence amphibians? To address this, Schmeller and his collaborators exposed susceptible tadpoles to a mixture of zoospores and different microfaunal predators. Mimicking the results from natural ponds, they found that predators significantly reduced the incidence and intensity of Bd infection. Indeed, in the presence of one particular Notommatid rotifer predator, the prevalence of infection declined to zero. These experiments thus established a crucial causal link between zoospore consumption of Bd microbial predators and amphibian disease.

Two clear messages for conservation emerge from this study. First, by seeding microbial predators into ponds it might be possible to directly and rapidly reduce amphibian Bd infection rates by removing infectious Bd zoospores. Solutions to amphibian decline are critically needed and this novel approach certainly warrants further consideration. Second, even with successful intervention, this study highlights the fact that amphibian conservation requires habitat preservation, not only to support the direct physical requirements of amphibians but also to protect the species that are not themselves threatened but whose presence can dramatically influence those that are. Saving rotifers may not be high on the agenda of Greenpeace, but doing so might be the difference between a twilight chorus of frogs and a silent spring.

References

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Microscopic aquatic predators strongly affect infection dynamics of a globally emerged pathogen
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Curr. Biol.
24
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1
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5
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