Researchers may have finally solved the mystery of the fungal pathogen that has been devastating amphibian populations worldwide. The fungus, known as Batrachonchytrium dendrobatisdis (Bd), appears to alter the permeability of amphibian skin, which can lead to a fatal osmotic imbalance, according to a study published this week in Science.

The endangered corroboree frog infected with chytridiomycosis. Image: Jamie Voyles, Alex Hyatt and Frank Fillipi

"It's a great study," said ecologist Karen Lips of the University of Maryland, who did not participate in the research. "It's another small step forward in the hope that we can maybe save some amphibians."

Bd can spread rapidly through amphibian populations and has been blamed for numerous extinctions around the globe. The mechanism by which the fungus killed these animals, however, was unknown. Histological preparations of the skin of infected frogs showed clear signs of infection, but other known cutaneous infections are rarely fatal and infected animals showed no obvious damage to their internal organs. "The idea that some skin fungus could cause death was pretty incredible," said Lips.

One possibility for how skin alterations could have such a devastating effect on amphibian health was the skin's unique role in gas, water, and electrolyte exchange. Unlike the skin of other vertebrates, amphibian skin is a key player in maintaining homeostasis. If the fungus were somehow able to disrupt that balance, infected animals could suffer from an osmotic imbalance that could ultimately cause their hearts to stop beating. Previous findings of diseased frogs with low electrolyte levels in their blood indicated that this might be the case, but no one had ever examined if these low levels were a direct result of the fungal infection.

To test this hypothesis, disease ecologist Jamie Voyles of James Cook University in Australia and her colleagues measured electrolyte transport across the skin of infected and uninfected green tree frogs, as well as sodium and potassium concentrations in the body. They found that diseased animals had lower levels of epidermal electrolyte transport as well as lower concentrations of sodium and potassium in their blood. Body mass and protein concentrations, however, remained stable, indicating that the observed osmotic imbalance could not be due to dilution caused by increases in water uptake. Together, these results suggested that the imbalance was caused by the skin's failure to properly maintain its osmoregulatory functions.

"We expected to find reductions in electrolyte levels," Voyles said in an email to The Scientist. "However, we were surprised the electrolyte levels dropped as low as they did. In some cases, plasma sodium levels were below the detection limit of the available equipment."

By the process of elimination, the researchers determined that this electrolyte imbalance caused by the fungus was the most likely explanation for the heart failure that ultimately killed the diseased frogs. The researchers were able to effectively treat the diseased animals by pumping an electrolyte supplement directly into their stomachs, where it could be absorbed. After receiving this treatment, frogs that had lost their ability to right themselves when turned on their backs were climbing out of the water onto the container walls and even jumping to avoid capture. Treated frogs also lived 20 hours longer than untreated frogs, but despite this initial improvement, all diseased animals eventually died.

"It is the damage to the skin that is the initiating factor in the pathogenesis," Voyles said. "Without treating the skin, electrolyte treatments will not prevent death."

Still, understanding the mechanism by which this pathogen causes disease "brings up all sorts of possibilities" for how to stop its spread, Lips said. "Once you know the mechanism then you can at least have a conversation about what you want to do about this."

In addition to providing possible treatment options for diseased amphibians, understanding the fungal pathogenesis and the importance of certain skin characteristics may help identify susceptible species that could serve as vectors to spread the disease, Voyles added. "This work needs to be repeated in other susceptible amphibians, but given the physiological importance of the skin for all amphibian species, disruption to the skin function may be the primary mechanism."

"Anytime you learn something about the mechanism of what's causing the death, it opens up the possibility of finding a way to mediate the disease in the future," said microbial ecologist Reid Harris of the James Madison University in Virginia, who was not involved in the study. "This was the necessary first step along that road."


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