Water is key for amphibians, without it, they wouldn’t survive. Maintaining moist skin is the top priority for these toads because the sponginess of their skin enables them to remain hydrated and breathe.

But toads are not the only life frequenting these ponds – the deadly fungus in swimming in them as well.

Cynthia Carey, one of the leading amphibian decline researchers, first noticed the disappearance of Colorado’s boreal toads in 1973. In less than a decade Carey observed the extinction of 11 distinct boreal toad populations in Western Colorado alone. From 1982 to 1992 a separate study surveyed 38 toad-breeding sights in Colorado and by the end of the survey, toads were only found at one site. And these toads weren’t just disappearing in Colorado – significant population declines were observed in Wyoming, Idaho and Montana as well.

But the cause of death remained a decades-long mystery. It wasn’t until 1998 that the fungus was confirmed as the killer according to Carey.

The fungus itself is a swimming aquatic spore with an extremely short lifespan, only a few hours to be exact. So it needs to find a host, fast, according to McKenzie. And in an alpine environment, boreal toads make an ideal host.

The fungus will attach to the surface skin of the toad and enter its skin cells – it targets areas that contain keratin proteins according to a study published in Science. This invasion creates an imbalance within the individual and over time the toad’s skin thickens. Thicker skin limits their ability to breathe and absorb water. The toad’s physiological makeup is corrupted, and it eventually dies of heart failure.

The fungus is also able to replicate itself within the skin cells of a toad, producing the next generation of spores. A young spore army is sent into the world after the fungus ruptures the skin cell according to McKenzie.

“And then those spores can swim in the water and go infect another toad,” she said.

In 2014 scientists produced a global wide map of the fungus spread. Evidence of the fungus was detected in 50 percent of the 1,377 amphibian species samples. This is the most up-to-date global study of fungus spread. Scientists hypothesize that the number of infected individuals has only grown in recent years.

“One fungus is systematically wiping out a huge amount of amphibian diversity,” said McKenzie. “It blows my mind.”

And it wasn’t until May of this year that researchers were able to pinpoint the origin of the fungus.

***

Historically the fungus had little impact on native amphibian population levels. It wasn’t until the twentieth century, when globalization of the economy quickened significantly, that this fungus made its deadly debut worldwide.

One of the first documented cases of amphibian trade goes back to the 1930s when zoologist Lancelot Hogben made a groundbreaking discovery. Hogben found that South African clawed frogs could detect if a woman was pregnant.

Urine samples were injected into the hind legs of female frogs. If the frog laid eggs overnight, this indicated the woman was pregnant. Here’s how it worked: The trace of a pregnancy hormone in the woman’s urine sample was found to set off the ovulation of the frog. This became known as the Hogben test. Between the 1930s and 1950s thousands of frogs were exported from Africa to labs all over the world.

“We didn’t just move an amphibian from Southern Africa to North America,” said McKenzie. “We also moved their microbes.”

Traces of the fungus have been in detected in African clawed frogs imported to the United States, according to a team of researchers from San Francisco State.

“People moving amphibians around the globe allowed distant, ancient strains to come together, hybridize and produce a terrible strain,” said McKenzie.

Humanity’s global expansion paved the way for this rapid hybridization of the fungus.

Researchers originally hypothesized that the fungus derived from South Africa. But this idea is no longer correct – a false positive some may even say.

A ten-year global investigation pinpointed East Asia, specifically Korea, as the birthplace of this deadly fungus, according to a study published in the journal Science this May. Researchers detected four distinct lineages of the fungus. Of these four, traces of the lineage from the Korean peninsula had the greatest global genetic overlap. Meaning that evidence of the Korean lineage was found in the majority of fungus strains, confirming it as the “mother strain.”

***

When exactly the fungus made its way to Colorado is still unknown. But one thing is for sure – a changing climate helped it spread.

Many historical breeding grounds found in Gunnison National Forest no longer exist due to the decrease in snowpack levels according to McKenzie. Occurring within the past decade this is a fairly recent disappearance. Less snowpack means less habitat.

Higher densities of toads are now observed in the remaining breeding ponds. Toads from miles away are congregating in the remaining pools. The likelihood that infected individuals are mixing in with healthy individuals exponentially increases.

“If they’re all congregated in one place, then they’re exposing each other to the pathogen verses if they’re spread out on the landscape or over multiple breeding ponds,” said McKenzie.

Climate change can also have a sort of “psychological” impact on the toads, according to McKenzie. Amphibians are highly sensitive creatures. Even the slightest change is stressful whether it’s a fluctuation in temperature or access to water. Stress weakens their immune system, making the toads more susceptible to the fungus.

But McKenzie isn’t giving up hope. Instead, she’s taking a novel approach in her fight against fungus.

Her team identified a bacterium, native to boreal toads, that prevents the fungus from growing on the individual, preventing it from entering its skin cells.

“We’ve learned as scientists that it’s a bad idea to go putting animals or microbes or anything in a place that doesn’t belong,” said McKenzie. “So we’re using a native microbe.”

In the lab, the survival rate of toads increased by 40 percent.

This summer the team graduated from the lab to the field. In June the team collected individuals that were still in their tadpole state – 200 of them. Half were identified as the control group and the others were treated with the native probiotic bacteria. The team also collected a skin swab of each individual before and after treatment to establish a baseline. All 200 were marked and then released into a toad hotel – a large plastic container filled with the necessary muddy water and aquatic plants that provide “stylish comfort” for the toads during the experiment.

“We want them to live like normal toads,” said McKenzie. “But we also need to be able to collect them at the end of the trial.”

These toad hotels enabled the team to monitor and easily collect the subjects.

This winter the team will start extracting DNA from the toads. The goal is to analyze a specific section found in one particular gene that can identify bacteria – this in turn will establish if any fungus growth occurred on the toad.

“If we get proof that this approach is working in one place, then we can go around and isolate native bacteria from lots of other boreal toad sites,” said McKenzie.

Her goal is to eventually have a site-specific fungus-fighting bacteria for every subpopulation of boreal toads in Colorado. But it doesn’t end there. This approach could also benefit captive breeding programs of boreal toads.

“We could potentially use this approach to treat toads before they go out into the wild,” said McKenzie. “Essentially boosting their defenses against the fungus before they’re released.”