Same Fungus, Same Species, Different Fates: Why Some Toads Live

A fungus that has contributed to the decline of at least 501 amphibian species ^[3] has left some Pyrenean toad populations standing, and a study published July 15, 2026 offers a clue to why: skin defences that switch on early ^[4].

The finding is narrow and it is not a cure. But it is a specific lead in a pandemic that has run for decades.

What is the fungus, and what does it do?

The culprit is Batrachochytrium dendrobatidis, usually shortened to Bd. It causes a disease called chytridiomycosis, which damages the skin of amphibians. That matters more than it sounds. An amphibian's skin does far more than cover the body. The disease can disrupt the animal's regulation of water, salts and minerals ^[1][4].

The fungus feeds on keratin, the tough protein that also makes up our hair and nails. Tadpoles do not have much keratinized skin. Adults do. So the animals become vulnerable as they metamorphose, the change from tadpole to adult, when the tissue the fungus likes grows in ^[4].

There is a second chytrid fungus, Batrachochytrium salamandrivorans, which prefers newts and salamanders. It plays a small part in the global count. Of the 501 declines tallied in a major 2019 assessment, 500 were attributed to Bd and one to its cousin ^[3].

Where did it come from?

Nobody has settled that, but there is an old and rather lovely line of evidence. In 2004, researchers examined 697 archived specimens of three Xenopus species, the African clawed frogs, collected in southern Africa between 1879 and 1999. Nineteen showed infection compatible with Bd. The earliest was a Xenopus laevis collected in 1938 ^[2].

An archive shelf, in other words, turned out to hold a medical record. Frogs collected decades ago still carried the traces of the disease.

From that survey, the authors proposed that Bd originated in Africa and that international trade in Xenopus frogs helped spread it ^[2]. That is their hypothesis, built on the specimens and on historical evidence. It is not a closed case.

The 2019 assessment's lead author reached a similar practical conclusion about the present. The lead author called for stronger global biosecurity and wildlife-trade regulation, saying globalization and wildlife trade were enabling the spread of disease ^[3]. We are not the fungus's first cause, perhaps, but we appear to be its carriers.

How bad was it?

The 2019 assessment, published in the journal Science, drew on published and unpublished information from amphibian experts around the world and on the IUCN Red List, the international register of threatened species. Its authors found chytridiomycosis in more than 60 countries. The most extensive losses were in Australia, Central America and South America ^[3].

The numbers are stark. Of the 501 species affected, 90 are confirmed or presumed extinct in the wild. Another 124 have fallen by more than 90 percent ^[3]. According to the University of Maryland's account, declines peaked in the 1980s ^[3].

There is a less grim half of the ledger. Of the affected species, 39 percent are still declining and 12 percent show signs of recovery ^[3]. Research in El Copé, Panama, had found some species able to coexist with Bd, and conservation and reintroduction work in Australia helped prevent further extinctions ^[3].

So the pandemic is not uniform. In some places the animals vanished. In others, something let them hang on. That is the question the new study takes up.

What did the Pyrenean study look at?

The researchers worked with common midwife toads from four lakes in the Pyrenees, the mountain range between France and Spain. All four populations had suffered severe Bd outbreaks.

Their fates then diverged. Three shifted to more stable disease dynamics. The fourth, at Lac d'Arlet, kept suffering high infection and seasonal die-offs and is close to disappearing locally ^[4].

That split is what makes the lakes useful. Same species, same fungus, different outcomes.

The team looked at antimicrobial peptides, short molecules in the skin secretions that form part of an animal's innate immune defence. Innate means built in and ready, as opposed to the learned immunity that develops after an infection. They used mass spectrometry, which weighs and identifies molecules, together with molecular diagnostics, laboratory tests of whether peptides inhibit Bd, and confocal microscopy, which builds sharp images from light focused on a single point ^[4].

They found 1,152 peptides in the toads' skin secretions. Only seven had been identified before ^[1][4]. That alone says how little anyone knew about the chemical armour of these animals.

What separated survivors from the doomed?

Timing, it seems. Toads with more diverse peptide defences already at the tadpole stage were associated with the populations coping better with Bd. Populations with fewer peptides at that stage continued to have high mortality ^[1][4].

The logic fits what the fungus does. If the animals are most vulnerable around metamorphosis, a toad that has its chemical defences in place before that moment has a better chance of getting through it. The authors associate earlier maturation of these defences with survival and with populations living alongside Bd ^[4].

The word to hold on to is associated. The study compares populations. It does not prove that early peptide maturation caused recovery.

Is this frogs evolving tolerance?

It is tempting to say so, and the story of survivors adapting is a good one. But the study does not show it. It does not establish that the difference between populations is genetic, or that natural selection produced it ^[4].

The lead author said that genetics could affect when the immune system develops, but so could environmental factors, including temperature or the presence of trout ^[1]. The study itself says environmental as well as genetic factors may shape that timing ^[4]. If the answer is the environment, the toads may not have changed at all. Their surroundings may have.

That difference matters for anyone hoping to help. A trait that is inherited can, in principle, be bred or selected for. A trait set by temperature or by which fish share the lake points toward managing habitats.

Does this lead to a treatment?

Not yet, and the senior author did not claim it does. The senior author described the peptides as leads for future research, not as treatments already shown to work in people ^[1].

The authors name two next steps. One is to find out which factors affect when immune defences mature. The other is to work out which of the 1,152 peptides actually act against microbes ^[1]. Whether any single peptide does the work, or whether they act together, is open.

What does it mean?

The frog story, or here the toad story, makes a case against fatalism. A pathogen that has been linked to the extinction of 90 species, confirmed or presumed, has still not finished off every population it reached. Some animals cope, and now there is a chemical lead on how.

It also makes a case against complacency. One of the four Pyrenean lakes holds a population near local extinction, and the study cannot say whether it can be saved.

The wider estimate of 501 species dates from 2019, and no figures in hand say how many populations have recovered or been lost since. Nor is there a count of what biosecurity or trade controls have been adopted since researchers asked for them.

The fungus is here to stay. Whether the toads can keep living with it depends partly on peptides nobody has yet tested, and partly on what happens to the lake at Arlet.