The killer fungus ravaging amphibian populations around the world is so deadly because it secretes a chemical that causes its hosts’ white blood cells to self-destruct. Once the molecule responsible for this attack is identified, it may be possible to combat the disease by bolstering species’ immune systems.
Since the 1980s, many species of frogs and salamanders have been wiped out. Scientists agree that the chytrid fungus, Batrachochytrium dendrobatidis, is at least partly responsible for these mass die-offs. The fungus attacks the amphibians’ skin cells, upsetting their fluid balance and, in severe infections, causes death by heart failure.
But this vulnerability is surprising. After all, amphibians spend a lot of their lives in pools of murky water, teeming with all kinds of microorganisms. “Amphibians have really capable immune systems, yet here they are stumbling against this skin pathogen,” says Louise Rollins-Smith, an immunologist at Vanderbilt University in Nashville, Tennessee. “Why does this pathogen seem to fail to activate that robust response?”
To find out, Rollins-Smith and her colleagues tested the effect of chytrid fungal cells on white blood cells, or lymphocytes, cultured from frogs. They found that both live and heat-killed chytrids inhibited the production of lymphocytes and made them more likely to self-destruct in a process called apoptosis – the way old or damaged cells are naturally cleared from the body. The loss of these cells leaves the animals unable to eradicate the chytrid infection before it does further damage to their skin cells.
The same effect was seen when the researchers inserted a permeable membrane between the chytrids and the lymphocytes, suggesting that the culprit is a soluble molecule released by the chytrids.
James Collins, an ecologist at Arizona State University in Tempe, who specialises in amphibian disease, calls the experiments thoughtful and thorough, and says they help answer the question of how the chytrid fungus is able to overcome amphibians’ usually robust immune system.
Potent immune suppressant
Rollins-Smith’s team has not yet identified the molecule responsible. So far, tests have shown that it is not a protein. They suspect it may be part of the chytrid’s cell wall since chytrid spores, which lack such architecture, do not have the same effect.
Whatever the immune-suppressing chemical is, it seems to be unusually broad in its effect, acting on a wide range of amphibians and even mammalian cell cultures, the team found. Indeed, the molecule may be worth investigating as a potential source of new immune-suppressing drugs for people, Collins suggests.
The discovery may also lead to new ways to manage chytrid infections in amphibians. Once researchers identify the molecule and how it disables the immune system, the hope is that conservationists may be able to block that action or find a way to boost the frogs’ immunity, says Rollins-Smith.
Journal reference: Science, DOI: 10.1126/science.1243316
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