August 07, 2007

Bad, Bad Fungus

When I write here about fungi, I typically talk about their good side. Some are very beautiful and the majority of them are necessary to preserving maintaining the health of ecosystems by acting as agents of decay, delignifying wood. We're finding new applications for them all the time in areas as diverse as medicine and nanotechnology. Still, there's a dark side to them as well. When we talk about fungi, after all, we're talking about a taxonomic kingdom as large and diverse as animals and plants.

One of the worst challenges the world faces from fungi right now is from a microscopic fungus with the mouth-filling moniker Batrachochytrium dendrobatidis. This nasty fungal bug is a pathogen that affects frogs; nobody is quite sure yet how it works, but it's theorized that it blocks the ability of the amphibians to absorb water through the skin. Amphibians don't drink water like most dedicated land animals, so if this is indeed the case then infected frogs die of dehydration even while surrounded by water.

Until very recently, it was thought that B. dendrobatidis reproduced amost exclusively asexually in nature. Spores produced by asexual reproduction are relatively thin-walled, and that was a little bit of good news in terms of how it spread. Thin-walled spores become dessicated quickly after leaving water, and that in turn meant that we could expect the rate at which the chytrid to spread would be limited by the distance between bodies of water that provide favorable conditions for germination. If it took too long for the spores to be transported from pond to pond, the spores would die before they had the chance to grow and the fungus wouldn't be spread efficiently.

Unfortunately, it looks like that estimation was incorrect. Based upon new genetic analysis in a study to be published next week in the Proceedings of the National Academy of Sciences, it now appears that sexual reproduction occurs frequently in B. dendrobatidis, and that's very bad news indeed. As is the case in many of the more-familiar macrofungi, sexual reproduction in this chytrid produces resting spores. Resting spores have thick, dehydration-resistant walls and can survive for decades (in some cases even centuries) in conditions unfavorable for germination. This means that the chytrid in question can spread over almost unlimited distances. For example, a person could pick up spores on their shoes from the mud near an infested pond. The mud could then dry out and fall off leaving just a few spores clinging to his boot. Weeks or even months later, this hypothetical human could visit a chytrid-free pond and deposit the resting spores. The pond is now infected, and within a year or two the frogs start dying. A wading bird could function in the exact same capacity and, since birds can migrate thousands of miles, spread sexually-engendered spores from North America to Asia along a migratory route.

Of course, there's an even worse scenario. In cases where the chytrids inhabit an ephemeral body of water, wind could act as the dispersal agent. When such a body of water dried out, spore-bearing dust can be picked up by a breeze and swept high into the atmosphere, remaining there sometimes for years at a time before being deposited in a new location and traveling around the whole planet in the meantime. If that's going on, we may well be looking at the extinction of frogs. The other factor here is sexual recombination; frogs may be resistant to the local strain of the fungus, but if new strains are introduced and interbreed with them, fungus that overcomes this natural resistance has a competitive advantage and the frogs are done for. The study referenced above makes this is a strong possibility. If that's the case, I'm not sure what can be done about the situation. Because both frogs and fungus are eukaryotes, we can't just go dumping fungal antibiotics into the habitat. This would be likely to kill not only the chytrids but also harm the frogs themselves and would almost certainly wipe out beneficial and necessary fungi. If you've ever had a case of athlete's foot, you already know how tough fungi are. To top it all off, it's likely that the introduction of various chemical pollutants into the frogs' habitat is already diminishing their immune response, so even those frogs that have evolved natural resistance to B. dendrobatidis infection are more likely to contract the disease and provide a rookery for more virulent strains.

Long story short, sexually-reproducing pathogenic chytridia means curtains for our croaking friends. That's an important trophic link to lose; everything from snakes to birds depends on frogs for a high-protein snack, and frogs are themselves important in controlling insect populations. Their loss would mean big changes in your local woodlands. At the current rate of spread, it probably won't take more than a couple of decades before you start noticing the difference.

Now, to be entirely "fair and balanced," I want to include a creationist take on all of this. Since they know that neither frog nor fungus evolves, the alternative theory can be summed up very simply in phraseology fit for any bumper sticker upon which rides a Jesus-fish:

I'll leave it to a theologian to explain why Jehovah/Allah/Flying Spaghetti Monster would decide to spend His time tinkering with frog-slaying microfungi.

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