Way back in a few editions of Animalcules, several of the submissions mentioned a fungus that was killing frogs. Wednesday at the ASM meeting suggested that there may be a way to protect these amphibians:
First in a petri dish and now on live salamanders, probiotic bacteria seem to repel a deadly fungus being blamed for worldwide amphibian deaths and even extinctions. Though the research is in its early stages, scientists are encouraged by results that could lead the way to helping threatened species like mountain yellow-legged frogs of the Sierra Nevada mountains of southern California.Experiments have shown that Pedobacter cryoconitis, bacteria found naturally on the skin of red-backed salamanders, wards off the deadly chytridiomycosis fungus. In late 2004, Australian researchers cited chytridiomycosis as one of the main factors imperiling up to one third of the world's amphibian populations.
"The exciting aspect is that we identified at least one bacterium from the skin that in both the dish and on the salamander aids the healing process...one species of bacteria which you could tentatively view as a probiotic," says Reid Harris, biology professor at James Madison University.
Harris hatched the idea of using the bacteria to fight the skin fungus while researching another amphibian killer, a fungus that attacks their eggs and embryos. Research by other scientists indicated bacteria on some amphibians produced compounds that were active against the egg fungus.
"There will have to be careful testing," says Harris. "Just because on the Petri plate you find a species of bacteria that is anti-chytrid doens't mean it's going to be anti-chytrid on the amphibian. So we're going to have to do some tests to make sure which ones are actually most effective on the organism. But we did find one."
Eventually, the research could lead to procedures for "vaccinating" endangered populations, Harris said. Other questions, such as whether bacteria from one species could be used to help another, could also be addressed with future research.
Source: ASM press release.
Image from http://www.the-ba.net/NR/rdonlyres/FB0C0DB4-5D14-414A-B112-5ADD692125B7…
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This relates to my research on commensal autotrophic ammonia oxidizing bacteria. I have found that they are commensal surface bacteria on a variety of diverse eukaryotes, including clams, lobsters, turtles, earthworms, and mammals.
These bacteria are obligate autotrophs, form biofilms, are ubiquitous in the environment where they perform the first step in the process of nitrification, the oxidation of ammonia to nitrite. I suspect they are one of the first lines of defense against heterotrophic organisms, via oxidation of quorum sensing compounds. A biofilm of them does suppress heterotrophic bacteria on a human host.
They are inhibited by light, and use the NO they produce as a quorum sensing compound. At high NO levels they form a biofilm, at low NO levels they become planktonic.
I suspect that their natural history is that during the night the biofilm grows thicker, then with some inhibition by light during the day it gets thinner as the NO level goes down and they disperse.
Xenobiotic chemicals also inhibit them, a particularly bad actor is atrazine (which is the largest tonnage herbicide used in the US, and which has been associated with amphibian abnormalities). I suspect that atrazine inhibits the natural biofilm, the NO levels go down, the bacteria go planktonic, the biofilm disperses to zero, then heterotrophic bacteria overgrow, detect quorum sensing compounds, express virulence factors and cause an infection. I think this may be what is causing lobster shell disease.
I did look at one species of adult frogs and was unable to find any on the skin, but they might be present at different life stages and in different species.
These bacteria in part, set the basal NO level. NO regulates steroid synthesis (in a feedback loop), by inhibiting the cytochrome P450 enzymes that are the rate limiting step. Changing the basal NO level will affect steroid synthesis WITH NO THRESHOLD. That is, because NO is already in the "active feedback range", and the "NO signal" is the sum of NO from all sources, a change in the basal NO level will affect the operating point of NO regulated pathways including steroid synthesis.
Thus inhibition of these bacteria in a biofilm would be expected to cause endocrine disruption. That is a mechanism by which atrazine (or other xenobiotics) could have endocrine disruption effects even if atrazine had no direct endocrine activity. These effects could occur even at very low levels where there was no overt toxicity to the bacteria, simply sufficient inhibition to increase their planktonic dispersal faster than they proliferate.
I have emailed you what I presented at a Gordon Conference 2 years ago.
Tara, if this research pans out, do you have an idea of how the practicalities of using a vaccine in the field would pan out? Especially given that chytridiomycosis affects a third of amphibian populations, and seems to affects species that live in some pretty hard-to-reach places.
Realistically, what could we expect conservation agencies to be able to do with a new vaccine at this stage? Could such a vaccine be manufactured in enough quantities? How would it be delivered to threatened populations? Would some species/regions need to be prioritised over others?