Vultures: our best defense against the damned geese

Browsing Promed-mail this morning I saw an article documenting some botulism duck die offs in Idaho, and that led to something really cool (IMHO).  You can always tell when I am avoiding work or a stressful situation – tunneling through literature like this is intensely escapist.

Background (minimal): botulism is caused by one of several toxins produced by bacteria in the Clostridium genus.  Clostridia (plural) are anaerobic (grow only in the absence of oxygen), love to gnosh on protein, and produce crazy resistant spores that can be found all over the natural environment (so: dirt, water etc).  Human disease generally arises from food contamination and improper canning, but this bacteria also slays birds.  If you see a decaying fish in the mud, I would bet you could find Clostridia inside its rotting meat, munching away. They didn’t kill the fish (I don’t think), but are ubiquitous in the environment and can’t say no to a giant rotting anaerobic fishburger.  Every year there are natural cycles of fish die offs that trigger something with the Reader’s-Digest-Ready name of the “Carcass-maggot cycle of avian botulism”.  It’s something that happens frequently (as in, every year) in natural populations of ducks, geese (good riddance), gulls and other shore birds.

More reasons to hate geese.

More reasons to hate geese.

Source:http://www.nwhc.usgs.gov/publications/field_manual/chapter_38.pdf

All that is wonderfully disgusting, but old news to me.  In the chapter from which the maggot cycle picture came is a fascinating sentence:

“The exception is vultures, which are highly resistant to type C toxin.”

Interesting.  Given their ghoulish tastes, vultures presumably are exposed to a lot of Clostridia and their toxins.  Could their resistance be the result of a long ago natural selection event?

Ridiculously oversimplified uninformed speculation:

Population of proto-vultures, pushed to find other sources of food engages in a little grazing at the Dirty Hamburger Bar.  Some die from botulism, but some do not. Lather, rinse repeat and some generations later you have botulism-proof vultures.  It could happen.  One slight complication however, is that not all vultures are closely related to each other: “vultures” evolved separately at least twice and from different ancestries to form the New World Vultures and the Old World Vultures.  No idea which group was tested with the toxin (I have searched, can’t find the study).  I also hate “just so stories” like this, so let’s move on.

Warning: the next two paragraphs are rough hewn and tangled/tortured technical “thinking” out loud.  Normal English (well….) resumes in the third.

How resistant are they?  Pubmed is mute about this, but I found one review article stating that vultures can take  “100,000 times as much type C toxin as it is required to kill a pigeon” (ref). One simple explanation for that result would be that vultures are 100,000 times larger than pigeons, and hopefully we can all laugh that one off. When I was a bench scientist I would have killed for a phenomenon showing a difference of 5 orders of magnitude; I seemed to attract projects in the 1.5 – 3x range*.  I really wish I could see how they did that study, but I assume they fed the vultures (??).  Imagine the simplest case of the vulture expressing a protein that binds to the toxin, and when bound by the vulture protein the toxin is dead in the water (could also be a polysaccharide or smallish molecule I guess)…. I can’t make my brain decide if having 100,000 times more of a gene product in one species than a different species in the same class (Aves in this case) is a big deal, though I guess within Mammalia there are examples of some species having a functional copy of a gene and another mammalian species having that gene inactivated (like olefactory receptors, for instance) – that would be “infinite times more” protein.  So maybe the magnitude of the vulture resistance isn’t such a big deal; the pigeons would beg to differ, but they are very very dead.

Then there is this dissertation (here) with a title suggesting that something in vulture blood puts the Bruce Lee on the toxin.  I am surprised that its hard to find out much information about this as Molecular Bruce Lees that fight off such nasties usually end up being developed as therapies.  Perhaps its all bogus; I can’t say as there is not a stitch of data to be seen.   A separate dissertation (here) from the same university suggests that its fragments of the vulture’s Immunoglobulin G (antibody) protein that are doing it, but that phrasing makes it sound like it ISNT the IgG binding via the normal antibody-antigen interaction site (the tips of the “Y”), otherwise why would you be looking at “fragments” when the whole antibody would work?  Adaptation of the non-antigen binding site part of your antibodies to inactivate a toxin?  That’s HOT.  Even if it isn’t true, I love the thought.

I have always hated geese .  They are aggressive, they bite (personal experience) and have bad attitudes.  They are also lazy about migrating, collecting in large groups in Atlanta pooping in parking lots and chasing young children.  Ducks, on the other hand, act in real life just like they do in Disney movies.   Anyone who has had the experience of feeding bread to ducks on a beautiful Fall day and witnessed a herd/gaggle/murder/whatever of geese arrive like a Canadian Biker Gang and chase away the baby ducklings knows the feeling.  I am sure that the Carcass-maggot cycle of avian botulism is a suicidal goose plot to kill off the ducks and/or make us feel sorry for them and forget their evil ways.

On the other hand, I have always had respect for vultures, tinged with a little throw up in the back of my throat at their culinary preferences.  Watching them soar effortlessly high in a beautiful California sky as a child made a strong impression on me.  They are huge and majestic in flight, and they may just be our best defense against the damned geese.

* – Just to be clear: “1.5x -3x” meaning “15%-30% of 1 order of magnitude (which would be 10x)”.  In graduate school I once had a result which showed a reproducible 90x difference in viral gene expression.  It was so stunning that I told no one while I repeated it several times over several days to make sure and labored at the math (maybe I was missing something, this was too good to be true).  I finally told my dissertation advisors (there were 2) and both were impressed; it was exhilarating.  Experiments were planned.  Acceptance speeches were framed.  Then over the course of a few weeks the air began to leak out of my 90x difference.  50x.  30x.  20x.  Finally 5x.  Sometimes 2x in some experiments, despite not changing anything I was doing.  I spent 6 months trying to figure out what happened; new lot of same cells, different lab’s culture of same cells, different lot of virus, re-grow & purify a new lot of virus. All for nothing. I still published the result (the 2.5x – 5 fold one) and expanded off of it.  The valuable lesson was that bigger is not better, and that in the complex system of a cell small changes in gene expression can lead to radical and pleasing effects.  But damn, I loved that week where I had a reproducible 90 fold effect.
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About SubOptimist

I am an Associate Professor in the Science Department at Georgia Perimeter College, Clarkston. I teach introductory biology courses at both the majors and non-majors level in addition to microbiology. Previous to that I spent 7 years as a postdoctoral researcher on different viruses. While I don't miss being on the "grant treadmill", I think better when I write and miss writing up data for papers and grants; this blog helps me with that a little. And sometimes my kids' insanely funny and cute antics need to be shared with the world. Any view expressed in this blog is that of me personally and not Georgia Perimeter College or the GPC Clarkston Science Department.
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