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The Emergence of a Strange and Novel Pathogen
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As I mentioned, my research focuses on emerging infectious diseases--that is, diseases that have been newly discovered, or are expanding in geographic range, or perhaps moving into new populations. Typically when we see organisms in that first group--novel to man--we think of bacterial or viral pathogens, such as SARS or E. coli O157:H7. However, sometimes things get even more weird, such as the strange case of the contagious Tasmanian devil facial cancer.
It's long been known that viruses can cause cancer. The first "cancer virus," which caused sarcoma in chickens, was discovered in 1911 by Peyton Rous, who later won the Nobel Prize for his work. Since this time, we've seen that viruses such as Hepatitis B and the human papilloma virus (HPV) can also cause liver and cervical cancer, respectively---so the idea of cancer caused by an infectious agent isn't new.
However, things are much different regarding the cancers in Tasmanian devils. First, the infectious organism isn't a bacterium or virus at all--it's a cancer cell that originated in a Tasmanian devil, and then took on a life of its own as a distinct pathogen, transmitted between animals as they fight and bite each other around the face and mouth. These wounds provide an opportunity for direct inoculation of the cancerous cells into the bloodstream of the next animal, allowing these transmissible tumor cells to find a home and proliferate, seeding the new animal with the disease. First seen in 1995, this highly lethal pathogen has since spread widely, and is almost 100% fatal. Death comes either from metastasis of the cancer throughout the body, or more commonly, because of starvation as the mouth tumors make it impossible for the animals to eat.
A new report in the Proceedings of the National Academy of Sciences notes that one reason these tumor pathogens have been able to spread so widely in the Tasmanian devil population is because these animals have little genetic diversity. The animal where the cancer originated was genetically very similar to all other animals in the current population--and so none of them are recognizing the tumor cells as "foreign" when they're infected. Typically, when one is infected with a pathogen, the body's immune system reacts in a number of ways to eliminate the foreign substance. However, in this case, because the devils are all so genetically alike, the immune system thinks the tumor cells are simply a normal part of the body--so they can proliferate unchecked.
This is potentially very bad news for the Tasmanian devils. Because these cells are so like their own, something like a vaccine won't work to stem the spread of disease. Rather, a better way to protect uninfected devils is to remove a cancerous animal from the population as soon as they're seen to be diseased. And while the issue of this particular cancer is unique to Tasmanian devils, other species of animals are also at risk because of their low genetic diversity:
"What also worries me is that many other wildlife populations are going through similar bottlenecks - koalas on Kangaroo Island, platypuses on King Island," she said.
"Loss of genetic diversity in these genes just opens the door for emergence and rapid spread of new and old disease."
For the devils, this spreading infection puts the entire species in peril:
Once the cancer becomes visible and spreads internally through the body, the animal usually dies within a few months from starvation and the breakdown of body functions.
Scientists predicted at a devil forum in Hobart earlier this year that the species faced extinction within 10 to 20 years at the current rate of decline.
Reference
Siddle et al. 2007. Transmission of a fatal clonal tumor by biting occurs due to depleted MHC diversity in a threatened carnivorous marsupial. PNAS. Link.
Image from http://en.wikipedia.org/wiki/Image:Tasdevil_large.jpg
Tags: cancer, emerging diseases, epidemiology
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October 9, 2007 5:58 PM
Alan Kellogg
Tara,
The invading cells don't cause the cancer, they are the cancer. DFTD is more a parasite than a cancer insofar as the invading cells are capable of existence independent of the parent organism, the one the cells originated in.
It's tempting to try fitting something new in an old cubbyhole, but sometimes you do need to think outside the usual mailslots.
October 9, 2007 7:07 PM
AK
Actually Alan, it's a semantic quibble. All cancers are parasites in a way.
If your identical twin had this sort of cancer and you caught it via a blood transfusion I would call it a cancer because it is infecting a host with the same genetic sequence as the original. You probably couldn't catch it from a fraternal twin, because your immune system would destroy it. Here, the lack of genetic diversity is making it more like an identical twin.
If the cause of the "immune evasion by tumors" were "down-regulation of classical cell surface MHC molecules", you would be right, but according to the abstract they show that it isn't. In the full article they mention that CTVT (canine transmissible venereal tumor) "avoid[s] immunological recognition by down-regulating classical class I (class Ia) expression and up-regulating nonclassical class I (class Ib) expression (10, 21, 22)". Thus, it qualifies as a parasite, unlike DFTD. But note that in the article they refer to CTVT as a "parasite" (their quotes).
Besides, the term "cancer" can be used in the sense of "tumor", and it certainly causes tumors in the newly infected hosts.
October 10, 2007 11:38 AM
Jon Howard Old
West VA. people, don,t bite each other!
October 10, 2007 12:08 PM
jspreen
>> It's long been known that viruses can cause cancer.
Wrong. It's long been suspected that viruses can cause cancer. That's what you shoud have written.
Now, why don't you take a closer look at sarcoma with virus activity, Tara? I can tell you beforehand that all the concerned tissue originates from the ectoderm. And that all the sarcoma you'll be watching were preceded by tissue necrosis. But nobody noticed because more often than not the necrosis is a silent process.
The cause of the Tasmanian devil facial cancer is not a virus. And the cancer is not contagious. How do I know that? Google Antoine Bechamp. And, after having read and understood what you read, google Ryke Geerd Hamer. That'll will do the job to put you on your way to new and exciting discoveries.
October 10, 2007 12:46 PM
Tara C. Smith
Sorry to inflict jspreen on everyone; he's a germ theory denier and a regular troll on my home blog. Jan, because this isn't my own, I'll be a lot less tolerant of your nonsense here than I am at Aetiology, just to warn you. Keep it over there from now on if you want your comments to remain up.
October 11, 2007 1:21 PM
Eric
Good lord Tara, they followed you to your shiney new blog. Pity that.
October 11, 2007 8:19 PM
Ian
they mention that CTVT (canine transmissible venereal tumor) "avoid[s] immunological recognition by down-regulating classical class I (class Ia) expression and up-regulating nonclassical class I (class Ib) expression (10, 21, 22)".
First, I'm not sure where they get the bit about "up-regulating non-classical MHC" because as far as I can see it's neither in the reference they cite, nor in the literature on CTVT. Second, the notion that CTVT can spread because it has downregulated its MHC is at best incomplete, since downregulation of MHC is so common as to be almost universal among tumors -- and yet CTVT is completely unique in its transmissibility and longevity. I talk a bit more about CTVT at my own blog, though I don't have much to add beyond those points.
October 11, 2007 9:06 PM
Tara C. Smith
Thanks Ian--I hadn't looked into that very much. A very interesting area of research...
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