Devils: It might have begun with atrazine, 1080, or even with tree cloning experiments, but the scientists say it’s transmitted by biting…

I’ve read the complete Conversation articles, both the Jody Warren/Brian Martin “What’s killing Tassie devils if it isn’t contagious cancer?” [TT Here] and also the Greg Woods counter article “Tassie devil facial tumour is a transmissible cancer” [TT Here]

Whereas Warren/Martin do not accept that DFTD is a contagious cancer, and point to the wide use of atrazine and 1080, Woods insists that the disease is transmissible from one animal to the next. Who to believe? It should be noted that Woods in his article does not rule out the possibility that a carcinogen could have ‘played a role’ in the first instance, in one of “patient zero’s” cells becoming cancerous. Woods concludes…

We may never know what caused DFTD in patient zero. It was most likely an accident of nature. Carcinogens may have played a role.

Although it would be of scientific interest to know the answer and undertake a large and expensive survey, the most important challenge is to save the devils in the wild. This is one of the major aims of the Save the Tasmanian Devil Program.

The past is history and the present learns from the past to inform the future. Habitat destruction does add extra stresses on our native wildlife and the future must take this into account.

The immediate task for us is to pursue vaccine development with the aim of protecting the healthy devils and repopulating the state with devils that have resistance to DFTD.

Where Woods and Warren/Martin differ is not so much in the cause of the tumour, but in how it has spread through the devil population. Warren/Martin dismiss the ‘transmission by biting’ theory on the grounds that devils’ ”… teeth are not sharp and not an obvious mechanism for spreading cancer”. I think at that stage of their article they needed to cite a study which would justify such a claim. “Predators with Pouches : The Biology of Carnivorous Marsupials” / Menna Jones et al. is hyperlinked by Warren/Martin to the admission that devils do bite each other. But, ambiguously, it is yet not clear to this Tasmanian Times reader that the ‘Predators with Pouches’ book actually does contain material supporting a rejection of the transmission theory … a theory which posits the transmission of the DFTD via biting behaviours and devil dentition.

There is a further difficulty in the Warren/Martin article. They write:

To spread from one devil to another, the genetics of the devils have to be similar so rejection of the foreign cells does not occur. It was proposed that devils had limited genetic variability, but later this turned out to be incorrect.

This statement, in my opinion, confuses what Kathy Belov told Rachel Carbonell [Here]. Kathy Belov actually said that

We’ve believed that the reason the devil facial tumour disease is spreading so quickly and so fast is because devils have very low levels of genetic diversity and essentially the tumour and the devil are genetically identical.

And that’s why the devil’s immune system doesn’t see it as a foreign cancer and doesn’t try to attack it or reject it. But this recent study has actually shown that even devils that are genetically different from the tumour still get sick.

Whereas Professor Belov had originally believed that “the reason the devil facial tumour disease is spreading so quickly and so fast is because devils have very low levels of genetic diversity” and whereas she has since found that “devils that are genetically different from the tumour still get sick”, we are still entitled to resist throwing the ‘spread by biting’ baby out with the ‘bathwater’ of ‘limited genetic variability’.

Indeed, Professor Belov, [17Nov14: Here] tweeted what amounts to her own rejection of the Warren/Martin account. Belov tweets:

“Devil facial tumour disease is irrefutably clonal and transmissible. Lots of genomics and cytogenetics data from different labs to back up.”

Arguments ad or pro hominem aside, I prefer the views of Woods and Belov who are both scientists credentialled and working in fields directly related to the TDFT disease. I feel that the Warren/Martin article is essentially speculative. I agree with David Obendorf that

With respect to the authors [Warren/Martin] I feel that where they are on firm ground is their call for a knowledge on the index genesis/origin of this malignant Schwann cell sarcoma of devils.

Effectively, it seems that Obendorf, Woods and Warren/Martin all agree that the origin of the cancer could be chemical. Incidentally David O. and Neil McGlashan [2008, Here] co-authored an interesting paper which explored a transmission mechanism. Yet the Warren/Martin article does canvass questions that deserve answers. For example, some are familiar with the disease-front scenario, wherein – like the world-changing ape that picked up a stick in Kubrick’s “2001…” – a cell in a single devil in the north-east of Tasmania turned ‘cancerous’, and that devil became the tumour’s first victim (c. 1996?) and that devil bit another devil, and spread her cancer, and tumour begat tumour… It spread, we’ve been told, from the north-east, fanning out from that original location and like a fire-front travelling westwards, and to the south.

However, what do we make of Warren’s [Here: The Devil Undone : The Science and Politics of Tasmanian Devil Facial Tumour Disease ]

[…] Steve Marvanek, a Commonwealth Scientific and Industrial Research Organisation (CSIRO) expert in applying geographical information systems (GIS) to resources and environmental problems, reported a further discrepancy. He noted that DFTD appears to ‘have broken out spontaneously’ in three separate locations ‘rather than moved in from nearby’, as might have been expected if the disease was contagious and spread via biting.86 […] The possibility that the spread of the disease was an artifact of reporting rather than a real event has not been resolved…

Can this spontaneous break-out in three separate locations be substantiated?

Finally, Karl Stevens [Here] presents an interesting view on the cause of the original tumour, when he identifies agrobacterium, used as a vector to transport genetic material into the tree genome, as the cause of the first instance of the DFTD. He concludes

If agrobacterium is genetically linked to devil facial tumour disease a prediction can be made. The ‘oncogenic potential’ or tumour generating properties of the chromosome will be found on the marker genes of the DFTD genome. The deleted chromosomes and lack of sex chromosomes, which I understand are not needed by trees, confirm the tumours could have jumped from the plant kingdom to devils with a dead browsing animal as an intermediary. It is known that the terpene producing properties of the trees was genetically enhanced. It would only require a single poisoning of a possum or wallaby, killed by plant terpenes or some other transgenic property of the trees, to infect devils with T-DNA bacterium in the same way plants are infected – through cellular damage. The two significant strains of DFTD may be caused by two separate poisoning events.

I wish I was a scientist. I would be delighted if Woods or Belov were able to offer some feedback on Karl’s prediction that the “’oncogenic potential’ or tumour generating properties of the chromosome will be found on the marker genes of the DFTD genome” prediction.

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[Pic taken this Sun morning, 23 Nov 2014], between Liffey and Launceston: plantation immediately adjoins a small town, which lies on the windward side of the plantation.]

Garry Stannus in the Liffey, and also in Launceston. He’s an amateur (musician, song-writer, performer, photographer, writer, gardener, cyclist, environmentalist and researcher). He offers this piece, assessing two recent TT articles on the causes/transmission of the devil-facial-tumour-disease (DFTD), for public analysis. Given certain devil-related announcements on the weekend, for light relief Garry offers [A Writer’s Dream: Here] and yet warns that premature release of ‘clean devils’ (from the insurance populations) might well see them also succumb to the disease; if not from transmission by biting, then perhaps in plantations to continued exposure to carcinogens from the air and from poisonous carrots on terra firma. What say ye all?